General Orthopaedics and Basic Science (2019)

Orthopaedic Study Guide Series
Nikolaos K. Paschos
George Bentley Editors
General
Orthopaedics
and Basic
Science
Series Editors:
Nikolaos K. Paschos
Harvard Medical School
Boston Children’s Hospital
Boston, USA
George Bentley
Royal National Orthopaedic Hospital
Stanmore, UK
Orthopaedics has many different specialisations such as trauma, spine, sports
medicine, arthroplasty, oncology, paediatric orthopaedics, hand surgery and
microsurgery to name just a few. This means that residents preparing for their
exams have a broad field to study and to remember. In addition, orthopaedics
is a surgical specialty, thus knowledge of orthopaedic techniques is necessary
and is tested during these exams. To cover all these fields and aspects of
orthopaedics, this book series has volumes dedicated to each study area and
provides a guide for all orthopaedic residents in preparation for residency and
fellowship exams.
More information about this series at http://www.springer.com/series/13489

Nikolaos K. Paschos • George Bentley
Editors
General Orthopaedics
and Basic Science
Editors
Nikolaos K. Paschos George Bentley
Harvard Medical School Royal National Orthopaedic Hospital
Boston Children’s Hospital Institute of Orthopaedics and
Boston, MA Musculo-Skeletal Science, U.C.London
USA Stanmore, Middlesex
UK
ISSN 2520-1115 ISSN 2520-1123 (electronic)

ISBN 978-3-319-92191-4 ISBN 978-3-319-92193-8 (eBook)
https://doi.org/10.1007/978-3-319-92193-8
Library of Congress Control Number: 2018966999
© Springer Nature Switzerland AG 2019

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Foreword
Knowledge expands exponentially and it has been increasingly difficult for

orthopedic residents to stay abreast of the recent and meaningful advances in
this most wonderful of surgical disciplines.
Recent reports of the rising epidemic of resident burnout reflect the chal-
lenges orthopedic surgeons in training face in attempting to retain the knowl-
edge necessary not only to pass their Board Examination but also to provide
responsible care.
Nikolaos Paschos, MD, PhD, has compiled a brilliantly succinct and well-
organized study guide aimed at providing orthopedic residents with an essen-
tial knowledge base. This wonderfully crafted work will spare surgeons in
training needless hours of anguish as they seek to fulfill their professional
requirements.
I know Dr. Paschos well and his opus “The Orthopedic Study Guide”
reflects his true genius and mastery of basic science and general orthopedic
principles. Furthermore, this innovative publication was conceived out of the
kindness and generosity of Dr. Paschos’ heart. He is a brilliant educator with
an absolutely selfless disposition. His chief goal in the production of this
work was to lessen the burden of effective orthopedic training.
He has succeeded beyond measure.
Philadelphia, PA, USA John D. Kelly IV
v
Contents
Part I Musculoskeletal System Anatomy
1 Spine�� 3
William D. Long III and Todd J. Albert
2 Pelvis and Hip�� 9
Gregory Pereira, Nikolaos K. Paschos, and John D. Kelly IV
3 Shoulder�� 17
Jason Somogyi, Jonathan Twu, and J. Martin Leland III
4 Knee�� 31
Nikolaos K. Paschos and Chadwick C. Prodromos
5 Foot and Ankle Anatomy�� 37
Nicola Maffulli, Alessio Giai Via, and Francesco Oliva
Part II Musculoskeletal System Physiology
6 Bone Tissue Physiology�� 53

Ann Marie Kelly, Nikolaos K. Paschos, Dimitrios Giotis,
and John D. Kelly IV
7 Ligament Tissue Pathology �� 57
Simone Cerciello and Philippe Neyret
8 Musculoskeletal System Physiology:
Ligament Tissue Physiology�� 63
9 Articular Cartilage Physiology �� 69
Ann Marie Kelly, Nikolaos K. Paschos, Dimitrios Giotis,
Part III Musculoskeletal System Pathology
10 Metabolic Bone Diseases�� 73

Miguel Botton, António Robalo Correia,
and Manuel Cassiano Neves
vii
viii Contents
11 Orthopaedic-Related Issues with Genetic Disorders�� 83

António Robalo Correia, Miguel Botton,
12 Infectious Diseases of the Musculoskeletal System �� 95
Theofanis Kalathas and Nikolaos K. Paschos
13 Musculoskeletal Pain Management�� 105
Avraam Ploumis and Ioannis Gkiatas
14 Bone Healing�� 111
K. Osman, Ayman Gabr, and Fares S. Haddad
15 Osteoarthritis�� 121
Ayman Gabr, Sunil Gurpur Kini, and Fares S. Haddad
16 Inflammatory Arthropathies (Rheumatic Disorders)�� 133
George Bentley
17 Repair of Osteochondral Defects in the Knee by Cellular
(Chondrocyte and Stem Cell) Transplantation �� 145
George Bentley and Panos D. Gikas
18 Heterotopic Ossification�� 153
Gregory Pereira, Nikolaos Paschos, and John Kelly IV
19 Metastatic Bone Tumors�� 159
20 Musculoskeletal Imaging Techniques�� 165
Ian Pressney and Asif Saifuddin
21 Ethics�� 183
Michael K. D. Benson
Contributors
Todd J. Albert Hospital for Special Surgery, New York, NY, USA

Michael K. D. Benson St Luke’s Hospital, Oxford, UK
George Bentley Institute of Orthopaedics and Musculo-Skeletal Science,
University College London, London, UK
Royal National Orthopaedic Hospital, Stanmore, UK
Miguel Botton Centro Hospitalar Lisboa Norte, Lisbon, Portugal
Simone Cerciello Casa Di Cura Villa Betania, Rome, Italy
Centre Albert-Trillat, CHU Lyon Croix-Rousse, Hospices Civils de Lyon,
Lyon, France
António Robalo Correia Department of Orthopaedic Surgery, Hospital
José Joaquim Fernandes, Beja, Portugal
Ayman Gabr Department of Orthopaedic Surgery, University College
London Hospitals, London, UK
Panos D. Gikas Bone Tumour Unit, Royal National Orthopaedic Hospital
NHS Trust, Stanmore, UK
Royal National Orthopaedic Hospital, Stanmore, UK
Dimitrios Giotis Panepistimion Ioanninon, Department of Orthopaedic
Surgery, Ioannina, Greece
Department of Orthopedic Surgery, University of Pennsylvania, Philadelphia,
PA, USA
Ioannis Gkiatas Departments of Orthopaedics and PMR, University of
Ioannina, Ioannina, Greece
Fares S. Haddad Institute of Sport, Exercise & Health, University College
Hospital, London, UK
Theofanis Kalathas Department of Internal Medicine, Boston Medical
Center, Boston, MA, USA
Ann Marie Kelly Department of Orthopedic Surgery, University of
Pennsylvania, Philadelphia, PA, USA
ix
x Contributors
John D. Kelly IV Department of Orthopedic Surgery, University of

Sunil Gurpur Kini Department of Orthopaedics, Manipal Hospitals,
Bangalore, India
William D. Long III Orthopedic Spine & Sports Medicine Center, Paramus,
NJ, USA
Nicola Maffulli Department of Musculoskeletal Disorders, School of
Medicine and Surgery, University of Salerno, Salerno, Italy
Queen Mary University of London, Barts and the London School of Medicine
and Dentistry, Centre for Sports and Exercise Medicine, Mile End Hospital,
London, UK
J. Martin Leland III University Hospitals Geauga Medical Center and UH
Solon/Twinsburg/Streetsboro Health Centers, Cleveland, OH, USA
Manuel Cassiano Neves Hospital CUF Descobertas, Lisbon, Portugal
Philippe Neyret University Lyon 1, La Tour-de-Salvagny, France
Centre Albert-Trillat, CHU Lyon Croix-Rousse, Hospices Civils de Lyon,
Lyon, France
Francesco Oliva Department of Orthopaedic and Traumatology, University
of Rome “Tor Vergata”, School of Medicine, Rome, Italy
K. Osman School of Biosciences, University of Birmingham, Birmingham,
UK
Nikolaos K. Paschos Division of Sports Medicine, Department of
Orthopaedic Surgery, Boston Children’s Hospital, Harvard Medical School,
Boston, MA, USA
Department of Orthopedic Surgery, University of Pennsylvania, Philadelphia,
PA, USA
Gregory Pereira Department of Orthopedic Surgery, University of
Avraam Ploumis Departments of Orthopaedics and PMR, University of
Ioannina, Ioannina, Greece
Ian Pressney Department of Radiology, The Royal National Orthopaedic
Hospital Trust, Stanmore, Middlesex, UK
Chadwick C. Prodromos Illinois Sports Medicine and Orthopaedic Center,
Glenview, IL, USA
Department of Orthopedic Surgery, Rush University Medical Center,
Chicago, IL, USA
Asif Saifuddin Department of Radiology, The Royal National Orthopaedic
Hospital Trust, Stanmore, Middlesex, UK
Contributors xi
Jason Somogyi Carl R. Darnall Army Medical Center, Fort Hood, TX, USA
University Hospitals: Geauga Medical Center, Cleveland, OH, USA
Jonathan Twu Department of Orthopedic Surgery, University of Chicago,
Chicago, IL, USA
University Hospitals, Geauga Medical Center, Cleveland, OH, USA
Alessio Giai Via Department of Orthopaedic and Traumatology, University
of Rome “Tor Vergata”, School of Medicine, Rome, Italy
Part I
Musculoskeletal System Anatomy
Spine
1
William D. Long III and Todd J. Albert
Case Examples ion with complete resolution of his pain by

2 weeks postoperatively.
51-Year-old male presents to the office with a 47-Year-old female presents for evaluation of
2-month history of severe pain originating in his severe pain and dysfunction in her left upper
low back. The pain travels down the posterior extremity. She works as a hairstylist, and has
aspect of his thigh down into the bottom of his been unable to perform her duties at work due to
foot. The pain is associated with subjective complaints of pain and weakness in her wrist.
numbness and a sensation of pins and needles Her symptoms began 6 weeks ago after suffering
across the lateral aspect of his foot. He notes a fall while walking her dog, landing hard on her
weakness in his “calf” muscle. Conservative left knee and jarring her neck. She describes the
measures initiated by his primary care physician pain as a burning down her left arm starting from
6 weeks ago included nonsteroidal anti- her shoulder and ending at her thumb and index
inflammatories, a Medrol dose pack, and physi- finger. It is associated with subjective weakness
cal therapy. Lumbar epidural injections performed in her left wrist. Physical therapy, nonsteroidal
by a physiatrist 2 weeks ago failed to provide any anti-inflammatories, and narcotic medications
relief of his symptoms. Physical examination of failed to provide relief. Physical examination
the patient showed subjective numbness along showed a positive Spurling’s sign to the left, with
the plantar aspect of the foot, 4/5 strength in numbness of the left thumb to pinprick, and 4/5
ankle plantar flexion, and an inability to heel strength in the left wrist extensors. Brachioradialis
raise ten times on the right. A MRI of the lumbar reflex was 1+, with a negative Hoffman’s sign.
spine revealed a herniated intervertebral disc at MRI of the cervical spine shows a herniated
the L5–S1 level, causing severe right-sided S1 nucleus pulposus at C5–6 causing left-sided
nerve root compression (Fig. 1.1). The patient foraminal stenosis and C6 nerve root compres-
underwent a right-sided L5–S1 microdiscectomy, sion (Fig. 1.2). The patient underwent an anterior
and recovered 5/5 strength in ankle plantar flex- cervical decompression and fusion, with resolu-
tion of her left-sided pain but persistent numb-
W. D. Long III ness in the thumb at 4 weeks.
Orthopedic Spine and Sports Medicine Center,
Paramus, NJ, USA
e-mail: LongW@hss.edu
T. J. Albert (*)
Hospital for Special Surgery, New York, NY, USA
e-mail: Albertt@hss.edu
© Springer Nature Switzerland AG 2019 3

N. K. Paschos, G. Bentley (eds.), General Orthopaedics and Basic Science, Orthopaedic Study
Guide Series, https://doi.org/10.1007/978-3-319-92193-8_1
4 W. D. Long and T. J. Albert
Fig. 1.1 T2-weighted axial and sagittal cuts from an MRI of the lumbar spine showing a right-sided herniated interver-
tebral disc at the L5–S1 level
Fig. 1.2 T2-weighted sagittal and axial cuts from an MRI of the cervical spine showing a left-sided herniated interver-
tebral disc (yellow arrow) at the C5–6 level
Main Topics • Chondrification and ossification occur

between days 40 and 60, leading to the forma-
Embryology of the Spine tion of distinct vertebral units.
• Caudal cells from the sclerotome migrate
• The vertebral column is formed from 42 to 44 to form the annulus fibrosus, and a regress-
somites that ultimately differentiate into ven- ing notochord forms the nucleus
tromedial sclerotomes and dorsolateral pulposus.
dermomyotomes. • The posterior elements of the spine are formed
• Sclerotomes develop into definitive vertebrae, from cells adjacent to the neural tube that
causing myotomes to bridge the intervertebral form the vertebral arches.
spaces, and this permits movement of the • Vertebral unit morphology is regulated by the
spine. HOX family of genes.
1 Spine 5
• The neural elements of the spine are formed • Fifty percent of flexion and extension of the
from the notochord, which is formed by day neck occurs at the articulation of the occiput
18 of gestation from migrating epiblasts fol- and atlas.
lowing gastrulation. • Fifty percent of rotation of the neck occurs at
the atlantoaxial joint.
• The vertebral artery courses through the trans-
Functional Spinal Unit (FSU) verse foramen of C2 and C1 before penetrating
the atlanto-occipital membrane and becoming
• The FSU is the smallest physiological motion intradural.
unit of the spine, consisting of two adjacent • C1 vertebra has no body or spinous process, and
vertebrae, the intervertebral disc, and all the superior concave articular surfaces accom-
adjoining ligaments between them. modate the occipital condyles of the skull.
• The basic bony anatomy of a vertebra can be • C2 vertebra has a traditional vertebral body
broken into three sagittal columns: anterior, with the projecting odontoid process, the site
middle, and posterior. of multiple ligamentous attachments to the
• The anterior column consists of the anterior ring of C1; it has distinct pedicles and pars as
half of the vertebral body. well as a large spinous process.
• The middle column consists of the posterior
half of the vertebral body and pedicle, includ-
ing the level of the canal. Cervical Spine
• The posterior column is made up of the facet
joints, laminae, and spinous processes. • The subaxial cervical spine includes C3
• The anterior longitudinal ligament (ALL) cov- through C7.
ers the anterior aspect of the vertebral bodies • The normal posture of the cervical spine is
and limits spinal extension. one of lordosis, approximately 15–25°.
• The posterior longitudinal ligament (PLL) • There are eight cervical nerve roots, each tak-
covers the posterior aspect of the bodies and ing off and coursing above the corresponding
limits spinal flexion. pedicle (e.g., the C7 root takes off above the
• The ligamentum flavum connects the laminae C7 pedicle, while the C8 roots take off below
of adjacent vertebrae from the axis to the first the C7 pedicle).
segment of the sacrum. • The anterior tubercle of the C6 transverse pro-
• Interspinous ligaments connect the spinous cess is frequently palpable and used as an ana-
processes, acting as a posterior tension band tomic landmark for incision placement, and is
preventing spinal flexion. commonly called the carotid or Chassaignac
tubercle.
• The hyoid bone is commonly at the level of
Craniovertebral Junction C3, while the thyroid cartilage corresponds to
C4, and the cricoid at C6.
• The craniovertebral junction is comprised of • The spinal canal is triangular with a larger lat-
the base of the occiput, the atlas (C1), and the eral compared to anteroposterior dimension.
axis (C2). • The uncovertebral joints are identified along the
• Primary stability is achieved through the sup- lateral aspect of the endplates and assist to define
porting ligamentous complex that spans the the margin for discectomy or corpectomy.
bony architecture. • The cervical plexus is comprised of the ante-
• The apical, alar, cruciate ligaments as well as rior rami of C1 to C4.
the tectorial membrane prevent abnormal • The brachial plexus is comprised of the ante-
motion between the three articulations. rior rami of C5 to T1.
• The vertebral arteries originate from the sub- • The pars interarticularis is the region between
clavian and enter the transverse foramen of C6. the superior and inferior articulating facets, a
• The carotid sheath houses the carotid artery, fracture of which is termed spondylolysis, and
the internal jugular vein, and the vagus nerve. can occur in 5–6% of the population.
• The spinal cord ends at the conus medullaris,
typically at the level of the L1 body or L1–L2
Thoracic Spine disc; caudal to this nerve roots descend within
the thecal sac as the cauda equina.
• The thoracic spine is composed of 12 rib- • Posterolateral disc herniations compress the
bearing vertebrae with occasional enumerat- traversing nerve root at the lateral recess of the
ing variations. spinal canal, prior to reaching the interverte-
• The thoracic cage commonly limits motion of bral foramen; this results in compression of
the thoracic spine secondary to the osteoliga- the inferior nerve root; hence a L4–5 disc
mentous relationship of the ribs and vertebrae. compresses the L5 nerve root.
• The normal posture of the thoracic spine is • Far lateral disc herniations compress the ceph-
one of kyphosis, approximately 10–40° with alad exiting nerve root close to the superior
an apex at T7. pedicle; hence a L2–3 disc would compress
• Vertebral body morphology demonstrates a the L2 nerve root.
wedge shape with the posterior height being • Facet joint and ligamentum flavum hypertrophy
greater than the anterior, facilitating the secondary to degeneration can lead to stenosis
kyphotic posture of this region. at the lateral recess and intervertebral foramen.
• Thoracic facet joints are intermediately ori- • The lumbosacral plexus is comprised of the
ented compared to the cervical (coronal) and ventral rami from the T12 though S3 nerve
lumbar (sagittal) spine, offering stability roots, and travels posterior to the psoas.
through both flexion and extension. • The sciatic nerve arises from the ventral rami
• The diameter of the spinal canal is less than of L4 through S3, with a preaxial tibial divi-
that of the cervical and lumbar spine. sion and postaxial peroneal division.
• Nerve roots at each level exit below their cor- • The main blood supply to the region comes
responding pedicle; hence the T5 nerve root from the segmental arteries arising from the
exits below the T5 pedicle. lumbar, iliolumbar, and median sacral arteries.
• Nerves innervate the thorax and abdomen, • The bifurcation of the aorta and inferior vena
with T4 at the level of the nipples and T10 at cava commonly occurs at the level of the L4–5
the level of the umbilicus. disc space.
• The artery of Adamkiewicz provides the main • The erector spinae is composed of the iliocos-
blood supply to the cord from T8 to the conus, talis, longissimus, and spinalis muscles, and is
with segmental arteries from the lumbar and responsible for extension and lateral rotation
intercostal arteries supplying the remainder. of the vertebral column.
Lumbar Spine Sacroiliac Spine
• The lumbar spine is typically comprised of • Five sacral vertebrae fuse to form the wedge-
five vertebras, with occasional counting shaped kyphotic sacrum.
anomalies due to a sacralized L5 or lumbari- • The coccyx is formed from four fused coc-
zed S1 vertebra. cygeal vertebras, possibly the remnant of a
• Compared with the cervical and thoracic tail.
spine, the spinal canal and bony architecture • The sacrum distributes force to the pelvis
are much larger in diameter. through the paired large vertical sacroiliac
1 Spine 7
(SI) joints, a true synovial diarthrodial joint d escending tracts that allow for the transmis-
that has negligent motion. sion of stimuli to and from the brain.
• The pelvic splanchnic nerves arise from the S2 • The dorsal root (sensory) and ventral root
through S4 nerve roots, supplying autonomic (motor) coalesce to form the paired spinal
innervation to the abdominal and pelvic viscera. nerves at each level of the spine.
• The bulbocavernosus reflex also involves the • The spinal cord is covered in three protective
S2 to S4 nerve roots, and is the lowest measure- sheaths, from deep to superficial: pia mater,
able spinal reflex, useful for spinal cord trauma. arachnoid mater, and dura mater.
• The median sacral artery supplies the lower • Cervical nerve roots C5 through T1 are
lumbar vertebra, sacrum, and coccyx. responsible for innervation of the upper
• The posterior SI ligaments are thicker and extremities in a myotomal and dermatomal
more robust than the anterior SI ligaments. pattern, while the five lumbar and first
• The sacrotuberous and sacrospinous liga- sacral nerve roots supply the lower
ments attach the sacrum to the ischial tuberos- extremities.
ity and ischial spine, respectively, delineating • The lower 11 thoracic nerve roots have less of
the greater and lesser sciatic foramen. a motor role, providing sensation to the thorax
and abdomen.
• The American Spinal Injury Association
Neural Elements (ASIA) provides a guide for the myotomal
and dermatomal innervation of the body based
• The cross-sectional anatomy of the spinal on nerve root level (Fig. 1.3).
cord is divided among ascending and
Fig. 1.3 ASIA worksheet for documenting individual motor and sensory nerve root function based on level
Questions (a) T1
(b) T10
Which of the following statements is true? (c) T12
(d) T4
(a) Cervical nerve roots come off the spinal cord (e) T8
below their corresponding pedicle, and lum-
bar nerve roots come off above their corre- What superficial anterior landmark can be
sponding pedicle. palpated to approximate the level of C4?
(b) Both cervical and lumbar nerve roots come
off above their corresponding pedicle. (a) Thyroid cartilage
(c) Cervical nerve roots come off the spinal (b) Hyoid bone
cord above their corresponding pedicle, (c) Sternocleidomastoid muscle
and lumbar nerve roots come off below (d) Carotid tubercle
their corresponding pedicle. (e) Carotid pulse
(d) Both cervical and lumbar nerve roots come
off below their corresponding pedicle. A right-sided far lateral disc herniation at
L4–5 would be expected to produce what signs
At which level is the conus medullaris typi- and symptoms?
cally found?
(a) Right-sided quadriceps weakness, pain
(a) Foramen magnum extending down to the top of the foot.
(b) C7–T1 (b) Left-sided foot drop, left-sided numbness

(c) T7–T10 over the dorsum of the foot.
(d) L1–L2 (c) Bilateral hallux extension weakness, numb-
(e) L5–S1 ness at the right foot first webspace.
(d) Right-sided ankle dorsiflexion weakness,
The sensation of the abdomen and back at the pain down into the front of the leg.
level of the umbilicus corresponds to what tho- (e) Right-sided hip extension weakness, numb-
racic level? ness over the lateral aspect of the leg.
Pelvis and Hip
2
Gregory Pereira, Nikolaos K. Paschos,
Anatomy fibrocartilaginous pubic symphysis and resists

external rotation. The pelvic floor complex
The pelvis is formed by the two innominate includes the sacrospinous ligament that resists
bones that articulate posteriorly at the sacrum external rotation and the sacrotuberous ligament
and anteriorly at the pubic symphysis. These that resists shear and flexion.
attachments form the pelvic girdle, which links The hip has conferred stability from the bony
the axial skeleton to the lower extremities of the articulation of the femoral head in the acetabu-
body. Each innominate bone is formed by the lum. Additionally, the fibrocartilaginous labrum
fusion of the ischium, ilium, and ischium that increases the acetabular depth, and offers an
occurs during puberty. The fusion of these three attachment site for the adjacent ligaments,
bones forms cup-shaped, anteverted (15°) acetab- increasing joint stability. Finally, the hip capsule
ulum that articulates with the head of the femur composed of the iliofemoral, ischiofemoral, and
to form the diarthrodial hip joint. pubofemoral ligaments contributes to the stabil-
Pelvic articulations have limited intrinsic sta- ity of the hip joint. The iliofemoral ligament is
bility. Instead, key ligaments of the posterior, the strongest of the three ligaments and resists
anterior, and pelvic floor complex provide stabil- anterior dislocation and hyperextension. The
ity to the pelvis and resist deforming stresses. ischiofemoral ligament, the only ligament located
The complex consists of the sacroiliac and ilio- in the posterior hip, resists excessive internal
lumbar ligaments that prevent nutation and coun- rotation, extension, and posterior translation.
ternutation and are among the strongest ligaments Finally the pubofemoral ligament on the anterior
in the body. The anterior complex includes the aspect of the hip resists excessive abduction and
extension.
G. Pereira (*) · J. D. Kelly IV

Department of Orthopedic Surgery, University of
Pennsylvania, Philadelphia, PA, USA Hip Arthroscopy
e-mail: Gregory.Pereira@uphs.upenn.edu
N. K. Paschos Setup
Pennsylvania, Philadelphia, PA, USA • Patient positioned in supine or lateral decubi-
Division of Sports Medicine, Department of tus position.
Orthopaedic Surgery, Boston Children’s Hospital, • Requires traction (25–50 lbs) in line with the
Harvard Medical School, Boston, MA, USA femoral neck.
e-mail: Nikolaos.Paschos@childrens.harvard.edu

10 G. Pereira et al.
Portals • Requires disruption of the abductor

mechanism.
• Anterolateral portal • Complications: damage to obturator nerve,
–– Used as the primary viewing portal and for medial femoral circumflex artery, deep exter-
anterolateral access. nal pudendal artery.
–– Incorrect placement risks damage to supe-
rior gluteal nerve.
• Anterior portal Medial Approach
–– Placed with hip flexed in internal rotation.
–– Used for anterior access. • Provides excellent exposure to the psoas.
–– Incorrect placement risks damage to lateral • Complications: damage to the LFCN and fem-
femoral cutaneous nerve (LFCN). oral nerve.
• Posterior/posterolateral portal
–– Used for posterior access.
–– Incorrect placement risks damage to sciatic
nerve. Direct Lateral Approach (Hardinge)
• Distal anterolateral portal (may not be used
depending on indication) • Commonly used in THA.
–– Used to access the peripheral compartment. • Requires split of gluteus medius and vastus
–– Traction must be removed and hip is placed lateralis.
in neutral flexion/extension. • Complications: superior gluteal nerve and
femoral nerve injury.
The reported complication rate for hip arthros-
copy is between 1.3 and 6.4%. The most common
complications from hip arthroscopy are transient osterior Approach (Moore or
P
neuropraxias of the pudendal and peroneal nerve. Southern)
These injuries may be prevented with intermit-
tent release of traction. • Provides excellent exposure to acetabulum
and proximal femur.
• Requires release of the short external
Surgical Approaches to the Hip Joint rotators.
• Complications: injury to sciatic nerve, infe-
Anterior Approach (Smith Peterson) rior gluteal artery, superior gluteal artery/
nerve.
• Provides excellent exposure to the ilium.
• Requires ligation of the lateral femoral cuta-
neous artery.
• Complications: damage to the LFCN and fem- Pelvic Ring Injury
oral nerve.
General
nterolateral Approach (Watson

A • Mechanism: high-energy blunt trauma.
Jones) • High mortality rates ranging from 15 to
50%.
• Provides excellent exposure to the acetabulum • Hemorrhage is he major cause of death in
and proximal femur. these cases.
2 Pelvis and Hip 11
Anatomy Classification
• Pelvic ring is composed of the sacrum and the • Tile classification

two innominate bones. • Young-Burgess Classification
• Must be disruption of the ring in at least two
places if displacement occurred.
• Stability is reliant on the ligamentous struc- Complications
tures in the pelvis (anterior, posterior, and pel-
vic floor complex). • DVT (~60%) and PE (27%)
• Posterior ligaments are in close proximity to • Urogenital injury (12–20%)
key neurovascular structures (e.g., internal • Chronic instability (rare)
iliac artery, lumbosacral plexus).
ecent Developments in Pelvis/Hip

R
Exam Anatomy
• Inspection: look for abnormal lower extremity • A recent retrospective review studied sacral frac-
rotation, ecchymosis, limb length discrepancy, tures in the setting of pelvic ring injuries. Sacral
lacerations, flank hematoma. fractures were seen in 60% of pelvic trauma
• Neurologic exam: assess lumbosacral patients. Of these fractures, avulsion fractures
plexus. and longitudinal fractures of the sacrum are
• Urogenital: vaginal, rectal exam, assess urine almost always associated with anterior pelvic
for gross hematuria. ring injury. Conversely, the study found that
• Stability: gentle rotational force on each iliac transverse fractures of the lower sacrum and
crest (perform one time only). combined longitudinal and transverse sacral
fractures are prone to occur in isolation.
• The direct anterior approach (DAA) to the hip
Imaging for total hip arthroplasty (THA) has been
growing in popularity in recent years. The rate
Critical to look for signs of radiographic of revision after DAA versus non-anterior
instability: approaches to the hip is a rather unexplored
field. A recent study comparing DAA versus
1. Avulsion fracture (sacrum, ischial spine,
non-anterior approaches found that the mean
ischial tuberosity, transverse process of the duration from primary DAA THA to revision
fifth lumbar vertebrae). THA was 3.0 ± 2.7 years versus 12.0 ± 8.8
2. Sacral gap fracture. years for non-anterior approaches. Aseptic
3. >5 mm displacement of posterior sacroiliac loosening of the stem was found to be signifi-
complex. cantly more common in DAA THA (P < 0.001)
than in non-anterior approach THA leading to
The imaging to request for suspected pelvic earlier revision procedures.
ring injury: • Hip arthroscopy has grown in popularity
but outcome data from patient-reported
• AP pelvis metric and patient satisfaction scores are
• Inlet view not frequently reported. A recent study
• Outlet view evaluated 2-year patient-reported outcome
• CT pelvis scores and patient satisfaction scores after
hip arthroscopy using pre- and postopera- (C) Infection

tively four PRO measures: (D) Hemorrhage
–– The modified Harris Hip Score (mHHS) What should you perform on this patient as
–– Non-Arthritic Hip Score (NAHS) part of the physical exam?
–– Hip Outcome Score-Activities of Daily
Living (HOS-ADL) I. Rectal exam
–– Hip Outcome Score-Sport-Specific II. Vaginal exam
Subscale (HOS-SSS) III. Oral exam
IV. Neurological exam of the lower extremities
At 2-year follow-up all scores showed statisti- (A) I
cally significant improvements (P < .0001) in (B) I, II
all measures. As such, this study concluded that (C) I, III
primary hip arthroscopy had excellent clinical (D) I, II, IV
outcomes and patient satisfaction at short-term (E) II, III, IV
follow-up validating its use in recent years.
Name two radiographic indications of pelvic
• Each approach to the hip has strengths and instability:
weaknesses but minimizing loss of strength to
the hip after THA might allow for faster recov- 1. Sacral gap fracture
ery. A recent study compared leg press and 2. >5 mm displacement of posterior sacroiliac
abduction strength pre- and postoperatively in complex
patients undergoing THA with three different 3. Avulsion fracture (sacrum, ischial spine,
approaches (direct lateral, posterior, or ante- ischial tuberosity, transverse process of the
rior approach). Follow-up was conducted up fifth lumbar vertebrae)
to 3 months postoperatively. In the first post-
operative week the posterior and anterior What is the most common complication of
approaches produced significantly less pelvic ring fracture?
decrease in muscular strength than the direct
lateral approach. However, at 3-month follow- (A) Urologic injury
up there were no differences in leg press and (B) DVT
abduction strength between any of the groups. (C) Chronic instability
(D) Vaginal vault prolapse
Case Studies
Case 2
Case 1
A 46-year-old man with a MRI-confirmed labral
A 28-year-old female presents to the emergency tear is referred to you for labral repair. He is in
department after a motor vehicle collusion in which good health, clears preoperative evaluation, and
he was the passenger. He is arousable but a poor his- is scheduled for surgery.
torian. On exam, he is noted to have multiple lacera- The patient is concerned about complications
tions around his trunk and pelvis and flank hematoma. of arthroscopy and asks what the most common
His left leg appears to be externally rotated. complication is. What do you respond?
What is the major cause of death in pelvic ring
injury patients? (A) Transient neuropraxia of pudendal or
peroneal nerve
(A) Fat embolism (B) LFCN nerve injury
(B) Air embolism (C) Injury to the labrum
2 Pelvis and Hip 13
When positioning the patient traction should • Direct lateral approach (Hardinge)
be in line with which anatomic structure? • Posterior approach (Moore or Southern)
(A) Femoral head To emulate native anatomy how should the

(B) Femoral neck cup be placed?
(C) Femoral shaft
(D) Acetabulum (A) Anteverted
(B) Retroverted
What is the order the portals should be placed? (C) Neutral version
( A) Anterior, posterior, anterolateral What is the strongest ligament in the hip capsule?
(B) Posterior, anterior, anterolateral
(C) Anterolateral, anterior, posterior (A) Pubofemoral ligament
(D) Anterior, anterolateral, posterior (B) Iliofemoral ligament
(C) Ischiofemoral ligament
What nerve is most at risk to be injured with
improper positioning of the posterior portal? What ligament of the hip capsule resists
_____________________________ (sciatic nerve) excessive internal rotation, extension, and poste-
What is the mechanism for pudendal and pero- rior translation?
neal nerve injuries in hip arthroscopy?
_________________________ (traction injury) (A) Pubofemoral ligament
(B) Iliofemoral ligament
(C) Ischiofemoral ligament
Case 3
A 68-year-old man with crippling osteoarthritis Review Questions

presents to your clinic. He has had multiple corti-
costeroid and visco-supplementation injections In a THA with a direct anterior approach what are
with no relief of symptoms. Radiographs show the two most commonly injured structures?
bone on bone wear, joint space narrowing, and
prominent osteophytes. You counsel the patient ( A) LCFN, sciatic nerve
on the treatment options and he decides to (B) LCFN, femoral nerve
undergo total hip arthroplasty. (C) Medial femoral circumflex artery
Which of the following structures confer sta- (D) Obturator nerve, femoral nerve
bility to the native hip?
What approach to the hip is most likely to
I. Hip capsule injure the obturator nerve?
II. Obturator internus
III. Labrum ( A) Direct lateral approach (Hardinge)
(A) I (B) Anterolateral approach (Watson Jones)
(B) I, II (C) Anterior approach (Smith Peterson)
(C) I, III (D) Posterior approach (Moore or Southern)
(D) II, III
Which of the following statements is true?
Name three approaches to the hip that may be
used for THA? (A) There must be disruption of the ring in at
least two places if displacement occurred.
• Anterior approach (Smith Peterson) (B) Bony articulation is the primary source of
• Anterolateral approach (Watson Jones) stability of the pelvis.
(C) The anterior complex ligamentous structures (E) Posterior approach

are stronger than the posterior complex
ligaments. Which of the following nerves is at risk of
(D) The Garden classification is the most common being damaged during hip arthroscopy if the
system used to classify pelvic ring fractures. anterior portal is incorrectly positioned?
What approach requires release of the short (A) Femoral nerve

external rotators? (B) Sciatic nerve
(C) Obturator nerve
(A) Anterolateral approach (D) LFCN
(B) Anterior approach
(C) Posterior approach What ligamentous complex structures in the
(D) Medial approach pelvis resist external rotation, shear, and exces-
sive flexion?
Incorrect placement of the anterolateral portal
in hip arthroscopy is most likely to injure what (A) Posterior complex
structure? (B) Anterior complex
(C) Pelvic floor complex
(A) Femoral nerve
(B) Lateral femoral circumflex artery
(C) Lateral femoral cutaneous nerve Further Readings
(D) Sciatic nerve
(E) Obturator nerve Alwattar BJ, Bharam S. Hip arthroscopy portals. Oper
Tech Sports Med. 2011;19(2):74–80.
What is the normal version of the acetabulum? Beckmann N, Cai C. CT characteristics of traumatic
sacral fractures in association with pelvic ring inju-
ries: correlation using the Young-Burgess classifica-
( A) 30° of retroversion tion system. Emerg Radiol. 2017;24(3):255–62.
(B) 15° of retroversion Bentley G, editor. European surgical orthopaedics
(C) 15° of anteversion and traumatology: the EFORT textbook. Berlin,
Heidelberg: Springer; 2014.
(D) 30° of anteversion Byrd JWT. Hip arthroscopy utilizing the supine position.
Arthroscopy. 1994;10(3):275–80.
What approach to the hip is most likely to Byrd JWT. Hip arthroscopy. J Am Acad Orthop Surg.
damage the sciatic nerve and the inferior gluteal 2006;14(7):433–44.
Chang CY, Huang AJ. MR imaging of normal hip
artery? anatomy. Magn Reson Imaging Clin N Am.
2013;21(1):1–19.
(A) Anterior approach Cole JD, Blum DA, Ansel LJ. Outcome after fixation of
(B) Anterolateral approach unstable posterior pelvic ring injuries. Clin Orthop
Relat Res. 1996;329:160–79.
(C) Medial approach Dickson KF. Pelvic ring injuries. In: Surgical treatment
(D) Lateral approach of orthopedic trauma. New York, NY: Thieme; 2007.
(E) Posterior approach p. 448–53.
DiGioia AM, Plakseychuk AY, Levison TJ,
Jaramaz B. Mini-incision technique for total
What approach to the hip provides optimal hip arthroplasty with navigation. J Arthroplast.
exposure to the psoas? 2003;18(2):123–8.
Dutton M. Orthopaedic examination, evaluation, and
(A) Anterior approach intervention. 2nd ed. New York: McGraw Hill;
2008.
(B) Anterolateral approach Eto S, et al. The direct anterior approach is associated
(C) Medial approach with early revision total hip arthroplasty. J Arthroplast.
(D) Lateral approach 2017;32(3):1001–5.
2 Pelvis and Hip 15
Gautier E, Ganz K, Krügel N, Gill T, Ganz R. Anatomy Meneghini RM, et al. Muscle damage during MIS total
of the medial femoral circumflex artery and hip arthroplasty: Smith-Peterson versus posterior
its surgical implications. J Bone Joint Surg Br. approach. Clin Orthop Relat Res. 2006;453:293–8.
2000;82(5):679–83. Meneghini RM, Pagnano MW, Trousdale RT, Hozack
Gupta A, et al. Does primary hip arthroscopy result WJ. Muscle damage during MIS total hip arthro-
in improved clinical outcomes? 2-year clini- plasty: Smith-Petersen versus posterior approach. Clin
cal follow-up on a mixed group of 738 consecu- Orthop Relat Res. 2006;453:293–8.
tive primary hip arthroscopies performed at a Miranda MA, et al. Pelvic ring injuries: a long term
high-volume referral center. Am J Sports Med. functional outcome study. Clin Orthop Relat Res.
2016;44(1):74–82. 1996;329:152–9.
Hardinge K. The direct lateral approach to the hip. Bone Olson SA, Pollak AN. Assessment of pelvic ring stability
Joint J. 1982;64(1):17–9. after injury: indications for surgical stabilization. Clin
Hughes PE, Hsu JC, Matava MJ. Hip anatomy and bio- Orthop Relat Res. 1996;329:15–27.
mechanics in the athlete. Sports Med Arthrosc Rev. Pflüger G, Junk-Jantsch S, Schöll V. Minimally
2002;10(2):103–14. invasive total hip replacement via the anterolat-
Kennon R, et al. Anterior approach for total hip arthro- eral approach in the supine position. Int Orthop.
plasty: beyond the minimally invasive technique. 2007;31(1):7–11.
JBJS. 2004;86(suppl_2):91–7. Robertson WJ, Kelly BT. The safe zone for hip arthros-
Leone A, et al. Emergency and trauma of the pelvic copy: a cadaveric assessment of central, periph-
ring. In: Seminars in musculoskeletal radiol- eral, and lateral compartment portal placement.
ogy, vol. 21. No. 03. Stuttgart: Thieme Medical Arthroscopy. 2008;24(9):1019–26.
Publishers; 2017. Sampson TG. Complications of hip arthroscopy. Clin
Levangie PK, Norkin CC. Joint structure and function: Sports Med. 2001;20(4):831–6.
a comprehensive analysis. fourth ed. Philadelphia: Winther SB, et al. Muscular strength after total hip
F.A. Davis; 2005. arthroplasty: A prospective comparison of 3 surgical
Martin HD, et al. The function of the hip capsu- approaches. Acta Orthop. 2016;87(1):22–8.
lar ligaments: a quantitative report. Arthroscopy. Vrahas M, et al. Ligamentous contributions to pelvic sta-
2008;24(2):188–95. bility. Orthopedics. 1995;18(3):271–4.
Shoulder
3
Jason Somogyi, Jonathan Twu,
and J. Martin Leland III
Osseous [1–5] –– Acromion

Four ossification centers (basi, meso, meta,
• Scapula and pre-acromion).
–– Seventeen muscle attachments, four liga- Three types of morphology (I—flat, II—
mentous attachments. curved, III—hooked).
–– Scapular plane is 30° anterior to coronal plane. –– Suprascapular notch
–– Glenoid Covered by the superior transverse scapu-
Retroverted 5° compared to scapular plane. lar ligament.
Supraglenoid tubercle—origin of long Suprascapular Artery runs over ligament
head of biceps. (“Army OVER the bridge”).
–– Scapular spine Suprascapular Nerve runs under ligament
Separates supraspinatus and infraspinatus. (“Navy UNDER the bridge”).
–– Coracoid Compression here will paralyze the supra-
Attachments for ligaments (coracoacro- spinatus and infraspinatus.
mial and coracoclavicular), conjoined ten- –– Spinoglenoid notch
don and pectoralis minor. Suprascapular artery and nerve run around
Used as anterior landmark for surgical notch.
approaches and injections. Compression here will only paralyze the
infraspinatus.
J. Somogyi, M.D. • Clavicle
University Hospitals: Geauga Medical Center, –– Fulcrum for lateral movement of arm.
Cleveland, OH, USA
–– First bone to ossify (5-week fetal) and last
Carl R. Darnall Army Medical Center, to fuse (medial epiphysis—25 years).
Fort Hood, TX, USA
• Humeral head
J. Twu, M.D. –– Retroverted 30° from transepicondylar axis
University Hospitals: Geauga Medical Center,
Cleveland, OH, USA
of distal humerus.
–– Neck shaft angle is 130°.
Chicago, Chicago, IL, USA
–– Greater tuberosity (supraspinatus, infraspi-
natus, teres minor) and lesser tuberosity
J. Martin Leland III, M.D. (*)
University Hospitals Geauga Medical Center and UH
(subscapularis) are attachments for rotator
Solon/Twinsburg/Streetsboro Health Centers, cuff.
Cleveland, OH, USA

18 J. Somogyi et al.
–– Long head of the biceps runs through the –– MGHL: resists anterior and posterior trans-
bicipital groove (pectoralis major inserts lation in midrange abduction (45°) and
just lateral to the groove, latissimus dorsi external rotation (ER).
just medial to the groove). –– IGHL:
Posterior band: restrains posterior sublux-
ation at 90° of flexion/abduction and inter-
Joint [1–5] nal rotation (IROT) as well as 90° of
external rotation.
• Range of motion Anterior band: restrains anterior sublux-
–– Forward flexion: 0–170° ation at 90° of flexion/abduction and inter-
–– Extension: 0–60° nal rotation as well as 90° of external
–– Abduction: 0–170° rotation.
2:1 ratio of glenohumeral joint to scapulo- Superior band: most important static
thoracic motion during abduction. stabilizer.
Full abduction requires external rotation to • Coracoacromial ligament (CAL)
clear acromion. –– Important for superoanterior restraint in
–– Internal rotation: 70° rotator cuff deficiencies (should be pre-
–– External rotation: 80° served when debriding massive cuff
tears).
Labrum
• Creates cavity compression and 50% of the

glenoid socket depth.
• Fibrocartilaginous tissue that receives blood
supply from capsule and periosteal vessels.
• Anchors:
–– Anteroinferior labrum anchors the infe-
rior glenohumeral ligament: leads to
Bankart lesion (anteroinferior labral
tears; can be boney or non-boney) in dis-
location events.
–– Superior labrum anchors long head of
biceps tendon: associated with SLAP (supe-
rior labrum anterior to posterior) lesions.
• Anatomic variants:
–– Sublabral foramen.
–– Buford complex.
Ligamentous restraints
Arm Anterior Inferior Posterior
Ligamentous Stability position restraint restraint restraint
Neutral SGHL
• Three main glenohumeral ligaments: superior 45 ER MGHL
45 ABD
(SGHL), middle (MGHL), and inferior
90 ER IGHL IGHL IGHL
(IGHL): Ant band Ant band Post band
–– Act as static stabilizers of the shoulder. 90 FF IGHL IGHL
–– SGHL: restrains inferior translation at 0° of 90 ABD Ant band Post band
abduction (neutral). 90 IR
3 Shoulder 19
Muscles • Shoulder internal rotators are stronger than the

external rotators (this is why electrocution/sei-
• Rotator cuff muscles (supraspinatus, infraspi- zures lead to posterior shoulder dislocations).
natus, teres minor, and subscapularis), deltoid, • Long head of biceps originates from superior
and teres major act on the shoulder: glenoid and labrum; held in groove via the
–– Cuff muscles stabilize humeral head transverse humeral ligament as well as the
against glenoid (dynamic stabilizers). subscapularis tendon.
Muscles of the shoulder

Muscle Origin Insertion Action Innervation
Deltoid Clavicle, acromion Deltoid tuberosity Abduction Axillary n.
Supraspinatus Superior dorsal Greater tuberosity Abduction and Suprascapular n.
scapula ER
Infraspinatus Inferior dorsal scapula Greater tuberosity ER Suprascapular n.
Teres minor Scapula Greater tuberosity ER Axillary n.
Subscapularis Ventral scapula Lesser tuberosity IR Upper + lower subscapular n.
Pectoralis Sternum, ribs, clavicle Intertubercular IR and Medial + lateral pectoral n.
major groove adduction
Neurovascular Supplies motor to subscapularis and teres

major.
• Arteries –– Medial pectoral nerve
–– Ascending branch of anterior humeral cir- Comes off medial cord of brachial plexus,
cumflex artery C8–T1 fibers.
Supplies humeral head; runs parallel and Pierces pectoralis minor to supply motor
lateral to long head of biceps. for pectoralis minor and major.
–– The arcuate artery –– Axillary nerve
Interosseous continuation of ascending Innervation: motor for deltoid and teres
branch; penetrates humeral head. minor; sensory to lateral shoulder.
–– Posterior humeral circumflex artery Origin: off posterior cord of brachial
Recent literature supports this as main plexus, C5–C6 fibers.
blood supply to humeral head. Travels posteriorly behind the surgical
–– Acromial branch of thoracoacromial artery neck of humerus with posterior circumflex
Runs on the medial aspect of the coracoacro- humeral artery through the quadrangular
mial ligament, a common cause of bleeding space and then curves anteriorly 5–7 cm
during subacromial arthroscopy. inferior to the acromion.
• Nerves
–– Suprascapular nerve
Comes off upper trunk of brachial plexus, Surgical Approaches [5–20]
C5–C6 fibers.
Runs under ligament in suprascapular and • Arthroscopic portals
spinoglenoid notch. –– Posterior
Supplies motor to supraspinatus and Primary viewing portal.
infraspinatus. 2 cm inferior and 1 cm medial to postero-
–– Upper and lower subscapular nerve lateral corner of acromion.
Comes off posterior cord of brachial Passes through infraspinatus or between
plexus, C5–C6 fibers. infraspinatus and teres minor.
–– Anterior –– Space for olecranon process in full

Lateral to coracoid process and anterior to extension.
the AC joint. (b) Radial head
Passes between pectoralis major and • Stabilizer against valgus stress.
deltoid. • 280° covered by cartilage:
–– Lateral –– Safe zone for fixation of fracture:
1–2 cm distal to lateral edge of acromion. –– 90–110° arc from radial styloid to
Passes through deltoid. Lister’s tubercle with arm neutral.
• Anterior approach (deltopectoral) (c) Proximal ulna
–– Deltopectoral groove and coracoid as • Olecranon
landmark. • Greater sigmoid notch
–– Deltoid (axillary) and pectoralis major –– Articulates with trochlea.
(medial and lateral pectoral nerve) • Lesser sigmoid notch
interval. –– Articulates with radial head.
–– Dangers: musculocutaneous nerve, • Coronoid
cephalic vein, axillary nerve. –– Buttress to prevent posterior
• Lateral approach (deltoid split) subluxation.
–– No internervous plane. –– Loss of >50% of height →
–– Split deltoid inferior to acromion; do not instability.
go more than 5 cm inferior to the acromion • Sublime tubercle
(due to location of axillary nerve). –– Insertion of anterior bundle of ulnar
• Posterior approach collateral ligament.
–– Use acromion and scapular spine as (d) Carrying angle
landmark. • Angle between long axis of humerus and
–– Teres minor (axillary nerve) and infraspi- ulna:
natus (suprascapular nerve) interval. –– Measured in frontal plane with elbow
–– Dangers: suprascapular nerve and axillary extended.
nerve. • 11–14° in men.
• 13–16° in women.
Elbow Anatomy
Joint
Osseous
• Ulnohumeral articulation = hinge.
(a) Distal humerus • Radiohumeral articulation = pivot.
• Lateral epicondyle • Radioulnar = rotation.
–– Origin of lateral collateral ligament • Maximum capsule distension at 70–80°:
complex. –– Patients with effusion most comfortable in
–– Origin of extensor/supinator mass. this position.
• Medial epicondyle • Normal capsular volume = 25 mL.
–– Origin of medial ulnar collateral • Capsule attaches 6 mm distal to tip of
ligament. coronoid
–– Origin of flexor/pronator mass. –– Coronoid is intra-articular structure; can be
• Trochlea visualized during arthroscopy.
–– Medial and spool shaped. • Range of motion
• Capitellum –– 0–145° Flexion/extension.
–– Lateral and hemispherical. –– 90° Supination.
• Olecranon fossa –– 80° Pronation.
3 Shoulder 21
Ligamentous Stability • Provides stability to valgus stress:

–– Anterior bundle most important in
(a) Medial collateral ligament resisting valgus force.
• Originates from anteroinferior medial (b) Lateral ulnar collateral ligament complex
humeral epicondyle. • Originates from lateral humeral epicon-
• Components: dyle (near axis of rotation).
–– Anterior bundle (ulnar collateral). • Stabilizes against rotational/varus forces.
Inserts 18 mm posterior from coronoid • Components:
tip. –– Annular ligament.
Inserts on anteromedial aspect of coro- Attaches lesser sigmoid notch.
noid (sublime tubercle). Envelopes radial head.
–– Posterior bundle. Stabilizes proximal radius throughout
Inserts on posterior aspect of greater supination/pronation.
sigmoid notch. –– Radial collateral ligament.
Secondary stabilizer with elbow flexed Blends with annular ligament.
beyond 90°. –– Lateral ulnar collateral ligament.
–– Transverse ligament (Cooper Inserts on supinator crest.
ligament). Essential stabilizer against dislocation.
No humeral attachment. Deficient in posterolateral instability.
Muscles Inserts on posterolateral olecranon and

proximal ulna.
• Flexors
• Biceps
Distal insertion at radial tuberosity. Neurovascular
Also acts as main supinator.
• Brachialis • Nerves
Inserts 11 mm distal to coronoid tip. • Musculocutaneous (lateral cord of brachial
• Brachioradialis. plexus)
• Extensors Traverses with biceps/brachialis.
• Triceps (long/lateral/medial heads) Terminates as lateral antebrachial cutane-
Inserts on the tip of olecranon. ous nerve.
• Anconeus
• Radial (posterior cord of brachial plexus) (b) Posterior approach

Spiral groove of humerus 13 cm proximal • Detach extensor mechanism (olecranon
to trochlea. osteotomy).
Lies between brachialis/brachioradialis. • Triceps splitting, triceps reflecting,
Courses longitudinal/medial to capitellum. paratricipital.
Brachialis lies between capsule and radial • Danger: ulnar nerve.
nerve at joint line. (c) Medial approach (Hotchkiss).
Divides into posterior interosseous nerve • Proximal interval
and superficial radial nerve. –– Brachialis (musculocutaneous nerve)
• Median (medial/lateral cords of brachial and triceps (radial nerve).
plexus) • Distal interval
Travels with brachial artery medial to –– Brachialis (musculocutaneous nerve)
brachialis. and pronator teres (medial nerve).
Medial to biceps tendon and brachial artery • Danger: ulnar and medial antebrachial
in antecubital fossa. cutaneous nerves.
• Ulnar (medial cord) (d) Anterolateral (Henry)
Travels posterior to medial epicondyle • Proximal
through cubital tunnel. –– Brachialis splitting proximally.
Cubital tunnel floor: medial collateral liga- • Distal interval
ment/joint capsule/olecranon. –– Pronator teres (median nerve) and
Cubital tunnel roof: arcuate (Osborne’s) brachioradialis.
ligament. • Dangers: lateral antebrachial cutaneous,
• Artery radial nerve, brachial artery.
• Brachial (e) Lateral
Divides at elbow into radial/ulnar arteries. • Kocher
Courses medial to brachialis. –– Interval
Terminates into radial/ulnar arteries. Anconeus (radial nerve) and extensor
carpi ulnaris (posterior interosseous
nerve).
Surgical Approaches –– Danger: posterior interosseous nerve
Pronation moves PIN anteriorly/
(a) Arthroscopic portals radially.
• Anterolateral portal • Kaplan
–– 1 cm Lateral to epicondyle at joint line. –– Superficial interval: extensor digito-
–– Danger: radial nerve(4.8 mm)/poste- rum communis (radial nerve) and
rior antebrachial cutaneous (12.6 mm). extensor carpi radialis longus/brevis
• Anteromedial portal (radial nerve).
–– 2 cm Distal and 2 cm anterior to medial –– Deep: splits annular ligament.
epicondyle. –– Danger: posterior interosseous nerve.
–– Danger: medial antebrachial cutaneous
(8.9 mm)/median nerve (12.9 mm)/
ulnar nerve (22.1 mm). Cases
• Posterolateral portal
–– 2 cm Proximal to olecranon at lateral Spinoglenoid Cyst
edge of triceps.
• Posterior portal A 29-year-old male who was an avid weight lifter
–– 3 cm Proximal to olecranon at mid- and football lineman has been complaining of
point between condyles. shoulder weakness, clicking, and pain. He has
–– Danger: ulnar nerve (15–25 mm). tried multiple rounds of physical therapy but con-
3 Shoulder 23
tinues to complain of vague pain and weakness MRI of the shoulder revealed paralabral
when lifting or playing football. On physical cysts in the spinoglenoid notch, mild atrophy
exam of the shoulder, the patient has decreased of the infraspinatus, and a posterior-inferior
external rotation strength compared to the oppo- labral tear.
site site and has a positive O’Brien’s exam.
Due to continued pain and inability to play at

a competitive level, surgical intervention was rec-
ommended. The cyst was decompressed and the
labrum was repaired arthroscopically.
ubscapularis Tear, Subluxation Long

S
Head of Biceps
A 37-year-old male presents to your clinic with a

3-month history of shoulder pain, clicking, and
weakness after a volleyball injury. On physical
exam of the shoulder, he has weakness on inter-
nal rotation and a palpable click with arm abduc-
tion and external rotation. This weakness has
persisted despite multiple rounds of physical
therapy. Due to persistent pain and weakness, the
An MRI of the shoulder revealed a subscapu- bicipital groove was deepened and the subscapu-
laris tear with subluxation of the long head of the laris was repaired.
biceps.
Medial UCL Injury rehabbed but at the beginning of the next season,
the patient heard a pop while attempting to pitch
21-Year-old right-hand-dominant collegiate and was subsequently unable to continue. On
pitcher with right-elbow pain and inability to physical exam, there was tenderness to palpation
pitch: One year previously the patient had pain over the medial epicondyle and laxity to valgus
and difficulty pitching. He underwent elbow compared to the contralateral side.
arthroscopy and ulnar nerve transposition but no MRI of the elbow revealed an ulnar collateral
ligament tear was identified. Patient then ligament tear.
T1 coronal MRI arthrogram elbow images arm. On physical exam, the patient had no open
reveal complete rupture of medial ulnar collateral wounds with isolated tenderness about the lat-
ligament at insertion. eral aspect of the elbow. Forearm supination/
Due to pain, instability, and inability to pitch, pronation was limited secondary to pain
surgical intervention was recommended. Using a (20°/15°, respectively).
palmaris longus autograft the ulnar collateral X-rays revealed a mildly displaced radial head
ligament was reconstructed. fracture.
Radial Head Fracture
38-Year-old left-hand-dominant female pre-

sented to the ED with left-elbow pain, swelling,
and decreased ROM after fall on outstretched
3 Shoulder 25
The elbow was aspirated and injected with Using the Kocher approach, the radial head
local anesthetic with minimal improvement in was exposed. ORIF was performed with care-
range of motion. ful consideration to place the hardware in the
Due to the mechanical block of motion, safe zone.
surgical intervention was recommended.
3 months postoperatively the patient had no

pain and full return of supination (90°) and pro-
nation (80°).
Safe Zone What is the main blood supply to the humeral

head?
90–110° arc of non-articular radial head mea-
sured from Lister’s tubercle to radial styloid with (a) Anterior humeral circumflex artery.
arm in neutral. (b) Axillary artery.
(c) Profunda brachii artery.
(d) Posterior humeral circumflex artery.
(e) Thoracoacromial artery.
What structure is responsible for superoante-

rior restraint of the shoulder when there are rota-
tor cuff deficiencies?
(a) Superior glenohumeral ligament.

(b) Middle glenohumeral ligament.
(c) Inferior glenohumeral ligament.
(d) Coracoacromial ligament.
(e) Labrum.
What artery runs with the coracoacromial

ligament?
(a) Anterior humeral circumflex artery.

(b) Acromial branch of thoracoacromial
artery.
(c) Profunda brachii artery.
(d) Posterior humeral circumflex artery.
(e) Deltoid branch of thoracoacromial artery.
Compression at the suprascapular notch would

cause atrophy of which muscles?
Questions
(a) Supraspinatus
The superior glenohumeral ligament is the (b) Infraspinatus
main shoulder constraint when the humeral (c) Teres minor
head and arm are in which of the following (d) Subscapularis
positions? (e) a and b
(f) c and d
(a) Anterior translation, arm in 90° of abduction (g) All of the above
and IR.
(b) Inferior translation, arm in 45° of abduction What structure is responsible for anterior
and IR. restraint of the shoulder at 45° of abduction and
(c) Inferior translation, arm in 90° of abduction external rotation?
and neutral rotation.
(d) Posterior translation, arm in 90° of abduction (a) Superior glenohumeral ligament.
and IR. (b) Middle glenohumeral ligament.
(e) Inferior translation, arm in 5° od adduction (c) Anterior band of the inferior glenohumeral
and neutral rotation. ligament.
3 Shoulder 27
(d) Posterior band of the inferior glenohumeral Where does the anterior bundle of the medial
ligament. collateral ligament insert?

(e) Superior band of inferior glenohumeral
ligament. (a) Radial tuberosity
(b) Sigmoid notch
Os acromiale is usually seen between which (c) Anteromedial process of coronoid
two ossification centers? (d) Capitellum
(a) Basi and meso What repair/fixation of what structure is key

(b) Meso and meta to providing rotatory stability after posterolateral
(c) Meta and pre elbow dislocation with radial head and coronoid
(d) Basi and pre fracture?
(e) Basi and meta
(a) Coronoid fracture.
Damage to the axillary nerve would affect (b) Lateral collateral ligament.
which shoulder motions? (c) Anterior bundle of medial collateral
ligament.
(a) External rotation (d) Radial head fracture.
(b) Internal rotation
(c) Abduction What muscle lies between the radial nerve
(d) Adduction and the proximal aspect of the elbow joint
(e) a and b capsule?
(f) a and c
(g) b and c (a) Brachialis
(b) Biceps brachii
What structure is responsible for posterior (c) Supinator
restraint of the shoulder at 90° of abduction and (d) Flexor carpi ulnaris
external rotation?
What elbow structure is the primary stabilizer
(a) Superior glenohumeral ligament. to resist valgus stress at the elbow at mid arc
(b) Middle glenohumeral ligament. flexion?
(c) Anterior band of the inferior glenohumeral
ligament. (a) Posterior bundle of medial collateral
(d) Posterior band of the inferior glenohumeral ligament.
ligament. (b) Lateral ulnar collateral ligament.

(e) Superior band of inferior glenohumeral (c) Coronoid.
ligament. (d) Anterior bundle of medial collateral
ligament.
Compression at the spinoglenoid notch would
cause atrophy of which muscles? In evaluating placement of fixation for a
radial head fracture, you must consider the
(a) Supraspinatus placement of hardware to prevent impingement
(b) Infraspinatus with the ulna articulation. A 90° arc of motion
(c) Teres minor between these two structural landmarks is con-
(d) Subscapularis sidered safe:
(e) a and b
(f) c and d (a) Radial styloid and biceps tuberosity.
(g) All of the above (b) Lister’s tubercle and radial styloid.
(c) Radial styloid and lateral epicondyle. (a) Extensor digitorum communis (radial nerve)
(d) Lister’s tubercle and biceps tuberosity. and anconeus (posterior interosseous
nerve).
When performing open reduction/internal fix- (b) Anconeus (posterior interosseous nerve) and
ation of a displaced radial head fracture through a extensor carpi ulnaris (radial nerve).
Kocher approach, the arm should be held in what (c) Extensor digitorum communis (radial nerve)
position in an effort to protect the posterior inter- and extensor carpi radialis longus (radial
osseous nerve? nerve).
(d) Anconeus (radial nerve) and extensor carpi
(a) Supination ulnaris (posterior interosseous nerve).
(b) Flexion
(c) Pronation
(d) Extension
References
A 16-year-old male presents to your office
with persistent elbow pain and complains of 1. Adams JE, King GJW, Steinmann SP, Cohen
MS. Elbow arthroscopy: indications, techniques,
instability. On exam, you find a positive lateral outcomes, and complications. J Am Acad Orthop
pivot shift test. What ligament is most likely Surg. 2014;22:810–8. https://doi.org/10.5435/
incompetent? JAAOS-22-12-810
2. Alcid JG, Ahmad CS, Lee TQ. Elbow anatomy
and structural biomechanics. Clin Sports Med.
(a) Lateral ulnar collateral ligament. 2004;23(4):503–17, vii. https://doi.org/10.1016/j.
(b) Anterior medial bundle of the medial collat- csm.2004.06.008.
eral ligament. 3. Bekler H, Riansuwan K, Vroemen JC, Vroeman JC,
(c) Annular ligament. McKean J, Wolfe VM, et al. Innervation of the elbow
joint and surgical perspectives of denervation: a cadav-
(d) Cooper ligament. eric anatomic study. J Hand Surg. 2008;33(5):740–5.
https://doi.org/10.1016/j.jhsa.2008.01.029.
The ulnar nerve cross the elbow through the 4. Bruce JR, Andrews JR. Ulnar collateral ligament
cubital tunnel. Which of the following structures injuries in the throwing athlete. J Am Acad Orthop
Surg. 2014;22:315–25. https://doi.org/10.5435/
does not comprise part of the cubital tunnel floor? JAAOS-22-05-315.
5. Bryce CD, Armstrong AD. Anatomy and bio-
(a) Medial collateral ligament mechanics of the elbow. Orthop Clin North Am.
(b) Joint capsule 2008;39(2):141–54, v. https://doi.org/10.1016/j.
ocl.2007.12.001.
(c) Osborne’s ligament 6. Caputo AE, Mazzocca AD, Santoro VM. The non-
(d) Olecranon articulating portion of the radial head: anatomic and
clinical correlations for internal fixation. J Hand
At what degree of flexion is the elbow capsule Surg. 1998;23(6):1082–90. https://doi.org/10.1016/
S0363-5023(98)80020-8.
maximally distended? 7. Cheung EV, Steinmann SP. Surgical approaches to the
elbow. J Am Acad Orthop Surg. 2009;17:325–33.
(a) 0° 8. Cohen MS, Bruno RJ. Collateral ligaments of the
(b) 135° elbow: anatomy and clinical correlation. Clin Orthop
Relat Res. 2001;383:123–30.
(c) 75° 9. Elhassan B, Steinmann SP. Entrapment neuropa-
(d) 25° thy of the ulnar nerve. J Am Acad Orthop Surg.
2007;15:672–81.
When fixing a radial head fracture, a Kocher 10. Hughes M. Glenohumeral joint anatomy, stabi-

lizer and biomechanics. www.orthobullets.com
approach is often performed. What is the interval Published in 2012 and updated on December 18th,
for this approach? 2014.
3 Shoulder 29
11. Lieberman JR. AAOS comprehensive orthopaedic

16. Paxton ES, Backus J, Keener J, Brophy RH. Shoulder
review; 2013. arthroscopy: basic principles of positioning, anes-
12. Mathew PK, Athwal GS. Terrible triad injury of the thesia and portal anatomy. J Am Acad Orthop Surg.
elbow. J Am Acad Orthop Surg. 2009;17:137–51. 2013;21:333–42.
13. Miyasaka KC. Anatomy of the elbow. Orthop Clin 17. Rockwood CA, et al. The shoulder. Pennsylvania, PA:
N Am. 1999;30(1):1–13. https://doi.org/10.1016/ Elsevier; 2004.
S0030-5898(05)70057-2. 18. Smith GR, Hotchkiss RN. Radial head and neck
14. Nicholson GP, et al. Orthopaedic knowledge update: fractures: anatomic guidelines for proper place-
shoulder and elbow 4; 2013. ment of internal fixation. J Shoulder Elb Surg.
15. Omid R, Hamid N, Keener JD, Galatz LM,
1996;5:113–7.
Yamaguchi K. Relation of the radial nerve to 19.
Sokolowski MJ. Orthopedic surgery review.
the anterior capsule of the elbow: anatomy New York, NY: Thieme Medical Publishers; 2009.
with correlation to arthroscopy. Arthroscopy. 20. Thompson JC. Netter’s concise orthopedic anatomy.
2012;28(12):1800–18004. Philadelphia, PA: Elsevier; 2010.
Knee
4
Nikolaos K. Paschos and Chadwick C. Prodromos
Anatomy and Biomechanics In the knee joint, two cruciate ligaments, i.e.,

the anterior and the posterior ligament, help to
The knee joint represents a classic diarthrodial ensure further stability at the joint. Both cruciate
joint that has hyaline articular cartilage, synovial ligaments contribute mainly regarding the antero-
membrane, and intra-articular ligaments. The posterior instability, and less in tibial rotation.
knee joint is composed of two separate articu- Two extra-articular ligaments, i.e., the medial
lated surfaces, i.e., the tibiofemoral and patello- and lateral collateral ligaments, mainly assist in
femoral joints. varus/valgus stability.
The knee is composed of three bones, the The knee joint is often described as a simple
femur, the tibia, and the patella. In older reports, hinge joint, but it seems that its movement is
the fibula was considered to contribute to the more complex. As the knee flexes, a slight poste-
anatomy of the knee. rior sliding of the femur in relation to the tibia
There are two menisci located within the knee occurs, which places posteriorly the center of
joint. Their roles are: femoral rotation. Further, at the end of knee
extension, the tibia automatically performs an
• To deepen the concavity of the tibial articular external rotation, as part of the bony discrepancy
surfaces. between the femur and the tibia plateau. This
• To evenly distribute the load of the body and phenomenon is known as the screw home
therefore to protect the articular cartilage for mechanism.
degeneration and wear.
• To assist in knee rotation.
Knee Arthroscopy
Most commonly used anterior portals:
N. K. Paschos (*) • Anterolateral.

Division of Sports Medicine, Department of • Anteromedial.
Orthopedic Surgery, Boston Children’s Hospital,
• Suprapatellar.
Harvard Medical School, Boston, MA, USA
e-mail: Nikolaos.Paschos@childrens.harvard.edu • Posteromedial.
• The 30° arthroscope is most commonly used,
C. C. Prodromos
Illinois Sports Medicine and Orthopaedic Center, and the 70° scope is used for special
Glenview, IL, USA circumstances.

32 N. K. Paschos and C. C. Prodromos
Complications of knee arthroscopy are rare. Posteromedial Approach

However, due to the increasing number of
arthroscopic procedures conducted, the number • Used for the posterior horn of the medial menis-
of patients affected is not insignificant. These can cus and other posterior structures of the knee
be vascular or neurologic. Mechanisms of nerve joint (capsule, medial collateral ligament).
injury are considered: • Risk of vascular structure compromise.
• Direct injury.
• Lesion due to compartment syndrome or tour- Less Favored Approaches
niquet application.
• Complex regional pain syndrome. • Y-shaped approach (Mercedes-Benz star)
–– Despite good exposure, significant wound-
healing problems led to abandonment of
Surgical Approaches this approach in everyday practice.
• Posterior approach
Medial Parapatellar –– Due to the proximity to neurovascular
structures and accessibility of the posterior
• The most common surgical approach to the structures with knee arthroscopy, this
knee. approach is rarely used today for deep
• Allows adequate visualization of the knee structure.
joint. –– A transverse accessory approach in the
• It is relatively safe. popliteal fossa is however very useful in
• It can easily be expanded both distally and the harvest of hamstring tendons for ante-
medially. rior cruciate ligament reconstruction.
–– Risk for injury to the infrapatellar branch
of the saphenous nerve.
–– Risk of significant detachment of the patel- Recent Developments/Publications
lar ligament. in the Field
Due to the fact that most aspects of knee anatomy

Midline Approach are already known and published, a literature
search through the recently published studies
• The skin incision is conducted at the midline about knee anatomy revealed most interesting
over the patella and the tibia. findings.
• The arthrotomy is performed as described in It is controversial whether the anterolateral
the medial parapatellar approach. ligament (ALL) of the knee represents a distinct
• Safer for the saphenous nerve branch: structure; however, it is described in recent ana-
–– Associated with increased risk of wound tomic studies. It has been proven that it contrib-
healing complications. utes to tibial rotation stability. The anterolateral
ligament seems to play a major role in the patho-
genesis of Segond fracture as a result of the
Lateral Parapatellar Approach location of its attachment. Reconstruction of

ALL ligament of the knee seems to provide addi-
• It is mainly used for lateral compartment tional rotational stability that might be useful for
pathology, but when combined with osteotomy revision ACL reconstruction [1–5].
of the tibial tubercle it can be used for TKA. The anatomy of the proximal tibiofibular joint
• Main disadvantages are the long incision and and its implication in below-knee amputations
the healing at the osteotomy site. has been further studied [6, 7].
4 Knee 33
An increased interest in the ACL shape, mid- –– Unilateral versus bilateral.

substance cross section area, and attachment Bilateral is most probably a good sign ☺:
appearance is expressed with potential implica- –– Pain characteristics or associations.
tion in the future of ACL reconstruction [8–12]. Ask about night pain, relief with
Regarding knee anatomy and arthroplasty, a NSAIDs, or other characteristics of
great amount of variability regarding distal femo- tumor pain :
ral anatomic characteristics has been shown in a –– Presence of systemic symptoms.
retrospective evaluation of more than 13,000 CT Always ask everything to exclude most
scans of the knee and in a more detailed mapping serious non-orthopedic conditions (leu-
of distal femoral anatomy using MRI [13, 14]. kemia, systematic infectious diseases,
Furthermore, certain differences due to patient etc.) .
characteristics seem to also need to be considered • What is the next step? What imaging or lab
in implant design [15]. Even though this is com- tests would be useful?
mon knowledge among orthopedic surgeons, the –– X-ray.
recording of the amount of variability and its Simple, cheap, always think first!
potential implications in TKA design and perfor- –– CBC.
mance that can affect implant positioning and Exclusion of systemic disorders, etc., but
knee axes, and consequently TKA survivorship, not routinely indicated unless there is some
could influence joint arthroplasty techniques in clinical suspicion.
the near future [13, 14].
Finally, also regarding knee anatomy in • Main associations to remember.
arthroplasty, more information about the surgical –– Anterior knee pain that is bilateral in a
approaches and potential complications has been child at a growth peak age—think Osgood
highlighted. The potential disruption of patellar Schlatter.
vascularization and its role in patellofemoral –– Night pain that has relief with aspirin or
complications after TKA, but also the anatomy of NSAIDs—think of osteoid osteoma.
the infrapatellar branch of the saphenous nerve, –– Night pain that affects activity and has sys-
have been evaluated [16–18]. temic features—think of neoplasm or
infection.
–– Mild recent pain that occurs after extensive
Case-Based Discussions activity—think of trauma.
–– Do not forget.
Case 1 To examine other joints (e.g., hip).
Follow-up is critical in children.
A 13-year-old boy presents at the clinic with Make parents your allies, inform, and
complaints of intermittent knee pain. involve them.
• What are the main characteristics of the pain

that should be defined from the history? Case 2
–– Pain duration
Short duration—think trauma (mostly Case Presentation
benign) ☺. A 49-year-old woman presents at the clinic with
Long duration—think chronic conditions complaints of progressively increased left-knee
that could be developmental ☺, inflamma- pain and edema for the last month. There is no
tory , or malignant . history of trauma and it is the first time that she
–– History of trauma. had symptoms from the knee joint. Remaining
Most probably a good sign, but if chronic history is unremarkable. There is associated
this is an alarm for a complex condition: stiffness at both knee joints and hands that lasts
more than an hour in the morning and it gets bet- What is the most commonly injured nerve
ter with exercise. Her mother has rheumatoid branch during the median parapatellar approach?
arthritis and coronary artery disease. On physi-
cal examination, she is afebrile. She walks with • The infrapatellar branch of the saphenous
a limp because of her pain. The left knee is nerve.
warm, and tender, with mild edema. The remain- • The suprapatellar branch of the saphenous
der of the examination is unremarkable. nerve.
Laboratory studies are normal. • The medial cutaneous branch of the saphe-
Aspiration of the knee joint yields 20 mL of fluid nous nerve.
(leukocyte count, 45,000/μL; 87% neutrophils). No • The peroneal nerve.
crystals are seen on polarized light microscopy, and • The saphenous nerve.
Gram stain is negative. Results of mucosal, blood,
and synovial fluid cultures are pending. The cartilage in the patella is:
Case Discussion • Thicker than the lateral plateau but thinner

From the history and the clinical findings, the than the medial tibial plateau.
most likely diagnosis is rheumatoid arthritis. • Thicker than both the lateral and medial
There is typical description of a case with several plateaus.
characteristics that lead to this diagnosis. • Same as the lateral and medial plateaus.
Findings favoring RA: • Thinner than both the lateral and medial
plateaus.
• Progressive knee pain and swelling.
• Thinner than the lateral plateau but thicker
• Positive family history.
than the medial tibial plateau.
• Associated stiffness >1 h.
• Local temperature, tenderness, and edema.
Which of the following is the second longest
• Leukocyte count.
bone in the body?
Findings against RA:
• Femur
• WBC shift is rather increased with high neu-
• Tibia
trophil percentage—DD with septic arthritis.
• Fibula
• Patient is older—DD with OA.
• Humerus
• The presentation of knee pain, swelling, and
• Ulna
edema at the knee joint could be characteristic
• Which of the following is correct?
of calcium pyrophosphate crystals except that
• Lateral plateau is concave and the medial is
there are no crystals in the aspirate.
convex.
• Must be differentiated from other inflamma-
• Medial plateau is concave and the lateral is
tory arthritides.
convex.
• Both medial and lateral plateaus are concave.
• Both medial and lateral plateaus are convex.
Review Questions • None of the above.
• The patella reflex is generated by:
What is the angle of the most commonly used • L3 root
knee arthroscope? • L4 root
• L5 root
• 0° • S1 root
• 30° • S2 root
• 45° • Which of the above is the most common com-
• 70° plication of arthroscopy?
4 Knee 35
• Hemarthrosis • Varus—“the opposite,” have aiR between the

• Infection legs.
• Thromboembolism • Varus—bowlegged cowboy riding a horse
• Anesthesia complications with a rifle (R-R).
• Instrument failure • Valgus—from lateral force applied!
• Which arthroscopic procedure is associated • VaLgus—the left knee forms an L (valgus has
with the highest number of complications? an L in it).
• ACL reconstruction • VaRus—looks like a parenthesis ().
• PCL reconstruction
• Lateral meniscectomy
• Medial meniscectomy References
• Loose body removal
• Which of the above statements is correct? 1. Dodds AL, Halewood C, Gupte CM, Williams A,
Amis AA. The anterolateral ligament: anatomy,
• Increased tourniquet time is associated with length changes and association with the Segond frac-
increased rate of complications. ture. Bone Joint J. 2014;96-B:325–31.
• Patients <50 year old have lower incidence of 2. Pomajzl R, Maerz T, Shams C, Guettler J, Bicos J. A
complications. review of the anterolateral ligament of the knee: cur-
rent knowledge regarding its incidence, anatomy,
• Male patients have an increased rate of biomechanics, and surgical dissection. Arthroscopy.
complications. 2015;31:583–91.
• Instrument breakage was the most common 3. Claes S, Luyckx T, Vereecke E, Bellemans J. The
complication seen. Segond fracture: a bony injury of the anterolateral
ligament of the knee. Arthroscopy. 2014;30:1475–82.
• Compartment syndrome occurs in 20% of 4. Claes S, Vereecke E, Maes M, Victor J, Verdonk P,
patients with tourniquet application. Bellemans J. Anatomy of the anterolateral ligament
• DVT prophylaxis in a patient undergoing knee of the knee. J Anat. 2013;223:321–8.
arthroscopy would be more appropriate when: 5. Herbst E, Arilla FV, Guenther D, Yacuzzi C,
Rahnemai-Azar AA, Fu FH, et al. Lateral extra-
• A 50-year-old male smoker. articular tenodesis has no effect in knees with isolated
• Tourniquet time >90 min. anterior cruciate ligament injury. Arthroscopy. 2017;
• Previous history of DVT and pulmonary 6. Asa B, Payne MW, Wilson TD, Dunning CE, Burkhart
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movement in below knee amputations. Clin Biomech
• A 40-year-old female with diabetes mellitus (Bristol, Avon). 2014;29:551–5.
type 2. 7. Burkhart TA, Asa B, Payne MW, Johnson M, Dunning
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8. Iriuchishima T, Yorifuji H, Aizawa S, Tajika Y,
ACL Attachments Murakami T, Fu FH. Evaluation of ACL mid-
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stance and fan-like extension fibres of the anterior
ing ACL tunnel placement in a late-hour surgery cruciate ligament during knee motion, with special
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Foot and Ankle Anatomy
5
Nicola Maffulli, Alessio Giai Via,
and Francesco Oliva
Bony and Joint Anatomy body. The posterolateral process is larger than

posteromedial, and may have an accessory bone
The foot and ankle are complex structures which which is called the os trigonum (Fig. 5.1). The
absolve important functions as walking, weight os trigonum may be a source of posterior ankle
bearing, shock absorption, and proprioception. impingement and pain. The superior surface of
The talus forms the ankle joint together with the the talus forms the ankle together with the distal
distal tibia and fibula. The body of the talus is tibia and fibula. The posterior surface of the dis-
wider anteriorly than posteriorly by an average tal fibula has a sulcus for the peroneal tendons,
of 4.2 mm; this is important when performing and in about 20% of individuals this surface may
the stabilization of the syndesmosis. On its lat- be flat or convex. This anatomical configuration
eral surface, the lateral process of the talus forms may have implications during the surgical repair
the articular surface of the distal fibula as well of peroneal tendon dislocation, even if it not rec-
as a facet with the underlying calcaneus. A pos- ognized as a risk factor [1].
terolateral process and a posteromedial process The calcaneus is the largest bone of the foot.
are present in the posterior portion of the talar Its axis is directed laterally and it forms the lat-
eral column of the foot which includes also the
cuboid and the fourth and fifth metatarsal bones.
The peroneal tubercle is placed on the lateral
N. Maffulli (*) surface and it divides the two peroneal tendons,
Department of Musculoskeletal Disorders, School of
while the upper and forepart of the medial sur-
Medicine and Surgery, University of Salerno,
Salerno, Italy face contains the sustentaculum tali (Fig.5.2). The
sustentaculum tali gives attachment to the plantar
Queen Mary University of London, Barts and the
London School of Medicine and Dentistry, Centre for calcaneonavicular ligament (the spring ligament),
Sports and Exercise Medicine, Mile End Hospital, tibiocalcaneal ligament, and medial talocalca-
London, UK neal ligament [2]. The sustentaculum is typically
e-mail: n.maffulli@qmul.ac.uk
involved in subtalar or talocalcaneal tarsal coali-
A. Giai Via tion (Fig. 5.3). The flexor hallucis longus (FHL)
Department of Orthopaedic Surgery, Sant’Anna
runs in a groove in the inferior surface of the talus.
Hospital, San Fermo della Battaglia, Como, Italy
The superior face of the calcaneus presents three
F. Oliva
articulating facets, the anterior, middle, and poste-
Department of Orthopaedic and Traumatology,
University of Rome “Tor Vergata”, School of rior facets, which articulate with the inferior sur-
Medicine, Rome, Italy face of the talus, forming the subtalar joint. The

38 N. Maffulli et al.
joint allows inversion and eversion of the foot, sits lateral and congruent to the middle facet. The
and it contributes only 10% of dorsiflexion of the posterior facet is the largest one and it is separated
ankle. The sustentaculum tali articulates with and from the others by the tarsal canal.
forms the floor of the middle facet, and the ante- The ankle is stabilized by its bony configura-
rior facet articulates with the head of the talus, and tion, the syndesmosis, the lateral ankle ligament
complex, and the deltoid ligament medially [3].
The syndesmosis provides stability for the distal
tibiofibular joint. It is stabilized by the anterior-
inferior tibiofibular ligament (AITFL), the
posterior-inferior tibiofibular ligament (PITFL),
and the interosseous ligament, which continues
with the interosseous membrane. In syndesmosis
injuries, the AITFL and the anterior deltoid liga-
ments are the first to tear. In normal condition, the
Fig. 5.3 CT scans of subtalar coalition

Fig. 5.1 Os trigonum
Fig. 5.2 3D reconstruction of the calcaneus, showing its lateral and medial surfaces and the sustentaculum tali
5 Foot and Ankle Anatomy 39
distal tibiofibular joint only widens 1 mm, while alis posterior tendon inserts on the medial surface
tears of all three ligaments result in 7.3 mm of of the navicular. Sometimes a separation of a por-
widening and an increase in external rotation by tion of the medial tuberosity gives rise to an acces-
10.2° [4]. The lateral ligamentous complex of the sory navicular bone which may be cause of medial
ankle consists of the anterior talofibular ligament foot pain and swelling when injured (Fig. 5.4).
(ATFL), the calcaneofibular ligament (CFL), and The cuboid extends from the calcaneus to the
the posterior talofibular ligament (PTFL). The lat- bases of the fourth and fifth metatarsal bones. The
eral talocalcaneal ligament (LTCL) may or may not peroneus longus tendon crosses curves along the
be present. When present, it limits subtalar motion lateral surface of the cuboid; it crosses its inferior
[5]. The ATFL is the primary restraint to ankle surface and inserts on the base of the first metatar-
inversion [6]. It is often described as a thickening sal. The three cuneiforms contribute to the trans-
of the lateral joint capsule. When the foot is plantar verse arch of the foot. The talus, the calcaneus, and
flexed, the ATFL is vertical, and is the primary sta- the navicular bones form a particular joint called
bilizing structure of the ankle during an inversion “coxa pedis” [9]. The “coxa pedis” is an enarthro-
stress. The CFL is a round, cord-like extracapsu- sis in which it is possible to recognize an epiph-
lar structure that originates from the inferior distal ysis represented by the head and the neck of the
surface of the fibula, extends posteroinferiorly deep talus and an acetabulum which is formed by the
to the peroneal tendons, and attaches on a small posterior articular surface of the navicular and the
tubercle on the posterior aspect of the lateral cal- calcaneal surfaces, in particular the anterior and
caneal surface. The CFL is vertical when the foot middle facets (the sustentaculum tali). The acetab-
is dorsiflexed, when it becomes the primary ankle ulum is completed by a glenoid structure which
stabilizer and secondary subtalar joint stabilizer. is reinforced by the spring ligament. The spring
The PTFL is the strongest of the three ligaments.
It is a trapezoid-shaped structure, which originates
from the distal portion of the digital fossa of the
fibula and inserts on the posterolateral tubercle of
the talus, and on the os trigonum when present.
Strain to the ATFL increases progressively as the
ankle moves into plantar flexion and inversion. The
ATFL is the weakest of the three lateral ligaments,
and it is most frequently injured in ankle sprains,
while the CFL is involved in 50–75% of such inju-
ries; the PTFL is injured in less than 10% of cases
unless complete dislocation occurs [7].
The deltoid ligament extends from the medial
malleolus to the medial aspect of the talus. It is
formed by a strong deep layer which contributes
most to stability, and a superficial layer [8]. The
superficial component of the deltoid ligament
extends to the talar neck and the body of the navic-
ular bone, and contributes to the spring ligament.
The deltoid ligament complex is also covered by
the anterior tibial tendon, the posterior tibial ten-
don, and the flexor digitorum longus tendon.
The midfoot is formed by bones, joints, liga-
ments, and tendons which are structured in a com-
plex relationship that provide static and dynamic
stability. The navicular articulates with the head of
the talus and the three cuneiform bones. The tibi- Fig. 5.4 X-ray showing accessory navicular bone
ligament is a reinforcing fascicle of the talo-cal- column (Fig. 5.5). Ligaments are absent between
caneonavicular joint capsule. It begins at the base the medial and middle cuneiforms and the bases of
of the anteromedial outline of the sustentaculum the first and second metatarsal. Dynamic support
tali and inserts distally to the medial tubercle and to the midfoot is provided by tendons. The tibialis
to the corresponding posteroinferior surface of the posterior and the peroneus longus tendons both act
navicular. As a reinforcing fascicle, it is not a well- to preserve the longitudinal and transverse arches.
individualized anatomic formation, and is there- The tibialis anterior tendon, which inserts into the
fore only artificially dissociable by the capsular dorsomedial aspect of the first metatarsal base and
apparatus. The spring ligament is also reinforced the medial cuneiform, adds medial column support.
by the intermediate fibers of the deltoid ligament They work in conjunction with the intrinsic muscles
and the recurrent navicular fascicle of the tibial and the plantar fascia to further support the arches
posterior tendon. A proprioceptive function of the of the midfoot. Sports-related Lisfranc injuries
spring ligament has also been postulated given the are uncommon, and can be misdiagnosed in up
presence of proprioceptive corpuscles. The calca- to 20% of cases unless a high index of suspicion
neonavicular ligament or Chopart ligament rein- is not present, and they can become very serious
forces the inferior surface of the acetabulum. The and disabling conditions for athletes. Patients
coxa pedis is a fundamental structure because it
ensures the stability of the lower limb during the
load-bearing phase (closed kinetics chain) and,
with its rotational mechanism, the succession of
intercurrent mechanism in the frontal plane (lat-
eral translation of the load in starting load-bearing
phase) and in the sagittal plane (oscillating phase).
The tarsal joint formed by the talonavicular
and calcaneocuboid joints is also called Chopart’s
joint in honor of the French surgeon François
Chopart (1743–1795) by one of his students.
The Lisfranc joint is the tarsometatarsal joint,
which is a specialized bony and ligamentous struc-
ture, providing stability to the midfoot. The osse-
ous geometry between the cuneiforms, the cuboid,
and the metatarsals bones, as well as the capsulo-
ligamentous structures, is essential to the stability of
the Lisfranc joint and the maintenance of both the
transverse and longitudinal arches of the foot [10].
The five metatarsal bases form a “Roman arch”
configuration in the axial plane. The base of the
second metatarsal is the “keystone” recessed in a
mortise between the medial and lateral cuneiforms.
Plantar and dorsal ligaments cross the Lisfranc joint
and transverse ligaments connect the metatarsal
bases [11, 12]. The plantar ligaments are stronger
and larger than the dorsal ones. It may explain the
dorsal direction of dislocations. The Lisfranc liga-
ment is the largest and strongest of the interosseous
ligaments (1 cm in length and 0.5 cm in width) [13].
It is located plantarly between the medial cuneiform
and the base of the second metatarsal and acts as
an additional plantar reinforcement for the medial Fig. 5.5 MRI imaging of the Lisfranc ligament
usually present with midfoot pain, swelling, and often underestimate the injury, but the history of
pain or inability to bear weight. Passive dorsiflex- the mechanism of injury provides important clues.
ion and abduction of the forefoot may also produce The forefoot is formed by the metatarsal
pain. Classic findings include forefoot and midfoot bones and the phalanges. The first ray contains
edema, and plantar arch ecchymosis (Fig. 5.6). The only two phalanges. The flexor hallucis longus
“piano key test” is pathognomonic for Lisfranc and the extensor hallucis longus tendons insert on
injury (Fig. 5.7). The examiner moves the first and the distal phalanx. The other rays contain three
second metatarsals into plantar flexion/dorsiflexion phalanges with the proximal and middle pha-
and abduction/adduction, and subluxation or dis- langes acting as the insertion point for the short
comfort with this test suggests tarsometatarsal joint flexors, the interossei muscles, as well as the
injury. Low-energy injuries for which the index of lumbrical muscles. The second metatarsal is usu-
suspicion may be lower and the signs more sub- ally the longest one. The base of the fifth meta-
tle may be even more difficult to detect. In these tarsal contains a styloid process which allows the
cases, patients may refer inability and pain to bear insertion of the peroneus brevis tendon. The first
weight on the tiptoes. Furthermore, the diagnosis metatarsophalangeal joint capsule is reinforced
is not made easier by the athletes themselves, who by a fibrocartilaginous plate, which is formed by
the flexor hallucis, adductor hallucis, abductor
hallucis tendons, and deep transverse metatarsal
ligament (Fig. 5.8). The sesamoid bones are con-
tained within the fibrocartilaginous plate. The
Fig. 5.6 Plantar arch ecchymosis secondary to a Lisfranc

injury
4
6
5
2
Fig. 5.7 The “piano key test.” The test is positive if Fig. 5.8 Plantar plate of the first metatarsophalangeal
patient refers pain while the examiner moves the first and joint. (1) Abductor hallucis. (2) Flexor brevis hallucis. (3)
second metatarsals into plantar flexion/dorsiflexion and Flexor longus hallucis. (4) Deep transverse intermetatar-
abduction/adduction, or if a subluxation is perceived sal ligament. (5) Adductor hallucis. (6) Sesamoid bones
“turf toe” is an injury of the plantar capsule liga- The Achilles tendon is the thickest and the
ments which may occur in athletes. strongest tendon in the human body with a
tensile strength of 50–100 N/mm [15]. About
15 cm long, it originates in the midcalf and
Muscle and Tendon Anatomy extends distally to insert into the posterior
surface of the calcaneus. It is formed from the
The anterior ankle is crossed by the tibialis ante- joining of the two tendons of soleus (dorsally)
rior medially, the extensor hallucis longus, the and gastrocnemius (ventrally). Its insertion is
extensor digitorum longus, and the peroneus ter- crescent shaped, with the medial side exhibit-
tius, which is present in the 90% of people. The ing more extensive tendon substance, probably
tibialis anterior tendon inserts onto the medial from the contribution of the plantaris tendon. A
cuneiform and the first metatarsal base. The bursa is typically formed in the retrocalcaneal
extensor digitorum longus divides just proximal area. Achilles tendinopathy is a common cause
to the superior extensor of the retinaculum, and of disability, which occurs both in athletic and
again under the inferior retinaculum to form the sedentary people. It is a pathological condi-
tendons for the lesser toes. tion characterized by both pain and pathologic
The lateral portion of the ankle and foot con- changes in and around the tendon, and its inci-
tains the two peroneal tendons and the muscle dence has risen in the last few decades. The
belly of the extensor digitorum brevis. The pero- etiopathogenesis remains unclear. It is cur-
neal tendons share a common tendon sheath rently considered multifactorial and the inter-
proximal to the distal tip of the fibula with the action between intrinsic and extrinsic factors
peroneus brevis medial and anterior to the per- is crucial for the development of the pathology
oneus longus [14]. More distally, each tendon [16]. However, the precise role that each predis-
lies in its own sheath. The common sheath is posing factor plays has still to be understood.
contained within a sulcus, the fibular groove, on Changes in training pattern, poor technique,
the posterolateral aspect of the fibula, prevent- previous injuries, footwear, and environmental
ing subluxation. The primary restraint to ten- factors, such as training on hard, slippery, or
don subluxation is the peroneal retinacula. The slanting surfaces, are extrinsic factors that may
superior peroneal retinaculum originates on the predispose the athlete to Achilles tendinopathy
posterolateral aspect of the fibula and inserts onto (Table 5.1). Dysfunction of the gastrocnemius
the lateral surface of the calcaneus. The inferior soleus, age, body weight and height, pes cavus,
peroneal retinaculum is attached to the peroneal marked forefoot varus, and lateral instability
trochlea and calcaneus above and below the pero- of the ankle have also been recognized as pos-
neal tendons. Acute dislocation of the peroneal sible risk factors [17]. Currently, many stud-
tendons is uncommon, and often misdiagnosed ies emphasize the importance of extracellular
as an ankle sprain. However, recurrent or chronic
dislocation may occur when the acute injury is
Table 5.1 Risk factors for tendinopathy
misdiagnosed or not adequately managed.
The medial aspect of the ankle contains the Extrinsic risk
factors Intrinsic risk factors
flexor tendons. The tibialis posterior runs behind
Training errors Malalignment (i.e., flatfoot,
the medial malleolus in its own sheath. The flexor femoral neck anteversion, varus/
digitorum longus and the flexor hallucis longus valgus knee)
(FHL) cross run posteriorly to the tibialis poste- Training surfaces Limb-length discrepancy
rior tendons. The FHL runs though the posterior Footwear and Muscular imbalance
grove in the talus formed by the posteromedial equipment
Environmental Muscular insufficiency
and posterolateral process and it continues under
conditions
the sustentaculum tali. This fibro-osseous tunnel Metabolic disorders
also contains the tibial nerve and accompanies Hormonal diseases
the posterior tibial artery. Genetics
matrix (ECM) for the homeostasis of connec- arch with attachments on the cuneiform, and
tive tissue, and its physiologic and pathologic inserts distally on the lateral sesamoid.
modifications seem to be the most important
intrinsic factors involved in tendinopathies
and tendon ruptures. The turnover of ECM in Vascular and Nervous Anatomy
normal tendon is mediated by matrix metallo-
proteinases (MMPs) [18, 19]. And the increase The posterior tibial, anterior tibial, and peroneal
of MMP-1 and the reduction of MMP-3 and arteries provide the vascular supply to the foot.
MMP3 may be responsible for modification The anterior tibial artery runs between the two
of the tendon’s ECM [16]. Metabolic diseases malleoli. Above the ankle joint, it lies between
also seem to play a role. The role of hormonal the extensor hallucis longus and the tibialis ante-
and metabolic diseases in the pathogenesis rior tendons. The dorsalis pedis artery originates
of tendinopathy, such as diabetes mellitus, from the anterior tibial artery. The posterior tibial
hypercholesterolemia, and obesity, has been artery lies between the FHL and the flexor digi-
recently investigated [20, 21]. A recent study torum longus tendons. When it enters the plantar
detected the presence thyroid hormones’ aspect of the foot, it divides into the lateral and
nuclear receptors on the tenocyte membrane, medial plantar arteries.
and that, in vitro, thyroid hormones enhance The ankle is crossed by five major nerves, the
tenocyte growth and counteract apoptosis tibial nerve, the deep and the superficial peroneal
in a dose- and time-dependent manner [22]. nerves, and the sural and the saphenous nerves.
Some clinical observational studies showed Four of them are the terminal branches of the sci-
that the incidence of tendinopathy on tendon atic nerve (deep and superficial peroneal, tibial,
rupture is higher in patients with diabetes mel- and sural nerves), while the saphenous nerve is
litus. A possible reason is the development of the cutaneous branch of the femoral nerve. Two
advanced glycation end products (AGEs) in nerves, the posterior tibial and deep peroneal
ECM of tendons. Protein glycation is a spon- nerves, are deep to the fascia, while the saphe-
taneous reaction that occurs in the presence of nous, sural, and superficial peroneal nerves are
glucose, and it is directly proportional to the superficial. This is important for success of the
blood level of glucose. Glycated proteins can nerve blocks because the two deep nerves are
produce further reactions developing protein anesthetized by injecting local anesthetic under
cross-linking. Collagen proteins are particu- the fascia, whereas the three superficial nerves
larly susceptible to AGE formation, because are anesthetized by a simple subcutaneous injec-
of their long half-life, and this process may be tion of local anesthetic.
involved in physiopathology of tendinopathy At the ankle level, the deep peroneal nerve lies
[23]. A recent animal study showed that AGE- anterior to the tibia and the interosseous mem-
related collagen cross-links alter biologic and brane, and close to the anterior tibial artery. It is
mechanical properties of tendons and it may located immediately lateral to the extensor hallu-
predispose Achilles tendon to degeneration and cis longus tendon. The pulse of the anterior tibial
rupture [24]. artery (dorsalis pedis) can be felt at this location.
The midfoot contains also different muscle The nerve is positioned immediately lateral to the
bellies which originate on the plantar aspect artery. At this point, it divides into two terminal
of the calcaneus and interact with the extrin- branches for the foot, the medial and the lateral,
sic flexor muscles. The most superficial is the which provide innervation to the space between
flexor digitorum brevis. Just deep to this muscle the first and second toes, to the tarsometatarsal,
are the abductor hallucis medially, the abductor metatarsophalangeal, and interphalangeal joints
digiti minimi laterally, and the quadratus plan- of the lesser toes.
tae in the deep layer. The oblique head of the The superficial peroneal nerve provides inner-
adductor hallucis originates in the longitudinal vation to the dorsal skin of the foot. It divides into
two terminal cutaneous branches, the medial and injuries, and can have a devastating impact on a
the lateral dorsal cutaneous nerves. They usu- patients’ quality of life. When direct nerve repair
ally exit the crural fascia 4–5 cm above the ankle is not possible, autologous nerve transplantation is
joint, and they carry sensory innervation to the generally accepted as the clinical gold standard for
dorsum of the foot. These branches are located the reconstruction of large peripheral nerve defects
in the subcutaneous tissue and they can be easily (>3 cm) [25]. The sural nerve is the most com-
injured by the anterolateral portal during ankle mon autologous donor nerve to reconstruct severe
arthroscopy. nerve defects in both adults and children. It is also
The sural nerve accompanies the lesser saphe- a common donor site for nerve biopsies to assist
nous vein posterior to the lateral malleolus. It is a in diagnosing polyneuropathies of unclear origin.
sensory nerve which courses between the heads of Even if the donor-site comorbidities are the
the gastrocnemius muscle, and after piercing the most important long-term complications, har-
fascia covering the muscles it emerges on the lat- vest of the sural nerve was reported to be safe
eral aspect of the Achilles tendon 10–15 cm above with mild residual symptoms [26]. A sensory
the lateral malleolus. After providing lateral calca- loss at the foot in the skin around the heel is the
neal branches to the heel, the sural nerve descends most common symptom (90% of the patients).
behind the lateral malleolus, supplying the lateral However, interestingly the area of sensory loss in
malleolus, Achilles tendon, and ankle joint. The the skin decreases over time in a half of the cases.
sural nerve continues on the lateral aspect of the Mild or intermittent allodynia is also a com-
foot, innervating the skin, subcutaneous tissue, mon complication (50% of the patients), but the
fourth interosseous space, and fifth toe. majority of patients refer no or slight problems
The tibial nerve runs distally in the thick neu- from their foot, and usually few patients require
rovascular fascia and emerges at the inferior third painkillers. Cold intolerance may be present in
of the leg from beneath the soleus and gastrocne- 30% of cases, and a painful neuroma formation
mius muscles on the medial border of the Achilles has also been reported.
tendon. At the level of the medial malleolus, the
tibial nerve is covered by the superficial and deep
fasciae of the leg. It is positioned laterally and Clinical Cases
posteriorly to the posterior tibial artery and mid-
way between the posterior aspect of the medial Case 1
malleolus and the posterior aspect of the Achilles
tendon. Just beneath the malleolus, the nerve A 40-year-old man went to the emergency for
divides into lateral and medial plantar nerves. acute pain to the posterior aspect of the leg. The
The posterior tibial nerve provides cutaneous, patients told he was sprinting to catch the bus
articular, and vascular branches to the ankle joint, when he heard a snap and acute pain over the
medial malleolus, inner aspect of the heel, and heel. The patient was otherwise healthy and he
Achilles tendon. It also branches to the skin, sub- doesn’t reported any comorbidities.
cutaneous tissue, muscles, and bones of the sole. At the clinical examination a tendon gap was
The saphenous nerve is a terminal cutaneous palpable and a loss of plantar flexion strength was
branch of the femoral nerve. It runs with the long objectivable. The calf squeeze test or Thompson
saphenous vein anterior to the medial malleo- test and the flexion knee test were also posi-
lus in the subcutaneous tissue of the skin on the tive (Fig. 5.9). The X-ray of the ankle and foot
medial aspect of the ankle and foot. showed no bony fracture.
The sural nerve is a common donor site for
autologous nerve transplantation and biopsy. Question n.1
Peripheral nerve injuries usually afflict young and Which exams would you prescribe for a correct
healthy people who are most at risk of traumatic diagnosis?
Fig. 5.10 Surgical approach for minimally invasive AT

repair
vs 90.9%) [27]. According to AAOS guide-

lines for acute AT rupture there is not enough
evidence to recommend for or against the
routine use of US and MRI to confirm the
diagnosis [28]. US or MRI is useful in case of
doubt. A careful evaluation and judicious use
Fig. 5.9 The flexion knee test for Achilles tendon rup- of advanced imaging as needed are therefore
ture. This test is performed with the patient prone and the recommended [29].
ankles clear of the table. The patient is asked to actively Open surgery provides good strength to the
flex the knee to 90°. During this movement the foot on the repair, low re-rupture rates, and reliably good
affected side falls into neutral or dorsiflexion and a rup-
ture of the Achilles tendon can be diagnosed endurance and power to the gastrocnemius-
Achilles tendon complex. However, open
surgical approaches resulted in high risk of com-
1 . Ultrasound (US) of the Achilles tendon. plications, like wound breakdown and infection.
2. Magnetic resonance imaging (MRI) of the
Minimally invasive surgery has been developed
foot and ankle. to reduce this complication, and recent studies
3. CT scan of the foot and ankle. reported similar scores and functional results
4. No further imaging is needed for a precise between open and minimally invasive tech-
diagnosis. niques. Major advantages of minimally invasive
repair are less iatrogenic damage to normal tis-
Question n.2 sues, lower postoperative pain, accurate opposi-
Which treatment would you offer to this patient? tion of the tendon ends, and improved cosmetics
(Figs. 5.10 and 5.11). However management of
1. Nonsurgical treatment. acute ruptures of the AT is still controversial,
2. Open tenorrhaphy. especially for older people and in patients with
3. Minimally invasive repair. comorbidities such as diabetes or vascular dis-
eases with a higher risk of infection and wound
Correct response: n.3. complications. Recent well-conducted random-
ized controlled trials showed that conservative
Case Discussion management using functional bracing, early
The diagnosis of Achilles tendon rupture is a mobilization, and open surgery management
clinical one. Clinical examination is of pri- gave similar results with regard to re-rupture
mary importance. When three or more clini- rate, range of motion, and calf circumference.
cal tests, including Thompson test, the flexion So, mini-invasive surgery and nonoperative
knee test, a palpable defect, or others, are management are both suitable alternatives for
positive for acute ruptre of the Achilles ten- AT repair in older patients, in particular in the
don, the sensivity is higher than MRI (100% presence of comorbidities [30, 31].
Case 2
A 52-year-old woman came to consultant for

chronic bilateral foot pain. She referred 1 year
of intermittent pain and generalized fatigue of
the foot and ankle. The pain got worst in the last
few months, interfering with walking and daily
activities.
At clinical examinations a depression of the
medial longitudinal arch, valgus heel, and a
forefoot abduction (“too many finger signs”)
were detected. At the double-heel-rise test the
deformity of the hindfoot was not reducible. The
patient’s X-ray is showed in Fig. 5.12.
Question n.1
Which is the reasonable cause of pain?
1. Hallux valgus.
2. Midfoot osteoarthritis.
3. Adult acquired flexible flatfoot.
4. Adult rigid flatfoot and midfoot coalition.
Correct response: n.4
Question n.2
Which is the first management for this patient?
Fig. 5.11 Schematic figure showing the final configura- 1. Conservative management.
tion of AT minimally invasive repair
Fig. 5.12 X-ray of a 52-year-old woman with a painful flatfoot. A total talonavicular coalition is present
2 . Surgical resection of coalition. Questions

3. Arthrodesis.
1. What is the shape of the superior surface of
Correct response: n.1 the talus?
(a) Rectangular.
Question n.3 (b) Trapezoidal with a posterior wider base.
Which is the next treatment in case of failure of (c) Trapezoidal with an anterior wider
conservative management? base.
2. Which is the best imaging to evaluate a foot
1 . Resection of the coalition. coalition?
2. Subtalar arthroereisis. (a) RX
3. Arthrodesis (talonavicular). (b) CT scan
4. Realignment osteotomies. (c) MRI
5. Soft-tissue procedures (gastrocnemius reces- 3. The subtalar joint mostly contributes to:
sion, tibialis posterior tendon repair, or (a) Flexion-extension of the foot.
transfer). (b) Prono-supination of the foot.
6. Arthrodesis, realignment osteotomy, and (c) It does not contribute significantly to any
eventual soft-tissue procedures. movement of the foot.
4. Which is the most frequently involved liga-
Correct response: n.6. ment in case of a lateral ankle sprain?
(a) The anterior talofibular ligament
Case Discussion (ATFL).
Adult flatfoot is a common pathology which (b) The calcaneofibular ligament (CFL).
orthopedic surgeons have to deal with. (c) The posterior talofibular ligament (PTFL).
It may present as an incidental finding or as (d) The deltoid ligament.
a symptomatic condition with clinical conse- 5. The spring ligament is:
quences ranging from mild limitations to severe (a) A reinforcing fascicle of the talo-
disability and pain. The incidence of symptom- calcaneonavicular joint capsule.
atic flatfoot ranges from 5 to 15% of adult flatfoot (b) A constituent of the acetabulum of the
according to different authors. “coxa pedis.”
If symptoms do not improve after 3–6 months (c) It is reinforced by the fibers of the del-
of appropriate nonoperative treatment, surgery toid ligament and of the tibial posterior
should be recommended [32]. But, the adult tendon.
flatfoot is a complex disorder with a diversity (d) All these statements are correct.
of symptoms and various degrees of deformity (e) None of these statements is correct.
in any of the three cardinal planes, so rarely a 6. Which is the most important dynamic stabi-
single surgical procedure is able to solve all the lizer of the longitudinal arch of the foot?
deformities. Therefore, many different surgi- (a) The peroneus longus tendon.
cal techniques have been described including (b) The peroneus brevis tendon.
resection of the coalition, bony osteotomies, (c) The tibialis posterior tendon.
single- or multiple- joint arthrodesis, subtalar (d) The intrinsic muscles of the foot and the
arthroereisis, primary repair or posterior tibial plantar fascia.
tendon transfer, gastrocnemius muscle reces- 7. Which are the most typical signs off a
sion, or Achilles tendon lengthening, and sev- Lisfranc injury?
eral of these procedures are often performed at (a) Forefoot and midfoot edema.
the same surgical setting [33]. (b) Plantar arch ecchymosis.
(c) Positive “piano key test.” 8. McMinn RMH. Last’s anatomy regional and applied.
9th ed. Edinburgh: Churchill Livingstone; 1994.
(d) None of these signs is typical for
p. 265.
Lisfranc injury. 9. Pisani G. The coxa pedis. Foot Ankle Surg.
(e) All these signs are typical for Lisfranc 1994;1:67–74.
injury. 10. Peicha G, Labovitz J, Seibert FJ, et al. The anatomy
of the joint as a risk factor for Lisfranc dislocation
8. Sports-related Lisfranc injuries are: and fracture-dislocation. An anatomical and radio-
(a) Common sports injuries. logical case control study. J Bone Joint Surg Br.
(b) They are easy to diagnose due to their 2002;84:981–5.
clinical presentation. 11. Eleftheriou K, Rosenfeld PF. Lisfranc injury in the
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21. Oliva F, Via AG, Maffulli N. Physiopathology of intra-
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Part II
Musculoskeletal System Physiology
Bone Tissue Physiology
6
Ann Marie Kelly, Nikolaos K. Paschos,
Dimitrios Giotis, and John D. Kelly IV
Function Bone Composition

(Cells and Matrix)
• Structural support for body and protection of
internal organs. Bone Cell Types
• Provision of levers for muscles, allowing for
movement. Osteoclasts
• Storage of minerals/lipids and regulation of • Digest bone, break down bone tissue via bone
mineral homeostasis and pH balance. resorption.
• Production of blood cells. • Originate from macrophage cell line.
• Multinucleated, large cells.
The adult human body contains 206 bones. • Howship’s lacunae presence indicates bone
Bones undergo constant remodeling, adapting reabsorption.
to changes in biomechanical forces and maintain- • Activity regulated by osteoblasts via RANKL,
ing bone strength by removing/replacing old and IL-1.
damaged bone.
Approximately 20% of the adult skeleton is echanism of Bone Resorption
M
replaced per year. • Osteoclasts secrete acid phosphatase and
cathepsin K to aid in absorption.
• Bisphosphonates inhibit acid production [1].
A. M. Kelly (*) · J. D. Kelly IV • Resorption typically stimulated by RANKL
Pennsylvania, Philadelphia, PA, USA and by PTH amidst metastatic disease.
N. K. Paschos
Department of Orthopedic Surgery, University of Osteoblasts
Pennsylvania, Philadelphia, PA, USA • Form bone via synthesis of osteoid
Division of Sports Medicine, Department of –– Regulate osteoclast function.
Orthopaedic Surgery, Boston Children’s Hospital, • Manufactures type I collagen, alkaline phos-
Harvard Medical School, Boston, MA, USA phatase, bone sialoprotein, and RANKL.
e-mail: Nikolaos.Paschos@childrens.harvard.edu • Contains receptors for estrogen, parathyroid
D. Giotis hormone, and vitamin D.
Panepistimion Ioanninon, Department of Orthopaedic

54 A. M. Kelly et al.
Osteocytes Nutrition and Metabolism

• Former osteoblasts enmeshed by newly manu-
factured matrix. Key Regulators of Bone Metabolism
• Comprise 90% of cells in fully developed
skeleton. • PTH.
• Regulate calcium, phosphorous, and extracel- • Calcitonin.
lular calcium levels to maintain bone and cel- • Hormones (including sex hormones, growth
lular matrix. hormone, and thyroid hormone).
• Connect with other cells via canaliculi. • Steroids (glucocorticosteroids and vitamin D).
• Stimulated by calcitonin, inhibited by PTH.
Bone metabolic functions are dependent upon
Osteoprogenitor Cells the homeostasis of calcium and phosphate
• Develop from mesenchymal stem cells. levels.
• Differentiate into osteoblasts in the presence
of high oxygen tension.
• Transform into cartilage under low-oxygen- Calcium
tension milieu.
• Differentiate into fibrous tissue under high • Over 99% of calcium in the body is housed in
mechanical strain. bone.
• Plays critical role in nerve conduction, clot-
ting mechanisms, and muscle cell
Bone Matrix contraction.
• Calcium is absorbed via the digestive tract and
• Forty percent dry weight is organic, 60% resorbed from bone and kidneys.
inorganic.
• Components of bone matrix:
–– Collagen (mainly type I). Phosphate
Comprises most of the organic component
of matrix. • ~85% of phosphate in the body resides in
Affords tensile strength bone.
–– Cytokine and growth factors • Reabsorbed by proximal tubule of the renal
Assist in bone cell growth, turnover, activa- system.
tion, and differentiation.
–– Proteoglycans
Inhibit mineralization. Vitamin D
Supply compressive strength.
–– Matrix proteins • 1,25(OH)2-vitamin D3 is the active version of
Enhance formation of bone and the hormone.
mineralization. • Activates osteoclasts for bone resorption,
Three types of proteins involved in bone increases serum calcium levels.
matrix:
Osteocalcin.
Osteonectin.
Osteopontin.
6 Bone Tissue Physiology 55
Parathyroid Hormone Aging/Degeneration
• Produced by chief cells. With age the mechanical and homeostatic func-
• Modulates levels of calcium in plasma. tions of bone become impaired—bone weakens
• Activates osteoblasts. as calcium stores become depleted.
• Moderates phosphate filtration of kidneys.
• Bone mass is highest between 16 and 25 years
of age.
Calcitonin • 0.3–0.5% of bone mass is lost each year after
skeletal maturity.
• Derived from clear cells of the thyroid • Bone loss rate is influenced by metabolic and
gland. structural elements.
• Lowers calcium levels in serum.
• Inhibits bone resorption of osteoclasts.
ge-Dependent Changes in Bone
A
Mechanical Behavior
Response to Trauma/Healing
• Older individuals may have as high as a ten-
• Initial response to bone trauma/fracture is a fold increased risk of fracture compared to
decrease in the rate of bone blood flow at the younger counterparts who have the same bone
site of the fracture. mineral density (BMD).
• Within a relatively short period of time (hours • Age-related bone changes include:
to days), the blood flow in the bone increases— –– Increased nonenzymatic collagen cross-links.
its highest level ~2 weeks after the trauma. –– Cortical porosity.
• Blood flow within the bone is the chief deter- –– Absolute collagen content.
minant of healing.
• Stages of fracture repair
–– Inflammation otential Causes of Bone Damage
P
Provides hematopoietic cells that can Due to Aging
secrete growth factors.
Osteoprogenitor cells, fibroblasts, and • Damage to bone mineral crystallites.
mesenchymal cells form granulation tissue • Disturbance of collagen fibrils.
around the ends of the fracture site. • Debonding at the mineral organic border.
–– Remodeling • Disruption of osteocyte integrity
Collagen formation and intramembranous –– Exponential increase in age-related micro-
ossification. damage is manifest by a rise in bone micro-
Mesenchymal stem cells differentiate into crack densities and lengths.
osteoblasts. –– Inability to repair these cracks and their
Cartilaginous callus is replaced by bone increasing prevalence with age partly
callus (endochondral ossification). explains the reduced strength of cortical
and trabecular bone.
Aging in Bone Cells –– Impaired regulation of gene expression.

–– Alterations in intracellular signaling.
• The life spans of osteoblasts, osteoclasts, and
osteocytes are restricted by the number of
finite replication cycles.
• Upon aging, bone cells are more vulnerable to: Reference
–– Mechanical deterioration.
–– Dysregulation of apoptosis. 1. Patel A. Bone cells. Orthobullets; 2013.
Ligament Tissue Pathology
7
Introduction presence of a large extracellular matrix in which

a large amount of cells are present [1, 2].
Tendons are connective structures with mostly Tenoblasts and tenocytes constitute about
parallel fiber arrangement. Tendons are inter- 90–95% of the cellular elements of tendons [1].
posed between muscles and bones and transmit Tenoblasts are immature cells that evolve into
the force generated in the muscles to bone. In this tenocytes losing part of their metabolic activity.
way they are responsible for joint movement. The Both cells produce the extracellular matrix con-
point of connection with a muscle is called a sisting of ground substance and fibers and are
myotendinous junction (MTJ), and the point of active in energy production. The remaining
connection with a bone an osteotendinous junc- 5–10% of the cells are chondrocytes at the bone
tion (OTJ). The peculiar anatomic organization interface, synovial cells of the tendon sheath, and
and metabolism are responsible for their unique vascular cells, including capillary endothelial
function. cells and smooth muscle cells of arterioles.
The ground substance in which lay tenocytes
and tenoblasts surrounds the collagen. It consists
Anatomy and Histology of proteoglycans, glycosaminoglycans (GAGs),
structural glycoproteins, and a large number of
Tendons are bright, white-in-color structures different small molecules. These macromole-
with a fibroelastic texture and a great resistance cules (proteoglycans and GAGs) have important
to mechanical loads. They may be extremely water-binding capacities that improve the biome-
variable in terms of shape and in the way they are chanical properties (elasticity) of a tendon against
attached to bone. They are formed by soft and shear and compressive forces. In addition they
fibrous connective bands characterized by the are also important for stabilization of the whole
collagenous system of connective tissue and for
maintenance of ionic homeostasis and collagen
fibrillogenesis.
S. Cerciello
Casa di Cura Villa Betania, Rome, Italy Collagen represents the predominant part of
the tendon. In fact the dry weight of a tendon rep-
Marrelli Hospital, Crotone, Italy
resents approximately 30% of the total tendon
P. Neyret (*) mass, with water accounting for the remaining
Centre Albert-Trillat, CHU Lyon Croix-Rousse,
Hospices Civils de Lyon, Lyon, France 70%. Collagen type I accounts for 65–80% and
elastin accounts for approximately 2% of the dry
University Lyon 1, Lyon, France

58 S. Cerciello and P. Neyret
mass of tendons [3–6]. Collagen mainly trans- network of connective tissue binding collagen
mits large forces between muscle and bone [7]. fibers and contaminating the vascular, lymphatic,
The parallel arrangement of tendon collagen and neural transmission routes to fibroblasts [15].
fibers resists to tension so that contractile energy This peculiar organization is responsible for the
is not lost during transmission from muscle to the viscoelastic behavior of the tendons.
bone. For this reason tendons are a slightly stron- They Tendons have high mechanical strength,
ger tissue than ligaments, and are composed of good flexibility, and elasticity [8, 16, 17] in rela-
more collagen fibers (roughly 85% vs. 70%). tion to the number and types of intramolecular
Tenocytes and tenoblasts lie between the colla- and intermolecular links [18].
gen fibers along the long axis of the tendon [8].
Collagen is organized in hierarchical levels of
increasing complexity, beginning with tropocol- Function and Metabolism
lagen (a triple-helix polypeptide chain, which
unites into fibrils). Tropocollagen fibers aggre- The major function of tendons is to transmit the
gate progressively into microfibrils and then into muscle contraction to bones, thus ensuring
units that are visible at electron microscope: the motion. To fulfill this goal they have to be highly
collagen fibrils. Bunch of collagen fibrils form a resistant to traction. Although the majority of col-
collagen fiber, which is the basic unit of a tendon lagen fibers have a longitudinal orientation, it has
and the smallest tendon unit visible using light been clearly demonstrated that they are also
microscopy. Collagen fibers are mainly aligned arranged transversely and horizontally, with the
to reach both tendon ends [9] and are surrounded longitudinal fibrils also crossing each other [19].
by a sheath of connective tissue called endotenon. This complex architecture, which is variable
Endotenon binds fibers together to create a pri- between different tendons and within the same
mary fiber bundle (subfascicle) [10, 11]. Several tendon, provides good resistance against longitu-
primary bundles form a secondary bundle (fasci- dinal, transversal, horizontal, as well as rotational
cle). The number of subfascicles constituting a forces [20]. In addition the peculiar aspect of the
fascicle is variable from 3/4 to 10/12 [12]. In a collagen fibers increases the resistance of the ten-
similar way, several secondary bundles form a don. At rest they are not stretched but have a
tertiary bundle. At the end, groups of tertiary bun- wavy configuration, which is called crimping.
dles constitute the tendon itself, which is sur- When the tendon is stretched the fibers elongate
rounded by the paratenon. The diameter of avoiding damages or ruptures. The recovery of
secondary and tertiary bundle is variable with the wavy configuration after muscle stretch could
values ranging from 150 to 1000 μm and from be facilitated by the presence of elastic fibers
1000 to 3000 μm, respectively. In addition the [21]. Although this disposition is visible and
diameters of both bundles vary proportionally to definable at light microscope, and even better
the size of the tendon itself; smaller tendons have under the scanning electron microscope, the
thinner secondary and tertiary bundles [10]. crimp angle may vary between 0° and 60° [22].
Besides this hierarchical network of bundles the The crimp angle decreases with age leading to
tendon is covered by a loose connective tissue, decreased resistance to mechanical stretch.
which is called paratenon. It is formed by type I Tendons have an active metabolic activity
and type III collagen and elastic fibrils [4] and mainly focused on energy production and synthe-
acts as an elastic sleeve allowing the movement sis of matrix and collagen [3]. Tenoblasts and
of the tendon itself against the surrounding ana- tenocytes may produce energy using the three
tomic structures [13]. A fibrous sheath called epi- major pathways: the aerobic Krebs’ cycle, the
tenon, which is in continuity with the endotenon, anaerobic glycolysis, and the pentose phosphate
covers the deep surface of the paratenon [14]. As shunt. The three pathways are active at the same
already stated the endotenon is a thin reticular time in young tendons when the growth rate is
7 Ligament Tissue Pathology 59
high. Later the contribution of Krebs’ cycle and and a decrease in their water and proteoglycan
the pentose phosphate shunt decrease whereas the content. The content and also quality of colla-
glycolysis remains stable, thus leading to a more gen fibers also change; in degenerated tendons
anaerobic metabolism [10]. This change has a rel- there is increased rate of type 3 collagen. It is
evant impact on tendons’ function. The oxygen normally less than 5% and forms smaller diam-
consumption decreases with age and is 7.5 times eter fibrils. During healing processes it converts
lower than that of skeletal muscles in adults [23]. to type 1, which promotes more cross-linking,
The shift toward glycolytic activity with reduction forming larger, stronger fibers. Finally the ten-
of energy production has a positive influence on don insertion into the bone becomes weakened
the ability of maintaining tensions and withstand- due to osteoclastic activity destroying their
ing prolonged loads reducing the risk of ischemia fibers. On the contrary moderate exercise has
and subsequent necrosis. In other words, the ten- positive effects. Gradually increasing loads
don tolerates low oxygen tension well without induce collagen cross-linking and production of
injury. However, a decreased metabolic rate new microfibrils, which can group together to
results in slow healing after injury [24]. form new fibrils. The new microfibrils can also
Besides energy production, tendon cells syn- be added to existing fibrils, increasing their size.
thesize and degrade all components of the ten- There is now added validation that exercise
don matrix: the collagen and elastic fibers, increases collagen synthesis, concentration of
proteoglycans, and structural glycoproteins. metabolic enzymes, and the size, number, and
The production of these last two components strength of fibers [28–30]. Finally it has been
occurs in different parts of the tendon cells: pro- shown that mechanical stretching of fibroblasts
tein component is synthesized at the rough also stimulates their proliferation.
endoplasmic reticulum and the glycidic part in
the Golgi apparatus [25]. The degradation seems
to occur following two different ways: produc- Conclusion
tion of lysosomal or cytoplasmic degradative
enzymes from tenocytes, which are then released Tendon function is essential for joint motion
into the extracellular space where degradation and correct sport performance. Comprehension
of the matrix components occurs. In addition of the ultrastructural anatomy as well as
the degradation of the matrix may occur through metabolism and function is crucial to under-
direct cellular phagocytosis and pinocytosis stand the etiology of tendon damages. In the
[26]. The balance between anabolism and catab- same way it is crucial to prevent sports inju-
olism is quite rapid with the turnover of proteo- ries and to plan individualized treatment and
glycans being completed between 2 and 10 days rehabilitation protocols once the damage has
[3]. However whereas the anabolic activity is occurred.
intense in young subjects, it decreases along
with age. Collagen content and turnover as well
as fiber area and strength decreases in old sub- Multiple-Choice Questions
jects. In a similar way, water content declines
and there is an increase in cross-linking of the The percentage of tenocytes/tenoblasts in a ten-
tropocollagen molecules. For these reasons tendon is
don becomes smaller, weaker, and more prone
to overuse injuries. Similarly, tendons may 1. 5–10%
undergo anatomic and functional variations as a 2. 30–35%
consequence of training and disuse [27]. After 3. 50%
prolonged immobilization, tendons show disor- 4. 65–70%
ganization of their parallel fiber arrangement 5. 90–95%
Which structure is biomechanically stronger? 8. Kirkendall DT, Garrett WE. Function and biomechan-
ics of tendons. Scand J Med Sci Sports. 1997a;7:62–6.
9. Curwin S. Biomechanics of tendon and the effects of
1. Muscle immobilization. Foot Ankle Clin. 1997;2:371–89.
2. Tendon 10. Jozsa L, Kannus P, Balint BJ, Reffy A. Three-

3. Ligament dimensional ultrastructure of human tendons. Acta
Anat. 1991;142:306–12.
4. Fat 11. Elliott DH. Structure and function of mammalian ten-
don. Biol Rev. 1965;40:392–421.
Age-related changes in tendons include: 12. Kastelic J, Galeski A, Baer E. The multicom-

posite structure of tendon. Connect Tissue Res.
1978;6:11–23.
1. Decrease in oxygen consumption, water con- 13. Kvist M, Jozsa L, Järvinen M, Kvist H. Fine struc-
tent, and cross-linking. tural alterations in chronic Achilles paratenonitis in
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18. Fyfe I, Stanish WD. The use of eccentric training and
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Musculoskeletal System
Physiology: Ligament Tissue 8
Physiology
Introduction components. The water contributes to cellular

function and is responsible for the viscoelastic
Human ligaments are dense bands of collagenous behavior. The solid components are principally
tissue (fibers) that bind bone ends, spanning constituted by collagen, which accounts for
joints. They may be internal or external to the approximately 75% of the dry weight. Type I col-
joint capsule ensuring additional stability to lagen is predominant, representing around 85%
articular geometry and active muscular function. of the whole collagen amount and being respon-
They vary in size, shape, and orientation accord- sible for the resistance to tensile stresses [2]. The
ing to their location and bony attachments. rest is made up of types III, VI, V, XI, and
XIV. Collagen fibrils have different diameters,
with the large ones being more than 150 nm and
Anatomy and Histology the small ones being less than 50 nm.
Ultrastructural studies have revealed hierarchical
Ligaments are collagen structures with complex arrangement of the collagen fibers: with the asso-
ultrastructural architecture and function that con- ciation of several collagen fibrils constituting the
nect bones through a transition structure named fascicles, and several fascicles forming collagen
junction. A lax and finely vascularized layer bundles. Collagen bundles are sheathed in a loose
named the “epiligament” often surrounds them connective tissue. The organized, parallel colla-
[1]. This layer is often indistinguishable from the gen fibers are oriented along the major axis of the
actual ligament and merges into the periosteum ligament itself. The fibers are rather undulated or
of the bone around the attachment sites of the helicoidal at rest [3]. This disposition, which is
ligament. Ligaments are formed by approxi- called “crimping,” has different wave sizes and
mately two-thirds water and one-third solid gives rise to a process called “recruitment.” Upon
load bearing, certain areas of the ligament crimp,
S. Cerciello allowing the tissue to elongate without sustaining
Centre Albert-Trillat, CHU Lyon Croix-Rousse, structural damage [4, 5]. The recruitment of the
Hospices Civils de Lyon, Lyon, France collagen fibers is selective. Once an axial stretch-
Casa Di Cura Villa Betania, Rome, Italy ing is applied, fibers or bundles with a small heli-
P. Neyret (*) cal wave appearance straighten first and begin to
Centre Albert-Trillat, CHU Lyon Croix-Rousse, offer resistance (increased stiffness) to stretch.
Hospices Civils de Lyon, Lyon, France As long as the ligament is stretched, there is pro-
University Lyon 1, Lyon, France gressive involvement of fibers with larger helical

organization with further increase of ligament insertion sites and middle part of the ligaments.
stiffness. Once all the fibers are straightened a These cells, which lay between the rows of col-
sudden increase in stiffness is observed. For these lagen fibers, produce and maintain the extracel-
reasons the whole process has a nonlinear length– lular matrix. Recent studies suggest that
tension behavior. fibroblasts in normal ligaments may be capable
In addition it seems that some fibers tighten or of cell-to-cell communication, allowing the coor-
loosen depending on musculoskeletal positioning dination of cellular and metabolic processes
and applied forces. throughout the tissue [5, 12, 13]. Proteoglycans
The large content of water (70%) and the which represent <3% of the dry weight constitute
cross weave of the long fibers by short fibers the extracellular matrix, bind water, and contrib-
provide the necessary lubrication for bundles to ute to the viscoelastic properties of ligaments.
slide relative to each other, yet to remain bun- Decorin is the most abundant proteoglycan in the
dled together and generate stiffness in the trans- matrix of ligaments [14]. It is a small leucine-rich
verse directions [6]. proteoglycan that binds to collagen fibrils and
The dry part is mainly formed by collagen. At actively participates in fibrillogenesis [15]. The
the molecular level, collagen is synthesized as viscoelastic properties, in association with the
procollagen molecules and these are secreted into “crimp” shape of the collagen fibers, allow liga-
the extracellular space through structures in the ments to progressively lengthen when under ten-
cells called microtubules. Once outside the cell, a sion and return to their original shape when the
post-transitional modification takes place and the tension is removed. These progressive stresses
triple-helical collagen molecules line up and are transmitted to bone through the junction.
begin to form fibrils and then fibers. A special- Osteoligamentous junction acts as a stress con-
ized enzyme called lysyl oxidase, which pro- centration site where soft ligamentous tissue
motes cross-link formation, carries on this step. meets hard bone. According to the type of tissue
These cross-links occur both within and between present at the attachment site, two types have
the collagen molecules and contribute to the tre- been described: fibrous and fibrocartilaginous
mendous strength that ligaments have [7]. During [16]. This corresponds to the classification by
growth and development, cross-links are rela- Woo et al. where indirect and direct attachments
tively immature and soluble but with age they were described, highlighting the absence of a
mature and become insoluble and increase in periosteum at fibrocartilaginous entheses (indi-
strength. Collagen has a relatively long turnover rect) or the direct attachment of the ligament to
rate; its average half-life is between 300 and the bone [17].
500 days, which is slightly longer than that of At fibrous entheses, the ligament attaches
bone. Therefore, several months may be required either directly to the bone or indirectly to it via
for a ligament to alter its structure to meet the periosteum with no evidence of fibrocartilage
changes in physical loading conditions or to differentiation in the cellular elements. At fibro-
repair itself after injury. cartilaginous entheses the chondrogenesis occurs
The remaining part of the dry weight is formed and four zones of tissue are commonly present:
by cells, proteoglycans (<1%), elastin, and other pure dense fibrous connective tissue, uncalcified
proteins and glycoproteins such as actin, laminin, fibrocartilage, calcified fibrocartilage, and bone.
and integrins. However not all of the dry-weight
components have been characterized. Previous
studies have demonstrated two major cell types Function
in the ligaments. One is fusiform or spindle-
shaped fibroblast with negative toluidine blue The ligaments act as a passive restraint increas-
staining. The other type is round or oval, resem- ing the intrinsic joint stability. In addition they
bling fibrochondrocytes with lacunae [8–11]. The guide joints through their range of motion when
chondrocyte-like cell is mainly located at the a tensile load is applied. This happens as a
8 Musculoskeletal System Physiology: Ligament Tissue Physiology 65
c onsequence of the “crimp pattern” and the inter- degradation, collagen synthesis [20], and disor-
action and cross-linking of elastic, reticular, and ganization of collagen fibrils [21, 22].
collagen fibers is critical. These features allow Finally it also depends on the frequency of
ligaments to have a limited range of strains over load and unloading application, such as in repeti-
which they produce minimal resistance to move- tive occupational tasks. Cyclic loading of a liga-
ment. Thus joints move among certain ranges and ment with the same peak load, but at a higher
directions without a major increase in ligament frequency, results in larger creep development
stiffness. However if a joint is displaced toward and longer period of rest required for the full
the outer limit of the normal range of motion, recovery of the creep [23]. The process of recov-
there is a recruitment of collagen fibers from their ering a physiological creep status after ligament
“crimp” state to a straightened condition. Fiber strain is a relatively unexplored issue. Studies in
recruitment causes the ligament to quickly healthy humans and in vivo animal models show
increase its resistance to further elongation, that creep developed over relatively short periods
hence stabilizing the joint. For this reason with of 10–60 min of loading did not fully recover at
increasing loads there is an increase in ligament the end of up to 2 h of rest [24–26].
stiffness. At higher loads the ligaments exhibit Conversely the exposition to loading over an
nearly linear stiffness; beyond that point although extended period of time causes an increase in
they can absorb additional loads this results in mass, stiffness, and load to failure of the liga-
tensile failure and ligament rupture. ments [20]. However, when they are overloaded,
Ligament response to strain depends on sev- or exposed to strains that exceed the limit they
eral extrinsic factors. Firstly it is related with can sustain, the tissue fails, resulting in partial or
maturation and therefore with aging. In young complete ligament discontinuity, or tears. The
animals the bone-ligament junction is consis- bundles of fibers fail at different locations due to
tently weaker than the ligament substance. shear and tensile mechanisms between fibers.
However, along with time the structure and This is the most common mode of failure of the
mechanical properties of collagenous tissues ligaments (among three) as described by Butler
change with an increase in collagen cross-linking, et al. [18]. When these events occur, the body
collagen glycosaminoglycan, and collagen-water responds by attempting to heal the injury through
ratios [18, 19]. The stabilization of collagen with a specialized sequence of cellular events. They
maturity enhances tissue strength while the loss can be categorized by three consecutive phases
of water and elastin reduces tissue plasticity [19]. that occur over time: the acute inflammatory
The elastic elements become coarser and more phase, the proliferative or regenerative/repair
easily fractured. In any case it must be high- phase, and the tissue-remodeling phase.
lighted that the effects of aging on ligaments are Ligament also acts as sensory organs and
individual and depend on multiple factors such as plays a crucial role in joint proprioception, which
genetics, previous diseases and traumas, and life- is the perception of limb position in space. Acting
style. Similarly, the alterations at the bone- as sensory organs, ligaments can protect the joint
ligament junction that occur in later years in life and prevent injury when they are under stress.
are due to a combination of aging factors, dis- Ligaments contain sensory receptors such as
eases, and decreased physical activity. In addition mechanoreceptors and nerve endings called
the mechanism is also temperature dependent, Pacinian corpuscles, Golgi tendon organs, and
showing reduced capability to sustain loads as Ruffini endings [6]. They may detect joint posi-
temperature increases [17]. Moreover it is influ- tion, velocity, and acceleration and may indi-
enced by disuse; in some tests, ligaments that rectly contribute to maintain joint integrity by
have been immobilized for 8 weeks showed initiating the recruitment (or decruitment) of
decrease in strength and in the measurements of dynamic stabilizers such as muscles [27]. The
load to failure of 35–40%, respectively. This is function of receptors is activated by ligament
probably the consequence of increased collagen strain. This event invokes neurological reflex,
which is called “ligamento-muscular reflex” with ment. Knee Surg Sports Traumatol Arthrosc. Mar.
2006;14(3):204–13.
efferent feedback signals that activate muscular 3. Zhu J, Zhang X, Ma Y, Zhou C, Ao Y. (2012)
contraction. This contraction has a role in joint Ultrastructural and morphological characteristics of
position sense. human anterior cruciate ligament and hamstring ten-
Apart from the ligaments themselves, inser- dons. Anat Rec (Hoboken)Sep;295(9):1430–1436.
https://doi.org/10.1002/ar.22527.
tion sites play an important role in joint function 4. Amiel D, Constance C, Lee J. Repetitive motion
since they are well suited for dissipating force. disorders of the upper extremity: effect of loading
As the ligament passes through the insertion site, on metabolism and repair of tendons and ligaments.
it changes from ligament itself to fibrocartilage Rosemont, Illinois: Am Acad Orthop Surg; 1995.
p. 213–7.
and then to bone. The transition areas are less 5. Frank CB. Ligament structure, physiology and function.
susceptible to disruption than the extremes on J Musculoskelet Neuronal Interact. 2004;4(2):199–201.
either side (bone or peri-insertional ligament sub- 6. Solomonow M. Ligaments: a source of work-related
stance). At this level bony avulsion may occur, as musculoskeletal disorders. J Electromyogr Kinesiol.
2004;14:49–60.
a consequence of slow loading applied through 7. Hauser RA, Dolan EE, Phillips HJ, Newlin AC,
the cancellous bone beneath the insertion site Moore RE, Woldin BA. Ligament injury and healing:
[18]. Another mode of failure is the pullout at the a review of current clinical diagnostics and therapeu-
ligament-bone interface. This mode is less com- tics. Open Rehab J. 2013;6:1–20.
8. Duthon VB, Barea C, Abrassart S, Fasel JH, Fritschy
mon due to the efficient force dissipation that D, Menetrey J. Anatomy of the anterior cruciate
occurs through the insertional zone. When a fail- ligament. Knee Surg Sports Traumatol Arthrosc.
ure of this type does occur, it generally occurs 2005;14:204–13.
through the mineralized fibrocartilage [18]. 9. Murray MM, Spector M. Fibroblast distribution in the
anteromedial bundle of the human anterior cruciate
ligament: the presence of alpha-smooth muscle actin-
positive cells. J Orthop Res. 1999;17:18–27.
Conclusion 10. Jiang Q, Lin G, Qu M, Cui G, Teng H. Cartilage-like
phenomenon in the anterior cruciate ligament. Chin
Med Sci J. 2001;16:103–6.
Ligaments act together with other ligaments and 11. Wang YJ, Ao YF. Histologic study of semitendinosus
with joint surface geometry, to maintain joint tendon autograft used for anterior cruciate ligament
integrity and promote joint motion. The compre- reconstruction in a rabbit model. Chin J Sports Med.
hension of the functional role of ligaments 2004;23:609–12.
12. Lo IK, Chi S, Ivie T, Frank CB, Rattner JB.

requires deep analysis of all joint structures. In The cellular matrix: a feature of tensile bearing
addition ligaments act as sensory organs ensuring dense soft connective tissues. Histol Histopathol.
proprioception and regulating muscle function 2002;17:523–37.
that enhances joint stability. 13. Benjamin M, Ralphs JR. The cell and developmen-
tal biology of tendons and ligaments. Int Rev Cytol.
Finally they can change their structure and 2000;196:85–91.
mechanical properties in response to environ- 14. Ilic MZ, Carter P, Tyndall A, Dudhia J, Handley

mental changes. All these aspects need to be con- CJ. Proteoglycans and catabolic products of pro-
sidered prior to the onset of training program, teoglycans present in ligament. Biochem J.
2005;385:381–8.
when planning injury treatment, or rehabilitation 15. Reed CC, Iozzo RV. The role of decorin in collagen
programs. fibrillogenesis and skin homeostasis. Glycoconj J.
2002;19:249–55.
16. Benjamin M, Toumi H, Ralphs JR, Bydder G,

Best TM, Milz S. Where tendons and ligaments
References meet bone: attachment sites (‘entheses’) in rela-
tion to exercise and/or mechanical load. J Anat.
1. Chowdhury P, Matyas JR, Frank CB. The “epiliga- 2006;208:471–90.
ment” of the rabbit medial collateral ligament: a quan- 17. Woo S, Buckwalter J. Injury and repair of musculo-
titative morphological study. Connect Tissue Res. skeletal soft tissue. Park Ridge, IL: AAOS; 1988.
1991;27:33–50. 18.
Butler DL, Grood ES, Noyes FR, Zernicke
2. Duthon VB, Barea C, Abrassart S, Fasel JH, Fritschy RF. Biomechanics of ligaments and tendons. Exercise
D, Ménétrey J. Anatomy of the anterior cruciate liga- Sports Sci Rev. 1978;6:125–81.
8 Musculoskeletal System Physiology: Ligament Tissue Physiology 67
19. Menard D, Stanish WD. The aging athlete. Am J responses to cyclic lumbar flexion. J Biomech.
Sports Med. 1989;17(2):187–96. 2004;37(6):845–55.
20. West RV, Fu FH. Soft-tissue physiology and repair. In: 24. McGill S, Brown S. Creep response of the lum-

Vaccaro AR, editor. Orthopaedic knowledge update 8. bar spine to prolonged full flexion. Clin Biomech.
Chapter 2. Rosemont, IL: AAOS; 2005. p. 15–27. 1992;7:43–6.
21. Woo SL, Gomez MA, Sites TJ, Newton PO, Orlando 25. Ekstrom L, Kaigle A, Hult E, Holm S, Rostedt M,
CA, Akeson WH. The biomechanical and morpho- Hansson T. Intervertebral disc response to cyclic
logical changes in the medial collateral ligament of loading: An animal model. Proc Inst MechEngr.
the rabbit after immobilization and remobilization. J 1996;209:249–58.
Bone Joint Surg Am. 1987;69(8):1200–11. 26. Crisco J, Chelikani S, Brown R. Effects of exercise
22.
Woo SL, Abramowitch SD, Kilger R, Liang on ligamentous stiffness in the wrist. J Hand Surg.
R. Biomechanics of knee ligaments: injury, healing, 1997;22A:44–8.
and repair. J Biomech. 2006;2(39):1–20. 27. Skinner H, Barrack R. Joint position sense in the
23. Lu D, Solomonow M, Zhou B, Baratta RV, Li L. normal and pathologic knee joint. J Electromyogr
Frequency dependent changes in neuromuscular Kinesiol. 1991;1:180–90.
Articular Cartilage Physiology
9
Ann Marie Kelly, Nikolaos K. Paschos,
Dimitrios Giotis, and John D. Kelly IV
Articular cartilage is mainly hyaline articular car- Articular Cartilage Composition [1–4]
tilage. It is an avascular and aneural tissue; thus
its potential for healing is limited—if not Extracellular Matrix
nonexistent.
Articular cartilage matrix is composed of 75%
water.
Role The rest is 15% collagen and 10%
proteoglycans.
• Shock absorption From its dry components,
• Protection of the ends of bones that comprise
synovial joints • 50–75% is composed of collagen and
• Friction reduction and lubrication • 15–30% of proteoglycans
• Load distribution
The matrix is further divided into:
• Superficial
• Middle
• Deep
• Calcified zones
A. M. Kelly (*) · J. D. Kelly IV
Pennsylvania, Philadelphia, PA, USA Type II collagen is the most collagen type in
articular cartilage. Other types present are type V,
N. K. Paschos
Department of Orthopedic Surgery, University of type VI, type IX, and type XI
Division of Sports Medicine, Department of • Collagen structure and orientation are impor-
Orthopaedic Surgery, Boston Children’s Hospital, tant for tensile but also compressive
Harvard Medical School, Boston, MA, USA properties.
e-mail: Nikolaos.Paschos@childrens.harvard.edu • Proteoglycans are produced from chondro-
D. Giotis cytes and are critical for compressive proper-
Department of Orthopedic Surgery, University of ties. Due to its negative charge aggrecan can
retain water, therefore increasing the amount
Panepistimion Ioanninon, Department of Orthopaedic of compressive load withstand, but also

ensures nutrient inflow for the chondrocytes • Loss of foundational bone structure.
during loading/unloading cycles. • Lacerations.
• Proteoglycans are composed of glycosamino-
glycan (GAG) subunits:
–– Chondroitin sulfate ey Changes with Aging/
K
–– Keratin sulfate Degeneration [1–5]
Lubricin or superficial zone protein (SZP) is Chondrocytes

responsible for the low friction in the joint. It is
produced by the superficial zone of articular car- • Chondrocytes progressively become less
tilage and by the synovial cells. active metabolically.
• Diminished number of chondrocytes:
–– Senescence markers.
Chondrocytes [2–5] –– More lysosomal enzymes.
• Reduced response to growth factors (TFG-b):
Chondrocytes are the sole cells of the articular –– Lower matrix density.
cartilage. They are responsible for producing and –– Diminished chondroitin SO4−.
maintaining the extracellular matrix.
Proper function of chondrocytes is dependent
on the cytoskeletal organization of actin fibers for Extracellular Matrix
maintenance of their phenotype.
Chondrocytes, which also require correct • Shrunken proteoglycan molecules.
mechanical loading to maintain the articular car- • Extracellular matrix loses collagen content
tilage matrix, employ multiple methods of sens- and proteoglycans.
ing loading. • Loss in level of tensile strength.
Several growth factors, such as TGF-β, BMP, • Greater protein content.
and VEGF, are responsible for cartilage mainte- • Water content decreases with age.
nance. Osteoarthritis is believed to be a result of • Shrunken proteoglycan molecules.
malfunction of the signaling pathways regulating • Higher levels of water seen with
cartilage function. osteoarthritis.
Response to Trauma/Healing
References
Cartilage homeostasis may be disrupted by:
1. Wheeless MD, Clifford R. Articular cartilage.
Wheeless’ textbook of orthopedics; 2016.
• Trauma and excess or inadequate forces. 2. Miller MD, Thompson SR, Hart J. Miller’s review
• Extreme levels of stress: of orthopaedics. 7th ed. Philadelphia, PA: Elsevier
–– Obesity, varus/vulgus. Health Sciences; 2012. p. 40.
–– Lack of adequate use/activity. 3. Moore D. Articular cartilage. Orthobullets; 2013.
4. Miller MD, Thompson SR, Hart J. Miller’s review
• Chemical/enzymatic threats: of orthopaedics. 7th ed. Philadelphia, PA: Elsevier
–– pH variation. Health Sciences; 2012. p. 44.
–– Metalloproteases. 5. Miller MD, Thompson SR, Hart J. Miller’s review
• Genetic abnormalities in structure/function. of orthopaedics. 7th ed. Philadelphia, PA: Elsevier
Health Sciences; 2012. p. 45.
Part III
Musculoskeletal System Pathology
Metabolic Bone Diseases
10
Miguel Botton, António Robalo Correia,
Overview Zooming In
Causes of Osteoporosis in Childhood Rickets
1. Endocrine: Hyperthyroidism; hyperparathy-

Definition: Failure of mineralization of cartilage
roidism; hypogonadism; glucocorticoid and osteoid tissue because of disruption of cal-
excess. cium/phosphate homeostasis.
2. Metabolic: Homocystinuria; gastrointestinal
Decreases longitudinal bone growth and
malabsorption; idiopathic hypoproteinemia; weakens mechanical properties of tubular bone.
vitamin C deficiency; rickets. Manifestations around growth plates and long
3. Liver disease. bones. Increased thickness of physis; abundant
4. Renal disease: Chronic tubular acidosis; idio- and widened osteoid; abnormal arrangement of
pathic hypercalciuria; Lowe syndrome; ure- collagen fibers in compact bone. Occurs at zone
mia; regular hemodialysis. of provisional calcification.
5. Bone diseases: Osteogenesis imperfecta; idio- After physeal closure called osteomalacia.
pathic juvenile osteoporosis; idiopathic oste-
olysis; Turner syndrome. Nutritional Rickets
6. Malignant diseases: Leukemia; lymphoma. • Vitamin D deficiency.
7. Miscellaneous: Disuse of paralyzed limbs;
• Inability to absorb calcium and phosphorus
heparin therapy; anticonvulsant drug therapy. from the gut.
• Children between 6 months and 3 years old.
Risk factors: Developing countries, premature

infants, prolonged breastfeeding, vegetarian diet,
M. Botton black children, celiac disease, hepatic disease.
Centro Hospitalar Lisboa Norte, Lisbon, Portugal
A. R. Correia Clinical Presentation
Department of Orthopaedic Surgery, Hospital José • Lethargy, irritability.
Joaquim Fernandes, Beja, Portugal • Hypocalcemic seizure.
M. C. Neves (*) • Listlessness.
Hospital CUF Descobertas, Lisbon, Portugal • Muscular weakness.
e-mail: Manuel.CassianoNeves@jmellosaude.pt; • Periarticular swelling.
Manuel.CassianoNeves@efort.org

74 M. Botton et al.
• Angular deformities (bowleg, genu varum, Vitamin D-Resistant Rickets

genu valgum, coxa vara).
• Short stature. Genetics
• Rachitic rosary. Hereditary of familial hypophosphatemic:
• Harrison’s groove. X-linked dominant, autosomal dominant, or
• Pectus carinatum. autosomal recessive.
• Affected dentition.
• Stress fractures. • X-linked dominant (more fre-
• Kyphoscoliosis (later). quent—1/20.000): Mutation in gene PHEX:
PHEX produces elevated levels of FGF23
Laboratory (hormone produced by osteoblasts and osteo-
cytes that reduces renal phosphate reabsorp-
Radiographic Findings tion and the conversion of 25(OH)D to its
active form by suppressing 25-hydroxyl-1a-
• Widened growth plate. hydroxylase activity).
• Cupped metaphysis. • Autosomal dominant: Mutations in FGF23.
• Osteopenic bone with thinning of cortices. • Autosomal recessive with mutations in DMP1
• Looser’s lines (20%). gene and ENPP1: DMP1 is a regulatory pro-
• Angular deformities. tein produced by osteoblasts and osteocytes
• Thoracolumbar kyphosis. that regulates the growth of dentin, bone, and
cartilage and also plays a role in matrix
Bone scintigraphy in neonates to diagnosis. mineralization. DMP1 produces elevated lev-
els of FGF23.
Treatment • Autosomal recessive with mutations in
• Vitamin D: 5000 IU daily (6–10 weeks). SLC34A3 (rare) leads to hypercalciuria.
• Radiograph improvement in 2–4 weeks. • Autosomal recessive with mutations in
• Tetracycline in older children. SLC34A1 (rare) leads to Fanconi syndrome.
• Suspect vitamin D resistant if not responding
to therapy. Clinical Presentation
• Age older that nutritional rickets (1 and
Rickets of Prematurity 2 years old).
• Systemic manifestations are minimal. Delayed
Risk Factors walking.
• Hepatobiliary disease. • Physical findings more severe: Angular defor-
• Total parenteral nutrition. mities, spinal deformities, periarticular
• Diuretic therapy. enlargement.
• Physical therapy with passive motion and • Height is 2SD below.
chest percussion therapy. • Dietary intake of vitamin D is insufficient
because of pathologic renal phosphate wasting.
Resolution as infants gain weight.
Rachitic changes and fractures. Radiographic Findings
Same as nutritional rickets.
Drug-Induced Rickets
Seizure medications that affect liver (cytochrome Treatment
P-450) decrease levels of vitamin D. Medical:
Hypocalcemia develops.
Suspect in patients with seizures and frequent • Oral replacement of phosphorus.
fractures. • Vitamin D.
10 Metabolic Bone Diseases 75
• Calcitriol and analogues of vitamin D3. (b) Low-turnover disease: Adynamic disorder

• Deformities improve with medical therapy. due to high doses of exogenous calcium.
• Nephrocalcinosis is a complication of treat- More frequent in rapidly progressive forms
ment (79%)—severity correlated with dose of of renal disease.
phosphorus.
• Growth hormone increases height and bone Pathophysiology
density and reduces phosphate retention. • Damaged glomerulus results in
hyperphosphatemia.
Orthopedic: • Decrease production of dihydroxyvitamin D.
• Results in diminished absorption of calcium.
• Orthotic treatment not efficacious. • Hypocalcemia triggers hyperparathyroidism
• Pain or difficulty walking demands surgical which worsens the bony changes.
correction of angular deformities.
• Multilevel osteotomy with overcorrection of Pathology
mechanical axis with external fixation, intra- • Rachitic changes: Failure to replace physeal
medullary fixation, or plating. chondrocytes by endochondral ossification.
• Recurrent deformity is a common sequela Widened physis. Provisional calcification
(younger patients have higher risk). zone irregular. Bony trabeculae with abundant
• Adults prone to arthritis. osteoid and widened osteoid seams.
• Hyperparathyroidism changes: Bone marrow
Tumor-Related Hypophosphatemic replaced by hyperplastic fibrous tissue.
Rickets Osteosclerosis.
Oncogenic hypophosphatemic osteomalacia.
Older children. Laboratory findings (Table 10.1): Urea
Certain tumors secrete phosphatonins (FGF23); nitrogen and creatinine in serum are elevated.
others disrupt renal tubular resorption of phosphate. Albumin in serum is low. Acidosis.
Tumors: Neurofibromatosis, fibrous dysplasia, Diagnosis: Bone biopsy necessary for accu-
osteoblastoma, hemangiopericytoma, and skin tumors. rate diagnosis and guide treatment.
Resolves with excision of the tumor. Clinical presentation: Resemble rickets:
• Short children.
Renal Osteodystrophy • Fragile bones.
• Skeletal deformities.
• Prevalence risen with successful kidney trans- • Periarticular enlargement of long bones.
plants in children. • Rachitic rosary.
• Renal failure triggers high levels of serum • SCFE.
phosphate.
• Manifestations in 66–79% of children with Radiographic Findings
renal failure (chronic pyelonephritis, congeni- • Osteopenia.
tal abnormalities, polycystic kidney disease). • Thinning cortices.
• Indistinct bony trabeculae.
Two types: • Physes increased in thickness.
• Osteosclerosis at base of the skull and
(a) High-turnover disease (osteitis fibrosa cys- vertebrae.
tica): Driven by presence of secondary • Rugger jersey spine.
hyperparathyroidism—(activation of osteo- • Brown tumors.
clasts and resorption of bone). More frequent • Corticosteroid-associated osteonecrosis of the
in progressive forms of renal disease. femoral heads.
76 M. Botton et al.
Table 10.1 Biochemical abnormalities in rickets

Ca Pho Alk PTH 25(OH) 1,25(OH)2
Condition Genetics Ph Vit D Vit D
Vitamin D deficiency Nutricional N⇑ N⇓ ⇑ ⇑ ⇓⇓ ⇓
Vitamin D resistant Xlinked dominant N ⇓ ⇑ N N N
Renal osteodystrophy Renal disease ⇓ ⇑ ⇑ ⇑ N ⇓⇓
Hyperparatyroidism Adenoma ⇑ ⇓ ⇑ ⇑
Hypoparathyroidism ⇓ ⇑ ⇓
Hypophosphatasia ⇑ N ⇓⇓ N
Medical Treatment Radiographic findings: Similar to renal

• Underlying renal disease treatment (dialysis osteodystrophy.
and transplantation). Laboratory: See Table 10.1.
• Vitamin D. Treatment: Directed toward the cause.
• Sodium bicarbonate. Hypercalcemic crisis treated by hydration,
• Phosphate-binding agents. calciuresis, inhibition of bone calcium
• Growth hormone. resorption.
• Parathyroidectomy.
• Serum alkaline phosphatase above 500 U/L is
a marker of ongoing metabolic bone disease. Hypoparathyroidism
Orthopedic Treatment Overview

• Angular deformities: Genu valgum is the most Result from failure to synthetize or secrete PTH
common. Osteotomy. or from tissue resistance to PTH.
• SCFE: Patients younger compared to idio- Distinguish from pseudohypoparathyroidism
pathic SCFE. Bilaterally common. In situ with PTH infusion test.
fixation. Clinical presentation: Results from
• Avascular necrosis: Associated with pro- hypocalcemia.
longed steroid use after renal transplantation. Laboratory: See Table 10.1.
Symptomatic treatment. Treatment: Calcium and vitamin
D. Nephrocalcinosis is a complication.
Primary Hyperparathyroidism
Pseudohypoparathyroidism
Overview
Results from hyperplasia (1/3) or adenoma (2/3) • Genetic cause.
of parathyroid glands. Can also be MEN syn- • Similar to hypoparathyroidism in clinical and
dromes (inherited). radiographic manifestations.
Increased secretion of PTH. • PTH levels are elevated: Skeleton responds as
osteitis fibrosa cystica (Albright
Clinical Presentation osteodystrophy).
• Nonspecific with lethargy. • Kidneys resistant to PTH: Hypocalcemia
• Bone pain and abdominal complaints. and hyperphosphatemia resembling
• Diagnosis late and missed. hypoparathyroidism.
• Treatment with vitamin D.
Vitamin Disorders • Rare inheritable disorder, caused by defi-

ciency of TNSALP (tissue-nonspecific isoen-
Hypervitaminosis D zyme of alkaline phosphatase).
Overview: Patients at risk are taking vita- • Wide variation in severity of disease.
min D for metabolic bone diseases. • Various forms:
Hypercalcemia drives laboratory and clini- –– Perinatal lethal.
cal features. –– Perinatal benign.
Treatment: Cessation of vitamin D, diuretics, –– Infantile.
steroids, and bisphosphonates. –– Childhood.
–– Adult.
Scurvy –– Odontohypophosphatasia.
Overview Clinical presentation: Similar to rickets.

• Nutritional deficiency of vitamin C. Widening of physis.
• Develops after 6–12 months of deprivation Laboratory: See Table 10.1.
(anorexia nervosa). Phosphoethanolamine in urine is diagnostic.
• Rare. Treatment: No approved therapies. NSAIDs
• Collagen synthesis is impaired. Osteoblasts improve pain in childhood.
dysfunctional.
Clinical Presentation Idiopathic Hyperphosphatasia

• Loss of appetite.
• Irritability. Overview
• Hemorrhage. • Extremely rare.
• Impaired wound healing and fractures. • Known as juvenile Paget disease of bone.
• Increased bone turnover.
Radiographic Findings • Autosomal recessive with mutations in
• Osteopenia. TNFRSFIIB gene (encodes OPG).
• Thinning of cortices.
• Frankel’s line. Treatment: Antiresorptive drugs.
• Wimberger sign.
Differential diagnosis: Osteomyelitis, leuke- Growth Hormone (GH) Deficiency

mia, and purpuric diseases.
Treatment: Vitamin C. Overview
• Congenital or acquired.
Hypervitaminosis A • Various mutations in the genes for GH1 (most
Very rare. Caused by vitamin supplements. common), GHRHR, and SOX3.
Clinical Presentation
Hypophosphatasia 1. Congenital forms: The infant is of normal size
but diminished growth is noted within the first
Overview 6 months.
• Generalized impairment of bone 2. Acquired forms caused by a pituitary lesion,
mineralization. signs of neurologic deficit are present.
78 M. Botton et al.
Radiographic findings: Skeletal maturation Radiographic Findings

is delayed. Osteoporosis of the long bones and • Skeleton immature for infant’s chronologic
skull. age.
Laboratory findings: GH serum levels will • Epiphyseal dysgenesis.
be low or absent. Stimulation test (insulin or • Irregular physis and widened (similar
L-arginine) is usually needed. rickets).
Treatment: Synthetic growth hormone. • Thoracolumbar kyphosis.
• Transverse radiopaque bands in metaphyseal
areas and thickened cortices.
Hypothyroidism
Diagnosis: TSH level measurement is diag-
Overview nostic. High serum calcium levels.
• Disturbed enchondral bone formation. Treatment: Thyroxine. If treatment begun by
• Common (1/4000); 15–35% of infants with 24 months of age, growth normal by 5 years.
Down syndrome have congenital
hypothyroidism.
• Degree of deficiency, age of onset, and dura- Idiopathic Juvenile Osteoporosis
tion determine the severity of disease.
• Cretinism is the congenital form: most com- Overview
mon endocrine disorder in neonates. • Extremely rare disorder characterized by
• Can lead to dwarfism and mental retardation. reduction in bone mass—decreased remodel-
• More common in girls. ing activity and bone formation.
• Causes: Structural (80%) range from aplasia • Cardinal features:
of the thyroid, hypoplasia to goiter. Synthesis –– Onset before puberty.
defects responsible for 20%. –– Compression fractures of the vertebrae and
long bones.
Clinical Presentation –– Formation of new but osteoporotic bone.
• Jaundice. –– Spontaneous recovery after skeletal
• Lethargy. maturity.
• Sleepiness. • Diagnosis of exclusion.
• Feeding difficulties and constipation.
• Overweight. Clinical presentation: Mean age at onset is
• Dry skin. 7 years. Back and leg pain.
• Scanty coarse hair. Radiographic findings: Diffuse generalized
• Enlarged tongue. osteoporosis.
• Umbilical hernias. Treatment: Controversial. Isolated reports of
• Associated malformations: Heart defects. successful medical treatment with calcitonin, cal-
• In an older child, SCFE may be the first mani- citriol, bisphosphonates, and estrogen.
festation. Contralateral prophylactic pinning
should be performed (bilateral SCFE in 61%).
ecent and Future Developments

R Medical treatment with high-dose vitamin D
[1–6] is standard therapy. Corrective surgery can be
considered to correct severe tibial bowing. When
T Shimada. Updates on rickets and osteomalacia: gait is compromised or pain is present, osteotomy
anti-FGF23 antibody, a new therapeutic approach should be considered even if recurrent deformity
for hypophosphatemic rickets/osteomalacia. is a common sequel.
Clinical calcium 23(10): 1469–1475. 2013.
Winer KK et al. Synthetic human parathyroid
hormone 1-34 replacement therapy: a random-
ized crossover trial comparing pump versus
injections in the treatment of chronic hypopara-
thyroidism. J Clin Endocrin Metab 97:391, 2011.
JE Gordon et al. Bone Mineral Density after
Immobilization for fractures in adolescents. JBJS
Am. Feb 01;94. 2012.
Itai Pashtan et al. Primary hyperparathyroid-
ism in adolescents: the same but different.
Pediatric Surgery International. Volume 29, issue
3, pp 275–279. March 2013.
Case Studies/Discussion
Case 1
8-year-old girl with vitamin D-resistant rickets,

presents with skeletal deformity and characteris-
tic findings of rickets.
Is the family history relevant to this case?
As the most frequent form of vitamin
D-resistant rickets is X-linked, family history
should be present in this case.
What would be your expectations regarding
the laboratory findings?
The most common form of heritable rickets
is caused by the inability of renal tubules to
absorb phosphate; so, we should expect a low-
serum phosphorus and an elevated alkaline
phosphatase.
Would you consider any surgical approach at
this age?
80 M. Botton et al.
Case 2 weight so we can classify the SCFE as unstable

(Loder) and associated with high risk of
10-year-old girl with Down syndrome presents to osteonecrosis.
emergency room with bilateral hip pain and What would be your approach in this clinical
inability to tolerate walking. case?
What is the diagnosis? This patient should be screened to rule out
According to frog leg bilateral lateral X-rays, renal failure and hypothyroidism. Although con-
we can see a left slipped capital femoral epiphy- troversial, we would consider prophylactic pin-
sis. If we draw a line along the superior border of ning of the contralateral hip in patients at high
the femoral neck, it does not touch the femoral risk (as in this case).
head (Klein’s line). The patient is unable to bear
Review Questions 3. In RENAL OSTEODYSTROPHY the

pathological findings are characterized by
1. The BLOOD CALCIUM LEVEL is normal the following except:
or low in all the conditions below except: (A) Failure to replace physeal chondrocytes
(A) Vitamin D-deficiency rickets by endochondral ossification
(B) Vitamin D-resistant rickets (B) Widened physis
(C) Renal osteodystrophy (C) Provisional calcification zone irregular
(D) Hyperparathyroidism (D) Bony trabeculae with abundant osteoid
(E) Hypoparathyroidism and widened osteoid seams
2. The most common radiographic findings in (E) Bone sclerosis
HYPOTHYROIDISM are the following 4. In a patient with SCFE secondary to
except: hypothyroidism:
(A) Immature skeleton for infant’s chrono- (A) The “in situ” fixation should be per-
logic age formed with Kirschner wires.
(B) Epiphyseal dysgenesis (B) If the slip angle is > 45° it should be
(C) Narrow physis corrected by surgical dislocation of
(D) Thoracolumbar kyphosis the hip
( E) Transverse radiopaque bands in (C) AVN is observed in 73% of the cases
metaphyseal areas and thickened (D) Prophylactic pinning of the contralat-
cortices eral hip is mandatory
(E) All the above (D)

Autosomal recessive mutations in
5. Regarding VITAMIN D-RESISTANT SLC34A3
RICKETS which below sentence is (E) Autosomal recessive mutations in
appropriate: SLC34A1
(A) The orthotic treatment should be the ini- 11. Which sentence below does not apply to

tial treatment. IDIOPATHIC JUVENILE
(B) Surgical correction of angular defor- OSTEOPOROSIS?
mities is fundamental. (A) Characterized by increased remodel-
(C) Multilevel osteotomy with undercorrec- ing activity
tion of mechanical axis is the rule. (B) Onset before puberty
(D) Recurrent deformity is a rare sequel. (C) Compression fractures of the vertebrae
(E) Younger patients have lower risk. and long bones
6. Which of the following is NOT a known risk (D) Formation of new but osteoporotic bone
factor for NUTRITIONAL RICKETS? (E) Spontaneous recovery after skeletal
(A) Premature infant maturity
(B) Celiac disease 12. Which of the following diseases has SCFE
(C) Prolonged breastfeeding as a clinical manifestation?
(D) Hypocaloric diet (A) Renal osteodystrophy
(E) Hepatobiliary disease (B) Nutritional rickets
7. Which symptom is NOT a typical RICKETS (C) Drug-induced rickets
physical finding? (D) Vitamin D-resistant rickets
(A) Rachitic rosary (E) Scurvy
(B) Harrison’s groove 13. In a child with osteopenia, jaundice, leth-
(C) Pectus excavatum argy, sleepiness feeding difficulties, and con-
(D) Short stature stipation the most probable diagnosis is:
(E) Periarticular swelling (A) Growth hormone deficiency
8. Regarding VITAMIN D DEFICIENCY, (B) Idiopathic hyperphosphatasia
(A) Serum calcium is usually above normal (C) Hypervitaminosis D
levels. (D) Hypothyroidism
(B) Serum phosphorus is above normal (E) Hypoparathyroidism
levels. 14. Which of the following radiograph signs are
(C) Alkaline phosphatase is below nor- not common in HYPOTHYROIDISM?
mal levels. (A) Skeleton immature for infant’s chrono-
(D) 25(OH) vitamin D is below normal
logic age
levels. (B) Epiphyseal dysgenesis
(E) Serum PTH is below normal levels. (C) Narrow and irregular physis
9. Which of the following are radiographic (D) Thoracolumbar kyphosis
findings of RICKETS? (E) Transverse radiopaque bands in metaph-
(A) Widened growth plate yseal areas and thickened cortices
(B) Cupped metaphysis 15. In a child with loss of appetite, irritability,
(C) Looser’s lines hemorrhage, impaired wound healing, frac-
(D) Angular deformities tures, osteopenia, and thinning of cortices all
(E) Thickening of cortices the above should be considered except:
10. Which is the most frequent inherited form of (A) Scurvy
VITAMIN D-RESISTANT RICKETS? (B) Osteomyelitis
(A) X-linked dominant (C) Leukemia
(B) Autosomal dominant mutations in (D) Purpuric diseases
FGF23 (E) Pseudohypoparathyroidism
(C) Autosomal recessive mutations
82 M. Botton et al.
References
4. Prentice A. Nutritional rickets around the World.
The Journal of Steroid Biochemistry and Molecular
Biology. 2013;136:201–6.
1. Tachdjian pediatric orthopaedics, 5th ed. Saunders.

5. Elder CJ, et al. Rickets. The Lancet.
Chapter 42. Elsevier; 2014.
2014;383(9929):1665–76.
2. Canale T, Beaty J. Campbell’s operative orthopaedics.

6. Mornet E. Hypophosphatasia. Best Pract Res Clin
12th ed. Mosby; 2012.
Rheumatol. 2008;22:113.
3. Glorieux FH. Pediatric bone. Elsevier; 2012.
Orthopaedic-Related Issues
with Genetic Disorders 11
António Robalo Correia, Miguel Botton,
“Nature is nowhere more openly to display her secret mysteries than in cases where she
shows traces of her workings apart from the beaten path”
Victor A. McKusick, Heritable Disorders of Connective Tissue, 1973
Overview • According to the level of limb affection, we

can distinguish between proximal (rhizo-
• More than 200 bone dysplasias have been melic), middle (mesomelic), and distal
identified and the majority of them are rare. (acromelic).
• Genetically transmitted dysplasias present • In some cases, the form of the skeleton makes
with growth modifications of the trunk and/or it possible to further classify the bone dyspla-
extremities due to structural abnormalities of sias into diastrophic (twisted) or campomelic
the bone and/or cartilage. (bent).
• These changes usually result in short stature • There are two major classification systems
(“dwarfism”), which can be proportionate or accepted worldwide:
disproportionate; in the last case, dysplasias
can be “short trunk” or “short limb.”
A. Dynamic Classification of Bone Dysplasiasa

Epiphyseal Physeal Metaphyseal Diaphyseal
B. International Nomenclature of Constitutional Disease of Boneb
Osteochondrodysplasias Dysostoses Idiopathic Chromosomal Primary metabolic
(cartilage and bone (malformation of osteolyses aberrations abnormalities
growth) individual or associated
bones)
Mnemonics: COP ID (chromosomal aberrations—osteochondrodysplasias—primary metabolic abnormalities—idio-
pathic osteolyses—dysostoses)
a
Rubin P. On organizing a dynamic classification of bone dysplasias. Arthritis Rheum. 1964;7:693–708
b
Rimoin DL, Francomano GA, Giedion A, Hall C, Kaitila I, Cohn D, et al. International nomenclature and classification
of the osteochondrodysplasias (1997). International Working Group on Constitutional Diseases of Bone. Am J Med
Genet. 1998;79(5):376–82
A. R. Correia M. Botton · M. C. Neves (*)

Department of Orthopaedic Surgery, Hospital José Hospital CUF Descobertas, Lisbon, Portugal
Joaquim Fernandes, Beja, Portugal e-mail: Manuel.CassianoNeves@jmellosaude.pt

84 A. R. Correia et al.
Zooming In Mnemonics: ARMS DO

(autosomal-rhizomelic-metaphyseal-stenosis-
Achondroplasia (A) dominant-osteotomies).
Definition: “Classic” rhizomelic dwarfism,

with metaphyseal involvement only. Short Pseudoachondroplasia (PA)
stature, one of the most striking features, is a
consequence of enchondral ossification fail- Definition: Similar to achondroplasia, but with
ure; intramembranous and periosteal ossifica- normal head and face and epiphyseal involve-
tion rest intact. The width of the long bones ment also.
depends on intramembranous and periosteal Genetic transmission: Heterogeneous, both
ossification, so the bones have a normal diam- autosomal dominant and recessive.
eter. Frontal bossing and trident hands are Gene defect: COMP gene, which encodes carti-
some other key clinical features. The intelli- lage oligomeric matrix protein, mapped to 19p13.1.
gence is normal and life expectancy is just Clinical aspects:
slightly diminished.
Genetic transmission: Autosomal dominant; 1 . Not apparent until 2 years of age.
80% have de novo mutation. 2. No interpedicular narrowing and no spinal

Gene defect: Mutation in fibroblast growth stenosis.
factor receptor-3 gene (FGFR3), on chromo- 3. Cervical instability due to odontoid hypoplasia.
some 4P, resulting in a reduction in number and 4. Platyspondyly and lumbar lordosis.
disarray of chondrocytes in the proliferative 5. Genu valgum.
zone of the physis, with loss of columnization 6. Pelvis: Shallow acetabulum and widening of
and normal proliferation, with the presence of the great sciatic notch.
fibrous tissue in the zone of provisional 7. Hip and knee arthritis.
calcification.
Clinical aspects: Treatment points:
1. Short stature. 1. Atlantoaxial posterior fusion and immobiliza-

2. Foramen magnum stenosis. tion in a halo brace.
3. Spinal stenosis (especially lumbar). 2. Osteotomies, taking into account the ligamen-
4. Thoracolumbar kyphosis. tous laxity and the possibility of recurrence.
5. Genu varum. 3. Difficult, due to the incongruity femur-

6. Pelvis: Horizontal acetabulum and narrowing acetabulum; valgus osteotomy of the proxi-
of greater sciatic notch. mal femur may improve joint congruity and
7. Upper extremities: Flexion contractures of the Chiari osteotomy or shelf acetabular aug-
elbows and subluxation of the radial heads. mentation may improve coverage of the fem-
oral head; hip replacement is technically
Treatment points: demanding.
1. Bone lengthening.
2. Decompressed symptomatic stenosis. Osteogenesis Imperfecta (OI)
3. Brace if mild curves; anterior strut corpec-
tomy and posterior fusion if curve is >60° by Definition: Abnormal bone fragility, with an
age 5. incidence of 1 in 20,000 children. It is often
4. Osteotomies or hemiepiphysiodesis for genu called brittle bone disease. Histologically, it is
varum if symptomatic. characterized by a decreased number of trabecu-
11 Orthopaedic-Related Issues with Genetic Disorders 85
lae and cortical thinning, with an increased num- Treatment points:

ber of osteoblasts and osteoclasts.
Genetic transmission: Autosomal dominant 1. Fracture prevention: Through bracing (?) and
and recessive forms. bisphosphonates; fracture treatment: conser-
Gene defect: Mutations in the genes coding vative <2 years old and fixation with telescop-
for type I collagen (COL1A1- mapped to ing rods if >2; bowing deformities:
17q21.33 and COL1A2- mapped to 7q21.3). realignment osteotomy with rod fixation.
Clinical aspects: 2. Scoliosis: Operate when curves >45° in mild
forms and >35° in severe forms.
1. Fractures occur during childhood, heal at the 3. Basilar invagination: Bone resection via tran-
normal rate, but with impaired remodelling. soral approach.
2. Scoliosis.
3. Compression vertebral fractures. Mnemonics: AS BOBS (autosomal-Sillence-
4. Ligamentous laxity. blue sclerae-osteotomies-basilar invagination-
5. Basilar invagination. scoliosis).
Modified Sillence classification:

Mucopolysaccharidoses (MPS)
1. Blue sclerae; preschool, mildest form; normal
or low-normal height; multiple bone fractures Definition: A group of metabolic syndromes
occur during childhood, but are less common presenting proportionate dwarfism, caused by
after puberty. the absence or malfunctioning of lysosomal
2. Blue sclerae; perinatal lethal; the child has enzymes which break down glycosaminogly-
short, crumpled femurs and ribs as well as cans. The incomplete degradation product accu-
hypoplastic lungs. Commonly, central ner- mulates in lysozymes in tissues such as the
vous system malformations and haemorrhage brain, viscera and joints. In the intramedullary
are present. space, this accumulation contributes to symp-
3. More severe survivable form, with fractures toms of spinal cord compression. These syn-
presenting at birth; there is a large skull and an dromes can be divided into Hurler (MPS I),
underdeveloped conformation of the facial Hunter (MPS II), Sanfilippo (MPS III), Morquio
bones in a triangular shape; the sclerae are pale (MPS IV), Scheie (MPS V) and Maroteaux-
blue at birth, becoming normal at puberty; mul- Lamy (MPS VI). Morquio and Scheie have the
tiple long bone and vertebral fractures are pres- better prognosis, with normal or near-normal
ent, leading to kyphosis and a severe scoliosis. life expectancy. Cardiopulmonary pathology
4. Moderate form of OI characterized by short severely affects the four other forms.
stature, bowing bones and vertebral fractures. Genetic transmission: Autosomal recessive,
Most of these patients are ambulatory, being except for X-linked Hunter syndrome.
less severely affected than in type III. The Gene defect: Each type has a deficiency of a
sclera typically is white. specific lysosomal enzyme.
5. Characteristic hypertrophic callus after frac- Clinical aspects:
ture, with ossification of the interosseous
membrane between the tibia and fibula and 1. Odontoid hypoplasia or aplasia, with resulting
the radius and ulna. C1–C2 instability.
6. Moderate form, similar to type IV, but with 2.
Progressive platyspondyly with thoracic
abnormalities of mineralization rather than kyphosis.
collagen. 3. Early knee and hip arthritis, with progressive
7. Rhizomelia and coxa vara. acetabular dysplasia.
4. Genu valgum. Treatment points: Enzyme replacement, sub-

5.
Finger triggering and carpal tunnel strate reduction and bone marrow transplant.
syndrome. Bone complications treated accordingly to the
pathology present.
Treatment points: Mnemonics: FEEL OP (fracture-enzyme-
Erlenmeyer-lysosomal-osteomielitis/
1. C1–C2 fusion. necrosis-pseudarthrosis).
2. A progressive deformity should be surgically
stabilized.
3. Total joint arthroplasty. Neurofibromatosis (NF)
4. Guided growth and realignment osteotomies
may restore limb alignment, although recur- Definition: Congenital disorder of the neural
rence is common. crest with spinal and extremity involvement,
5. Surgical releases. being the most common single-gene disorder in
6. Marrow transplantation: Can increase life
humans. There are three forms of presentation:
span, although most children develop the typi-
the NF1 (von Recklinghausen disease), the most
cal skeletal phenotypic features despite its common. For diagnostic purposes, there must
success. be at least two of these cardinal clinical find-
ings: (1) Six or more café-au-lait spots (larger
Mnemonics: SHAMES OH MVP (Scheie- than 5 mm in diameter in a child or 15 mm in an
Hurler-acetabular dysplasia-Morquio-enzyme- adult); (2) two neurofibromas or a single-plexi-
Sanfilippo-odontoidhypoplasia-Hunter-Maroteaux- form neurofibroma; (3) freckling in the axilla or
valgum-proportionate dwarfism). inguinal region; (4) an optic glioma; (5) two or
more Lisch nodules (hamartoma of the iris); (6)
a distinctive osseous lesion such as vertebral
Gaucher Disease (GD) scalloping or cortical thinning; (7) a first-degree
relative with neurofibromatosis type 1. The two
Definition: The most frequent lysosomal storage other forms are NF2 (associated with bilateral
disease. vestibular schwannomas) and segmental NF.
Genetic transmission: Autosomal recessive. Genetic transmission: Autosomal dominant.
Gene defect: GBA gene, mapped to 1q21, Gene defect: Mutation in NF1 gene on chro-
which encodes the beta-glucocerebrosidase mosome 17q21.
enzyme. Clinical aspects:
Clinical aspects: Bone-related manifestations:
fracture, osteomyelitis, osteonecrosis, osteopenia, 1. Scoliosis (not present in NF2):
pseudarthrosis and distal femur (Erlenmeyer flask (a) Idiopathic: Similar to idiopathic scoliosis
deformity—80%), and proximal tibia deformi- with a large curve.
ties. There are three different types: (b) Dystrophic: Short segmented and sharp
curve.
1. Adult (type 1): Easy bruising, anaemia,
2. Anterolateral bowing and pseudarthrosis of
fractures. the tibia.
2. Infantile (type 2): Lethal. 3. Pseudarthrosis of a long bone typically is

3. Juvenile (type 3): Onset in teen years, throm- associated with NF.
bocytopenia, anaemia, enlarged liver, frac- 4. Limb overgrowth associated with neurofibro-
tures, gradual brain involvement. mas, which can turn malignant into neurofi-
brosarcomas. Malignancy in patients with NF Metaphyseal Chondrodysplasia (MC)

ranges from less than 1% to more than 20%.
Definition: Disease caused by metaphyseal bone
Treatment points: changes, at the level of the proliferative and
hypertrophic zone of the physis, maintaining nor-
1. Operative for dystrophic form: High rates of mal epiphyses.
pseudarthrosis, even with anterior and poste- Genetic transmission: Autosomal recessive
rior fusions. (McKusick); autosomal dominant (Schmid and
2. Bone grafting plus surgical fixation in frac- Jansen).
tures or pseudarthrosis (vascularized fibula) or Gene defect: Three main subtypes can be
amputation followed by prosthetic replace- found:
ment in selected cases.
1. McKusick: RMRP gene, which has been
mapped to chromosome 9.
Marfan Syndrome (MS) 2 . Schmid: COL10A1 gene, on chromosome
6.
Definition: Connective tissue pathology with mul- 3. Jansen: PTH/PTHrP (parathyroid hormone-
tiorganic manifestations due to a mutation in the related peptide) receptor gene on chromo-
gene encoding for the fibrillin protein. There is an some 3.
increased availability of transforming growth
factor-β, responsible for an increase in cellular and Clinical aspects:
longitudinal bone growth, leading to tall stature.
Genetic transmission: Autosomal dominant. 1. Angular deformities, particularly genu varum;
Gene defect: Mutation in the fibrillin-1 gene coxa vara produces a waddling gait.
(FBN-1) mapped to 15q21. 2. Hindfoot varus, with midfoot and forefoot

Clinical aspects: valgus.
1. Hyperlaxity: Responsible for subluxation of Treatment points:

joints, sprains and scoliosis.
2. Arachnodactyly. 1. Hemiepiphysiodesis; valgus osteotomy of
3. Protrusio acetabuli (present in one-third of the proximal femur for significant coxa
patients). vara.
4. Pes planovalgus. 2. Calcaneal sliding osteotomy.
5.
Non-skeletal deformities: Cardiovascular
changes of the mitral valve and dilatation of
the aorta; ophthalmology—characterized by Spondyloepiphyseal Dysplasia (SED)
myopia and superior lens luxation; pectus
excavatum. Definition: Short-trunk dwarfism, resulting from
an epiphysary defect caused by abnormal synthe-
Treatment points: sis of type II collagen.
Genetic transmission: Autosomal dominant
1. Surgery has a role in fast-progressing curves (SED congenita) and autosomal recessive
in skeletally immature patients or large curves (X-linked SED tarda). Half of the cases result
in skeletally mature patients. from a random mutation.
2. Mainly nonoperative. Gene defect: COL2A1 on chromosome 12.
Clinical aspects: Treatment points:
1. C1 to C2 instability causing cervical

1. Surgically improving acetabular coverage in
myelopathy. early years; joint replacement in adulthood.
2. Scoliosis. 2. Early corrective osteotomy or
3. Hip dysplasia due to coxa vara. hemiepiphysiodesis.
4. Genu valgus.
5. Breathing problems related to thoracic

dysplasia. Cleidocranial Dysostosis (CD)
6. High-grade myopia and retinal detachment.
Definition: Proportionate dwarfism in which there is
an abnormal intramembranous ossification, result-
Treatment points:
ing in affection of clavicles (hypoplastic or even
absent), cranium and pelvis. Enchondral growth is
1. Posterior atlantoaxial fusion in the case of
also, disturbed, although to a lesser degree. Affects
myelopathy or atlantoaxial instability.
approximately 1 in 1,000,000 children.
2. Bracing for mild scoliosis or posterior instru-
Genetic transmission: Autosomal dominant.
mentation if curvatures >50°.
Gene defect: Defect in CBFA1 gene located
3. Valgus intertrochanteric osteotomy if coxa

on chromosome 6p21 (transcription factor which
vara angle <100°; progressive coxa vara; or
regulates osteoblastic differentiation).
symptomatic hip arthritis.
Clinical aspects:
1. Loss of the lateral end of the clavicle; scapular

Multiple Epiphyseal Dysplasia (MED) winging may be painful or symptomatic.
2. Unossified pubic rami.
Definition: Large spectre of disorders of short- 3. Coxa vara.
limb dwarfism caused by multiple delayed and 4. Scoliosis.
irregular epiphysary ossification. 5. Delayed fontanelle ossification.
Genetic transmission: Autosomal dominant.
Gene defect: Cartilage oligomeric matrix pro- Treatment points:
tein (COMP) on chromosome 19; mutations that
code for type IX collagen (COL9A1, COL9A2, 1. Majority do not need intervention; scapulo-
COL9A3) have an impact on type II collagen, thoracic arthrodesis for symptomatic scapular
impairing its function. winging.
Clinical aspects: 2. Valgus osteotomy of the proximal femur; pel-
vic osteotomy in older children.
1. Late childhood presentation. 3. Same as idiopathic scoliosis.
2. Epiphyseal deformation of large joints result-
ing in early arthritis.
3. Similar to Perthes disease. But in this case, Diastrophic Dysplasia (DD)
bilateral presentation with same staging
degree. Definition: Rare form of micromelic dwarfism
4. Progressive genu valgum. that results from impairment of enchondral
5. Abnormal ossification (tibial “slant sign” and growth and articular cartilage vulnerability and
flattened femoral condyles, patella with dou- early degeneration, with progressive deformity
ble layer). (“twisted dwarf”).
Genetic transmission: Autosomal recessive. showed foramen magnum stenosis with spinal
Gene defect: Mutation in DTDST gene on cord compression at the C1 level.
chromosome 5.
Clinical aspects:
1. Spinal deformity is universal, presenting cer-

vical kyphosis and scoliosis.
2. Hip degenerative disease, because of femoral
head deformity and joint contractures.
3. Genu valgum.
4. Clubfeet and skewfeet.
5. “Hitchhiker’s thumb” (shortening of the trian-
gular first metacarpal and radial subluxation
of the metacarpophalangeal joint).
6. Cauliflower ears (80%).
7. Cleft palate (60%).
Treatment points:
1. Monitor cervical kyphosis and fuse if found

increasing; early surgery—anterior and poste-
rior spinal fusion—is indicated for severe sco-
liosis, as any delay only leads to stiffer This is mandatory for surgical decompression.
deformities. After partial resolution of symptoms with otolar-
2. Hips are very difficult to reduce, even openly; yngological treatment, she was then submitted to
osteotomy is often done to improve gait in C1 laminectomy and posterior fossa craniectomy.
patients with joint contractures; proximal val-
gus extension femoral osteotomy has had pos-
itive results in some cases. Joint replacement
can be beneficial in young adults.
3. Genu valgum does not usually require
correction.
4. Equinovarus requires surgical correction,

when the child is about to learn to walk; talec-
tomy and talar decancellation are sometimes
necessary if surgical releases fail.
Case Studies
Case 1: Female child diagnosed at birth with

achondroplasia. At 2 months old, she presented
with severe sleep apnoea and hypotonia.
How to investigate this child?
One of the major features in achondroplasia is We would like you to pay attention to the clin-
a foramen magnum stenosis. The brain MRI ical alarm signs of foramen magnum stenosis
presenting in an achondroplasic child: hypotonia of the telescopic nail and to replace it by a solid
and sleep apnoea. The prognosis is time depen- nail. The question is how to extract the nail.
dant. This is why we should be alert by the clini- One possibility is to straighten the nail under
cal signs, in order to have a fast diagnosis and general anaesthesia, and then proceed to the
early treatment. extraction. In case it fails, the fracture should be
Case 2: 13-year-old skeletally mature girl approached directly and the nail cut with a Midas
with the diagnosis of osteogenesis imperfecta, Rex tool and then proceed to the extraction. Since
made at age of 2 months. She has been treated it is a mature girl, the nail can be solid and can be
with bisphosphonates therapy and telescopic introduced in a regular way by the fossa pirifor-
nail. mis, as seen below.
She presents in the emergency room with
acute pain on the left thigh after a fall.
The X-ray below shows a diaphyseal fracture
over a bending rod.
Case 3: 32-month-old female child that pres-

ents in the emergency room complaining of pain
in the left thigh after a minor trauma. In the previ-
ous medical history, it is referred a fracture of the
wrist that healed uneventfully with normal callus
What would be your attitude towards this formation. At the clinical exam, she has blue
complication? This is a complicated case and the sclerae and proportionate trunk-limb ratio and
surgeon should be prepared to different hypothe- the right femur has a slight valgus/flexum
ses: the main idea is to proceed to the extraction deformity.
How would be your diagnosis? The associa- mandatory to treat the left femur with a growing
tion of the clinical features with one previous nail and it should be considered also the insertion
fracture associated with a femur fracture with a of a prevention rod on the right femur.
minor trauma is very suspicious of osteogenesis Case 4: 17-year-old boy, complaints of non-
imperfecta, probably type I. irradiated right trochanteric pain with reduced
The second question is how to treat this girl? range of motion, already for 4 months. It had
She is more than 2; it’s a second fracture and has started right after a football game. At physical
a deformity on the contralateral femur that exam, it was noticed a large liver and his blood
predisposes to a fracture. For these reasons, it is tests showed anaemia. The X-rays below reveal:
An enlargement of the distal metaphysis of 3. Which of the listed below is not a

both femurs, compatible with an Erlenmeyer- M U C O P O LY S A C C H A R I D O S I S
flask deformity, is a typical bone-related manifes- subtype?
tation of the Gaucher disease. We also can see a (a) Hurler.
pseudarthrosis of the femoral neck over a scle- (b) Sanfilippo.
rotic bone marrow, involving the proximal femur. (c) McKusick.
These features, associated with the clinical and (d) Scheie.
laboratory exam, are typical for a Gaucher (e) Maroteaux-Lamy.
disease. 4. Which one is true about the
How would you treat this adolescent and “HITCHHIKER’S THUMB”?
which inherent complication would you fear the (a) It occurs in multiple epiphyseal dyspla-
most? sia and consists of shortening of the tri-
The initial treatment of this disease should angular second metacarpal and cubital
always start with an enzyme-replacement ther- subluxation of the metacarpophalangeal
apy. The pseudarthrosis of the femoral neck joint.
should be treated by internal fixation plus valgus (b) It occurs in metaphyseal chondrodysplasia
osteotomy and bone grafting. The most feared and consists of shortening of the triangular
complication would be avascular necrosis of the first metacarpal and radial subluxation of
femoral head. the metacarpophalangeal joint.
(c) It occurs in diastrophic dysplasia and
consists of shortening of the triangular
Review Questions first metacarpal and cubital subluxation
of the metacarpophalangeal joint.
(d) It occurs in multiple epiphyseal dyspla-
1. About the SKELETAL DYSPLASIAS, sia and consists of shortening of the tri-
which of the sentences below is false: angular second metacarpal and radial
(a) To observe the patient’s facies is impor- subluxation of the metacarpophalangeal
tant to pick up diagnostic clues. joint.
(b) To distinguish the dysplasias with fre- (e) It occurs in diastrophic dysplasia and
quent spinal involvement from those consists of shortening of the triangular
without can be very useful in patient first metacarpal and radial subluxation
management and follow-up. of the metacarpophalangeal joint.
(c) Those with metaphyseal involvement 5. About the ACHONDROPLASIC PELVIS,
have the most augmented risk of which is true?
developing degenerative joint disease. (a) The ilium is broad because the pelvis is
(d) Pseudoclaudication and standing dis-
formed almost entirely by enchondral
comfort can be a clinical sign of spinal ossification, which is undisturbed in
stenosis in an achondroplasic patient. achondroplasia.
2. Which of the ones below is not a clinical or (b) The sciatic notches are normal.
imagiologic feature of (c) The acetabula are vertical.
ACHONDROPLASIA? (d) Enchondral ossification pathology at the
(a) Normal intelligence. triradiate cartilage leads to abnormal
(b) Delayed motor milestones. horizontal growth of the iliac contribu-
(c) Presence of frontal bossing, button noses tion to the acetabulum and therefore to
and small nasal bridges. radiographic flattening.
(d) Trident hands, bowed legs and radial
(e) The pelvis takes on the appearance of
head subluxation. a champagne glass because the width
(e) Short lumbar pedicles, with increased of the pelvic inlet is greater than its
interpedicular distance from L1 to S1. depth.
6. Which of the deformities below is not com- (d) Reduction in the number of chondro-

mon in DIASTROPHIC DYSPLASIA? cytes in the hypertrophic zone of the
(a) Cervical kyphosis. physis.
(b) Scoliosis. (e) Increase in the number of chondro-

(c) Hip degenerative disease. cytes in the degenerative zone of the
(d) Genu valgum. physis.
(e) Flatfeet. 12. In PSEUDOACHONDROPLASIA one of
7. In the SPONDYLOEPIPHYSEAL the sentences below does not apply:
DYSPLASIA (SED)—tarda form, the (a) Apparent at birth.
genetic transmission is: (b) No interpedicular narrowing and no spi-
(a) Autosomal dominant inheritance. nal stenosis.
(b) Autosomal recessive inheritance. (c) Cervical instability due to odontoid
(c) X-linked dominant inheritance. hypoplasia.
(d) X-linked recessive inheritance. (d)
Platy-spondylolyses and lumbar
(e) Mitochondrial inheritance. lordosis.
8. The MARFAN SYNDROME is character- (e) Genu valgum.
ized by all the above except: 13.
In a patient with OSTEOGENESIS
(a) Scoliosis. IMPERFECTA which of the following is
(b) Arachnodactyly. false?
(c) Protrusio acetabuli. (a) Clinical picture characterized by abnor-
(d) Talipes equinovarus. mal bone fragility.
(e) Changes of the mitral valve and dilata- (b) Has an incidence of 1 in 20,000

tion of the aorta. children.
9. Regarding ACHONDROPLASIA which of (c) Mutations in the genes coding for type I
the sentences below does not apply: collagen (COL1A1 and COL1A2).
(a) Short stature recognized at birth. (d) Histology shows decreased number of
(b) Foramen magnum stenosis. trabeculae and cortical thickness.
(c) Spinal stenosis (especially lumbar). (e) Fractures heal at a slower rate.
(d) Thoracolumbar kyphosis. 14. In a patient with
(e) Genu valgum. MUCOPOLYSACCHARIDOSES which
10. All sentences below are common in
of the clinical aspects below is not common?
NEUROFIBROMATOSIS except: (a) Odontoid hypoplasia or aplasia, with
(a) Long-ray scoliosis. resulting C1–C2 instability.
(b) Anterolateral bowing tibia. (b) Progressive platyspondyly with thoracic
(c) Pseudarthrosis of the tibia. kyphosis.
(d) Limb overgrowth. (c) Early knee and hip arthritis, with pro-
(e) “Café au lait” spots. gressive acetabular dysplasia.
11. The gene defect in ACHONDROPLASIA (d) Cavus foot.
is characterized by a mutation in fibroblast (e) Finger triggering and carpal tunnel
growth factor receptor-3 gene (FGFR3), on syndrome.
chromosome 4P, resulting in: 15. MULTIPLE EPIPHYSEAL DYSPLASIA
(a) Reduction in the number of chondro- is characterized by except:
cytes in the proliferative zone of the (a) Short-limb dwarfism.
physis. (b)
Autosomal dominant genetic
(b) Increase in the number of chondrocytes transmission.
in the proliferative zone of the physis. (c) Epiphyseal deformation of large joints.
(c) Increase in the number of chondrocytes (d) Progressive genu valgum.
in the hypertrophic zone of the physis. (e) Progressive cavus foot.
References 11. Unger S. Pseudoachondroplasia and multiple epiphy-

seal dysplasia: new etiologic developments. Am J
Med Genet. 2001;106:244.
1. Neves C, et al. Lesões Osteoarticulares na Doença de
12. Wynne-Davies R, et al. The prevalence of skeletal
Gaucher (A propósito de um caso clínico). Rev Ortop
dysplasias, an estimate of their minimum frequency
Traum. 1987;13P, 1B, n°1:55–8.
and the number of patients requiring orthopaedic care.
2. Dietz FR, et al. Update on the genetic bases of dis-
Edinburgh: JBJS; 1984.
orders with orthopaedic manifestations. J Bone Joint
13. http://www.orthobullets.com/pediatrics.
Surg Am. 1996;78:1583.
14. http://www.omim.org.
3. Gonçalves L, et al. Fetal biometry of skeletal dys-
plasias, a multicentic study. J Ultrasound Med.
1994;13(12):977–85.
4. Gordon N. The neurological complications of achon- Future Directions: Promising Articles
droplasia. Brain and Development. 2000;22:3.
5. Gregory D, et al. Genetic causes of chronic musulo-
Baldridge D, et al. Signaling pathways in human skel-
skeletal disease in childhood aare common. Am J Med
etal dysplasias. Annu Rev Genomics Hum Genet.
Genet. 1984;19:533–8.
2010;11:189–217.
6. Horan F, et al. Orthopaedic problems in inherited
Foldynova-Trantirkova S, et al. Sixteen years and count-
skeletal disorders. New York: Springer; 1982.
ing: The current understanding of fibroblast growth
7. Orthopaedic Knowledge Update (OKU) 10. Chapter
factor receptor 3 (FGFR3) signaling in skeletal dys-
62 (Skeletal dysplasias, connective tissue diseases,
plasias. Hum Mutat. 2012;33(1):29–41.
and other genetic disorders, 797:810), AAOS; 2011.
Krakow, et al. The skeletal dysplasias. Genet Med.
8. Rubin P. Dynamic classification of bone dysplasias.
2010;12:327–41.
Chicago: Year Book; 1964.
Riminucci, et al. Stem cells and bone diseases: new tools,
9. Sillence DO, et al. Genetic heterogeneity in osteogen-
new perspective. Bone. 2015;70:55–61.
esis imperfecta. J Med Genet. 1979;16(2):101–16.
Yasoda A, et al. Translational research of C-type natri-
10. Tachdjian Pediatric Orthopaedics. 5th edn., Chapter
uretic peptide (CNP) into skeletal dysplasias. Endocr
40 (Skeletal dysplasias, e360:e472), Philadelphia:
J. 2010;57(8P):659–66.
Elsevier Saunders; 2014.
Infectious Diseases
of the Musculoskeletal System 12
Osteomyelitis • Secondary to a contiguous focus of infection

associated with vascular insufficiency.
Risk Factors –– ~35% of cases
–– Primary in patients with diabetes mellitus
• Recent trauma or surgery. or peripheral vascular disease.
• IV drug use. • Hematogenous.
• Immunocompromise. –– ~20% of cases
• Diabetes mellitus. –– Most common site: Vertebrae; mainly lum-
• Peripheral vascular disease. bar spine.
• Peripheral neuropathy. –– Most common in children affecting the
metaphyses of long bones.
–– Most common organism: S. aureus.
hree Major Categories Based
T
on Mechanism of Spread
Classification Based on Duration
• Secondary to a contiguous focus of infection.
–– ~45% of cases • Acute—lasts less than 2 weeks.
–– For example after surgery, trauma, pres- • Subacute—lasts from 2 to 6 weeks.
ence of foreign bodies or wounds. • Chronic—lasts more than 6 weeks.
–– Typically bacterial, but fungal also
possible.
Prognosis
• Recurrence rate of chronic osteomyelitis

T. Kalathas (*) (despite adequate operative and antimicrobial
Department of Internal Medicine, management): 30%.
Boston Medical Center, Boston, MA, USA –– Reasons for recurrence:
N. K. Paschos Inadequate duration of treatment.
Division of Sports Medicine, Department of Improper antibiotic selection.
Harvard Medical School, Boston, MA, USA Necrotic bone/sequestrum formation.
e-mail: Nikolaos.Paschos@childrens.harvard.edu Defective immune system.

96 T. Kalathas and N. K. Paschos
• Chronic osteomyelitis only treated with radi- –– If blood culture positive with consistent
cal resection due to avascularity of bone. radiologic findings biopsy may be omitted.
• Chronic osteomyelitis may recur as acute –– If clinical suspicion high but blood culture
exacerbations suppressed by debridement fol- and needle biopsy negative, repeat needle
lowed by antibiotics. biopsy or perform an open biopsy.
• Rare complications: • Imaging studies:
–– Pathologic fractures. –– X-ray of involved area.
–– Secondary amyloidosis. Used always first.
–– Squamous cell carcinoma at the sinus tract Changes evident after 10–14 days in adults
orifice. and 5–7 days in children when at least
50–75% of bone matrix is destroyed (low
sensitivity).
Symptoms Changes associated with acute osteomyeli-
tis: periosteal thickening or elevation, cor-
• Nonspecific symptoms: tical thickening, sclerosis, irregularity, loss
–– Fever, of trabecular architecture, osteolysis, new
–– Fatigue, bone formation.
–– Lethargy, Sequestrum: devitalized bone that may
–– Irritability. lead to infection.
• Classic signs of inflammation: local pain, Involucrum: formation of new bone around
swelling, redness, warmth. a necrotic area.
–– Disappear after 5–7 days. –– MRI of involved area:
Used if X-ray negative but suspicion high.
Can detect abnormalities as early as
Workup 24–48 h after onset.
High sensitivity (~95%).
• Labs. –– Bone scan:
–– CBC: Used if X-ray negative but suspicion high
Anemia of chronic disease and leukocytosis and MRI contraindicated.
present. High sensitivity.
Chronic osteomyelitis typically with nor- Low specificity (increased metabolic activ-
mal WBC count. ity often present in posttraumatic injury,
–– ESR, CRP: post-surgery, cancer as well).
Useful in assessing effectiveness of –– CT scan of involved area:
treatment. Useful for: guiding needle biopsy, preop-
Should be checked every 48–72 h. erative planning.
If not reducing while on therapy suspect
and seek for occult abscesses.
• Blood culture: Staging
–– Sensitivity ~50%.
–– Obtain before or at least 48 h after treatment. • Cierny-Mader classification system most
–– Culture of the sinus tract may be useful if S. commonly used.
aureus or Salmonella species isolated on First part:
blood culture. Stage 1—medullary bone affected by a
• Bone biopsy: single organism.
–– Definitive diagnosis. Stage 2—surfaces of bones affected and
–– Perform either before or more than 48 h may occur with deep wounds or ulcers.
after discontinuance of treatment and Stage 3—advanced polymicrobial, local
through uninfected tissue. infection of bone and soft tissue associ-
12 Infectious Diseases of the Musculoskeletal System 97
ated with an intramedullary rod or open –– Marginal resection in immunocompe-

fracture. tent hosts.
Stage 4—extensive disease involving mul- –– Extensive resection in immunocom-
tiple layers. promised hosts.
Second part: • Management of dead space:
Class A—normal physiologic, metabolic, –– Typically, filled with vascularized tis-
and immune functions. sue from the fibula or ilium.
Class B—systematically (Bs) or locally –– Antibiotic-impregnated beads may be
(Bl) immunocompromised. used but replaced within 1–2 weeks
Class C—treatment poses a greater risk with cancellous bone graft.
than the infection itself. –– The Ilizarov method may be used if
correction of the deformity or length-
ening is needed.
Medical Therapy • Adequate soft-tissue coverage:
–– For small defects: Split-thickness skin
• Antibiotic therapy is based on the results of graft.
bone culture. –– For large defects: Local muscle flaps
• Start parenteral antimicrobial treatment after and/or free vascularized muscle flaps.
bone cultures obtained and modify if needed • Stabilization:
when results available. –– External fixation preferred:
• In open fractures start prophylactic treatment May be related to improved
combining systemic antibiotics with antibiotic angiogenesis.
beads. Adjunctive hyperbaric oxygen therapy
• Duration of treatment: typically, 4–6 weeks. may also be used to promote healing.
• Antibiotics that can be used: clindamycin,
rifampin, TMP-SMX, fluoroquinolones.
• Typical organisms involved: Complications
–– Hospital-acquired: MRSA.
–– Community-acquired: polymicrobial. • Recurrence of bone infection (even in 5–10%
• Suppressive oral antibiotic therapy used for of patients treated appropriately).
6–9 months to prevent recurrence; TMP-SMX • Persistence or extension of infection.
has proven most useful. • Amputation.
• If relapse after 6 months of suppressive therapy, • Sepsis.
try lifelong regimen of suppressive therapy. • Marjolin’s ulcer (skin squamous cell carci-
noma developed in the setting of draining
sinus tract).
Surgical Therapy • Pathologic fracture.
• Secondary amyloidosis.
(a) Surgery indications:
• Stage 3 or 4 (Cierny-Mader classification).
• Abscess formation. Septic Arthritis
• Draining sinus.
(b) Preoperative CT may be used: Risk Factors
• To assess bone quality, demonstrate
intraosseous fistula and detect devitalized • Age >80 y.o.
bone areas or cortical defects. • Presence of prosthetic joint (most common).
(c) Operative treatment includes: • History of joint disease (e.g., osteoarthritis,
• Adequate drainage. rheumatoid arthritis, crystal arthropathy,
• Extensive debridement of necrotic tissue. recent joint surgery).
• Immunocompromise (e.g., AIDS, diabetes –– If crystals present and Gram stain negative,
mellitus, cirrhosis). treat as crystal-induced arthropathy.
• Bacteremia. –– If no crystals present, treat the patient for
presumed infection (even if gram stain neg-
ative—sensitivity: ~50%).
hree Major Categories Based
T –– WBC count in septic arthritis: typically,
on Mechanism of Spread >50,000/μL with >75% PMNs.
• CRP, ESR—useful for monitoring response to
• Bacteremia (e.g., infectious endocarditis, therapy.
IVDU)—most common route. • Obtain at least two sets of blood cultures to
• Direct inoculation (e.g., trauma, surgery). rule out bacteremia.
• Contiguous spread (e.g., adjacent osteomyelitis). • If gonococcal arthritis suspected, obtain also
cultures from rectum, cervix, urethra, phar-
ynx, and any skin lesions.
ost Common Organisms Associated
M • X-ray/CT scan/MRI of the joint:
with Septic Arthritis –– Of limited value in septic arthritis.
–– Mostly used to rule out underlying osteo-
• Staphylococcus aureus—50% of cases in myelitis, periarticular abscesses or joint
adults and children >2 years old. effusions.
• Neisseria gonorrhea—mainly in young sexu- • Radionuclide scan:
ally active patients. –– May be used in diagnosing septic arthritis
• Streptococcal species—20%. in sequestered areas, such as the hip or sac-
• Gram-negative bacilli—20%. roiliac joints.
• Polymicrobial—5–10%.
Medical Therapy
Most Common Joints Affected
• Antibiotics:
• Knee—50%. –– Evaluate each case separately and initiate
• Hip—20%. empirical ABX based on the sensitivity
• Shoulder—8%. pattern of the pathogens of the
• Ankle—7%. community.
• Wrists—7%. –– MRSA, MSSA: need at least 4 weeks of IV
ABX.
–– Prosthetic joint infections (PJI): always use
Symptoms combination including rifampin.
–– Gonococcal arthritis: oral ABX typically
• Pain in affected joint. used administered concurrently with ther-
• Fever (in 60% of patients). apy for chlamydia.
• May lead to septic shock. –– If after 5 days of empirical treatment the
• Signs of inflammation present in affected joint patient responds well, consider an empiri-
(pain, redness, increased temperature, swell- cal trial of an NSAID,
ing, loss of function). –– If after 5 days of empirical treatment the
patient does not respond as expected
consider:
Workup Fluid reexamination for crystals.
Lyme disease serology.
• Joint aspiration—screen for polarizing crystals, Synovial biopsy for fungal or mycobacte-
send for Gram stain, culture, and WBC count: rial infection.
Use of NSAIDs for suspected reactive • Gas in the tissue.

arthritis. • Hypotension.
Imaging studies for superimposed
osteomyelitis.
• Immobilization of the joint. Workup
–– Needed during the first 5 days.
–– After that, begin gentle mobilization of the • No workup is needed if mild symptoms present.
joint with physical therapy. • If signs of systemic toxicity (e.g., fever, chills,
• Synovial fluid drainage: malaise) present:
–– 2–3 times per day over the first days using a –– CBC with diff.
needle; if fails consider surgical drainage. –– Blood cultures.
–– Gonococcal arthritis does not need –– Creatinine, bicarbonate, CPK, CRP levels.
aspiration. • U/S if formation of abscess is suspected.
• Surgical therapy in prosthetic joint infection. • Needle aspiration performed only in patients:
–– Debridement with retention of the prosthe- –– With immunocompromise.
sis possible if infection within 30 days of –– With bullae formation.
implantation. –– Not responding to initial therapy.
–– If not, remove the prosthesis and follow –– With Hx of animal bites.
with 6 weeks of ABX.
Consider Hospitalization if
Complications
• Creatinine elevated.
• Osteomyelitis. • CPK > ×2–3 times than normal.
• Fibrous ankylosis. • CRP > 13 mg/L.
• Sepsis. • Serum bicarbonate decreased.
• Marked neutrophilia present.
Cellulitis
Treatment
Signs and Symptoms
• Antibiotics:
• Signs of inflammation (pain, erythema, swell- –– In mild cases: oral cloxacillin, amoxicillin,
ing, warmth). or cephalexin.
• Fever, chills. –– In severe cases: IV cefazolin, cefuroxime,
• Malaise. ceftriaxone, nafcillin, or oxacillin.
• Lymphangitic spread (red lines). • Drainage:
–– If abscess is present.
–– If abscess isolated, drainage alone may
mergent Surgical Evaluation
E suffice.
Needed if
• Violaceous bullae. Necrotizing Fasciitis

• Cutaneous hemorrhage.
• Skin sloughing. Overview
• Skin anesthesia.
• Rapid progression. • Mortality: 20–80%.
• Average age of patients: 38–44 y.o. –– BMP.

• M:F ratio: 2:1. –– ABGs.
–– U/A.
• Blood and deep tissue culture.
Risk Factors • Rapid Strep Diagnostic kit and PCR assay for
tissue specimens.
• Immunocompromise such as: • Imaging.
–– Diabetes mellitus. –– CT, MRI scans of significant value.
–– Cancer. Early diagnosis of the disease.
–– Alcoholism. Delineation of the extent of the disease.
–– AIDS. –– Bedside U/S of limited value.
–– Neutropenia. –– Plain X-rays of no value.
• Bacterial introduction such as: • Finger test.
–– Insect bite, minor abrasion, boil, IVDU. • Tissue biopsy for frozen section analysis.
–– Thoracic or abdominal surgery. • Percutaneous needle aspiration followed by
• One half of the cases occur in young and pre- Gram staining.
viously healthy people. –– When suspicion of the disease is high,
never delay surgical intervention for diag-
nostic workup.
lassification Based on the Causative
C
Organisms
Medical Therapy
• Type I, or polymicrobial:
–– 90% of cases. • Aggressive resuscitation to maintain hemody-
–– Seen in immunocompromised patients. namic stability.
–– Typically, in abdomen or perineum. • Start empirical broad-spectrum IV antibiotic
• Type II, or group A streptococcal: therapy.
–– 5% of cases –– Typically, combination of penicillin G,
–– Seen in healthy patients. aminoglycoside, and clindamycin.
–– Typically, in extremities. –– Adjust per culture results.
• Type III, or clostridial myonecrosis. • Transfer to surgical ICU (burn or trauma cen-
ter ideally).
Signs and Symptoms
Surgical Therapy
• Intense pain that progresses later to anesthesia.
• Tenderness over the involved skin and muscle. • Primary treatment for necrotizing fasciitis.
• Local edema, erythema, skin vesicles, crepi- • Wide, extensive debridement of all tissues that
tus, hardened feel over the involved area. can be easily separated from the fascia fol-
• Fever. lowed by application of daily antibiotic
• Malaise. dressings.
• Amputation can be considered in life-
threatening extensive disease.
Workup • Soft-tissue reconstruction can be
considered.
• Labs: • Hyperbaric oxygen therapy can be considered
–– CBC with diff. if anaerobic organisms identified.
Complications –– Occurs within 30 days of the operation or

within 1 year if an implant is present.
• Renal failure. • Organ/space SSI:
• Septic shock. –– Involves organs or spaces other than the
• Scarring with cosmetic deformity. incision.
• Limb loss. –– Occurs within 30 days of the operation or
• Toxic shock syndrome. within 1 year if an implant is present.
Wound Infection Presentation
• Account for 15% of the hospital-acquired • Purulent drainage.

infections. • Signs of inflammation at incisional site (pain,
• ~70% of the deaths of surgical patients are warmth, edema, redness).
related to surgical site infections (SSIs). • Diagnosis can be suspected even if neither of
the above symptoms is present. In these cases,
clinical judgment and well-defined follow-up
Risk Factors visits may assist in establishing the
diagnosis.
• Immunocompromise (malnutrition, steroids,
AIDS, DM, old age).
• Wound characteristics (necrotic tissue, foreign Workup Possible to Use
body, hematoma, dead space).
• Operative characteristics (poor technique, • Gram and fungal stain.
lengthy operation, prolonged stay in the hos- • Culture.
pital, intraoperative contamination). • ELISA/EIA.
• Northern, Southern, or Western blotting.
• PCR.
Most Common Causes • U/S can be performed in the area to assess if
there is a collection that needs to be drained.
• Staph. aureus—20%.
• Coagulase-negative Staph.—14%.
• Enterococci—12%. Prevention
• E. coli—8%.
• P. aeruginosa—8%. • Use IV antibiotics preventively generally
• Enterobacter species—7%. 30 min before surgery in:
–– Procedures of high risk of infection.
–– Procedures associated with disastrous
lassification Based on Depth
C complications if infected (e.g., total joint
of Spread replacement).
–– Patients with high NNIS risk index consti-
• Superficial incisional SSI: tuted by:
–– Involves skin and subcutaneous tissue. Preoperative patient physical status.
–– Occurs within 30 days of the operation. Operation status.
–– Accounts for the majority of the SSIs. Operation lasting longer than the 75th per-
• Deep incisional SSI: centile of the specific operation
–– Involves fascial or muscle layers. performed.
• Preventive antibiotics may be used up to 24 h Case-Based Discussions

postoperatively.
• Choose antibiotics effective against the most Case 1
likely contaminating microorganism.
A 36-year-old diabetic male presents to the emer-
gency department with a deteriorating rash over
Treatment the last 2 days on his right calf complaining of
severe pain on the same area. When asked, he
• Dressing changes to improve healing (second- admits of frequent IV drug use. His temperature
ary intention healing). is 39 °C and his BP 110/80. On physical exami-
• Wound debridement with subsequent packing nation crepitus is noted and severe tenderness on
may be necessary. the affected area. Which of the following is the
most appropriate next step?
Complications ( A) Right leg X-ray.

(B) CT angiography of chest.
• Increased morbidity and mortality (associated (C) CT of right leg.
with 75% of deaths of surgical patients). (D) MRI of right leg.
• Increased stay in the hospital by 7–10 days. (E) Ultrasound of right leg.
• Increased hospitalization cost by 20%. (F) Tissue biopsy for frozen section analysis.
Recent Developments/Publications Correct answer. F.

in the Field The patient most likely suffers from necrotizing
• According to the results of a recent RCT that fasciitis of his right leg as a result of bacteria
was published in Annals of Internal Medicine, introduction secondary to his immunocompro-
it was shown that in patients with pyogenic mised status (diabetes mellitus) and his IV drug
vertebral osteomyelitis, 6 weeks of antibiotic use. Even though presence of bullae and instabil-
therapy was noninferior to 12 weeks of ther- ity of vital signs are not present at the present
apy for clinical cure [1]. moment they may appear as the disease pro-
• According to the results of a recent study pub- gresses. Since the patient is hemodynamically
lished in July 2016 in the Archives of stable indicating an early state of the disease, we
Orthopaedic and Trauma Surgery, joint should first confirm the diagnosis with tissue
arthrodesis with the external AO frame fixator biopsy before proceeding with antibiotic treat-
is a probable tool to achieve union in septic ment and surgical debridement.
ankle joints, although it is associated with a (A) X-ray has no value in diagnosing necro-
high complication rate such as wound-healing tizing fasciitis. Even though the presence
problems, nonunion, and need for surgical of air may be a sign of the disease, it is
revision. The possible advantage of intramed- neither sensitive nor specific.
ullary nailing has yet to be shown by future (B) Chest CTA is needed to diagnose pulmo-
studies comparing the two methods [2]. nary embolism. There is no sign or symp-
• According to the results of a recent study pub- tom that the patient suffers from a PE.
lished in April 2016 in the Archives of (C, D) Even though CT and MRI scans can dem-
Orthopaedic and Trauma Surgery, it was onstrate significant changes in necrotizing
proved that two-stage treatment of destructive fasciitis, they do not provide the defini-
septic arthritis of the hip joint combined with tive diagnosis.
spacer implantation leads to a high rate of (E) Ultrasound is of limited value in diagnos-
infection control but is associated with a high ing necrotizing fasciitis. It’s mostly
mortality rate between stages. important for deep venous thrombosis.
Case 2 • X-ray should always be performed first when

osteomyelitis suspected.
A 24-year-old driver is involved in a motor vehicle • Blood cultures are typically positive in
accident and suffers an open fracture of humerus. osteomyelitis.
Over the following 10 years he suffers from a persis- • Suppressive antimicrobial therapy typically
tent wound draining malodorous pus whereas over lasts 6–9 weeks.
the last month he has noted a “strange mass” on the • The most common way of spread is
same site. What is the most likely diagnosis? hematogenous.
• The risk for pathologic fracture is decreased in
( A) Basal cell carcinoma. osteomyelitis.
(B) Squamous cell carcinoma.
(C) Melanoma. How long does it take for a regular X-ray to show
(D) Cellulitis. abnormalities in osteomyelitis?
(E) Erysipelas.
(F) Normal posttraumatic reaction. • 2–4 days
• 5–7 days
Correct answer: B. • 7–10 days
The most likely diagnosis in this case is Marjolin’s • 10–14 days
ulcer which most often (90%) represents a type • 14–17 days
of squamous cell carcinoma of the skin that • 17–21 days.
develops in the setting of chronic osteomyelitis,
burns, and skin ulcers. A small percentage of What is the most common cause of early (within
these cancers is basal cell carcinoma, melanoma, 3 months of implantation) prosthetic joint
or sarcoma. infection?
Marjolin’s ulcers are more aggressive compared
to other types of skin cancer (except melanoma) • S. aureus.
with higher rates of metastasis and mortality. The • S. epidermidis.
most typical treatment used for Marjolin’s ulcers is • N. gonorrhea.
amputation of the affected extremity. • Strep. pyogenes.
• P. aeruginosa.
Review Questions What is the most common route of joint

infection?
How long does the antimicrobial treatment of
osteomyelitis typically last? • Contiguous spread.
• Via the bloodstream.
• 1–2 weeks. • Direct inoculation.
• 2–4 weeks.
• 4–6 weeks. What is the most common cause of septic arthri-
• 6–8 weeks. tis in a sexually active 22-year-old man?
Which of the following sentences regarding • S. aureus.

osteomyelitis is correct? • S. epidermidis.
• N. gonorrhea.
• The most sensitive test for diagnosing osteo- • Strep. pyogenes.
myelitis is MRI. • P. aeruginosa.
What is the most common joint affected by septic What is the imaging modality of choice in diag-
arthritis? nosing necrotizing fasciitis?
• Hip. • U/S.
• Knee. • X-ray.
• Shoulder. • CT scan.
• First interphalangeal joint. • MRI scan.
• Scintigraphy.
Which of the following sentences regarding sep-
tic arthritis is correct? Which of the following is the main diagnostic
method for cellulitis?
• It is more common in young adults.
• The best initial test is X-ray of the affected • Physical exam.
joint. • Blood culture.
• Patients with osteoarthritis have lower risk to • Gram stain.
be affected. • CBC.
• S. epidermidis is the most common culprit in • CRP levels.
delayed-onset prosthetic joint infection. • Ultrasound.
Which of the following is typically the treatment

of choice for septic arthritis? References
• IV antibiotics for 3–4 weeks. 1. Zervou FN, Zacharioudakis IM, Mylonakis E. ACP
Journal Club. 6 weeks of antibiotics was noninferior
• IV antibiotics for 4–6 weeks. to 12 weeks for clinical cure in pyogenic vertebral
• IV antibiotics for 1–2 weeks. osteomyelitis. Ann Intern Med. 2015;162(10):JC7.
• Oral antibiotics for 4–6 weeks. https://doi.org/10.7326/ACPJC-2015-162-10-007.
• Direct installation of antibiotics into the joint 2. Suda AJ, Richter A, Abou-Nouar G, Jazzazi M,
Tinelli M, Bischel OE. Arthrodesis for septic arthri-
cavity 2–3 times per day. tis of the ankle: risk factors and complications. Arch
Orthop Trauma Surg. 2016;136(10):1343–8. https://
Which of the following patients is most likely to doi.org/10.1007/s00402-016-2520-y.
have been affected by necrotizing fasciitis?
• A 70-year-old male. Sources for Additional Studying

• A 70-year-old female.
• A 40-year-old male. European Surgical Orthopaedics and Traumatology-
The EFORT Textbook Editors: Bentley,
• A 40-year-old female. George, Springer, EFORT; 2014. https://doi.
org/10.1007/978-3-642-34746-7.
Which type of necrotizing fasciitis is caused by Infections in Orthopaedics and Fractures Eivind Witso.
Clostridium perfringens (gas gangrene or clos- p. 331–356.
http://www.orthobullets.com/trauma/1057/osteomyelitis
tridial myonecrosis)? %2D%2Dadult?expandLeftMenu=true
http://emedicine.medscape.com/article/1348767-
• Type I. overview
• Type II. http://www.orthobullets.com/trauma/1058/septic-
arthritis%2D%2Dadult
• Type III. http://emedicine.medscape.com/article/236299-overview
http://emedicine.medscape.com/article/2051157-
overview
http://emedicine.medscape.com/article/214222-overview
Musculoskeletal Pain Management
13
Avraam Ploumis and Ioannis Gkiatas
Musculoskeletal pain is a result from a complex well localized. It can also present as neuropathic
interplay of mechanical, biomechanical, psycho- pain from inflammation of nerves innervating
logical, and social factors. It is a subjective expe- the musculoskeletal system and it is more dif-
rience, involving sensations and perceptions, fuse pain.
which may or may not be the result of tissue dam- The pain is transmitted at three distinct
age or physical injury. Generally the meaning of levels:
pain will differ among individuals depending on
how pain affects their lives [1]. • Peripheral level
Management of musculoskeletal pain includes • The peripheral nervous system includes affer-
pharmacologic agents, non-pharmacologic (phys- ent neurons, the nociceptors, which are capa-
ical, psychological, social/environmental) inter- ble of detecting noxious stimuli. They are
ventions, and invasive (surgical) methods [2]. divided into two different types:
–– The myelinated delta fibers which transmit
the precise location and quality of a nox-
Pathophysiology ious stimulus rapidly.
–– The unmyelinated C fibers that slowly
Pain is classified as nociceptive and neuropathic transmit sensations of burning, cramping,
pain. Nociceptive is pain produced by stimula- warmth, and itching [3].
tion of specialized receptors of an intact neural • Spinal level
fibers. There are two types of nociceptive pain, The axons of peripheral nociceptors form syn-
somatic (direct pain) and splanchnic (reflex pain). apses with interneurons of the central nervous
Neuropathic pain is pain originating from disor- system in the dorsal horns of the spinal cord.
dered neural fibers. The transmission between peripheral and cen-
Musculoskeletal pain can appear in the form tral nervous system is modulated by the pres-
of somatic nociceptive pain received at skin, ence of local neurotransmitters and descending
muscles, ligaments, joints, and bones and it is supraspinal regulatory signals [4].
• Supraspinal-cerebral level
At this level the ultimate perception of pain is
modulated through a complex interplay of bio-
A. Ploumis (*) · I. Gkiatas chemical, neurologic, and psychological influ-
Departments of Orthopaedics and PMR, University
of Ioannina, Ioannina, Greece ences [3, 5]. The intensity of a painful stimulus
e-mail: aploumis@uoi.gr as well as its character, duration, and quality

106 A. Ploumis and I. Gkiatas
correlate significantly with varying concentra- • Manual therapy (manipulation) with exer-
tions of central neurotransmitters [3]. cise regimen is preferred compared with
exercise regimen alone for the management
Chronic pain can be defined as unremitting of nonspecific chronic neck pain [8] (Akhter
pain lasting more than 6 months [5]. However, et al. Role of manual therapy with exercise
there are certain pathophsyiological mechanisms regime versus exercise regime alone in the
that are involved in chronicity of musculoskeletal management of non-specific chronic neck
pain and it’s not strictly its duration that specifies pain).
acute or chronic pain. The concept of neuronal • Comparing the effects of trigger-point dry
plasticity (the ability of neurons to profoundly needling and trigger-point manual therapy,
alter their structure, function, or biochemical pro- there are similar outcomes as far as it con-
file in response to repeated afferent sensory cerns the pain, disability, and cervical range
input) is now central to the understanding of the of notion. There is greater improvement in
development of chronic pain from acute pain. neck pain intensity, cervical range of motion,
Local inflammation in injured tissue increases and pressure pain thresholds after trigger-
the sensitization of specialized peripheral sen- point dry needling [9] (Liamas-Ramos et al.
sory neurons (nociceptors), leading to repeated Comparison of the short-term outcomes
afferent input into the central nervous system [6]. between trigger dry needling and trigger
point manual therapy for the management of
chronic mechanical neck pain: a randomized
Classification of Musculoskeletal clinical trial).
Pain • For the management of hip pain, ultrasound-
guided hip injections were found more conve-
Musculoskeletal pain is divided into four major nient and less painful than fluoroscopy-guided
categories: hospital-based injections [10]. (Ultrasound-
guided hip injections: a comparative study
• Acute postoperative/posttraumatic musculo- with fluoroscopy-guided injections).
skeletal pain.
• Chronic posttraumatic musculoskeletal/neu-
ropathic pain. Case-Based Discussion
• Arthritic pain.
• Low back or spinal pain. Case 1
• Myofascial pain syndromes (MPS) and fibro-
myalgia (FM). Starting from the spinal pain, a characteristic
example is the low back pain. It is very common
in the general population, affecting both sexes
Recent Developments/Publications and all age groups, and ethnic and socioeconomic
(Last 3 Years) classes [11, 12]. In most of the cases, there is no
specific pathoanatomic underlying cause [13].
• Kinesiophobia predicts greater pain intensity The annual incidence of low back pain ranges
and activity interference. Interventions in the from 15 to 45% [14]. The patient presents with
workplace should be taken into consideration, pain that typically increases with activity and
due to the fact that employment status and decreases with rest (mechanical pain). The goals
race serve as predictors of pain-related out- in the treatment are:
comes [7] (Ang et al. Predictors of pain out-
comes in patients with chronic musculoskeletal • Education of the patients.
pain comorbid with depression: results from a • Relief of the pain.
randomized controlled trial). • Function improvement.
13 Musculoskeletal Pain Management 107
• Minimizing of any adverse effects of the

treatment.
• Prevention of chronicity [13].
As far as it concerns the medication, it includes

analgesics, nonsteroid anti-inflammatory drugs
(NSAIDS), and muscle relaxants. The analgesics
are divided into nonnarcotic analgesics, such as
acetaminophen, which are effective for mild acute
pain; however they are hepatotoxic [15]. Narcotic
analgesics (i.e., tramadol, codeine, morphine) can
be used in patients whose pain is unresponsive to
other medications [16]. Topical analgesics such as
capsaicin or lidocaine or diclofenac can be used to
relief pain in combination with other medications.
NSAIDs in combination with muscle relaxants
seem to be the most effective therapy for the acute
pain in lumbar spine [17, 18]. In a meta-analysis
[19], it is supported that NSAIDs did not provide
greater relief for low back pain than placebo,
despite the fact NSAIDs are widely used for the
treatment of low back pain.
Physical therapy (TENS, acupuncture, elec-
trotherapy) (Fig. 13.1), steroid epidural injection
(Fig. 13.2), and behavioral therapy are second-
line treatments that can be started in the acute Fig. 13.2 Lumbar spine radiograph with dye during
phase but certainly should be included in the transforaminal epidural steroid injection
physician’s armamentarium to treat patients in
the subacute or chronic phases. Together with tance to NSAIDs and muscle relaxant cases.
pharmacologic agents such as anticonvulsants Interventions are applied as a last resort option
and antidepressants, they are indicated for resis- when low back pain is nonresponsive to other
treatments. Options include radiofrequency
nerve root or disc ablation, surgical nerve root
decompression, and fusion.
Case 2
The arthritic pain may be of different severity and

duration. The main causes are:
• Inflammation of the joints.

• Damage to joint tissues caused by the disease
process or from wear and tear.
• Muscle strain caused by overworked muscles
Fig. 13.1 Photo with application of electrotherapy trying to protect joints from painful
patches on shoulder area movements.
• Fatigue caused by the disease process which Case 3

can make the pain seem worse and harder to
handle. Another category of musculoskeletal pain is the
posttraumatic or postoperative pain. It can be
It can be characterized mostly as chronic mus- characterized as acute pain. It can be broadly cat-
culoskeletal pain. It is supported that 50% of egorized as either adaptive or maladaptive pain
patients with chronic pain have mood disorder [28]. A stubbed toe results in minor but persistent
[20] and the incidence of anxiety disorders pain that leads to protection of the toe from fur-
among chronic pain patients is also approxi- ther injury (adaptive pain). On the other hand,
mately 50%, with many patients experiencing maladaptive pain occurs when the nervous sys-
symptoms of both types of disorders [12]. tem is overwhelmed by pain stimulation, result-
A characteristic example is the osteoarthritic ing in a chronic disease state such as a severe
pain of the knee. Among the most frequently rec- phantom pain that persists for years after wound
ommended drugs by orthopedic surgeons for the healing in a person who suffered traumatic foot
arthritic pain relief are the NSAIDs. Their analgesic amputation [29].
effects are closely related to their ability to decrease It is generally accepted that poorly managed
local inflammatory mediators [4]. Prostaglandins pain following trauma or surgery has a negative
and leukotrienes are local hormones known to sen- impact on all major organ systems, i.e., cardio-
sitize C-fiber nociceptors in the peripheral nervous vascular or pulmonary insults [30].
system [21]. The clinical practice guidelines on the Surgical procedures and trauma tissue injury
treatment of symptomatic osteoarthritis of the knee may result in the production and release of chem-
developed by the American Academy of ical mediators that are thought to be responsible
Orthopaedic Surgeons (AAOS) include the use of for activating pain pathways. All joint surgeries
selective, nonselective, and topical NSAIDs [22]. including arthroscopic surgery cause some pain
According to these guidelines, the use of NSAIDs and effusion due to an inflammatory reaction
over placebo for the treatment of osteoarthritic knee mediated by prostaglandins [1].
pain is acceptable [4]. A very common situation of posttraumatic
The potential complications of the wide use of pain is the ankle sprain. Rest, ice, compres-
NSAIDs should also be taken into consideration. sion, and elevation (RICE) is the standard of
The prolonged use of NSAIDs has been associ- initial care of all soft-tissue injuries.
ated with gastrointestinal as well as cardiovascu- Furthermore, NSAIDs that inhibit the cyclo-
lar disorders [23, 24]. The COX-2 selective oxygenase pathway and affect the lipoxygen-
inhibitors may be less harmful for gastrointesti- ase activity of the arachidonic acid cascade
nal toxicity; nevertheless the cardiologic, renal, have been shown to be effective analgesics and
and cerebrovascular threats remain [24]. the reasonable alternatives to oral narcotics in
An anti-arthritic, which is also widely used, is the management of moderate posttraumatic/
the glucosamine. It is the same substance that is postoperative pain [1].
naturally produced and enables the building of Generally the oral route of drug administra-
new cartilage. It combats the osteoarthritis by tion is the preferred route for the management
stimulating the manufacture of glycosaminogly- of pain. It is well tolerated, convenient, and
cans, a natural lubricant and shock absorber, the least expensive mode of treatment and has
which enables the smooth and painless move- the fewest side effects [31]. Intramuscular
ment of the joints [25]. In several double-blind administration of opioids is not recommended
medical studies, it is supported that glucosamine [31, 32]. The administration of intramuscular
not only reduces the symptoms of osteoarthritis, opioids before discharge to home from the
but can also stop the disease in its beginning, and ambulatory setting is particularly dangerous
may even repair some of the damage that has because of unpredictable absorption [31]
already occurred [26, 27]. (Fig. 13.3).
13 Musculoskeletal Pain Management 109
(d) Are often given rectally to patients who

cannot take oral analgesics.
5. Which is the second line in the pain

management?
(a) Analgesics.
(b) Physical therapy.
(c) Steroid.
(d) Intervention.
(e) All of the above.
Mnemonic tricks
Types of pain
NOCICEPTIVE: Noxious Stimuli
Fig. 13.3 Photo of knee injection with hyaluronic acid
Perception
NEUROPATHIC: Nerve Pathology
Soft-tissue injury management
eview Questions (You Can Choose
R RICE: Rest, Ice, Compression, Elevation
More than One Answer) Musculoskeletal pain management levels
Management So Good But Pain Insists 1.
Muscle relaxant, Analgesic, Anti-inflammatory
1. Which is/are the best route for the opioid use? (NSAID) 2. Steroid, Opioid, Glucosamine,
(a) Intravenous (i.v.) Behavioral Therapy, Physiotherapy 3.
(b) Intramuscular (i.m.) Intervention.
(c) Orally.
(d) All the above.
2. Which is/are the most common side effects of References
the use of NSAIDs?
(a) Gastrointestinal. 1. Fetrow KO. The management of pain in orthopae-
dics. Clin J Pain. 1989;5(Suppl 2):S26–32; discussion
(b) Renal. S33–4
(c) Cardiovascular. 2. Nicholas MK. Pain management in musculoskel-
(d) All the above. etal conditions. Best Pract Res Clin Rheumatol.
3. Patients who have underlying chronic (persis- 2008;22(3):451–70. https://doi.org/10.1016/j.
berh.2007.11.008.
tent) pain: 3. Apkarian AV, Baliki MN, Geha PY. Towards a theory
(a) Should stop all of their pain medications of chronic pain. Prog Neurobiol. 2009;87(2):81–97.
before surgery. https://doi.org/10.1016/j.pneurobio.2008.09.018.
(b) Rarely undergo orthopedic surgery. Epub 2008 Oct 5
4. Uhl RL, Roberts TT, Papaliodis DN, Mulligan MT,
(c) Should not be given anticonvulsants Dubin AH. Management of chronic musculoskeletal
postoperatively. pain. J Am Acad Orthop Surg. 2014;22(2):101–10.
(d) May take opioids preoperatively and often https://doi.org/10.5435/JAAOS-22-02-101.
require higher opioid dose 5. Main CJ, Spanswick CC. Pain management: an
interdisciplinary approach. Edinburgh: Churchill
postoperatively. Livingstone; 2000.
4. Nonopioids such as acetaminophen and non- 6. Ekman EF, Kmoan LA. Acute pain following musculo-
steroidal anti-inflammatory drugs (NSAIDs): skeletal injuries and orthopaedic surgery: mechanisms
(a) Should not be given to patients with and management. Instr Course Lect. 2005;54:21–33.
7. Ang DC, Bair MJ, Damush TM, Wu J, Tu W, Kroenke
chronic pain. K. Predictors of pain outcomes in patients with
(b) In combination with opioids have not been chronic musculoskeketal pain co-morbid with depres-
shown to reduce opioid requirements. sion: results from a randomized controlled trial. Pain
(c) Cannot be given preoperatively. Med. 2010;11(4):482–91.
8. Akhter S, Khan M, Ali SS, Soomro RR. Role of of the Cochrane Collaboration Back Review Group.
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T, Liamas-Ramos I, Plaza-Manzano G, Ortega- Am. 2006;88(Suppl 2):58–62.
Santiago R, Cleland J, Fernandez-de-Las-Penas 22.
American Academy of Orthopaedic Surgeons.
C. Comparison of the short-term outcomes between Clinical practice guideline on treatment of osteoar-
trigger dry needling and trigger point manual therapy thritis of the knee: evidence-based guideine. 2nd ed.
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Bone Healing
14
K. Osman, Ayman Gabr, and Fares S. Haddad
Pathophysiology • Repair—The callus response usually occurs

within 2 weeks. It can occur by two distinct
Bone healing is a continual process that is initi- mechanisms.
ated at the time of the initial injury or fracture and –– Enchondral ossification (indirect/second-
is completed with the establishment of mature ary bone healing)—Where the fracture
lamellar bone and repopulation of the bone fragments are not opposed, initially there is
marrow. formation of soft bridging callus rich in
Fracture healing occurs in the following type II collagen which is replaced by hard
stages: callus (woven bone) rich in type I collagen.
Medullary callus is formed more slowly.
• Inflammation—A fracture haematoma is Soft callus is composed of fibrous tissue
established providing a source of haemato- and cartilage and becomes progressively
poietic cells producing cytokines and growth calcified. Starting at the periphery, perios-
factors that promote the migration and pro- teal progenitor cells differentiate into
liferation of fibroblasts, osteoblasts and osteoblasts and migrate through the calci-
osteoprogenitor cells. An organised haema- fied callus replacing soft callus with woven
toma is formed containing a network of bone with capillary ingrowth.
fibrin, reticulin and small amounts of colla- –– Intramembranous ossification (direct/pri-
gen fibrils that are gradually replaced by mary bone healing)—Where the fracture
granulation tissue alongside osteoclast ends are anatomically opposed with rigid
resorption of necrotic bone. stabilisation. There is direct heeling with-
out visible callus via Haversian
remodelling.
K. Osman • Remodelling—Woven bone is subject to
School of Biosciences, University of Birmingham, the process of Haversian remodelling
Birmingham, UK involving osteoclast cutting cones followed
A. Gabr by osteoblasts laying new organised lamel-
Department of Orthopaedic Surgery, University lar bone. It begins in the repair phase and
College London Hospitals, London, UK
continues for many years allowing the bone
F. S. Haddad (*) to regain its full properties and architecture
Institute of Sport, Exercise and Health, University
College Hospital, London, UK in response to the stresses it endures
e-mail: secretary@fareshaddad-clinic.co.uk (Wolff’s law).

112 K. Osman et al.
There are multiple biological and mechanical –– Sequential radiographs to monitor the
factors affecting the speed, quality and type of stages of bone healing.
bone healing. Listed are some of the most clini- • Radiographic union scores:
cally important factors but there are many more. –– Usually assess four cortices on plain AP
and lateral radiographs and provide a score
indicating the degree of healing.
Biological Factors –– For example Radiographic Union Score for
Hip (RUSH) and Radiographic Union
• Bone blood supply (most important). Score for Tibia (RUST)
• Infection. • Computed tomography (CT):
• Non-steroidal anti-inflammatory drugs –– Superior to plain radiographs in visualising
(NSAIDs). callus especially in the presence of an over-
• Nicotine. lying caste.
• Nutritional status. –– High sensitivity but a low specificity for
• Hormones, Vit D and C. non-union (can misdiagnose non-union) [2].
• Ultrasound:
–– Can detect callus formation earlier than
Mechanical Factors plain radiographs [3].
–– High sensitivity for predicting healing [3].
• Extent of bone loss. –– User dependent and uncommonly used.
• Excessive fracture gap.
• Stability.
• Strain across the fragments. Non-union and Delayed Union
• Anatomical site of fracture.
• Severity of injury (energy imparted). A non-union is defined as a fracture that lacks the
potential to heal without further intervention. It is
identified by cessation of all reparative processes of
Signs of Bone Healing [1] healing without radiological or clinical union and is
usually determined at least 6 months after the injury.
Clinical signs Types of non-union
• Clinical signs used to assess fracture union • Septic—Will not heal unless infection is
include: eradicated.
–– Weight-bearing ability (perhaps the most • Hypertrophic—Usually good biological fac-
important). tors but inadequate immobilisation.
–– Fracture pain and pain on weight bearing. • Oligotrophic—Inadequate reduction or frac-
–– Bony tenderness on palpation. ture displacement.
Stability or lack of movement at the frac- • Atrophic—Inadequate immobilisation and/or
ture site. poor biological factors.
Radiological signs Delayed union is when the adequate expected

period of time has elapsed without achieving
• Plain radiographs: bony union. It can be difficult to differentiate
–– Used to visualise calcified callus formation, between delayed and non-union as duration of
cortical continuity and loss of fracture line. normal fracture healing varies according to mul-
–– Bone resorption at the fracture edges in the tiple factors including site of fracture, degree of
early reparative phase may be the first sign soft-tissue injury and age of patient. Non-union is
of healing. one possible outcome of a delayed union.
14 Bone Healing 113
Bone Grafts • For example demineralised bone matrix

(DBM), coral, surgical polymers, hydroxyap-
Bone grafts are used to encourage bone forma- atite (HA), human/animal collagen and vari-
tion across a fracture gap. There is a wide range ous combinations of the above [5].
of different graft options available and it is • Often combined with an osseoinductive agent
therefore important for the surgeon to consider in various preparations.
the different properties of the products and their • Their efficacy may vary at different body sites
constituents when selecting a material. Most and there is large variability between brands
graft materials contain osseoconductive compo- and in some cases limited regulation, which is
nents, which by definition encourage bone especially true of DBM [5].
growth preferentially along their surface. Many
are arranged in a scaffold similar to structure of
cancellous bone. Such materials should be bio- Recent Developments/Publications
degradable allowing them to be replaced by new in the Field
bone. Osseoinductive agents cause differentia-
tion of osteoprogenitor cells into osteoblasts Due to the complexity and multifactorial nature
and thereby encourage new bone formation. of bone healing, the literature is abundant with
Some graft materials also include structural ele- new advancements in the basic science and its
ments that enhance their mechanical integrity, clinical application. We present some of the most
which may be favourable in weight-bearing interesting and clinically important develop-
situations. ments in the field.
Autologous bone graft
• Bisphosphonates are normally used for the
• Remains the gold standard for the treatment primary prevention of osteoporotic frac-
non-unions. tures; however over recent years they have
• Disadvantage of donor-site morbidity and sac- been implicated in causing delayed union
rificing host structures. and non-union. The evidence so far sug-
• Contain osseogenic cells, osseoinductive fac- gests that bisphosphonates may cause
tors, osseoconductive matrix as well as struc- delayed union in wrist fractures but their
tural elements coupled with a lack of host effects on lower limb fractures remain con-
immune response making them the ideal troversial [6].
material. • Osseoinductive agents such as bone morpho-
genic proteins (BMPs) and growth factors
Cadaveric allografts have been shown to be an effective alterna-
tive to bone grafting in both clinical and pre-
• Readily available. clinical trials [7, 8]. The efficacy of
• Sterilisation processes (freezing or irradia- platelet-rich plasma (PRP) is yet to be firmly
tion) affect structural strength and modify established [9].
graft incorporation. • The potential use of mesenchymal stem cells
• There is evidence that they can be as effective (MSCs) in the treatment of non-unions is an
as autografts when combined with bone mar- evolving science and the clinical application
row aspirate concentrate (BMAC) [4]. is yet to be established [10]. Percutaneous
injection of stem cell-rich BMAC combined
Bone graft substitutes with an osseoinductive agent may offer a less
invasive option for the effective treatment of
• The expanding use of bone grafts has led to a non-unions [11]. However the future proba-
growing market in substitute materials. bly lies in the use of isolated and cultured
114 K. Osman et al.
allogenic MSCs without the need for bone

marrow aspiration [8].
• There is increasing evidence that electrical
stimulation, low-intensity pulsed ultrasound
(LIPUS) and pulsed electromagnetic fields
can be used effectively to enhance the suc-
cess of treatment and accelerate the time to
union in acute fractures, non/delayed unions
as well as spinal/foot/ankle fusion [12, 13].
Although the exact mechanism is not fully
understood, LIPUS is thought to work by
inducing small mechanical forces at the frac-
ture site, thereby positively influencing bone
healing in the reparative phase. Whilst elec-
trical stimulation is invasive, LIPUS is non-
invasive and has no major safety concerns.
The patient usually administers it on a daily
basis for 20 min at a time via an ultrasound
probe in contact with the skin overlying the
fracture site. Although there is evidence to
support the use of LIPUS as an adjunct to
established treatment for acute fractures [14],
a more recent update of the same systematic
review suggests that the evidence is insuffi-
cient to support routine clinical use [14]. The
National Institute for Health and Clinical
Excellence (NICE) 2010 guidelines support
the use of LIPUS for the treatment of
delayed-union, non-union and fresh fractures
with risk factors for poor healing [15].
• CT-based finite element analysis (FEA) uses
computerised models to give accurate predic-
tions of bone structural strength. This innova-
tive technique is being developed to enable
virtual stress testing (VST) of bones in order
to determine the likelihood of refracture prior
to removal of fixation methods [16].
How do you dynamise the IM nail and what is

Case 1 the rationale?
The IM nail is usually inserted in a static mode
A 38-year-old gentleman had a twisting injury to where the nail is fixed distal with screws in the
his right leg while playing football. He sustained a static as well as in the dynamic nail holes.
closed fracture to his tibia as shown in the X-rays. Dynamisation of the nail can be achieved by
He is a taxi driver and smokes 20 cigarettes a day. removing the screw from the static hole and leav-
He was treated with intramedullary nail fixation ing the dynamic hole screw. The nail can then
for his tibial shaft fracture. The nail was dyna- slide over the screw in the dynamic hole increas-
mised 10 weeks following the operation. ing the mechanical load across the fracture site.
14 Bone Healing 115
The patient returns back 8 months following over the fracture site. Plain X-rays are shown
the index procedure complaining of right leg pain below.
What is the diagnosis? • The patient needs to be counselled regarding

The plain X-rays are showing signs of hyper- the effect of smoking on bone union with
trophic non-union. strong advice on smoking cessation.
What is the likely cause? • Mechanical stability at the fracture site
Failure of a fracture to progress to union could could be improved with different methods
be related to various factors. These factors could including plate and screw fixation, external
generally be categorised into host-related, fixation and exchange nailing. The latter
fracture-related and fixation-related factors. In involves reaming of the medullary canal
this case, mechanical instability is the most likely that increases the periosteal blood flow and
cause for developing non-union due to excessive stimulates new bone formation. This
motion at the fracture site. Smoking is also improves the biological environment for the
another important host-related factor that con- fracture to heal. After removing the nail and
tributed to non-union. reaming the canal, a larger diameter nail is
What are the treatment options? inserted.
116 K. Osman et al.
Case 2 tia and normally lives in a nursing home. She had

a left humerus fracture 4 years ago that was treated
An 87-year-old woman presented with 3-week conservatively. The swelling is pulsatile on exam-
history of painful large swelling in the left upper ination. The radial and ulnar pulses were present
arm. She has got a background of vascular demen- in the right arm. Plain X-rays are shown below.
What can you see? • A CT angiogram: to establish the nature of the

The plain radiographs are showing established swelling and its relation to the bony spikes of
non-union of the proximal third humerus shaft the humeral ends.
with wide displacement. There is also large soft-
tissue shadow surrounding the proximal third. What was the investigations outcome?
What is the provisional diagnosis?
A pulsatile swelling is suggestive of either a • Hb was 7.
true aneurysm or a pseudoaneurysm. • CT angiogram: 16 × 15 × 12 cm pseudoaneu-
What investigation would you request for this rysm arising from the brachial artery with an
patient? extensive thrombus within the aneurysm wall.
The sharp edge of the distal end of the proxi-
• A full blood count: possible bleeding in the mal humeral fragment was in contact with the
swelling sac. pseudoaneurysm sac. Images are shown below.
14 Bone Healing 117
follow-
up for patient with long bone non-
union is recommended especially in mobile
non-union [17].
MCQs
1. All the following are prerequisites for pri-

mary bone healing except:
(A) Anatomical reduction
(B) A strain of 10% at the fracture site
(C) Interfragmentary compression
(D) Absolute stability
2. The most important factor in fracture healing
is:
(A) Blood supply
(B) Degree of bone comminution at the
fracture site
(C) Serum calcium level
(D) Patient’s age
3. Secondary (indirect) bone healing occurs in
all the following except:
(A) Bridging plate
(B) Intramedullary nailing
(C) Compression plate
(D) Cast immobilisation
(E) External fixator
4. With regard to primary (direct) bone healing,
which of the following statement is correct?
(A) Primary bone healing occurs without

callus formation
(B) Primary bone healing is faster than sec-
ondary (indirect) bone healing
(C) Osteoblasts form cutting cones that tun-
What was the management? nel across the fracture site
A combined vascular and orthopaedic team (D) Bone healing occurs through contact

undertook surgical excision/repair of the pseu- healing and gap healing
doaneurysm and humeral fracture fixation. 5. Direct gap healing occurs at the fracture site
An anteromedial approach was used by a vas- when there is a gap of:
cular surgical team, and the pseudoaneurysm was (A) <1 mm
excised and vein patch graft was performed. The (B) <10 mm
approach was extended proximally, and the frac- (C) <20 mm
ture ends were debrided. The humeral shaft was (D) <40 mm
stabilised with an anterior ten-holed large- 6. Which of the following statements is
fragment locking plate. correct?
What is the learning point? (A) Osteoclasts are bone-forming cells
Non-union of long bone fracture could (B) Osteoblasts may eventually turn into
potentially result in a vascular injury. Regular osteocytes
118 K. Osman et al.
(C) Osteoblasts are bone-resorbing cells (D) The average healing time for metacarpal
( D) Bisphosphonate stimulates osteoclast fracture is 12 weeks.
activity 13. Wolff’s law states that:
7. All the following promote bone healing (A) Compression across the growth plate

except: increase longitudinal growth.
(A) Calcium (B) Bone remodels in response to mechani-
(B) Vitamin D cal stress.
(C) Silicon (C) Tension across the growth plate inhibits
(D) Corticosteroids longitudinal bone growth.
(E) Copper (D) Bone does not remodel in response to
8. All the following decrease the rate of bone mechanical stress.
healing except: 14. With regard to non-union, all the following
(A) Associated head injury statements are correct except:
(B) Infection (A) Non-union is defined as progressive evi-
(C) Diabetes mellitus dence of non-healing of the fracture
(D) Non-steroidal anti-inflammatory drugs within the expected time.
(E) Alcohol (B) Hypertrophic non-union occurs when
9. Smoking may affect bone healing through: there is inadequate stability and poor
(A) Nicotine in high doses which inhibits blood supply.
osteoblast proliferation (C) Atrophic non-union occurs when there
(B) High risk for atherosclerosis to the large is inadequate blood supply.
and medium blood vessels of the (D) Abundant callus can be seen on plain
extremities radiographs of hypertrophic non-union.
(C) Low concentration of antioxidant 15. Which of the following hormones promotes
vitamins bone healing?
(D) All the above (A) Insulin
(E) None of the above (B) Thyroxin
10. The following factors are associated with
(C) Growth hormone
lower rates of fracture healing except: (D) Calcitonin
(A) Inadequate reduction of the fracture (E) All the above
(B) Elderly patients 16. Low-intensity pulsed ultrasound (LIPUS)

(C) Fractures at the metaphysis of long bone enhances bone healing through one of the
(D) Fractures at the diaphysis of long bone following mechanisms:
(E) Malnutrition (A) Integrin stimulation
11. In distraction osteogenesis, the optimal rate (B) Stimulates the release of IL-1
of distraction to achieve bone regeneration (C) Produces a thermal reaction
is: (D) Stimulates osteoclast activity
(A) 1 mm/day 17. Which of the following statements is

(B) 5 mm/day correct?
(C) 10 mm/day (A) Demineralised bone graft has no osteo-
(D) 15 mm/day inductive properties.
12. Which of the following statements is correct? (B) Cancellous allograft has strong osseo-
(A) The average healing time for femoral genic properties.
shaft fracture is 6 weeks. (C) The infection risk from allograft is 10%.
(B) The average healing time for tibial shaft (D) Xenografts are the most commonly

fracture is 16 ± 4 weeks. used graft type.
(C) The average healing time for distal 18. The histological phases of distraction osteo-
radius fracture is 20 weeks. genesis are in the following order:
14 Bone Healing 119
(A) Distraction phase>latency early diagnosis of tibial fracture healing after static
interlocked nailing without reaming: clinical results. J
phase>consolidation phase Orthop Trauma. 1998;12(3):206–13.
(B) Latency phase>distraction 4. Johnson RG. Bone marrow concentrate with allograft
phase>consolidation phase equivalent to autograft in lumbar fusions. Spine.
(C) Latency phase>consolidation 2014;39(9):695–700.
5. Greenwald AS, Boden SD, Goldberg VM, Khan
phase>distraction phase Y, Laurencin CT, Rosier RN. Bone-graft substi-
(D) Consolidation phase>latency tutes: facts, fictions, and applications. J Bone Joint
phase>distraction phase Surg Am. 2001;83-A(Suppl 2 Pt 2):98–103. Epub
19. Bone morphogenic proteins (BMPs): 2001/11/20
6. Molvik H, Khan W. Bisphosphonates and their influ-
(A) Induce metaplasia of mesenchymal
ence on fracture healing: a systematic review. Osteop
cells into osteoblasts Int. 2015;26(4):1251–60.
(B) Stimulate new blood vessel formation 7. Fisher DM, Wong JML, Crowley C, Khan
(C) Decrease intracellular calcium WS. Preclinical and clinical studies on the use of
growth factors for bone repair: a systematic review.
(D) Increase cell apoptosis Curr Stem Cell Res Ther. 2013;8(3):260–8.
8. Smith B, Goldstein T, Ekstein C. Biologic adjuvants
Answers: and bone: current use in orthopedic surgery. Curr Rev
Muscoskelet Med. 2015;8(2):193–9.
9. Lenza M, SDB F, DCM V, OFP d S, Cendoroglo Neto
1. B M, Ferretti M. Platelet-rich plasma for long bone
2. A healing. Einstein (Sao Paulo). 2013;11(1):122–7.
3. C 10.
Khojasteh A, Behnia H, Dashti SG, Stevens
4. C M. Current trends in mesenchymal stem cell applica-
tion in bone augmentation: a review of the literature. J
5. A Oral Maxillofac Surg. 2012;70(4):972–82.
6. B 11. Desai P, Hasan SM, Zambrana L, Hegde V, Saleh
7. D A, Cohn MR, et al. Bone mesenchymal stem cells
8. A with growth factors successfully treat nonunions and
delayed unions. HSS J. 2015;11(2):104–11.
9. D 12. Hannemann PFW, Mommers EHH, Schots JPM,

10. C Brink PRG, Poeze M. The effects of low-intensity
11. A pulsed ultrasound and pulsed electromagnetic
12. B fields bone growth stimulation in acute fractures:
a systematic review and meta-analysis of random-
13. B ized controlled trials. Arch Orthop Trauma Surg.
14. B 2014;134(8):1093–106.
15. E 13. Ebrahim S. Low-intensity pulsed ultrasonography

16. A versus electrical stimulation for fracture healing: a
systematic review and network meta-analysis. Can J
17. C Surg. 2014;57:E105–18.
18. B 14.
Griffin XL, Parsons N, Costa ML, Metcalfe
19. A D. Ultrasound and shockwave therapy for acute
fractures in adults. Cochrane Database Syst Rev.
2014;6:58.
15. Excellence NIfHC. Low-intensity pulsed ultrasound
to promote fracture healing. Interventional procedure
References guidance 374, London: NICE; 2010.
16. Petfield JL, Kluk M, Shin E, et al. Virtual stress testing
1. Morshed S. Current options for determining fracture of regenerating bone in Tibia fractures. Proceedings
union. Adv Med. 2014;2014:12. of the 23rd Annual Scientific Meeting of Limb
2. Bhattacharyya T, Bouchard KA, Phadke A, Meigs Lengthening and Reconstruction Society, New York,
JB, Kassarjian A, Salamipour H. The accuracy of NY; 2013.
computed tomography for the diagnosis of tibial non- 17. Gabr A, Kumar G, Narayan B. Brachial artery pseu-
union. J Bone Joint Surg Am. 2006;88(4):692–7. doaneurysm, a late complication of humeral non
3. Moed BR, Subramanian S, van Holsbeeck M, Watson union. Eur J Trauma Orthop. 2010;21–2:123–6.
JT, Cramer KE, Karges DE, et al. Ultrasound for the
Osteoarthritis
15
Ayman Gabr, Sunil Gurpur Kini,
and Fares S. Haddad
Introduction • Females are more commonly affected than

males.
• Osteoarthritis (OA) is a chronic joint disorder • The prevalence of OA varies greatly depend-
characterized by a progressive softening and ing on the joint involved, age, sex, and geo-
disintegration of articular cartilage accompa- graphical area studied.
nied by new bone formation and, often, syno- • In the United States, it was estimated that 26.9
vial proliferation. million adults aged 25 years or older have
• Although OA is considered a degenerative joint symptomatic OA in 2005 [1].
disease, the disease process is not purely degen- • Worldwide estimates are that 9.6% of men and
erative. The loss of articular cartilage leads to 18.0% of women aged ≥60 years have symp-
changes in the loading surfaces at the joint mar- tomatic osteoarthritis [2].
gins with new bone formation and remodeling. • Oliveria et al. reported that the age and sex
These changes, together with the joint synovitis, standardized incidence of symptomatic OA in
lead to pain, loss of joint function, and disability the knee, hip, and hand were 240, 88, and 100
with consequent reduction in quality of life. per 100,000 persons per year, respectively [3].
Epidemiology Etiology
• OA is the commonest of all joint disorders. It is well known that the etiology of OA is multi-
• The commonly affected joints with OA are factorial. The disease could be classified into pri-
knee, hip, hand, and facet joints. mary or idiopathic OA and secondary OA. The
diagnosis of secondary OA could be made when
A. Gabr there is a distinct cause for the development of
Department of Orthopaedic Surgery, University joint OA. Causes of secondary OA include
College London Hospitals, London, UK inflammatory arthropathy, trauma, osteonecrosis,
S. G. Kini malalignment, and endocrine disorders such as
Department of Orthopaedics, Manipal Hospitals, acromegaly [4]. In contrast, primary OA is a
Bangalore, India
diagnosis made by exclusion when there is no
F. S. Haddad (*) clear antecedent factor for the development of the
Institute of Sport, Exercise and Health, University
College Hospital, London, UK disease. There are multiple risk factors associated
e-mail: secretary@fareshaddad-clinic.co.uk with the development of OA:

122 A. Gabr et al.
• Age: A strong correlation exists between aggrecan [10]. Signals that are generated by
increasing age and OA. Articular cartilage is cytokines, growth factors, and matrix regulate
subject to degenerative changes with aging chondrocyte metabolic activity [11].
that include fraying and softening of the artic- • In OA, there are excess catabolic and inflam-
ular surface, decreased size and aggregation of matory signals that result in increased produc-
proteoglycan aggrecans, and loss of matrix tion of matrix-degrading enzymes by the
tensile strength and stiffness. These changes chondrocyte, including matrix metalloprotein-
are likely caused by an age-related decline in ases (MMPs), aggrecanases, and other prote-
the ability of the chondrocyte to maintain and ases that degrade the cartilage matrix.
repair the tissue shown by decreased mitotic Aggrecanases that belong to the “a disintegrin
and synthetic activity, decreased responsive- and metalloproteinase with thrombospondin
ness to anabolic growth factors, and synthesis motifs” (ADAMTS) family of proteinases
of smaller less uniform aggrecans and less play a significant role in aggrecan degradation
functional link proteins [5]. The articular car- in osteoarthritic cartilage [12].
tilage also undergoes age-related changes in • Cytokines produced by the synovium and
the mechanical load on joint cartilage that chondrocytes, especially interleukin IL-1
may arise from altered gait, muscle weakness, and tumor necrosis factor alpha (TNF-α),
changes in proprioception, and changes in play a significant role in the cartilage degra-
body weight. dation. Prostaglandins (PG) and leukotrienes
• Sex: Women are more affected than men. may also be contributing to the induction of
Functional estrogen receptors have been iden- apoptotic processes in articular chondro-
tified in articular cartilage [6]. Postmenopausal cytes [13].
women in particular are at a greater risk and
this has been attributed to the decline in estro-
gen level at that time. Zhang et al. demon- Clinical Presentation
strated that postmenopausal women who take
estrogen replacement therapy have a decreased Symptoms are often insidious in onset:
chance of developing radiographic evidence
of knee arthritis [7]. • Joint pain.
• Obesity: The increased mechanical force on • Joint stiffness (usually less than 30 min in the
joint surfaces is the leading cause for cartilage morning or following a period of inactivity).
degeneration in obese patients. An obese per- • Joint swelling.
son is 14 times more likely to develop OA
compared to normal-weight person [8]. Signs:
• Race: The prevalence with osteoarthritis varies.
Results from the Beijing osteoarthritis study • Joint tenderness.
showed that the prevalence of hip OA in Chinese • Decreased range of motion.
elderly population was 80–90% less frequent • Effusion.
than in white persons in the United States [9]. • Crepitus.
• Genetics. • Malalignment/joint deformity.
Pathophysiology Imaging
• In a healthy cartilage, chondrocytes are respon- Plain radiographs: Radiographic evaluation

sible for maintaining equilibrium between syn- should include weight-bearing views to deter-
thesis and degradation of extracellular matrix mine the alignment of the limb. Findings in OA
(ECM) that includes type II collagen and include [14]:
15 Osteoarthritis 123
• Osteophyte formation. Recent Development/Publication

• Narrowing of the joint space. in the Field
• Subchondral sclerosis.
• Subchondral cyst formation. • Several agents have been developed in an
attempt to slow the progression of osteoarthri-
Magnetic resonance imaging (MRI) is some- tis. These agents are known as disease-
times used to aid the diagnosis in patients with modifying osteoarthritis drugs (DMOADs).
mild OA. Among these drugs are bisphosphonates, cal-
citonin, strontium ranelate, diacerein, tumor
necrosis factor (TNF) antibodies, matrix
Treatment metalloproteinase inhibitors, glucosamine,
and chondroitin sulfate. There is little evi-
Different treatment modalities are available for dence available in the literature to support
the management of patients with OA. The treat- their efficiency and cost-effectiveness.
ment usually often consists of combination of • Multiple randomized controlled trials were
these modalities. The decision on what treatment conducted to investigate the efficacy of glu-
modality should be individualized for the patient cosamine, chondroitin sulfate, and combina-
depends on age, pain level, activity level, and tion of both in OA treatment. The
comorbidities. Glucosamine/chondroitin Arthritis
Intervention Trial (GAIT) study examined
• Patient education and lifestyle modification: the differences in outcome between patients
including weight loss and the use of orthoses/ who had treatment with glucosamine, chon-
walking aids. droitin, and combination of both celecoxib
• Exercise program/physical therapy: to and placebo. The results showed no clinically
improve muscle strength and joint mobility. significant difference in pain and function
• Pharmacological measures: between the treatment groups at 2-year fol-
–– Acetaminophen. low-up [15]. The Long-term Evaluation of
–– Nonsteroidal anti-inflammatory drugs. Glucosamine Sulfate (LEGS) study followed
–– Tramadol. a similar methodology and reported no dif-
–– Opioids. ference in symptomatic outcomes between
–– Intra-articular injections including steroids the different treatment groups and placebo
and hyaluronic acid. group. However, there was radiological evi-
• Other non-pharmacological treatment: dence of reduction in joint space narrowing
–– Bracing (e.g., unicompartmental knee at 2-year follow-up in patients who had treat-
arthritis). ment with combined glucosamine and chon-
–– Acupuncture. droitin sulfate [16].
–– Dietary supplement: glucosamine and • The effect of intra-articular injection of hyal-
chondroitin sulfate. uronic acid or the plasma-rich protein (PRP)
• Surgical treatment: has been investigated as well [17–19]. There is
–– Arthroscopic joint washout. a lack of good-quality evidence to prove their
–– Arthroscopic debridement. efficacy and identify any significant difference
–– Osteotomy. between these two treatment modalities [20].
–– Partial joint arthroplasty. • There is a potential for intra-articular injection
–– Total joint arthroplasty. of sodium bicarbonate and calcium gluconate
124 A. Gabr et al.
to improve pain and function in patients with 6. Cartilage change in osteoarthritis involves

knee OA [21]. which of the following?
• Mesenchymal stem cell (MSC) therapy is (A) Decreased water content
also a new treatment strategy. MSCs are mul- (B) Increased proteoglycans
tipotent progenitor cells and thus have the (C) Decreased chondrocyte activity
potential for articular cartilage regeneration. (D) Increased subchondral thickness
The effect of intra-articular injection of (E) Increased collagen content
autologous adipose tissue-derived MSCs has 7. Poor prognostic factors for patellofemoral

been investigated with early promising arthroplasty in isolated patellofemoral arthro-
results [22]. sis include all except:
(A) BMI >30
1. Most uncommon region to be involved in
(B) Previous tibiofemoral arthritis
osteoarthrosis: (C) Age <50 years
(A) Ankle (D) Patella alta
(B) Shoulder (E) Ligamentous instability
(C) Elbow 8. Most common involved hand joint in osteoar-
(D) Wrist throsis is:
(E) Hand (A) First CMC joint
2. Which of the following is not a biomarker for (B) MCP joint
osteoarthrosis? (C) PIP joint
(A) Cartilage oligomeric matrix protein (D) DIP joint
(B) CTX 1
(C) Matrix metalloproteinase 3 Answers:
(D) IL 6
(E) Serum HA 1. D
3.
Characteristic radiographic findings in 2. D
osteoarthritis include all of the following 3. C
EXCEPT: 4. C
(A) Subchondral cysts 5. E
(B) Osteophytes 6. D
(C) Symmetrical joint space narrowing 7. C
(D) Subchondral bone sclerosis 8. D
(E) Subluxation
4. Contraindications to unicompartmental knee
arthroplasty for medial compartment osteoar- Case Discussions
throsis include all except:
(A) Inflammatory arthritis 1. A 66-year-old lady consults in the clinic with
(B) Knee instability complaints of right-knee pain from the past
(C) Patellofemoral wear 4 years that was aggravated since 6 months.
(D) Less than 90° flexion arc He says that pain is brought upon by weight-
(E) More than 10° coronal deformity bearing activities. He has no comorbidities
5. Which of the following nonoperative treat- apart from well-controlled diabetes mellitus.
ments for osteoarthrosis has best supportive He has tried a year of physiotherapy to his
evidence for use? knee that was arranged by his GP.
(A) Glucosamine On examination patient has an antalgic gait
(B) Intra-articular steroids with a fixed varus and fixed flexion deformity
(C) Analgesics in the knee of about 10 degrees. Knee ranges
(D) Hyaluronic acid injections from 10 to 90 with pain on terminal flexion.
(E) Supervised knee-strengthening exercises There is a grade 2 varus/valgus laxity with no
distal deficits. Standing AP, lateral, and sky-

line views are taken that confirm the presence
of advanced tricompartmental arthritis.
What would be the ideal line of treatment
in this case scenario?
The definitive line of treatment in this case
would be a total knee replacement.
The principle of surgery would be accurate
bony cuts, correction of fixed deformities
through soft-tissue release, and to create a bal-
anced knee both in flexion and extension.
Tranexamic acid is often used just before inci-
sion to reduce intra- and postoperative bleed-
ing. An additional dose can be given 6–8 h
postoperatively. All patients are usually
started on dalteparin postoperatively. This
changed to oral rivaroxaban 10 mg on dis-
charge from hospital and this is to be contin-
ued for 14 days postoperatively.
126 A. Gabr et al.
2. A 73-year-old gentleman presented to the

clinic with right-hip pain since 5 years. He
says that in the past few months there has
been increasing difficulty to walk for consid-
erable distance due to pain. He has no previ-
ous history of trauma.
On examination he has a shortening of
about 1 cm on the right side. Flexion is
restricted to about 90 with negligible rotations
with all movements terminally painful. X-ray
of the pelvis and the right hip show advanced
Grade 4 osteoarthrosis of left hip. What is the
ideal modality of management?
In the current scenario the best treatment
option for the patient would be a total hip
replacement. Cementless acetabular and fem-
oral components were selected for this patient
in light of having good bone stock. The socket
is always supplemented with two holding
screws and the stem that has the best proximal
fit and fill is chosen. Patients are usually
started on dalteparin postoperatively that is
changed to oral rivoroxaban 10 mg on dis-
charge from hospital. This is to be continued
for 35 days postoperatively.
3. A 50-year-old banker visits the orthopedic clinic

with complaints of left-hip pain from the past
3 months. The pain started about a year back
and has worsened since. He is keen for a solu-
tion to go back to his active lifestyle that includes
trekking and sports and is medically fit.
Examination reveals equal leg lengths with
terminal painful restriction of left-hip flexion
and rotations. X-ray shows early osteoarthritis
of left hip. What is the best line of treatment of
this patient?
Clinical and radiological correlation is sug-
gestive of surgical line of management for the
patient. Patient is a good candidate for hip 4. Sixty-year-old software professional pres-
resurfacing considering his age, early arthri- ents with left-knee pain since 6 months.
tis, and keenness to carry on with sports. Patient indicated that pain is predominant
However the surgery should only be advo- in the inner aspect of knee. Patient is
cated and carried out in a well-informed unable to go about his morning walks
patient explaining to him additional risks with and finds it increasingly difficult to do
this procedure that includes femoral neck stairs. Patient has no significant
fractures and occurrence of metal-on-metal comorbidities.
adverse reactions with the possible need for Examination reveals a fixed varus of about
revision surgery if indicated. He should also 5° with flexion up to 120°. There is no liga-
be consented for a total hip replacement pro- mentous laxity with fair patellofemoral track-
cedure concurrently if he was found intraop- ing. Radiograph of the knees shows grade 4
eratively to be unsuitable for resurfacing. OA changes in the medial compartment with
The surgery is contraindicated in patients preserved lateral and patellofemoral
with significant limb length discrepancy, sig- compartment.
nificant loss of femoral offset, renal insuffi- Optimal treatment in this case scenario
ciency, and head size of less than 50 mm. would to offer a unicondylar knee replace-
ment. The Kazinin and Scotts criteria for
UKA includes young patients with disease
limited to one compartment, noninflammatory
arthritis, coronal deformity less than 15°,
fixed flexion less than 5°, and BMI less than
30 kg/m2.
Advantages of UKA over TKA include
preservation of native bone stock, less peri-
operative morbidity, increased range of
motion, less blood loss, and a shorter post-
operative recovery.
128 A. Gabr et al.
the pain has largely limited his activities of

daily living.
Knee examination reveals medial joint-line
tenderness. His knee exhibits correctable
varus of 10° with a range of 5°–120° with
intact ligaments. X-rays reveal reduction of
the medial joint space with preserved lateral
and patellofemoral compartments. What is the
surgical line of management?
This patient is a suitable candidate for high
tibial osteotomy(HTO) procedure considering
his age, nature of work, and presentation. This
could either be a medial opening-wedge or
lateral closed-wedge procedure. The concept
of osteotomy is to shift the weight-bearing
axis of the limb to a more lateralized position
and thus halt or delay the wear in the involved
compartment.
Contraindications include flexion defor-
mity more than 15°, range-of-knee motion
less than 90°, wear in other compartments,
patella baja, and inflammatory arthritis.
Complications of HTO include patella baja,
5. A 50-year-old teacher visits the clinic with delayed union, bone fractures, peroneal
complaints of 1-year duration of right-knee nerve palsy, compartment syndrome, arte-
pain. The pain was initially intermittent and rial injury, arthrofibrosis, and loss of
brought about by ambulation but recently correction.
130 A. Gabr et al.
5. Martin JA, Buckwalter JA. Aging, articular car-

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Inflammatory Arthropathies
(Rheumatic Disorders) 16
(See Refs. 1 and 2 for Excellent
General Overviews)
George Bentley
The inflammatory arthropathies cover a range of patients with rheumatoid arthritis show increased
non-infective conditions characterised by inflam- frequencies of HLA-DR4. This occurs in 70% of
mation of synovial membranes of joints and ten- people with RA compared with 30% in normal
don sheaths which are associated with general controls. It is encoded in the major histocompat-
mesenchymal disorders. They are usually pro- ibility complex (MHC) region on chromosome 6.
gressive, although this varies, and lead to exten- Certain cytokines are important in RA. These
sive joint and soft-tissue disorganisation and include tumour necrosis factor (TNF), interleu-
consequent disability. kin 1 (IL1) and interleukin 6 (IL6). The synovitis
Rheumatoid arthritis affects 3% of the popula- both in joints and tendon sheaths is the hallmark
tion, occurring three times more often in women of early RA.
than in men. It usually starts in the fourth or fifth Important factors in the evolution of RA are:
decade.
1. Genetic susceptibility.
2. An immunological reaction possibly involv-
Aetiology ing a foreign antigen (such as a virus) prefer-
entially focussed on synovial tissue.
The aetiology is unknown but it is considered that 3. An inflammatory reaction in joints and tendon
some antigen, possibly a virus, sets off a chain of sheaths.
events culminating in the formation in the joint of 4. The appearance of rheumatoid factor (RF) in
antigen-antibody complexes which, after activa- the blood and synovium.
tion by complement, stimulate a local inflamma- 5. Perpetuation of the inflammatory process.
tory reaction. These immune complexes initiate 6. Articular cartilage destruction.
the production of auto-antibodies which appear
in the synovial fluid and blood as anti-IgG rheu-
matic factor. The abnormal immune response Rheumatoid Factors
may be genetically predetermined because
B-cell activation in RA leads to the production of
anti-IgG auto-antibodies which are detected in
G. Bentley (*) the blood as rheumatoid factor (RF).
Institute of Orthopaedics and Musculo-Skeletal Lower levels of RF can be found in many nor-
Science, University College London, London, UK mal individuals but when the levels are high an
Royal National Orthopaedic Hospital, Stanmore, UK inflammatory disease is likely.

134 G. Bentley
Chronic synovitis in joint destruction devel- The synovial membrane becomes inflamed
ops as the disease proceeds with the production and thickened, giving rise to a cell-rich effusion.
of proteolytic enzymes, prostaglandins and the The joints and tendons are still intact and the dis-
cytokine tumour necrosis factor (TNF) and inter- order is treatable by DMARDs and is potentially
leukins, IL1 and IL6. Complexes are deposited in reversible.
the synovium and on the articular cartilage which Stage III—destruction.
appear to augment the inflammatory process. Persistent inflammation causes tissue destruc-
This leads to depletion of the cartilage matrix and tion, articular cartilage is eroded and tendon
eventually damage to cartilage and underlying fibres may rupture.
bone. Vascular proliferation and osteoclastic Stage IV—deformity.
activity, most marked at the edges of the articular The combination of articular destruction, joint
surface, contribute further to cartilage destruction stretching and tendon rupture leads to progres-
and periarticular bone erosion. sive instability and deformity. Cartilage degrada-
tion and bone destruction are primarily due to
osteoclasts and fibroblast-like synoviocytes.
Genetic Susceptibility The most common and characteristic extra-
articular lesion is the rheumatoid nodule, a small
Genetic association is supported by the fact that RA granuloma occurring under the skin, especially
is more common in first-degree relatives of patients over bony prominences in the sclera and in vis-
than in the population at large. It is now known that cera. Other systemic features are lymphadenopa-
many genes are involved. The genes play a role in thy, vasculitis, muscle weakness and inflammatory
both susceptibility to RA and its severity. changes in the lungs, heart, kidneys, brain and
gastrointestinal tract.
Pathology (Fig. 16.1)

Clinical Features
Although tissues throughout the body are affected
the main disease is in the synovium and the path- Before RA becomes clinically apparent, the
ological changes are in four stages: immune pathology is beginning with raised ESR,
Stage 1—preclinical. C-reactive protein (CRP) and RF which may be
Stage II—synovitis. detectable years before the first diagnosis.
Fig. 16.1 Synovial membrane in pigmented villonodular Orthopaedics and Traumatology, ed. G. Bentley, Springer:
synovitis. From “Management of Synovial Disorders”; Heidelberg, London, New York. With kind permission of
Z.P. Stavrou and P.Z. Stavrou, 2014. In: European Surgical the Authors and Springer
16 Inflammatory Arthropathies (Rheumatic Disorders) 135
There is a gradual onset of symmetrical poly- ion or valgus, toes are clawed and there are pain-
arthritis affecting mainly the hands and feet ful callosities under the metatarsal heads. Muscle
together with early-morning stiffness and a lack wasting is often severe. Almost one-third of all
of well-being. patients develop pain and stiffness in the cervi-
During Stage I there is typically swelling, cal spine due to the inflammatory process which
increased warmth and tenderness of the proximal may progress to spinal cord compression. In
finger joints and the wrists as well as the sur- long-standing cases there may be vasculitis and
rounding tendon sheaths. Later the disease may peripheral neuropathy.
spread to involve the elbow, shoulders, knees,
ankles and feet.
In Stage II joint movements are limited and Radiographic Changes
isolated tendon ruptures occur. Nodules may be
felt which are pathognomonic of RA. In Stage I, X-rays show soft-tissue swelling and
In Stage III the diagnosis is obvious. The periarticular osteoporosis.
fingers are deviated ulnarwards, often with In Stage II, there is narrowing of the joint
subluxation of the metacarpophalangeal joints space and marginal bony erosions, especially
(Fig. 16.2). Elbows cannot be straightened, about the wrists and the proximal joints of the
shoulders lose abduction, knees may be in flex- hands and feet (Fig. 16.3).
Fig. 16.2 Rheumatoid arthritis of the hands—stage

II—with ulnar deviation of the fingers, early sublux- Fig. 16.3 Rheumatoid arthritis of the wrist, showing grade
ation of the MCP joints of the fingers and thumb, soft- II changes of para-articular osteoporosis and joint space
tissue swelling and para-articular osteoporosis. From narrowing. From “Surgical Management of the Rheumatoid
“European Surgical Orthopaedics and Traumatology”; Hand”; A. Lluch. 2014. In: European Surgical Orthopaedics
A. Lluch. 2014. ed. G. Bentley, Springer: Heidelberg, and Traumatology, ed. G. Bentley, Springer: Heidelberg,
London, New York London, New York
136 G. Bentley
In Stage III, articular destruction joint defor- with arthritic changes. It is regarded as a
mity is obvious. benign ageing process.
At later stages in the disease, flexion and exten- 2. Reiter’s disease, which affects the liver, large
sion views of the cervical spine show sublux- joints and lumbosacral spine. There is often a
ation of the atlanto-axial or mid-cervical joints. history of urethritis, colitis or conjunctivitis.
Surprisingly, these cause few symptoms but can 3. Ankylosing spondylitis.
eventually cause spinal cord compression.
This may involve the peripheral joints, but is
primarily a disease of the sacroiliac and interver-
Serology tebral joints causing back pain and progressive
stiffness.
In active phases the erythrocyte sedimentation
rate (ESR) and C reactive protein are raised. 4. Polyarticular gout affects large and small

Serological tests for rheumatoid factor are usu- joints producing tophi on fingers and toes.
ally positive and antinuclear factors are present. 5. Seronegative polyarthritis is a group of condi-
A normocytic hyperchromic anaemia is tions with features of rheumatoid arthritis,
common and is a reflection of abnormal eryth- including psoriatic arthritis, juvenile chronic
ropoiesis due to the disease activity. It may be arthritis, Reiter’s disease, Still’s disease, sys-
aggravated by chronic gastrointestinal blood temic lupus erythematosus (SLE) and poly-
loss caused by non-steroidal anti-inflammatory myalgia rheumatica.
drugs.
Serological tests for rheumatoid factor are
positive in about 80% of patients, and anti- Clinical Progress
nuclear factors are present in 30%. However, nei-
ther of these tests is specific and neither is In 8% of patients RA follows a periodic course
required for a diagnosis of rheumatoid arthritis. with flares during which symptoms and signs of
Newer tests such as anti-CCP antibodies have inflammation are more severe. These attacks
added much greater specificity but at the expense occur less frequency and the disease may become
of sensitivity. completely quiescent, but by then the joints are
permanently damaged.
In 5% it is a relentless disease increasing with
Diagnosis increasing inflammatory joint changes in muscle
and muscle wasting leading to early death.
The diagnosis is based on the clinical signs 10% are patients over 55, usually men, with
described above, together with typical X-ray symptoms which start dramatically, but the
appearances and serology. condition can subside completely. The condition
However, the chief value of the rheumatoid settles after the first or second attack and does not
factor is for assessing prognosis, high titres indi- require treatment.
cating more serious disease.
Management of Rheumatoid
Differential Diagnosis Arthritis Is based on Four
Principles [1]
The important differential diagnoses are as
folows: (a) Controlling pain and synovitis.
(b) Preventing deformity.
1. Heberden’s arthropathy, which causes nodular (c) Reconstruction of joints and tendons.
swellings on the distal interphalangeal joints (d) Rehabilitation.
A multidisciplinary approach is required

involving physician, surgeon, physiotherapist,
occupational therapists, orthodontist and social
workers.
(a) Anti-inflammatory treatment with NSAIDs

(non-steroidal anti-inflammatory drugs)
is not curative but controls pain and stiff-
ness and therefore improves some function.
However, side effects can be severe with
rashes, gastrointestinal symptoms and peptic
ulceration.
The disease-modifying anti-rheumatic Fig. 16.4 Pre-operative clinical photograph of both knees
drugs (DMARDs) and newer biological showing rheumatoid synovitis. From “European Surgical
agents—(e.g. methotrexate) alter the natural Orthopaedics and Traumatology”; Z.P. Stavrou and P.Z.
Stavrou, 2014. ed. G. Bentley, Springer: Heidelberg,
history of the condition and can control the London, New York
disease [2]. They are used primarily in severe
disease or if NSAID use fails, but increas-
ingly are used in all cases. Corticosteroids
have a dramatic effect on joint stiffness, but
have serious long-term problems and are
therefore only used in acute exacerbations.
If DMARDs fail, rapid progression to bio-
logical therapies such as the TNF inhibitors
infliximab, etanercept and adalimumab is
indicated
(b) Rest and splintage.
No drug will reduce joint information
more effectively than rest and this is indi-
cated for acute exacerbations.
Intra-articular injections: Corticosteroids,
disease-modifying drugs and radiocolloids
can be effective when injected into inflamed
joints. However, repeated injections can
cause serious joint damage and should not be
given.
Fig. 16.5 MRI scan showing the hypertrophied
synovium in the knee and suprapatellar pouch. From
“European Surgical Orthopaedics and Traumatology”;
Synovectomy Z.P. Stavrou and P.Z. Stavrou, 2014. ed. G. Bentley,
Springer: Heidelberg, London, New York
Synovectomy is generally reserved for patients
in whom there is a bulky proliferative synovi-
tis and can be carried out by arthroscopic or Physiotherapy and Rehabilitation
open operation or combined with joint arthro-
plasty (Figs. 16.4, 16.5, 16.6, 16.7 and 16.8). Whilst rest is useful for acutely inflamed joints,
Synovectomy of inflamed tendon sheaths relieves they must also be put through passive range of
pain, restores function and prevents subsequent motion regularly and then programmed activity
rupture (Fig. 16.8). should be encouraged by a physiotherapist on a
138 G. Bentley
daily basis to prevent muscle wasting. Early oper-

ations to prevent tendon rupture accompanied by
synovectomy should be applied as indicated.
Advanced joint destruction, instability and
deformity are clear indications for reconstructive
surgery combined with any necessary synovec-
tomy of the joint or tendons.
Arthrodesis and prosthetic arthroplasty are
appropriate at late stages of the disease in certain
joints particularly the knee hands, knees, feet,
wrists, elbows and hip, which often correct defor-
mity, relieve pain and restore joint function
(Figs. 16.7 and 16.9).
Fig. 16.6 Synovectomy—excision of the knee synovium
Rehabilitation should accompany all stages of
en bloc including the suprapatellar pouch. From
“Management of Synovial Disorders”; Z.P. Stavrou and treatment, and includes functional assessment,
P.Z. Stavrou, 2014. In: European Surgical Orthopaedics special training, social integration and psycho-
and Traumatology, ed. G. Bentley, Springer: Heidelberg, logical adjustment, together with family support.
London, New York. By kind permission of the Authors and
A full understanding of the specific needs of
Springer
Fig. 16.7 RA knee stage II showing the preoperative arthroplasty. From “European Surgical Orthopaeics and
joint damage and varus deformity treated by synovectomy Traumatology”; Z.P. Stavrou and P.Z. Stavrou, 2014. ed.
combined with medial unicompartment replacement G. Bentley, Springer: Heidelberg, London, New York
Fig. 16.9 Anteroposterior radiograph of the same hand as

in Fig. 16.2 showing complete correction of deformity by
the use of Swanson MCP replacement arthroplasties. From
“European Surgical Orthopaedics and Traumatology”; A.
Fig. 16.8 Photograph of the extensor tendons of the wrist Lluch, 2014. ed. G. Bentley, Springer: Heidelberg, London,
showing the preservation of the tendons by synovectomy. New York
From “Surgical Management of the Rheumatoid Hand”;
A. Lluch, 2014. From: European Surgical Orthopaedics
and Rheumatology. ed. G. Bentley, Springer: Heidelberg,
affected ten times more often than females and
London, New York
the usual age of onset is between 50 and 25 years.
The aetiology of the disease is unclear but it
patients must influence treatment, together with tends to run in families and close relatives may
the extent of family support required. have had an arthritic disease such as Reiter’s dis-
NOTE: The detailed management of RA of ease, psoriatic arthritis or enterohepatic arthritis.
the foot is well described by Amin and Singh These are all associated with the HLA-B 27 tis-
(2014) [3]. sue type and it is commonly thought that the spe-
cific clinical syndrome is triggered by some
recent event such as a genitourinary urinary or
Ankylosing Spondylitis bowel infection.
and Seronegative Spondarthritis
Ankylosing Spondylitis Pathology
This chronic inflammatory disorder affects the The disease starts as an inflammation affecting
sacro-iliac and spinal joints and is characterised the sacro-iliac joints with back pain with some-
initially by pain and stiffness in the back with times involvements of hips and shoulders and
variable involvement of the peripheral joints. Its rarely the peripheral joints.
prevalence is low, affecting 0.1% in Caucasians, There is a sequence of inflammation, gra
and is much lower in other races. Males are nulation tissue formation, erosion of articular
140 G. Bentley
Fig. 16.10 Ankylosing spondylitis. Anteroposterior

X-ray of pelvis and sacro-iliac joints showing erosion of
the SI joints and reactive bony sclerosis. From “Apley’s
System of Orthopaedics and Fractures”; L. Solomon,
D. Warwick and S. Nayagam, 2010. 9th. edition
c artilage and replacement by fibrous tissue and

ossification of the ligaments in the spine leading
to ankyloses. In some cases the costovertebral
joints may be involved which produces respira-
tory restriction. In addition to the spine, hips may Fig. 16.11 Ankylosing spondylitis. Anteroposterior
go on to complete ankyloses. view of the lumbar spine showing intervertebral ossifica-
tion at all levels producing the appearance of “bamboo
spine”. From “Apleys’s Orthopaedics and Fractures”;
L. Solomon, D. Warwick and S. Nayagam, 2010
Clinical Features
Most patients are young men with persis- (Fig. 16.11). Peripheral joints may show erosive
tent backache and stiffness, often early in the arthritis resembling that of RA.
morning and after activity. The most typical The ESR is usually elevated during active
sign is stiffness of the spine, especially exten- phases of the disease and HLA-B 27 is present in
sion, and in advanced cases the entire spine 90% of cases.
may be rigid with chest expansion decreased
to well below the normal 6 cm. Occasionally
peripheral joints are involved and also ocular Treatment
inflammation, aortic valve disease, carditis and
pulmonary fibrosis. There is no specific treatment but pain may be
controlled by analgesics and non-steroidal anti-
inflammatory drugs. Above all, patients must
Radiographs be encouraged to exercise and keep moving.
Postural training can prevent serious deformity
The specific sign on radiographs is the presence so that if ankyloses occurs in the spine it occurs
or erosion of the sacro-iliac joint which becomes in a good position.
sclerosed and eventually completely fused Severely stiff or painful hips can be treated by
(Fig. 16.10). Ossification occurs across the inter- prosthetic joint replacement, though the results
vertebral discs producing bony bridges between are only moderate and there is a tendency to form
adjacent vertebral bodies. The bridging at several extra-articular bone in the soft tissues which
levels gives the appearance of “bamboo spine” causes pain and recurrent stiffness.
Seronegative Spondarthritis J uvenile Chronic Arthritis (Still’s

Disease)
This is a group of conditions including psoriatic
arthritis, Reiter’s disease and arthritis accompa- Juvenile chronic arthritis (JCA) is the term used
nying ulcerative colitis and Crohn’s disease. to describe non-inflammatory non-infective
inflammatory disease of more than 3 months’
duration in children under 16 years. It is a group
Psoriatic Arthritis of disorders characterised by pain, swelling and
stiffness of joints.
The feature of this disease is the presence of pso- It may occur as a systemic disease with lymph-
riasis in the skin but also involvement of the adenopathy, splenomegaly and hepatomegaly
interphalangeal joints of the fingers and toes accompanied by joint swelling in children below
rather than the metacarpophalangeal joints. the age of 3 years which features fevers, rashes
The arthritis is not usually symmetrical and and malaise with lymphadenopathy, splenomeg-
bone destruction may be so severe that it is some- aly and hepatomegaly, but may resolve.
times called “arthritis mutilans” because of the Pauciarticular JCA is a seronegative variant
flail joints. HLA-B27 occurs in 6%. which usually affects girls below 6 years where
There is no specific treatment so that manage- only a few joints are involved and there is no sys-
ment is based on the same principles as those apply- temic illness. However, serious complications,
ing to the management of rheumatoid arthritis. such as iridocyclitis, occur in 50%.
JCA may occur also as a polyarticular sero-
positive disease which is usually seen in older
Reiter’s Disease children, mainly girls, and resembles classical
RA with multiple joint involvement and progres-
Reiter’s disease is a clinical triad of polyarthritis, sive articular destruction.
conjunctivitis and urethritis. It is also associated Seronegative spondarthritis occurs usually in
with non-specific urinary or bowel infection. older boys and is considered to be “juvenile anky-
The pattern is of joint polyarthritis and is accom- losing spondylitis” with involvement of spine,
panied by an increased frequency of HLA-B 27. hips and knees. HLA-B 27 is often positive.
In JCA general treatment is similar to that of
rheumatoid arthritis with non-steroidal anti-
Clinical Features inflammatory drugs, splints and carefully man-
aged physiotherapy and rehabilitation.
The disease may begin acutely with acute arthri- Custom-made joint arthroplasties can be very
tis of a large joint such as knee or hip. effective for hips and knees.
Tenosynovitis and plantar fasciitis, together with
backache and stiffness due to sacro-iliac joint
involvement and spondylitis often, follow. The Pigmented Villonodular Synovitis
diseases is said to be self-limiting but remains (PVNS)
persistent in 8% of patients.
Radiographs are often normal at first but after This rare disease of joints affects mainly the knee
many months erosive arthritis with sacro-iliac (80%), followed by the hip (15%), and other
and vertebral changes occur similar to those of joints are occasionally involved. It is a mono-
ankylosing spondylitis. articular disease involving also bursae and syno-
The treatment is based on the principles for vial sheaths. Bony involvement is rare, usually in
rheumatoid arthritis and ankylosing spondylitis the hip (Fig. 16.12). It has been very well
with prolonged anti-inflammatory drug treatment. described by Stavrou and Stavrou [4].
142 G. Bentley
Overall incidence is very low—one in one

million—and it constitutes 5% of all soft-tissue
tumours.
Classification
At operation the lesion presents as a villous nod-
ular tissue which is yellow-brown because of the
deposition of pigment. Mostly it can be classified
therefore as PVNS synovitis, PVNS bursitis or
PVNS tenosynovitis according to the site and it
may be nodular or diffuse. The first is more com-
mon in joints and the latter in tendon sheets.
Histology
Histological examination shows villous hyper-
trophy of the synovial membrane in both types
with active proliferation of the synovial cells
and variable fibrosis. There are stromal cells
Fig. 16.12 PVNS—radiograph showing bone cysts amongst which can be found multinuclear giant
in the femoral head and acetabulum with an intact hip
joint. From “Management of Synovial Disorders”; cells and cells containing lipids. Deposits of
Z.P. Stavrou and P.Z. Stavrou, 2014. In: European Surgical haemosiderin are prominent which may be either
Orthopaedics and Traumatology, ed. G. Bentley. Springer: extracellular or within histiocytes. The cellular
Heidelberg, London, New York. With kind permission of membrane is vascular when there is bony
the Authors and Springer
involvement and similar tissue can be found
nearby forming cysts.
Although the histological appearances are
similar to synovial sarcoma they are distinct Differential Diagnosis
conditions. The presence of multinuclear giant cells, haemo-
siderin and absence of spindle cells in active pro-
Aetiology liferation distinguish the disease from malignant
The aetiology is unknown but is considered to be conditions and also from inflammatory disorders
either due to microtrauma or changes in concen- such as rheumatoid arthritis and haemophilia.
tration of lipids in the blood. Chromosome abnor-
malities have also been described. It has been Symptoms
established that there are phenotypic differences These include persistent pain and swelling, which
in giant cells between PVNS and other condi- gradually increase, and nodular changes in the
tions such as RA and haemophilia. synovium and tendons.
Cysts are formed in PVNS though the mecha- If there is no bone involvement there are no
nism is not clear (Fig. 16.12). However in several radiological abnormalities. In advanced cases
studies giant cells in PVNS have been shown to there may be cysts some distance from the articu-
express all the phenotypic features of osteoclasts, lar surface and they may be well defined whilst
including the ability to induce lacunar absorption, the joint space is preserved (Fig. 16.12). In
which may account for the cysts in this condition. advanced cases there may be secondary degen-
It has a high rate of recurrence and a diffuse form erative changes and, in cases affecting the fin-
but otherwise local treatment is satisfactory. gers, pressure indentation of bone.
cho and the MRI Findings

E 5. Many patients will require a combination of
Both techniques may delineate the lesion, espe- DMARDs with or without biologics to
cially MRI, in which multiple synovial lesions achieve the target.
with low or intermediate signal intensity on 6. Many effective biologic DMARDs are
T1-weighted images or no signal intensity on available—all are more effective with
T2-weighted images and gradient echo images methotrexate.
can be seen. 7. NSAIDs may provide useful symptom con-
trol but are rarely indicate without DMARDs.
Treatment 8. Glucocorticosteroids are rapidly affective for
Surgical treatment may be open or arthroscopic. most but have side effects. Therefore use
Open treatment applies in the more diffuse type only with DMARDs and ideally only as a
of the disease affecting the joint and more so if bridge to effective DMARD therapy.
there are extra-articular masses in synovial 9. Open or arthroscopic synovectomy is very
sheaths and bursae. useful for relieving pain in patients, who are
Since the knee joint is a major joint and eas- stabilised on medication but who have a per-
ily accessible open synovectomy is often persistent proliferative synovium.
formed with excision of the synovium en bloc 10. Surgical excision of inflamed tendon sheaths
and meticulous excision of the margins of the improves function and prevents progressive
lesion (Fig. 16.6). tendon rupture.
Recurrence is reportedly low, although 11. Replacement arthroplasty dramatically relieves
arthroscopic synovectomy has a high incidence pain, corrects deformity and improves function
of recurrence of 40% after 42 months [4]. in the hands, knees, feet, hips and ankles.
Total prosthetic replacement is indicated in 12. Aggressive management of the comorbidi-
advanced cases in conjunction with synovectomy ties of RA, especially cardiovascular disease,
when there is secondary joint damage. is vital.
Radiation therapy has been tried in PVNS but
can have serious complications so is now rarely
employed. References
1. Solomon L, Warwick D, Hodder Arnold NS. Apley’s
system of orthopaedics and fractures. In: Inflammatory
Summary Management of RA [1, 2] rheumatic disorders. 9th ed. London: Hachette UK
Company; 2010.
1. Treat RA early and initiate disease-modifying 2. Firestein GS, Budd RC, Gabriel SE, IB MI, O’Dell
anti-rheumatic drug (DMARD) therapy at JR. Kelley’s textbook of rheumatology. 9th ed.
Philadelphia, PA: Elsevier Saunders; 2013.
the time of diagnosis. 3. Amin A, Singh D. Rheumatoid forefoot reconstruc-
2. Treat all patients to a disease activity tar- tion. In: Bentley G, editor. European surgical ortho-
get—remission or low disease activity. paedics and traumatology. Heidelberg, New York,
3. It is not so important what specific therapy London: Springer; 2014. p. 3963–73.
4. Stavrou ZP, Stavrou PZ. Management of synovial dis-
patients receive as long as they are treated orders. In: Bentley G, editor. European surgical ortho-
until they reach the target. paedics and traumatology. Heidelberg, New York,
4. For most patients methotrexate will be the London: Springer; 2014. p. 301–18.
cornerstone of DMARD therapy.
Repair of Osteochondral Defects
in the Knee by Cellular 17
(Chondrocyte and Stem Cell)
Transplantation
George Bentley and Panos D. Gikas
The factors favouring success are: Introduction
1. Early treatment. Osteochondral and chondral lesions of the artic-

2. Young active patients. ular surface of the knee are a major cause of
3. Absence of previous surgery on the knee. pain and disability in young people and may
4. Lesions on the femoral condyles. progress, if untreated, to “early-onset” osteoar-
5. Low BMI. thritis. Over the last 15 years numerous studies
6. Non-smoking patients. have shown the short-term benefit of regenera-
7. Absence of degenerative changes in the joint. tive procedures but few over the long term [1–4].
The incidence of osteochondral defects is not
Future developments are aimed at more precisely known but several authors have
sophisticated cell techniques (genetically selected reported between 10 and 25% of osteochondral
cells, growth factors and stem cells) like mini- defects in patients with an injury and a haemar-
mally invasive surgery and rapid rehabilitation throsis of the knee [5–7]. This is especially the
which promise to potentiate the results and lead, case with sports injuries, and particularly where
in the long term, to prevention of “early-onset” there is also ligament damage. Other causes of
osteoarthritis and treatment of established osteochondral defects such as osteochondritis
osteoarthritis. dissecans and chondromalacia patellae are
important but much rarer.
To carry out the management of these
G. Bentley (*) patients it is important that the surgeon and
Institute of Orthopaedics and Musculo-Skeletal
team are experienced in arthroscopy and the
Science, University College London, London, UK
treatment of all major causes of knee pain and
Royal National Orthopaedic Hospital NHS Trust,
disability.
Stanmore, UK
Clinically the patients present with deep pain,
P. D. Gikas
aggravated by exercise, often associated with
Royal National Orthopaedic Hospital NHS Trust,
Stanmore, UK “catching” and “giving way” and “locking”,
especially if there is a loose fragment of bone and
Bone Tumour Unit, Royal National Orthopaedic
Hospital NHS Trust, Stanmore, UK cartilage or a torn meniscus. A history of high-
e-mail: veronica.white@rnoh.nhs.uk intensity contact sport is frequent.

146 G. Bentley and P. D. Gikas
Indications for Surgery discomfort in the joint. The patient is carefully

counselled regarding the semi-experimental
The main indication is the presence of a painful nature of the procedure and the possible compli-
chondral or osteochondral defect in a knee which cations and is invited to join a clinical trial of the
is otherwise normal. procedure where appropriate. Full consent and
Contraindications are: ethical consent by the relevant authority are
obtained.
1 . Malalignment of the tibio-femoral joint.
2. Malalignment of the patellofemoral joint.
3. Inflammatory arthritis. Imaging
4. Established osteoarthritis.
1. Radiology. A weight-bearing anteroposterior
and 30° lateral radiograph of both knees are
Preoperative Investigations required with a tangential view of the patello-
femoral joint in 30° flexion. These X-rays
Any patient with a history of injury or haemar- may demonstrate an osteochondral defect but
throsis with persistent symptoms should be not a purely chondral defect. They also indi-
investigated. A full general physical examination cate the alignment of the tibio-femoral and
to exclude comorbidity is followed by a detailed patella-femoral joints and the presence of
assessment of both knees and hips. other pathology such as loose bodies.
In a straightforward case the physical findings 2. MRI Scanning. Gadolinium-enhanced T1-
will be: and T2-weighted images are required of the
knee to demonstrate the soft tissues, i.e.
1. A small effusion with a positive “stroke” test. medial and lateral collateral ligaments, ante-
No crepitus. rior and posterior cruciate ligaments, menisci
2. Wasting of the vastus medialis. and the quality of the cartilage and the sub-
3. Variable slight joint-line tenderness over the chondral bone. Subchondral bone oedema
affected side. beneath a cartilage defect often occurs and
restoration of normal subchondral bone fol-
Stable collateral and cruciate ligaments. lowing surgery is associated with a good out-
Terminal restriction of knee flexion with deep come (Fig. 17.1).
Fig. 17.1 MRI showing full-thickness articular cartilage defect of the medial femoral condyle (left) and 1 year post-
ACI with good border integration
17 Repair of Osteochondral Defects in the Knee by Cellular (Chondrocyte and Stem Cell) Transplantation 147
When the investigations show a chondral or a

osteochondral defect the next step is to perform
the necessary operative procedures.
Operative Technique
tage I: Diagnostic and Staging

S
Arthroscopy
The purpose of arthroscopy is to exclude other
joint problems such as:
• Torn menisci.
• Osteochondritis dissecans.
• Ligament damage (anterior and posterior
cruciate). b
• Chondromalacia patellae.
• Inflammatory joint disease.
• Early osteoarthritis.
The arthroscopy is carried out through a lat-

eral portal and the joint is examined for signs of
pathology by a routine arthroscopic examination
of the supra-patellar pouch, patellofemoral joint,
medial and lateral compartments, menisci and
cruciate ligaments.
The osteochondral defect is then assessed and
classified according to the ICRS (International
Cartilage Repair Society) criteria. (Please note that Fig. 17.2 (a) Arthroscopy of knee showing harvesting of
the final size of the defect is assessed at the second fragment of articular cartilage from the medial margin of
operation for implanting of the cartilage cells.) the trochlea. (b) Chondrocytes spreading out in culture
A small piece of full-thickness articular carti-
lage is removed from the non-load-bearing margin sequentially by exposure to trypsin and collage-
of the trochlea, usually medially, removing approx- nase (Fig. 17.2b). A sample of the isolated cells is
imately 200–300 g (or a piece the size of the little checked for viability and then culture is carried
finger nail) using a small-gauge and grasping for- out, beginning with calf serum and continuing
ceps (Fig. 17.2a). The joint is then washed clear of with the patient’s own serum, which has been
any debris and closed in a routine manner and a removed at the time of the arthroscopy. Culture is
compression bandage applied to the knee. then performed with several passages and after
Post-operative management for this procedure 3–4 weeks the cell numbers have multiplied by
is as for any other arthroscopy with gradual 20–30 times.
mobilisation and increased activity within the At this point the patient is readmitted for
limits of pain. second-stage implantation.
econd Stage: Cell Implantation

S
Cell Culture At the time of the second-stage implantation care
is taken to exclude any possible problem with the
The articular cartilage is transferred to the cell knee such as infection or large effusion prior to
culture laboratory where the matrix is removed the commencement of the second stage. It is
Fig. 17.4 Chondrocytes in suspension being injected

Fig. 17.3 A defect in the medial femoral condyle pre- behind the collagen type I/III membrane, which is sutured to
pared for chondrocyte implantation the margins of the defect. The “tidemark” can be clearly seen
extremely rare to have any problems at this stage the cells in solution wet the membrane progres-
and the patient is therefore advised again of the sively forming a tidemark (Fig. 17.4). Fibrin glue
procedure and possible complications. is applied to the margin of the defect in order to
It is possible to perform the MACI procedure ensure that the cells in solution do not leak. When
by arthroscopic implantation but generally it is the cells have completely filled the defect a suture
easier and quicker to perform a mini-arthrotomy. is placed superiorly where the catheter was
The defect is prepared carefully, excising passed and the defect is sealed with fibrin glue
damaged cartilage with a sharp knife down to the and, if necessary, one or two sutures where the
calcified zone of the cartilage. It is essential to cut catheter has been inserted.
back to healthy cartilage around the defect. The At the end of the procedure the knee is put
defect is then carefully and gently cleared of any through a gentle full range of motion. The graft
residual cartilage whilst, at the same time, is re-examined to ensure that there is no adhe-
attempting to avoid bleeding from the subchon- sion of the glue to the soft tissues in the knee
dral bone (Fig. 17.3). Bleeding of the subchon- and to the graft and also that there has been no
dral bone, if it occurs, can be arrested by the displacement.
application of noradrenaline solution on a small The joint is then closed in layers with intrader-
swab for a period of 1 min. mal sutures to the skin. The leg is then enclosed
In the case of ACIC the defect is then assessed in a compression bandage with a plaster-of-Paris
for size using a soft metal template and the mem- backslap. It is elevated and immediately post-
brane (type I/III collagen porcine) is cut to the operatively quadriceps-setting exercises and
size of the defect. It is important that the mem- active foot movement are encouraged.
brane is not too tight when sutured because this On the first day post-operatively the patient
will lead to leakage at the edges of the is allowed up, fully weight bearing, in the com-
membrane. pression bandage and backslap, and at 48 h this
The membrane is sutured with interrupted 5/0 is changed to a cylinder cast. The patient mobil-
or 6/0 vicryl sutures at 3–4 mm intervals and a ises with elbow crutches for general support, but
gap left at the upper end of the defect to allow for fully weight bearing from then onwards. After
passage of the catheter. 10 days the plaster cast is removed and active
The cells, in suspension, are then injected by a mobilisation through a strict physiotherapy pro-
micro-syringe through the 2 mm catheter behind tocol is carried out. Walking sticks are contin-
the membrane. If the membrane is maintained ued for 6 weeks just to aid the patient in
dry it is possible to see the filling of the defect as balance.
At 6 weeks the sticks are discarded and full a

knee movement is encouraged. At this stage the
patient will have begun gentle rowing exercises
and swimming and will progress according to the
freedom from pain within the physiotherapy
protocol.
At 6 months light jogging is allowed and nor-
mal everyday activities except for avoiding squat-
ting and kneeling impact loading on the knee and
torsional strains on the knee. By this time the
knee should be pain-free in normal activities.
MRI scanning is performed if progress is slow.
heck Arthroscopy at 1 Year

C
The check arthroscopy at 1 year is to ensure that
the graft is satisfactory and that the patient is safe b
to recommence full activities. At the check
arthroscopy the graft is examined and checked
according to the degree of incorporation and the
depth of filling of the defect, consistency of the
surface and smoothness of the surface, according
to the ICRS protocol. It is scored up to 2 for each
of these parameters (Fig. 17.5). If this is satisfac-
tory, return to full activity is allowed.
Biopsy of the Graft
Where possible it is the custom in our unit to
biopsy the graft in its centre using a 2.5 mm Fig. 17.5 (a) Arthroscopic appearances preoperatively
diameter Jamshidi needle. The entrance into the (showing full-thickness defect) and (b) 1 year post-
defect should be perpendicular to the surface. A operatively (showing complete healing by hyaline-like
cartilage)
core of cartilage and bone is removed from the
knee.
This is then subjected to histological examina- MRI scan—The MRI scan at 12 months is
tion employing routine haematoxylin and eosin performed to attempt to assess the quality of the
staining for cellular content and viability, but also cartilage repair but more importantly to assess
safranin-0 for proteoglycans and other stains the condition of the subchondral bone. The pres-
such as S100 for type II collagen. In addition the ence of subchondral bone oedema at this stage
sections are viewed by polarised light to indicate suggests that the repair is not complete and full
the orientation of the collagen fibres in the repair mobilisation is delayed until a further MRI scan
material and the presence of a “tidemark” (indi- after 6 months.
cating normal attachment of the graft tissue to the
subchondral bone).
The repair material is classified as: Matrix-Assisted Chondrocyte
Implantation (MACI)
1 . Hyaline-like cartilage (Fig. 17.6).
2. Mixed hyaline and fibrocartilage. A number of concerns have been expressed
3. Fibrocartilage. regarding the technique of ACI(C) and they
4. Fibrous tissue. include possible leakage of cells from the defect
Fig. 17.7 MACI membrane with attached cartilage cells

b
in Petri dish ready for cutting to size of the defect
Fig. 17.6 (a) Histological appearance of hyaline carti-

lage (safranin O×10), (b) high-power view showing hya-
line cartilage with “tidemark” indicating the fixation of
the cartilage to the subchondral bone
Fig. 17.8 MACI implant in position secured with fibrin

and damage to the surrounding host cartilage glue
from the multiple sutures. The MACI technique
was developed to avoid the use of sutures and
also to decrease the time taken for the proce- pressure for 2 min. It is important to moisten the
dure. The growth of cells on the membrane dur- gloves when applying pressure; otherwise the
ing the last week of the culture period ensures graft may stick to the glove and be inadvertently
an even spread of cells over the area of the removed when the hand pressure is released
defect. Also it prevents cell leakage from the (Fig. 17.8).
defect. The joint is then put through a full range of
In the MACI technique, the collagen I/III motion. If there is any tendency for it to lift or
membrane with its attached cells is delivered to move, then it should be secured with several
the operating theatre (Fig. 17.7). A small square sutures. Finally, a thin layer of glue is placed
is removed from the bottom left-hand corner so around the defect to complete the seal.
that the cell-bearing surface faces the surgeon. Finally, the joint is put through a full range of
The template of the defect in the articular carti- motion again to ensure that there is no adherence
lage is cut and then this is used to cut a piece of of the graft to the synovial membrane and no fur-
membrane together with the cells to fill the ther dislodgement.
defect. Several drops of fibrin glue are placed in The closure of the wound is the same as for
the defect and then the MACI graft is placed into ACI(C) and the post-operative rehabilitation
the defect and held in position by thumb or finger identical.
Results venous thrombosis, which was treated success-

fully, and 1 patient had septic arthritis of the knee
ACI(C) has been practiced at the Royal National treated successfully with arthroscopic washout.
Orthopaedic Hospital since 1998 and MACI 32 early cases had a problem with ACI using
since 2002. Various publications from this unit periosteum as a membrane, with associated
have indicated that the ACI(C) will survive for up hypertrophy of the membrane and/or attachment
to 10 years in 75% of patients. Recent work to the synovium, requiring arthroscopic shaving
studying a cohort of 831 patients followed for to release it. None of these cases had persistent
2–12 years indicates the survival of the graft and symptoms. The use of periosteum was abandoned
satisfactory results in 70–80% over a 10-year in 2001.
period [10].
Conclusions
Factors that Influence Outcome
ACI(C) and MACI have successful results in the
During a recent study of the cohort of patients treatment of osteochondral defects of the knee in
with ACI and MACI, it became apparent that a 70–80% of patients over a 10-year period. The
number of factors were key to the success of the procedure carries almost no adverse effects and is
implantation procedure [8, 9]. These were as the only reported technique, which results in
follows: graft survival of at least 10 years with satisfactory
results. There is no data as yet on the preventative
1. Patients 15–50 years of age except in excep- effect on early osteoarthritis but the relief of
tional circumstances symptoms for 10 years defers the requirement for
2. Patients who have not undergone previous
any other more radical treatment such as joint
procedures on the cartilage defect replacement.
3. Patients who do not have osteoarthritis or

inflammatory arthritis
4. Patients who have a normal BMI References
5. Patients who are not smokers
6. Patients with no malalignment of the tibio- 1. Bentley G, et al. A prospective, randomised compari-
son of autologous chondrocyte implantation versus
femoral and patellofemoral joints mosaicplasty for osteochondral defects in the knee. J
Bone Joint Surg Br. 2003;85(2):223–30.
It is possible to carry out anterior cruciate lig- 2. Bentley G, et al. Minimum ten-year results of a pro-
ament repair at the second-stage procedure, spective randomised study of autologous chondrocyte
implantation versus mosaicplasty for symptomatic
simultaneous with the chondrocyte implantation articular cartilage lesions of the knee. J Bone Joint
procedure or realignment opening wedge tibial Surg Br. 2012;94(4):50.
osteotomy. Additionally, the alignment of the 3. Beris AE, et al. Treatment of full-thickness chon-
patellofemoral joint should be checked carefully dral defects of the knee with autologous chon-
drocyte implantation: a functional evaluation
preoperatively and if there is malalignment this with long-term follow-up. Am J Sports Med.
should be corrected by doing a soft-tissue 2012;40(3):562–7.
realignment procedure of the patellar tendon
4. Filardo G, et al. Arthroscopic second generation
together with lateral release and medial reefing. autologous chondrocytes implantation associ-
ated with bone grafting for the treatment of knee
osteochondritis dissecans: results at 6 years. Knee.
2012;19(5):658–63.
Complications 5. Curl WW, et al. Cartilage injuries: a review of 31,516
knee arthroscopies. Arthroscopy. 1997;13(4):456–60.
6. Aroen A, et al. Articular cartilage lesions in 993
Complications have been very few. Over the consecutive knee arthroscopies. Am J Sports Med.
large series of 831 patients, 2 developed deep 2004;32(1):211–5.
7. Flanigan DC, et al. Prevalence of chondral defects in a case-controlled study. J Bone Joint Surg Br.
athletes’ knees: a systematic review. Med Sci Sports 2009;91(12):1575–8.
Exerc. 2010;42(10):1795–801. 10.
Nawaz SZ, Bentley G, Briggs TW, Skinner
8. Jaiswal PK, et al. The adverse effect of elevated JA, Carrington RWJ, Gallagher KR, Dhinsa
body mass index on outcome after autologous BS. Autologous chondrocyte implantation in the
chondrocyte implantation. J Bone Joint Surg Br. knee: mid- to long-term results. J Bone Joint Surg
2012;94(10):1377–81. Am. 2014;96(10):824–30.
9. Jaiswal PK, et al. Does smoking influence out-
come after autologous chondrocyte implantation?:
Heterotopic Ossification
18
Gregory Pereira, Nikolaos Paschos,
and John Kelly IV
Background [1–9] signs are often nonspecific loss of joint mobility

and subsequently loss of function. Patients may
Heterotopic ossification (HO) is the formation of also complain of edema, erythema, palpable
mature cellular bone in non-osseous tissues. mass, contracture formation, or fever.
While the exact biological etiology is unknown,
HO typically occurs spontaneously, postopera-
tively, or following trauma, notably after spinal Prevalence
cord injury or TBI (see below).
HO affects twice as many males as females Inciting event Prevalence (%)
Traumatic brain injury (TBI) 8–20
and has a particularly high incidence in men
Spinal cord injury (SCI) 10–53
with hypertrophic osteoarthritis. The most
Total hip arthroplasty (THA) 40–74
common overall location for HO to occur in is Lower extremity amputation 63
the hip, though other locations are common
after specific injuries (e.g., after TBI elbow is a
commonly affected site). Clinically, HO is
most often seen in the hip, elbow, knee, or Classification Systems
shoulder joints.
Signs and symptoms of HO typically appear • Brooker Classification of Heterotopic
from 3 to 12 weeks after initial trauma, spinal Ossification (Following THA) [10]
cord injury, and other inciting events. The first • Schmidt and Hackenbrock Classification of
Heterotopic Ossification (Following THA)
G. Pereira (*) · J. Kelly IV • McAfee’s Classification of Heterotopic
Department of Orthopedic Surgery, University of Ossification (Following Total Disc Arthroplasty
e-mail: Gregory.Pereira@uphs.upenn.edu
N. Paschos Imaging
Triphasic Bone Scan
Division of Sports Medicine, Department of
Orthopaedic Surgery, Boston Children’s Hospital,
Harvard Medical School, Boston, MA, USA • Most commonly used diagnostic study.
e-mail: Nikolaos.Paschos@childrens.harvard.edu • Most sensitive study for early diagnosis.

• Serial scans used to monitor progression and • Shown to decrease incidence of HO after THA
optimal timing for surgical intervention. with more pronounced effect on higher Booker
classes [6].
Ultrasound • Mechanism thought to involve inhibition of
osteoblast differentiation.
• Finding: echogenic surface with posterior • Can be used prophylactically or
acoustic enhancement. postoperatively.
• Early detection of HO (~2 weeks before
x-ray). NSAID (prophylaxis)
• Helps clinicians opt to begin preventative
measures. • Indomethacin most commonly used:
• More accurate than any laboratory test. –– Mechanism is thought to work through
inhibition of differentiation of mesenchy-
X-ray mal cells and posttraumatic bone remodel-
ing (via prostaglandin inhibition).
• First seen 4–6 weeks after injury (not useful
for early diagnosis). Bisphosphonates (prophylaxis)
• Monitor progression and maturation of bone.
• Often used to classify HO after THA. • Disodium etidronate commonly used.
CT Wide exposure and surgical resection

(treatment)
• Useful for preoperative planning.
• Indicated for severe loss of function and
ROM.
Labs • Identify all neurovascular structures involved
with exposure.
Labs are nonspecific and no single lab is needed • Timing is controversial but current recom-
for the diagnosis of HO. Often used as an adjunct mendations based on etiology:
during workup for HO. –– 6 months for general trauma
–– 12 months for SCI
• Elevated serum alkaline phosphatase –– 18 months for TBI
(>250 IU). • Post-op oral indomethacin to lower risk of
• Elevated CRP. recurrence.
• Elevated ESR (>35 mm/h).
• Elevated CK (correlates with the extent of
muscle involvement). Recent Developments [11–35]
• THA has been known to be associated with

Treatment and Prophylaxis HO but differences related to the approach for
THA have not been well studied. A 2016 study
The management of HO is largely dependent on compared rates of HO after direct anterior
the location and amount of ectopic bone forma- approach (DAA) THA versus posterior
tion and functional capacity of the patient. If approach THA and found that rates of HO
there is concern for HO in an at-risk patient pro- after DAA were significantly lower. This may
phylactic treatment can be initiated, though lim- inform surgical planning for THA candidates
ited evidence of the efficacy in the literature. with many risk factors for the development of
Local radiation therapy (prophylaxis) subsequent HO.
18 Heterotopic Ossification 155
• The role of radiation prophylaxis in decreas- the patient’s vitals were unremarkable and
ing rates of progressing to HO has been there was mild erythema of the right hip. The
described in the literature though the opti- incision is well healed and intact. The patient
mal dose of radiation was unknown. In 2017, has globally decreased passive and active
a randomized control trial showed that 700 range of motion.
centigray showed superior results in decreas- What are these patients’ risk factors for het-
ing the rate of progression to HO after THA erotopic ossification?
compared to 400 centigray dosing. As such,
more standardized prophylaxis protocols I. Gender
utilizing radiation should be developed in II. Type 2 diabetes
the future. III. HTN
• The complex role of BMP in the pathogen- IV. Hypertrophic osteoarthritis
esis of HO has been well described but the (A) I
complex interplay between other transcrip- (B) I, II
tion factors and cell signaling molecules (C) I III
still remains unknown. A 2017 study found (D) II, III
signaling pathways for HIF-1α and hypoxia (E) I, IV
in the amplification of BMP signaling in
fibrodysplasia ossificans progressiva (FOP) Assuming this patient has HO, what studies
the most devastating form of HO. This would show evidence of disease at this point?
study provides insight into the underlying
cellular mechanism at play in HO and pro- I. Plain radiograph
vides HIF-1α as a potential therapeutic tar- II. Ultrasound
get for intervention in the treatment of HO III. Triphasic bone scan
and FOP. (A) I
• The histopathologic progression of HO has (B) II
been well described and the stages of bony (C) I, II
maturation have been well documented; how- (D) I, II, III
ever little was known about the vascular pat-
terning that occurs in HO. In 2017, a surgical Had this patient presented 2 weeks after THA,
pathology from HO cases was examined by what would be the most sensitive imaging modal-
vascular histomorphometric anaylsis and ity for early detection of HO?
showed pathophysiological processes of
osteogenesis and angiogenesis. (A) Plain radiograph
(B) Ultrasound
(C) Triphasic bone scan
Case-Based Discussions (D) CT
(E) MRI
Case 1
If surgical intervention was needed what
A 68-year-old male s/p right THA and a his- imaging modality would be most useful for oper-
tory of hypertension, type 2 diabetes, and ative planning?
hypertrophic osteoarthritis presents to the
clinic with R hip pain. The patient had an (A) Plain radiograph
uncomplicated THA 7 weeks ago and success- (B) Ultrasound
fully has been completing PT. He noticed mild (C) Triphasic bone scan
discomfort near the groin region but has not (D) CT
had any fevers, chills, night sweats. On exam, (E) MRI
Case 2 (C) Knee

(D) Shoulder
A 28-year-old M with a history of asthma pres- 5. If surgery were to be needed, what is the cur-
ents after head on collision in a football game rent guidelines regarding timing of surgical
in which he lost consciousness. He is found to intervention for HO after TBI?
have a traumatic brain injury. He was found to (A) 6 months
have no evidence of fractures and no intracra- (B) 9 months
nial bleeding. Two weeks after initial injury he (C) 12 months
presents with stiffness in his elbow. On exam, (D) 18 months
his vitals were unremarkable. He has a palpable
mass adjacent to his olecranon but no erythema
or edema. Case 3
1. What are the patients’ risk factors for HO? A 54-year-old female with a history of SCI pres-
I. Gender ents to your office for “problems with her knee.”
II. TBI She has recently noticed that it has been more
III. Asthma difficult to move her L knee though she has not
IV. Age had any associated pain or other associated symp-
(A) I toms during this time. On exam, her vitals are
(B) I, II unremarkable and she has decreased flexion at
(C) I, III her L knee.
(D) II, IV
(E) III, IV 1. What is this patients’ risk factors for HO?
2. What is the most appropriate single test to I. Gender
confirm the diagnosis of HO at this time II. SCI
(2 weeks after injury)? III. Age
(A) Triphasic bone scan (A) I
(B) Plain radiograph (B) II
(C) Ultrasound (C) I, II
(D) CT (D) III
(E) Serum alkaline phosphatase 2. If this patient had total disc arthroplasty, what
3. Which of the following would be appropriate would be the most appropriate classification
prophylaxis to start for this patient based on system to use?
current clinical practice? (A) McAfee’s Classification of Heterotopic
I. Methotrexate Ossification
II. Local radiation (B) Brooker Classification of Heterotopic
III. Indomethacin Ossification
(A) I (C) Schmidt and Hackenbrock Classification
(B) II of Heterotopic Ossification
(C) I, II 3. What would be the most appropriate time for
(D) II, III surgical intervention for a patient with HO s/p
(E) I, II,II SCI?
4. What is the second most common site of het- (A) 6 months
erotopic ossification after TBI (after hip)? (B) 9 months
(A) Hip (C) 12 months
(B) Elbow (D) 18 months
18 Heterotopic Ossification 157
Review Questions III) NSAIDs

IV) Radiation
What are the current recommendations for timing V) Methotrexate
of surgical treatment for HO s/p general trauma? (A) I
(B) I, II
(A) 6 months (C) II, III, IV
(B) 9 months (D) III, IV, V
(C) 12 months (E) I, IV, V
(D) 18 months
What is the proposed MOA of prophylactic

local radiation for HO? References
(A) Mechanism via inhibition of differentiation 1. Bentley G. European surgical orthopaedics and trau-
matology: the EFORT textbook. New York: Springer
of mesenchymal cells Berlin Heidelberg; 2014.
(B) Mechanism via inhibition of osteoclasts 2. Vanden Bossche L, Vanderstraeten G. Heterotopic ossi-
(C) Mechanism via inhibition of osteoblast fication: a review. J Rehabil Med. 2005;37(3):129–36.
differentiation 3. Liu K, Tripp S, Layfield LJ. Heterotopic ossifica-
tion: review of histologic findings and tissue dis-
(D)
Mechanism via inhibition of BMP tribution in a 10-year experience. Pathol Res Pract.
pathways 2007;203(9):633–40.
4. Cipriano CA, Pill SG, Keenan MA. Heterotopic
What lab values are needed for the diagnosis ossification following traumatic brain injury
and spinal cord injury. J Am Acad Orthop Surg.
of HO? 2009;17(11):689–97.
5. Board TN, et al. The prophylaxis and treatment of
I. Elevated alkaline phosphatase heterotopic ossification following lower limb arthro-
II. Elevated CRP plasty. J Bone Joint Surg Br. 2007;89(4):434–40.
6. Eggli S, Woo A. Risk factors for heterotopic ossifi-
III. Elevated ESR cation in total hip arthroplasty. Arch Orthop Trauma
IV. Elevated CK Surg. 2001;121(9):531–5.
(A) I 7. DeeLee J, Ferrari A, Charnley J. Ectopic bone forma-
(B) I, II tion following low friction hip arthroplasty of the hip.
Clin Orthop. 1976;121:53–9.
(C) I, III 8. Mavrogenis AF, Soucacos PN, Papagelopoulos
(D) II, III PJ. Heterotopic ossification revisited. Orthopedics.
(E) None of the above 2011;34(3):177.
9. Foruria AM, Augustin S, Morrey BF, Joaquin
S-S. Heterotopic ossification after surgery for frac-
What imaging modality can be used to help tures and fractures-dislocations involving the proxi-
determine the time of surgical intervention? mal aspect of the radius or ulna. J Bone Joint Surg
Am. 2015;95-A(10):e66(1)–7).
( A) Serial plain radiographs 10. Stover SL, Hataway CJ, Zeiger HE. Heterotopic ossi-
fication in spinal cord-injured patients. Arch Phys
(B) Serial ultrasounds Med Rehabil. 1975;56(5):199–204.
(C) Serial triphasic bone scans 11. Shehab D, Elgazzar AH, Collier BD. Heterotopic

(D) CT ossification. J Nucl Med. 2002;43:346–53.
(E) MRI 12.
Simonsen LL, Sonne-Holm S, Krasheninnikoff
M, Engberg AW. Symptomatic heterotopic ossifi-
cation after very severe traumatic brain injury in
Which of the following are used in the pro- 114 patients: incidence and risk factors. Injury.
phylaxis of HO? 2007;38(10):1146–50.
13. Banovac K, Williams JM, Patrick LD, Haniff

YM. Prevention of heterotopic ossification after
I) Surgical excision spinal cord injury with indomethacin. Spinal Cord.
II) Bisphosphonates 2001;39:370–4.
14. Wittenberg RH, Peschke U, Botel U. Heterotopic

agement of heterotopic bone formation. Clin Radiol.
ossification after spinal cord injury. Epidemiology and 1991;43(3):190–6.
risk factors. J Bone Joint Surg Br. 1992;74(2):215–8. 25. Firoozabadi R, Alton T, Sagi HC. Heterotopic ossi-
15.
van Kuijk AA, Geurts AC, van Kuppevelt fication in acetabular fracture surgery. J Am Acad
HJ. Neurogenic heterotopic ossification in spinal cord Orthop Surg. 2017;25(2):117–24.
injury. Spinal Cord. 2002;40:313–26. 26. Ayers DC, Pellegrini VD, Evarts CM. Prevention of
16. Hsu JE, Keenan MA. Current review of heterotopic heterotopic ossification in high-risk patients by radia-
ossification. UPOJ. 2010;20:126–30. tion therapy. Clin Orthop Relat Res. 1991;263:87–93.
17. Maloney WJ, et al. Incidence of heterotopic ossi-
27. McAuliffe JA, Wolfson AH. Early excision of hetero-
fication after total hip replacement: effect of the topic ossification about the elbow followed by radia-
type of fixation of the femoral component. JBJS. tion therapy. JBJS. 1997;79(5):749–55.
1991;73(2):191–3. 28. Fijn R, Koorevaar RT, Brouwers JR. Prevention of
18. Dalury DF, Jiranek WA. The incidence of heterotopic heterotopic ossification after total hip replacement
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2004;19:447–57. 29.
Mehren C, et al. Heterotopic ossification in
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JBJS. 2007;89(3):476–86. therapy in spinal cord injury patients with heterotopic
20. Hug KT, Alton TB, Gee AO. In brief: classifications ossification. Paraplegia. 1993;31(10):660–6.
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Res. 2014;473(6):2154–7. Relat Res. 1991;263:13–29.
21. Schmidt J, Hackenbroch MH. A new classification for 32. Pape HC, et al. Current concepts in the development
heterotopic ossifications in total hip arthroplasty con- of hetetrotopic ossification. Journ Bone and Joint
sidering the surgical approach. Arch Orthop Trauma Surg. 2004;86:783–7.
Surg. 1996;115(6):339–43. 33. Newman EA, et al. Incidence of heterotopic ossifica-
22. McAfee PC, et al. Classification of heterotopic ossi- tion in direct anterior vs posterior approach to total
fication (HO) in artificial disk replacement. J Spinal hip arthroplasty: a retrospective radiographic review.
Disord Tech. 2003;16(4):384–9. Int Orthop. 2016;40(9):1967–73.
23. Bodley R, Jamous A, Short D. Ultrasound in the early 34. Liu J, et al. 400 versus 700 CGY radiation in preven-
diagnosis of heterotopic ossification in patients with tion of heterotopic ossification after total hip arthro-
spinal injuries. Paraplegia. 1993;31(8):500–6. plasty. Bone Joint J. 2017;99(Suppl 4):125.
24. Thomas EA, Cassar-Pullicino VN, McCall IW. The 35. Cocks M, et al. Vascular patterning in human hetero-
role of ultrasound in the early diagnosis and man- topic ossification. Hum Pathol. 2017;63:165–70.
Metastatic Bone Tumors
19
Introduction –– Lung—Mainly osteolytic.

–– Thyroid—Mainly osteolytic.
• Most common sites affected by metastatic dis- • Multiple metastatic bone lesions typically
ease in general: present.
–– Lung. • Vascular spread through:
–– Liver. –– Batson’s vertebral plexus: responsible for
–– Bone. metastases to axial structure (skull, verte-
• Most common bones affected by metastatic bral bodies, pelvis, proximal limbs).
disease: –– Arterial tree metastases: responsible for
–– Spine (70%). metastases to distal extremities (mainly in
–– Pelvis (40%). lung and renal cancer).
–– Proximal femur (25%). • Most common and dominant symptom:
–– Humerus. –– Pain—more than 3/4 of patients.
• Most common site affected: Mechanical due to bone destruction or.
–– Thoracic spine. Tumorigenic—worst at night.
• Most common site of fracture secondary to • Other symptoms.
metastasis: –– Pathological fracture (8–30% at presenta-
–– Proximal femur. tion).
• Most common tumors metastasized to bones: –– Malignant hypercalcemia symptoms—
–– Prostate (32%)—90% osteoblastic lesions. confusion, muscle weakness, polyuria and
–– Breast (22%)—60% osteoblastic, 40% polydipsia, nausea/vomiting.
osteolytic lesions. –– Neurologic abnormalities (due to compres-
–– Kidney (16%)—Mainly osteolytic. sion of the spinal cord in case of disease to
the spine).
T. Kalathas (*)
Department of Internal Medicine, Boston Medical
Center, Boston, MA, USA
N. K. Paschos
Division of Sports Medicine, Department of
Harvard Medical School, Boston, MA, USA
e-mail: Nikolaos.Paschos@childrens.harvard.edu

Diagnosis • Negative prognostic factors.

–– Pathological fracture.
Workup for suspected metastatic lesion of –– Visceral metastasis present.
unknown primary origin: –– Hemoglobin <7 mmol/L.
–– Site of primary cancer—Lung.
1. Imaging: –– If more than one negative prognostic factor
(a) Assess the lesion: present, survival only a few months.
• X-rays—AP and lateral of involved area. • Scoring systems estimating survival proposed
• If not adequate, use CT scan. so far only of limited value.
• MRI used if radical resection considered.
(b) Detect possible primary cancer:
• CT—chest, abdomen, pelvis. Treatment Goals and Options
(c) Assess the whole skeleton:
• Technetium bone scan. (a) Goals of treatment:
–– If lesion present on bone scan • Analgesia.
- > X-ray; if X-ray equivocal - > use • Function maintenance.
CT scan or MRI. • Rarely cure.
–– Myeloma, some lymphomas, and thy- –– Rarely possible in patients with
roid cancer often cold on bone scan myeloma or breast cancer post-adju-
because solely osteolytic. vant chemotherapy, hormonal therapy,
If suspected evaluate with a skeletal or radiation.
survey (series of X-rays). (b) Bisphosphonates (BMAs).
–– High sensitivity, but low specificity. –– Strongly recommended in any skeletal
(d) Confirm diagnosis: related event (bone pain, impending or
• Bone biopsy. current fracture, spinal cord compression,
–– Needed in all patients without a history bone radiation, bone surgery).
of known bone metastatic disease to –– Most commonly BMA used: IV zoledro-
rule out primary bone lesion (NEVER nate, IV pamidronate, denosumab SC.
treat without tissue diagnosis first). –– Most common side effects of BMAs: ero-
2. Labs. sive esophagitis, osteonecrosis of the jaw,
(a) CBC, ESR. nephrotoxicity, hypocalcemia.
(b) BMP. (c) Pain alleviation options.
(c) Ca, phosphate. –– Mild analgesics.
(d) LFTs, ALP. –– Narcotics.
(e) Serum protein EP, urine protein EP. –– Radiation (single dose of 8 Gy).
–– Chemotherapy.
–– Hormone therapy (in breast cancer).
Survival –– Surgery (if fracture present or impending).
(d) Prophylactic fixation guidelines:
• Overall 1-year survival—40%. –– Fidler’s criteria:
• Long-term survivors—15%. Bone lesions >25 mm in long bones or
• Median survival in patients with metastatic Destruction of >50% of cortical bone.
bone disease per site of primary tumor: –– Mirel’s criteria (site, pain, lesion, size):
–– Thyroid: 48 months (best). Site, presence of pain, lesion, size.
–– Prostate: 40 months. Maximum score = 12—if calculated score
–– Breast: 24 months. 8 or above:
–– Kidney: varies depending on medical Prophylactic fixation needed before
condition. radiotherapy.
–– Lung: 6 months (worst). –– Harington’s criteria:
19 Metastatic Bone Tumors 161
However, fractures are possible even in Resection prosthesis used if great bone loss
lesions that do not satisfy the above present.
criteria. –– Wide resection:
Used in selected cases for patients with
potential for long-term survival.
Preoperative Care –– Amputation:
–– Rarely used only for palliation.
• Before consideration of surgery ask: • Procedures by location of the lesion.
–– Bone lesion—malignancy or not? • Humerus
–– Metastases or primary tumor? –– Proximal—Proximal humerus replacement
–– Biopsy needed? or plate with cement.
–– Solitary or multiple lesions? Anterior approach with patient in a supine
–– Site of primary cancer? sitting position.
–– Radical surgery considered? Sling used for 6 weeks postoperatively.
–– General health of the patient? MRI typically needed to assess extension
–– Expected survival of the patient? of lesion.
–– Profuse bleeding expected or not? –– Diaphysis—IM nail with or without cement.
• Goals of surgery: Proximal half—Lateral approach.
–– Patient survives. Distal half—Posterior approach.
–– Immediate stability of the implant. –– Distal—Total elbow arthroplasty or distal
–– Implant duration > patient survival. humerus replacement with cement.
• Hypercalcemia and dehydration: Posterior approach.
–– Provide adequate hydration. • Radius
–– Add bisphosphonates. –– Proximal—Proximal radial replacement or
–– Start low-dose heparin in patients on high small-fragment T plate with cement.
risk of thrombosis. Posterior approach.
• High risk for infection: –– Diaphysis—Small-fragment plate or flexi-
–– Anti-staphylococcal prophylactic antibiot- ble nail.
ics immediately before operation. –– Distal—Distal radius plate with cement or
Repeat possibly 3 h later. wrist fusion to ulna.
Avoid continuation after 24 h. • Ulna
• Preoperative embolization for: –– Proximal—Olecranon plate with cement or
–– Renal cell carcinoma. total elbow arthroplasty.
–– Thyroid carcinoma. Posterior approach.
–– Diaphysis—Small-fragment plate or flexi-
ble nail.
Operative Techniques –– Distal—Small-fragment plate with cement
or resection.
• Procedures of long bones: • Femur
–– Osteosynthesis with or without curettage –– Proximal—Proximal femoral replacement
and with or without additional PMMA. or calcar-replacing THA or long cephalom-
Simple procedure—performed even in edullary nail with cement.
patients in very poor condition. Prophylactic osteosynthesis needed even in
Goals: immediate stability, short rehabilita- minor lesions (due to high load).
tion period. –– Diaphysis—Long cephalomedullary nail
Osteosynthesis of choice: nailing. with or without cement.
–– Prosthesis: –– Distal—Distal femoral replacement or
Preferred when the metastasis is located plate with cement.
near joints.
• Tibia Recent Developments/Publications

–– Proximal—Plate with cement or proximal in the Field
tibia replacement.
–– Diaphysis—IM nail with or without • According to a recent RCT published in
cement. January 2017 in JAMA conducted in patients
–– Distal—Distal tibia plate or amputation. with bone metastases due to breast cancer,
• Fibula prostate cancer, or multiple myeloma, the use
–– P r o x i m a l / d i a p h y s i s — C o n s e r va t ive of zoledronic acid every 12 weeks compared
treatment. with the standard dosing interval of every
–– Distal—Distal fibula plate or ankle fusion. 4 weeks did not result in an increased risk of
• Spine skeletal related events over 2 years. This lon-
–– If life expectancy <6 months, only pallia- ger interval may be an acceptable treatment
tive care indicated. option for patients with the aforementioned
–– Surgery indicated for: primary cancers [1].
Metastatic lesions to spine with neurologic • According to a recent RCT published in
deficits in patients with life expectancy March 2016 in the Journal of Orthopaedic
>6 months. Science the rare condition of solitary bone
–– If life expectancy >6 months but surgery only metastasis (SBOM) should be treated
contraindicated use radiation alone. with wide resection or long-course radiother-
–– Be aware of complications such as hard- apy at doses 40–50 Gy to achieve long-lasting
ware failure, spinal instability, and non- local tumor control [2].
union of fracture. • According to a recent study published in
2016 in the Journal of Clinical Densitometry:
Assessment and Management of
Postoperative Care Musculoskeletal Health showed that routine
MRI sequences enable us to make an accurate
• Single-dose radiation (8 GY) to all patients for distinction between a vertebral fracture of
pain relief; repeat dose if pain persists. benign and malignant origin avoiding the need
• Adjuvant systemic medical therapy may be for a biopsy in most patients. In indeterminate
needed. cases, DW-MRI and/or chemical shift imag-
• Multiple lesions may require half-body radia- ing may help in this respect [3].
tion (7 GY). • According to a recent study published in
• Pain relief: 2016 in the Journal of Orthopaedic Surgery
–– In 50% patients within 2 days. and Research it was shown that modular tumor
–– The rest within 2 weeks. endoprosthesis may be an option in surgical
• High risk of infections and thromboembolic treatment of long-bone metastases providing
complications: fast pain relief and early mobilization but
–– Due to immobility and metabolic proximal humerus resections result in a
derangements. reduced shoulder mobility and weakening of
–– Consider anticoagulants. muscle strength which impair normal limb
• PMMA and intramedullary nailing associated functions [4].
with intraoperative MI and death.
19 Metastatic Bone Tumors 163
Case-Based Discussions Continuous.

May be the cause of both acute pain after
Case 1 trauma and chronic back pain.
–– Paraspinal muscle spasm:
A 64-year-old lady with PMHx significant for Pain typically comes and goes.
localized breast cancer s/p chemotherapy, radia- Starts out after trauma to the back (e.g.,
tion, hormonal therapy, and mastectomy presents sudden movement).
to the clinic with acute back pain. After ques- Does not radiate.
tioned she describes the pain as 9/10 in severity, Improves with pain medications.
sharp in quality, non-radiating, constant, located
in the lumbar area and started 30 min ago after
she tried to lift up the sofa. Case 2
• Differential diagnosis: A 74-year-old gentleman with Parkinson’s dis-

–– Vertebral fracture. ease comes to the clinic with severe right-elbow
–– Vertebral disc herniation. pain after a fall. X-ray of the right elbow reveals
–– Paraspinal muscle spasm. a distal humeral fracture and an osteolytic lesion.
• Workup: The patient is a former smoker of 50-pack-years.
–– Lumbar spine X-ray—may show a com-
pression fracture. • What are the next steps in the diagnosis?
–– Lumbar spine MRI—may show disc –– The osteolytic humeral lesion is suspicious
herniation. for metastatic bone lesion. Thus, the primary
• Main associations to remember: doctor orders CT scans of the chest, abdo-
–– Vertebral fracture: men, and pelvis to look for the site of the
Typically associated with Hx of osteoporo- suspected primary cancer. Indeed, he identi-
sis or cancer; if PMHx of cancer present fies a lesion consistent with lung cancer on
suspect recurrence and order tests to con- the chest CT scan. The pain does not respond
firm relapse (e.g., mammogram, breast to analgesics and the orthopedic surgeon is
MRI for breast cancer). consulted to take care of the fracture.
Very severe in intensity and does not • What should be the next step from the ortho-
radiate. pedic surgeon?
Typically starts out after minor injury to the –– Although the probability that the fracture is
back (e.g., sudden movement). pathologic secondary to metastatic lung
–– Vertebral disc herniation. cancer is high, biopsy should be performed
Typically associated with sciatica (radiat- first to rule out primary bone cancer since
ing pain down to the buttock and calf uni- incorrect treatment of this lytic bone lesion
laterally or bilaterally). with, e.g., intramedullary nailing could
May be associated with sensory and/or potentially represent a chondrosarcoma
motor abnormalities. that may lead to spread of the tumor to the
May be associated with urine or fecal entire length of the tumor and necessitate a
incontinence if leading to conus medullaris major amputation limiting the overall mor-
syndrome. bidity and mortality of the patient.
Review Questions treatment of pathological fracture caused by

metastatic bone disease in order to avoid long-
A 53-year-old lady is diagnosed with an osteo- term rehabilitation period and achieve imme-
lytic lesion in the right tibia. What is the most diate stability.
likely site of the primary cancer? • True.
• Prostate. • False.
• Lung.
• Kidney. In metastatic bone disease, the main treatment
• Breast. goal is pain relief and surgery is indicated only
when pathological fracture present.
A 53-year-old gentleman is diagnosed with an • True.
osteolytic lesion in his lumbar spine. • False.
What is the most likely site of the primary
cancer?
• Prostate. References
• Lung.
• Kidney. 1. Himelstein AL, Foster JC, Khatcheressian JL,
Roberts JD, Seisler DK, Novotny PJ, Qin R, Go RS,
• Multiple myeloma. Grubbs SS, O’Connor T, Velasco MR Jr, Weckstein
D, O’Mara A, Loprinzi CL, Shapiro CL. Effect of
What is the most common bone affected by longer-interval vs standard dosing of zoledronic acid
metastatic disease? on skeletal events in patients with bone metastases: a
randomized clinical trial. JAMA. 2017;317(1):48–58.
• Radius. https://doi.org/10.1001/jama.2016.19425.
• Tibia. 2. Hosaka S, Katagiri H, Honda Y, Wasa J, Murata H,
• Sternum. Takahashi M. Clinical outcome for patients of solitary
• Spine. bone only metastasis. J Orthop Sci. 2016;21(2):226–
9. https://doi.org/10.1016/j.jos.2015.12.005.
• Skull. 3. Torres C, Hammond I. Computed tomography and
magnetic resonance imaging in the differentiation of
A good friend of yours is diagnosed with met- osteoporotic fractures from neoplastic metastatic frac-
astatic bone disease. Which site would you prefer tures. J Clin Densitom. 2016;19(1):63–9. https://doi.
org/10.1016/j.jocd.2015.08.008.
the primary site to be? 4. Guzik G. Results of the treatment of bone metastases
• Lung. with modular prosthetic replacement—analysis of 67
• Breast. patients. J Orthop Surg Res. 2016;11:20. https://doi.
• Prostate. org/10.1186/s13018-016-0353-6.
• Thyroid.
• Kidney.
Sources for Additional Studying
How many doses of radiation should be used
European Surgical Orthopaedics and Traumatology- The
for pain relief in metastatic bone disease? EFORT Textbook Editors: Bentley, George, DOI
• One. https://doi.org/10.1007/978-3-642-34,746-7, Springer,
• Two. EFORT 2014 Bone Metastases of Long Bones and
• Three. Pelvis Johnny Keller. p. 4282–4293.
h t t p : / / w w w. o r t h o bu l l e t s . c o m / p a t h o l o g y / 8 0 4 5 /
• Four. metastatic-disease-of-extremity
• In a patient with long-term life expectancy h t t p : / / w w w. o r t h o bu l l e t s . c o m / p a t h o l o g y / 2 0 0 9 /
osteosynthesis is the preferred method of metastatic-disease-of-spine
Musculoskeletal Imaging
Techniques 20
Ian Pressney and Asif Saifuddin
With the increasing demand, availability and The Electromagnetic Spectrum

broad range of imaging techniques at the disposal
of the orthopaedic surgeon, it is paramount that • Two different theories: wave versus particle;
they must have at least a basic understanding of just models of what might actually be the
the principles around image acquisition. nature of radiation.
Ultimately, this increase in background knowl- • Increasing energy and decreasing wavelength
edge should augment and improve image inter- (energy = Planck’s constant × velocity/wave-
pretation skills and guide appropriate image length) (Fig. 20.1).
requesting, which carries inherent radiation risks
for patients. Properties of electromagnetic radiation:
• Travel at speed of light ~300,000 km/s.

Introduction • Travel in straight lines.
• Not affected by electric or magnetic fields.
Radiation is the process of energy transfer: • Travel through a vacuum.
• Absorbed or scattered by matter.
• Electromagnetic radiation—energy transfer • Exhibits inverse square law—intensity
by means of varying electric and magnetic decreases as the square of the distance from
fields, e.g. X-rays. the source increases.
• Beam of charged particles—kinetic energy
transfer by means of motion of particles, e.g.
radioactive emission. Ionising Versus Non-ionising
Radiation
Energy transfer by means of vibrated energy
through a material can also be used to create an • Ionisation is the removal of an orbital electron
image, e.g. ultrasound. from an atom.
• Some radiation, e.g. X-rays and gamma rays,
produces ionisation in material through which
it passes and others, e.g. ultrasound and radio
I. Pressney (*) · A. Saifuddin waves, do not.
Department of Radiology, The Royal National • Ionisation can produce chemical change which
Orthopaedic Hospital Trust, Stanmore, UK can lead to biological damage to tissue.
e-mail: ianpressney@nhs.net; Asif.Saifuddin@nhs.net

166 I. Pressney and A. Saifuddin
Increasing wavelength
Increasing energy
10-11 10-10 10-9 10-8 10-7 10-6 10-5 10-4 10-3 10-2 10-1 1 101 102 103
Wavelength (m)
Gamma Ultra-
X rays Infrared Microwaves Radio
rays violet
Frequency (s-1)
1020 1019 1018 1017 1016 1015 1014 1013 1012 1011 1010 109 108 107 106 105 104
Visible
400 500 600 700 750 mm
Fig. 20.1 The electromagnetic spectrum
Radiography [mA]). The kinetic energy of electrons is con-

verted into X-rays (1%) and heat (99%). The
Roentgen discovered radiographs in 1895 and kV and mA can be varied depending on imag-
they are the backbone and workhorse in investi- ing requirements.
gating and the follow-up of musculoskeletal X-ray interactions are determined by the type
pathology. and thickness of tissue:
Basic equipment consists of:
1. Transmitted—unaffected through matter.
• The generator, which produces the high- 2 . Attenuated—energy remaining in beam fol-
voltage current. lows exponential law.
• Glass X-ray tube, which contains the cathode 3. Photoelectric absorption—X-ray hits inner
and anode which produce the radiation. orbit electron and absorbed with ejection of
• The collimator, which guides the radiation to electron resulting in ion pair.
the patient. 4. Compton scattering—X-ray hits outer orbit
• Shielding, which protects staff and patient. electron with ejection from atom but X-ray is
• Filtration, which removes low-energy photons deflected or scattered and not absorbed con-
before reaching the patient to decrease radia- tinuing with lower energy (N.B. radiation haz-
tion dose. ard for surgeons during fluoroscopy).
The generator applies high voltage (applied

kilo-voltage [kV]; approximately 30–150 kV) Effects on Tissue
across the X-ray tube between the cathode (a
heated filament @ 2200 °C) and focal spot on 1. Direct—disrupt molecular bands of DNA and
the anode. The thermionic emission of elec- cell membranes.
trons from the cathode is guided towards the (a) To individual (somatic).
anode with a current (0.5–1000 milliamps (b) To descendants (genetic).
20 Musculoskeletal Imaging Techniques 167
2. Indirect. • Quicker.
(a) Stochastic (probabilistic)—probability of • Decrease X-ray dose (probable).
effect increasing as dose increases and a • Enhanced post-processing.
threshold does NOT exist. • Quantification.
(b) Non-stochastic (deterministic)—differ- • Can be sent via network and archived easily
ence is that a threshold is thought to exist (PACS—picture archiving communication
and is tissue specific, e.g. gonadal cell system).
damage leading to impaired fertility. • Easy retrieval from archiving system.
Conventional Radiography Fluoroscopy
• Now rarely available. • Flat screen versus image intensifier (II).

• Analogue image; continuous distribution; • Phosphor screen units converting incident
grey shade on photographic film. X-rays into corresponding patterns of lights
• X-ray cassette film lies between crystal inten- which are converted into direct digital image
sifying screens (silver iodobromide crystals) (flat screen) or electrons into light and digital
transforming X-ray to light photons which are image (II).
sensitive to electromagnetic radiation (X-rays
and light, hence use of darkroom).
• Developed and fixed. Computed Tomography (CT)
• Invented by Sir Godfrey Hounsfield; first used

Digital Radiography in 1972.
• Advance on tomography or the simultaneous
• Approximation of an analogue image; variation movement of X-ray tube and film in opposite
stored as numbers converted to greyscale with directions.
resolution dependent on image matrix size. • Multiple X-ray generators and detectors rotat-
ing around body as patient is moved through
Computed radiography (CR) scanner.
• New-generation scanners increase slice num-
• Indirect digital; X-rays → light → electrical bers and helical continuous rather than stop-
signal. shoot imaging.
• Film replaced by photostimulable phosphor • Image formation or tissue map of attenuation
luminescence plate inside cassette. profiles are secondary to linear attenuation
• They store energies following X-ray exposure coefficient (μ).
and emit light (scintillation). • μ = probability of attenuation per thickness of
• When put through CR laser with photomulti- material.
plier tube converting this light to digital image. • μ = mass attenuation coefficient x density.
• With CT Hounsfield unit (HU) num-
Direct radiography (DR) ber = (μobject − μH2O)/μH2O × 1000 (Table 20.1).
• These HU numbers are mapped onto a scale of
• Direct digital; X-rays → electrical signal. grey, from black to white, and can be interro-
• Digital X-ray sensors; amorphous selenium. gated based on the window level (WL; centre
• Images sent wirelessly to PACS. of represented range) and window width
(WW; range of field viewed).
Advantages digital versus conventional • Units outside the selected windowing would
radiography appear as undifferentiated white or black;
Table 20.1 Approximate CT Hounsfield units for matter and radiation controversial (www.rcr.ac.uk/
and their corresponding appearance on greyscale
guide-justification-clinical-radiologists).
Hounsfield unit 2. Optimisation—ALARA, As Low As Reason-
(HU) CT greyscale
ably Achievable.
Water 0 (by definition) Grey/isodense
3. Limitation—exposure subject to dose limits
Air −1000 Black/hypodense
or to some control of risk in the case of poten-
Fat −50–200 Grey/isodense
Bone 600–1000 White/hyperdense tial exposures; IR(ME)R; annual whole-body
Soft tissue 30–300 Grey/isodense dose limits for public (1 mSv) and for those
with occupational exposure (20 mSv that does
not include background radiation or personal
therefore decreasing window width reduces medical exposures).
noise.
• Commonly used parameters already pre-
assigned under ‘bone’, ‘soft tissue’ and ‘lung’ Measurement X-ray Radiation
windows on your workstations.
• CT monitor normally represents 256 • Dose, amount of energy absorbed per unit
greyscales (human eye can differentiate mass of matter (Gray).
between 10 and 15!). • Dose area product, absorbed dose multiplied
• CT contrast; ionic contrast can be injected by the area irradiated (Gray per centimetres
intravenously to increase tissue contrast squared).
dependent on enhancement characteristics • Equivalent dose, used to stipulate the radiobi-
with scan time (delay) optimised to take ological effect of dose as the energy absorbed
advantage of these characteristics, e.g. per unit mass (Sievert; Sv).
pulmonary arterial, arterial, portal- • Total effective dose, tissue-weighted sum of
venous, renal cortical and delayed-phase equivalent doses in all specified tissues and
imaging. organs of the body (Sievert; Sv) (Table 20.2).
Advantages:
I n Practice (See PRODUCT
• Rapid acquisition, e.g. trauma and CT-guided in Mnemonic Tricks)
intervention.
• High-resolution bone detail. • Minimisation of radiation use; ALARA; pulsed
• 3D reconstructions. fluoroscopy; patient close to intensifier; mini-
mise exposure time; smallest field size; use
Disadvantages: memory storage facilities; collimation.
• Maximising distance between the operator
• Radiation dose about 40% of total radiation and the X-ray source, beam and scatter.
dose by diagnostic imaging. • Use of lead screens; between operator/staff
and beam.
• Personal protective garments; handle with
Radiation Protection care—protective lining will crack and be inef-
fective with poor handling/storage; completely
1. Justification—produces significant benefit to ‘wrap’ around; thyroid and eye shields; 0.5 mm
exposed individual or society to offset the lead equivalence, i.e. the garment is equivalent
radiation detriment it causes N.B. research to this depth lead absorption properties.
Table 20.2 Dose and probabilities of fatal cancer induction for common orthopaedic investigations for patient
counselling
Approximate adult risk of fatal cancer Equivalent period of
Total effective per examination (prob fatal cancer natural background
Diagnostic procedure dose (mSv) 5 × 10−2Sv*procedure dose (Sv)) radiationa
Chest PA radiograph 0.02 1 in 1000,000b 2.4 days
Cervical spine XR (AP + lat) 0.08 1 in 30,000 1.6 weeks
Lumbar spine XR (AP + lat) 1.3 1 in 15,000 5.6 months
Pelvis XR (AP) 0.7 1 in 30,000 3.2 months
CT cervical spine 2.6 1 in 8000 13 months
CT lumbar spine 6 1 in 3300 2.3 years
CT abdomen/pelvis 10 1 in 2000 3.6 years
Fluoroscopy facet joint injection 1 1 in 22,000 4.3 months
Whole-body bone scan (Tc99m) 4 1 in 5000 1.6 years
Bone SPECT-CT 5 1 in 4000 1.8 years
2.5 mSv per year
a
Similar risk of death as 6000 miles on plane (cosmic rays) or 300 miles driving car (accident)
b
• Monitoring personal exposure dose; never • Allows characterisation of chemical com-

shared; constant position below protective position of material secondary to differen-
wear (body monitor) or collar/finger monitors; tial X-ray attenuation at these energy
optically stimulated luminescence dosimeter levels, i.e. directly related to atomic weight
(OSL) versus thermoluminescent dosimeter number and electron density.
(TLD); Ionising Radiations Regulations (IRR) • Potential MSK clinical applications; assess
1999 state that trust as employer ensures that for crystals in gout, reducing beam harden-
employees do not exceed relevant dose lim- ing from metal artefact, potential for
its—radioactive materials; prevent spills; clean assessing bone marrow oedema [2].
spills, protective clothing including syringe 3. Metal artefact reduction software (MARS).
shields; patient bodily fluids are radioactive. • Widely used; multiple vendor-specific
ways to reduce metal artefact and general
image noise reduction.
Advances in CT • Dual-energy CT (see above); iterative
reconstruction algorithm (correct for noise
1. Textural analysis. and artefact by linear interpolation or alge-
• Image post-processing by various methods braic technique) versus filtered back-
provides quantitative analysis of heteroge- projection (uses information from areas
neity rather than visual analysis. adjacent to metal artefact allowing replace-
• Both CT and MRI applications; utilised ment of metal corrupted raw data) [3, 4].
mainly in research. 4. Weight-bearing CT.
• Potential MSK clinical implications; • Increasingly available; cone beam technol-
tumour grading and predict outcome, ogy versus X-ray emitter and flat panel
tumour response to therapy, normal versus sensor rotate horizontally around feet.
dystrophic muscles [1]. • Patient stands in scanner.
2. Dual-energy CT. • Functional information about joint biome-
• Two X-ray tubes of different energy levels chanics where previously limited to supine
with simultaneous acquisition. CT with standing radiographs [5].
Ultrasound Probes
• Ultrasound transducer converts electrical • Each has specific frequency range.

energy into mechanical energy. • Probe frequency directly proportional to
• Ultrasonic energy = the power of the beam image resolution.
(Watts). • And inversely proportional to depth of
• This power propagates through medium penetration.
dependent upon width of the beam. • Linear array is utilised for many MSK investi-
• Transducer made of materials exhibiting piezo- gations which has higher frequency and
electric effect (from Greek ‘to press’—Piezen). therefore higher resolution of relatively super-
• Substance changes dimensions in response to ficial structures.
electrical charge and conversely an electric • Curved array has a lower frequency with
charge is developed when the substance is divergent beam and large field of view deeper.
distorted, e.g. lead zirconate titanate (PZT).
• As pulse propagates its intensity reduces as
energy is lost to the medium or attenuated. What Is an Ultrasound Image?
• Different mediums have different attenua-
tions, e.g. at low frequencies 0.2 cm of bone, • A 2D image.
1.5 cm of muscle, 5 cm of fat and 1360 cm of • Top of the image is superficial, bottom is deep.
water is required to reduce the intensity of an • A result of harmonic sounds being reflected
ultrasound beam by half. back to the transducer by difference in acous-
• Attenuation of ultrasound secondary to: tic impedance of different layers.
–– Absorption: ultrasound is lost from beam • Best possible image of a structure at 90° to
and converted to heat which increases with structure on linear array.
frequency.
–– Scatter: echoes scattered through uneven
surfaces and on scattered echoes. Doppler Ultrasound
–– Beam divergence: as echoes propagate the
cross-sectional area divergence increases • Phenomenon of changing frequency with
and results in decreased echo intensity. speed is known as the Doppler effect.
–– Refraction: bending of ultrasound beam when • That is, apparent wavelength compression
off axis with changes of speed, direction and when moving towards a stationary detector.
wavelength at interface but not frequency.
–– Reflection.
• Otherwise known as pulse echo. Ultrasound Artefacts
• Important as resultant ultrasound image.
• Propagated ultrasonic pulse reflects from • Anisotropy: artificially abnormal reflection
reflector to receiving transducer whose (dark/hypo-reflective) secondary to non-90°
energy is converted to electrical signal. positioning of probe compared to structure to
• These echoes are generated at tissue be assessed.
interfaces if acoustic impedance (AI) on • Reverberation: at strongly reflective surfaces
either side of the interface is different. where echoes are transmitted back and forth
• AI = density × propagation velocity. between probe and interface, e.g. bone interfaces.
• Therefore, 99% energy reflected at soft • Acoustic enhancement: fluid-containing struc-
tissue/air interface = hyper-reflective or tures allow more ultrasound through to deeper
bright echo (hence requirement for ‘con- structure giving brighter appearance.
ducting’ ultrasound gel); 50% at bone/fat • Acoustic shadowing: strong reflectors do not
interface; <1% at soft tissue/ allow through transmission of ultrasound giv-
water = hypo-reflective or dark echo. ing posterior ‘shadow’, e.g. bone and gas.
Advances in Ultrasound Principles
1. Elastography. 1. Each organ to be studied needs a suitable

• Based on general principle that stress pharmaceutical.
applied to tissue causes changes within it, 2. The uptake of the substance is different in the
dependent on their elastic properties normal versus clinical condition to be
(paper). assessed.
• Allows both qualitative visual and quanti- 3. The pharmaceutical is labelled with suitable
tative measuring of the mechanical proper- emitting radionuclide that does not alter the
ties of tissue. physiological properties of the pharmaceuti-
• Different types, strain (most common), cal, e.g. a radiopharmaceutical.
sheer wave, transient and acoustic radia- 4. After appropriate time delay (as radiation is
tion force. absorbed by the body) external imaging
• In MSK manual compression of tissue by device (e.g. gamma camera) can detect and
transducer causing axial tissue displace- measure the emitted radiation.
ment or strain which is then calculated by
comparing echo sets before and after the Types of radionuclide
compression.
• Potential MSK clinical implications, e.g. 1. Alpha particles; very short path with less

assessing tendon ‘softening’ or loss of energy therefore energy absorbed by patient
strain in focal tears, diseased skeletal mus- and increased radiation dose to patient.
cle and soft-tissue mass lesions [6]. 2. Beta emitters; excess of neutrons produced by
2. Contrast-enhanced ultrasound (CEUS). neutron bombardment or fission; short path
• Intravenous injection of microbubbles fol- length.
lows blood circulatory phases as per ionic 3. Gamma emitters; a by-product of neutron

contrast in CT studies. bombardment or fission; very good for imag-
• Microbubbles highly echogenic secondary ing, e.g. technetium.
to acoustic impedance and oscillate in 4. Positron emitters.
ultrasound field.
• Potential MSK clinical implications, e.g. What is a bone scan?
assessing muscle perfusion, assessing
‘active’ inflammatory conditions and
enhancement characteristics of soft mass • IV injection of specific radiolabelled
lesions [7–9]. pharmaceutical—Tc99mMDP.
• Technetium (Tc99m); pure gamma emitter
(limiting radiation dose), 1/2 life of 6 h, easily
radiolabelled, high energy to pass through
Nuclear Medicine body but low enough to be stopped by detector
of camera.
• It is the medical use of radionuclides: • Methylene diphosphonate (MDP); taken up
–– Diagnosis, e.g. in vivo as per radionuclide by osteoclasts.
imaging. • Emitted gamma rays are detected by gamma
–– Therapies, e.g. radiosynoviorthesis— camera.
image-guided intra-articular delivery of • Gamma camera; contains crystals that react to
radioactive agents, e.g. 90Y (yttrium sili- particles of radiation to produce a light source
cate/citrate colloid) with emittance of beta (scintillation) which is multiplied in a photo-
particles (short length) resulting in phago- multiplier tube and recorded; collimator to
cytosis and apoptosis of synovial mem- attenuate gamma rays not traversing perpen-
brane [10]. dicular to detector.
• Triple-phase imaging: tem, e.g. bone marrow, liver and spleen but
–– Vascular phase (less than 1 min). also areas of active infection.
–– Blood pool (3–5 min): assessing for hyper-
aemia, e.g. infection/inflammation.
–– Delayed phase (3–4 h). Advances in Nuclear Medicine
• Entire skeleton (anterior and posterior views
normally) with the option of targeted small 1. Hybrid PET-MRI: potential increase in bone
field-of-view imaging in different planes as metastasis assessment and response to treat-
clinically required. ment [11, 12].
• 50–60% radionuclide fixes in bone; the rest is
rapid renal excretion.
• Pitfall: uptake affected by quantity of miner- agnetic Resonance Imaging (MRI)
M
alised bone, vitamin and hormone levels. [13, 14]
• Based on nuclear magnetic resonance.

ingle Photon Emission Computed
S • Process of absorption and emission of energy
Tomography (SPECT) by atomic nuclei following applied external
magnetic field.
• Tomographic examination with planar • Applied energy is in the form of radiofre-
imaging. quency pulses.
• Emitted nucleus energy is as a magnetic reso-
nance signal introducing small voltage in
SPECT-CT receiver coil next to patient giving image.
• Based on the principle that active nuclei com-
• Gamma camera with additional CT compo- bine a net charge with net spin inducing a
nent on the same scanner, therefore multipla- magnetic moment about themselves.
nar imaging = increasing resolution, decreased • Therefore, the contrast in MRI signal is
noise and increased localisation. achieved by the differing magnetic moments
of tissues after applying various external mag-
netic fields.
Positron Emission Tomography-CT • The hydrogen nucleus is utilised in this modal-
(PET-CT) ity as it has an odd number of protons (effec-
tively a proton).
• Exploiting increased metabolic rate of • And is abundant in both water and fat within
tumours/inflammatory lesions, i.e. glucose the body, i.e. it possesses charge and ‘spin’
consumption. that acts like a tiny magnet.
• For example deoxyglucose-labelled • By putting this ‘tiny magnet’ in a magnetic
18Flourine (1/2 life 112 min). field it starts to rotate or ‘precess’.
• Utilises positron emission from radioactive • MRI signal is the result of how this rotation is
decay in body which interacts with electrons affected by magnetic and radiofrequency
in the body to produce two photons of gamma fields.
radiation. • In-phase; the magnetic moments of the nuclei
align and ‘spin’ at a specific frequency depen-
White Blood Cell (WBC) Scan dent on the applied magnetic field strength.
• A radiofrequency pulse of the same frequency
• Labelling patient’s own white blood cells with as the ‘precessing’ hydrogen nuclei and 90° to
radioactive tracer such as indium. the external magnetic field induces resonance,
• Accumulates in the reticuloendothelial sys- with resultant nuclei absorbing energy.
• The MRI signal is the voltage (energy) contrast between tissues on both T1 and T2
received from a receiver coil on the same signal weightings.
plane as the ‘precessing’ nuclei or ‘net mag- • Fast spin echo (FSE); multiple echoes per TR
netic vector’. acquired; decrease acquisition time but
• The RF pulse is removed and the ‘net mag- decrease signal-to-noise ratio: gradient echo
netic vector’ begins to decrease until the next (GE); gradient of pulsed echo and negative
RF pulse is applied. dephasing field echo applied.
• The time between the separate RF pulses is • T2*; faster than T2 relaxation due to magnetic
the TR or ‘time to repeat’ and is essentially field inhomogeneities.
responsible for T1 weighting of the signal. • Inversion recovery (IR) sequences; inver-
• A short TR maximises T1 signal and hence is sion of spins by radiofrequency pulse at
quite short, typically <800 ms (Fig. 20.2). 180° so no signal received until their ‘relax-
• The ‘time to echo’ or TE is the time from RF ing spins’ have a 90° RF pulse applied
pulse to signal collection which is generally allowing signal in plane of recovery, e.g.
responsible for T2 weighting. utilised in short tau inversion recovery
• A long TE maximises T2 signal differences (STIR) imaging.
between tissues. • STIR; aim to ‘null’ fat signal; fat has short T1
• T1 or T2 weighting is essentially the measure- relaxing quickly, therefore able to utilise this
ment of relaxation in different orthogonal and obtain no signal from fat protons.
planes with more relaxation equalling less
signal.
• T1 relaxation is back to equilibrium and T2 Diffusion-Weighted Imaging (DWI) [15]
relaxation is due to losing phase coherence.
• Based on Brownian motion.
• Random motion of water molecules moving
ther MRI Sequences (PD, FSE, GE,
O past and colliding with each other.
T2*, IR, STIR) (Table 20.3) • Diffusion is limited by barriers, e.g. neoplastic
infiltration of tissues.
• Proton density (PD) imaging aims to achieve • B value controls the amount of diffusion; with
pure signal secondary to protons therefore, greater value the stronger the diffusion
long TR and short TE which produce the least weighting.
• Apparent diffusion coefficient (ADC) increases
signal in areas of increased diffusion.
Longitudinal magnetization recovery
Mo
t T1
hor
Poor
ith s
Good contrast
contrast 1 Table 20.3 Typical parameters for various MR
gT
ue w
lon sequences, N.B. vendor and machine specific

ith
ew
Tiss
su
Tis Time to
inversion
TR TE Flip angle (1800 RF
Sequence (msecs) (msecs) (degrees) pulse) (msecs)
T1 <800 <30 90
Shorter TR Longer TR T2 >2000 >80 90
Time FSE T2 >1000 <30 90
T2* Variable <30 5–30
Fig. 20.2 Graph to illustrate how varying repetition time PD >1000 <30 90
(TR) can produce greater contrast between tissues with
STIR >2000 >60 90 120
different T1 relaxation curves
Contrast • Intrauterine contraceptive devices.

• Halo spinal vest.
• Paramagnetic contrast agent, e.g. gadolinium
(chelated to reduce toxicity of Gd-DTPA). http://www.mrisafety.com/TheList_search.asp
• Unpaired electron and permanently magnetic.
• Only affects relaxation of surrounding
protons.
• That is, shortens T1 relaxation, therefore Advances in MRI
increasing T1 signal.
• Dose = 0.2 mL/kg; max dose 20 mL. 1. Upright/weight-bearing MRI.
• Severe side effects = nephrogenic systemic (a) Previously only axial load whilst supine.
fibrosis with low eGFR. (b) Generally lower field strength; lower SNR.
• Contraindication = previous anaphylaxis, (c) Now higher field strengths; greater gradi-
nephrogenic systemic fibrosis, severe renal ent homogeneity.
failure, haemolytic anaemia and pregnancy. (d) Potential for flexion/extension studies.
(e) Assess spine under load/physiological
position/for spinal instability [16, 17].
MRI Artefacts 2. MRI-guided bone biopsy:
(a) Valuable for poorly visualised lesions on
1. Chemical shift artefact—dark band at fat/
CT; marrow signal abnormalities; viable
water interface—due to differing binding soft-tissue portions of lesions (better soft-
properties of protons in fat and water. tissue contrast) [18].
2. Susceptibility artefact—changes in local field (b) Radiation free.
strength through paramagnetic effects. (c) Need MRI-compatible instruments; opti-
mised pulse sequences for speed (FSE,
T2FS, GE).
Contraindications 3. Cartilage imaging:
(a) Early cartilage changes include altered

Strict contraindications; implanted electric and water content, glycosaminoglycan (GAG)
electronic devices are a strict contraindication to the depletion and alteration in proteoglycan-
magnetic resonance imaging, and in particular: collagen matrix.
• T2 mapping: T2* sensitive to water and
• Heart pacemakers (especially older types). interaction with collagen matrix [19].
• Insulin pumps. • dGEMRIC (delayed gadolinium-
• Implanted hearing aids. enhanced MRI of cartilage): sensitive
• Neurostimulators. to change in density of GAG content;
• Intracranial metal clips. Gd-DTPA accumulates in areas of low
• Metallic bodies in eyes. GAG as repelled by negatively charged
GAG, therefore these areas have
Relative contraindications: shorter T1 relaxation times [20].
4. Dynamic perfusion MRI:
• Surgical clips less than 6 weeks old. (a) IV gadolinium utilised with region
• Penile prosthesis and heart valves (compati- of interests (ROI) created in ‘vessel’,
bility must be checked). ‘healthy muscle’ and ‘at site of early
tumour enhancement’; enhancement of
MRI compatible: time-intensity curves formulated to assess
vascularisation and perfusion.
• Superficial staples. (b) Potential clinical implications; MSK

• Vascular lines. tumour assessment, response to treat-
ment, viable tumour for biopsy planning, risk should be stated as very low for this study
post-operative recurrence versus scarring (~0.06 mSv or three times dose of CXR). One
[21, 22]. could quote the risk of fatal cancer of 1 in 30,000 or
equivalent to 1.6 weeks of background radiation.
The correct patient and laterality combined
MSK Imaging Indications (Table 20.4) with clinical details should be checked prior to
confirming the radiation-based investigation.
What are the radiographic findings (Fig. 20.3)?
The radiographic findings include medial tib-
Case History iofemoral joint degenerative changes with rela-
tive preservation lateral tibiofemoral and
A patient is referred to general orthopaedic out- patellofemoral joint compartments. No joint effu-
patients with chronic knee pain: sion or focal bone lesion. Mild varus deformity
Clinical history suggests no red flag symp- and subluxation.
toms with medial joint-line tenderness on Could further imaging be helpful and what are
examination with minor varus deformity on
their disadvantages?
weight bearing. If unicompartmental joint replacement is to be
What would be your first imaging investiga- considered, then MRI to confirm articular carti-
tion of choice and how would you counsel the lage state in the other joint compartments and sta-
patient to make an informed decision regarding tus of ligaments could be utilised (see Fig. 20.4).
the investigation? CT—if the deformity is severe enough
Weight-bearing radiographs of the knee. to warrant CAD-CAM prosthesis. Again,
Counselling would involve highlighting the radia- informed consent for radiation procedure is
tion dose of the study and its risks, although this required.
Table 20.4 Musculoskeletal imaging indications: a guide for image requesting and justification for investigations
chondral depth
Pre/post-operative assessment Incl
CT Trauma X-ray complications
Preoperative planning (CAD-CAM joint Inflammatory, infection and
prostheses) degenerative conditions
Post-operative assessment Primary and metastatic bone tumours
Imaging when MRI contraindicated Developmental abnormalities
CT-guided intervention Fractures
Metabolic bone disease
Nuclear Detection and staging metastatic disease Ultrasound Soft-tissue disorders incl sports
medicine injuries
Bone pain in patients with normal Ultrasound-guided intervention
radiographs
Investigation of abnormal X-rays Soft-tissue mass interrogation
Prosthetic joints for signs of infection or Inflammatory disorders
loosening
MRI Soft-tissue disorders incl sports injuries
Primary and metastatic bone tumours
Soft-tissue mass interrogation
Bone pain in patients with normal
radiographs
Spinal instability incl cauda equina
Inflammatory, infection and degenerative
conditions
Fig. 20.3 Standing radiographs (AP and lateral) of the knee
The patient has an uncomplicated medial uni-

compartmental knee joint replacement.
What imaging studies could be utilised in the
post-operative period, including investigation of
acute, subacute or late complications?
Ultrasound (see Fig. 20.5)—good for soft-
tissue complications including joint effusion,
haemarthrosis and extensor mechanism rupture,
or for assessing deep venous system with Doppler
for embolism in acute, subacute and late stages.
Ultrasound is also good for guidance to targeted
injection therapies for soft-tissue abnormalities,
e.g. pes anserinus bursitis.
Radiographs: workhorse for routine post-
operative prosthetic check including for align-
ment and prosthetic or periprosthetic fracture.
Mainstay of routine follow-up assessment and
also for first-line investigation of late com- Fig. 20.4 Coronal PD (TR = 3640 ms, TE 50 ms) MRI
demonstrating medial tibiofemoral full-thickness chon-
plications, including loosening, fracture or dral loss with marginal osteophytosis and joint space nar-
bony abnormality inferring soft-tissue injury rowing. Relative preservation of the lateral tibiofemoral
(Fig. 20.6). joint compartment chondral depth
Fig. 20.5 Longitudinal ultrasound of the normal patel- (crosses) surrounding distal tendon fibres of sartorius,
lar tendon (fibrillary pattern) and at the anteromedial gracilis and semitendinosus consistent with pes anseri-
aspect of the knee demonstrating anechoic fluid nus bursitis
Fig. 20.6 Post-operative knee radiographs with no metalware complication
MRI: limited use in acute setting with metal late assessment of prosthetic alignment or for
artefact (see Fig. 20.7a). Late assessment of sur- prosthesis loosening. Late use in CAD-CAM
rounding soft-tissue structures. revision surgery planning.
CT (see Fig. 20.8)—limited use but may be Nuclear medicine: bone scan (see Fig. 20.8a)
utilised for equivocal acute periprosthetic frac- late (at least over 1 year) assessment of painful
ture on radiographs, much greater utilisation in replacement. Blood pool to assess for inflamma-
a
Review Questions
(Single Best Answer)
1. Electromagnetic radiation (EMR).

(a) All EMR produces ionisation in material
through which it passes.
(b) Includes radiowaves.
(c) Can behave both as a wave and as an ion.
(d) Includes alpha emission.
(e) Has energy proportional to its
wavelength.
2. Concerning the effects of ultrasound:
(a) Heat is produced when ultrasound inter-
acts with tissue.
b (b) Ultrasound causes ionisation.
(c) Compton scattering occurs with ultra-
sound echoes.
(d) Does not exhibit inverse square law.
(e) Higher probe frequencies are associated
with longer wavelengths.
3. Regarding gadolinium used as a contrast agent
in MRI:
(a) There are no contraindications to its use.
(b) Chelation to DTPA renders it non-toxic.
(c) Prolongs T1 relaxation.
(d) Has paired outer shell electrons.
(e) Dose = 2 mL/kg.
4. Regarding radiation hazards:
(a) Risk of radiation-induced cancer for an
effective does not vary with age at
exposure.
(b) Radiation-weighting factors are the same
for X-rays, gamma rays, protons and
Fig. 20.7 (a) Coronal PD (TR 3640 ms; TE 50 ms) dem-
onstrating metallic susceptibility artefact and develop- alpha particles.
ment of severe lateral compartment osteoarthritis (c) Deterministic effects such as erythema
(full-thickness chondral loss, marginal osteophytes and cannot occur as a result of radiological
subchondral cysts) with associated joint effusion and
procedures involving fluoroscopy.
synovitis. (b) Coronal CT reconstruction demonstrating
metal susceptibility artefact from the prosthesis. There is (d) Effective dose from a typical CXR is

minor periprosthetic lucency at bone-prosthesis interface about a tenth of the average annual effec-
that may indicate early loosening. (Please note these tive dose to the UK population.
images are not of the same patient)
(e) Effective dose of 10 mSv (CT abdomen/
pelvis) is associated with 1 in 2000 risk of
tion/infection with delayed imaging possibly radiation-induced fatal cancer.
helping to assess for aseptic loosening. 5. Regarding controlled areas:
Fluoroscopy: utilised in theatre by surgeons (a) The controlled area must only be entered
under general anaesthetic for assessment of joint by classified workers.
and also utilised for synovial biopsy in potential (b) A controlled area must be clearly demar-
late infection cases by radiologists (see Fig. 20.8b). cated.
Fig. 20.8 (a) Blood pool (perfusion) and delayed-phase screen-saved image demonstrating percutaneous fluoro-
imaging on bone scan demonstrating no significant uptake scopic guided coaxial needle technique to sample the bio-
on blood pool with linear uptake underlying the tibial film/synovium
prosthesis that may indicate early loosening. (b) Single
(c) Controlled areas may require written local (e) The main effect of detecting scattered
rules. gamma rays is to reduce image contrast.
(d) A nuclear medicine patient waiting area is 7. In the Ionising Radiations Regulations (IRR)
usually a controlled area. 1999:
(e) Personal dose monitoring is usually not (a) The annual dose limit for members of the
required. public is 6 mSv.
6. Regarding gamma camera imaging: (b) The installer must ensure that the equip-
(a) Attenuation in the body typically only ment is both installed and maintained so
stops 1% of gamma rays emitted from as to be capable of restricting exposure to
reaching the gamma camera. a patient.
(b) Following a bone scan with Tc99m,
(c) The annual dose limit for trainees aged
patients are expected to stay overnight in 16–18 is 1 mSV.
hospital so as to reduce their radiation risk (d) The employer is required to undertake a
on the public. quality assurance program for X-Ray
(c) The collimator aids detecting scatter. equipment.
(d) Following a bone scan the patient’s urine (e) The annual dose limit for a registered
is ‘radioactive’ for only 2 h. worker is 10 mSv.
8. The following causes of medical overexpo- sure alters the risk of radiation-induced fatal
sure need to be investigated as stipulated cancer with children and adolescents at greater
under Ionising Radiations (Medical Exposure) risk.
Regulations (IRMER) 2000: 5. b) A controlled area must be clearly demar-
(a) Patient identification error. cated. It must be under the control of the
(b) Wrong imaged anatomy. employer; must have a radiation protection
(c) Incorrect treatment dose given. supervisor attached; must have environmental
(d) Repeat of treatment planning X-ray pro- and personal monitoring taking place; should
cedures due to equipment failure. have local rules written up; and must be physi-
(e) All of the above. cally demarcated, with appropriate signage, red
warning light at entrance and restrictive con-
trols on access by non-radiation workers. A
controlled area (fluoroscopy room) is an area
Answers where a person is likely to receive more than
6 mSv effective annual dose (or an equivalent
1. b) Includes radiowaves. EMR can behave as a dose greater than three-tenths of any relevant
wave and as a particle with both ionising and dose limits) compared with 1 mSv (or an equiv-
non-ionising radiation included. Its energy is alent dose greater than one-tenth of any rele-
inversely proportional to its wavelength. vant dose limits) for supervised area (waiting
2. a) Heat is produced when ultrasound interacts room for nuclear medicine patients awaiting
with tissue. It does not cause ionisation and imaging study after radiopharmaceutical
obeys inverse square law with refraction and injection).
scatter affecting ultrasound but Compton scat- 6. e) The main effect of detecting scattered
ter refers to X-rays scattering after deflected gamma rays is to reduce image contrast. The
from atom after hitting outer orbit electron. collimator helps restrict scatter which
This scatter is the potential ionising radiation increases signal-to-noise ratio. Approximately
dose to operator during fluoroscopy. 10% of gamma rays emitted are attenuated by
Frequency and wavelength are inversely the body. Tc99m has a half-life of 6 h and an
proportional. overnight stay is therefore not required whilst
3. b) Chelation to DTPA renders it non-toxic. the urine will contain very small amounts of
Previous anaphylaxis, pregnancy, haemolytic radiation for several days.
anaemia, nephrogenic systemic sclerosis and 7. d) The employer is required to undertake a
severe end-stage renal failure are contraindi- quality assurance program for X-ray equip-
cations to its use. Dose = 0.2 mL/kg. It has ment. IRR 99 encompasses the appointment
unpaired electron and is therefore paramag- of radiation protection supervisors and advi-
netic. It shortens T1 relaxation providing sors, the control and restriction of exposure to
greater tissue contrast. ionising radiation (including dose limits), and
4. e) Effective dose of 10 mSv (CT abdomen/ requirement of local rules. The annual dose
pelvis) is associated with 1 in 2000 risk of limit for members of the public is 1 mSv,
radiation-induced fatal cancer. Annual whole- 20 mSv for adult workers and 6 mSv for train-
body dose limit for public is 1 mSv; therefore ees aged 16–18 years.
a tenth of this is 0.1 mSv (or 5 CXRs or AP 8. e) All of the above. IRMER stipulates that
pelvis radiograph). Radiation weighting ‘much greater than intended’ radiation doses
(which takes into account the relative biologi- to patients from human error require investi-
cal effectiveness of the radiation) is 1 for gation. This investigation paperwork must be
X-rays (and gamma rays/positrons) but 2 for kept for a minimum of 2 years with detailed
protons (alpha particles = 20). Age at expo- reports for 50 years.
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Ethics
21
Michael K. D. Benson
Introduction In essence Ethics is the science of human duty.

In medical terms moral principles should guide our
Even before medical school prospective doctors decision-making in the whole of our practice. These
should ask why a career in medicine might be ideals ensure that we remain properly professional
right for them: there are many things to consider. in our relationships with patients, colleagues, train-
It cannot just be a desire to make people better. It ees and the industries which service us.
must be recognised that learning is more than the One hundred years ago the relationship
need to pass exams to get to medical school and between doctor and patient was paternalistic: the
qualify: it is a lifelong commitment which will be doctor often told the patient what was to happen
regularly assessed by your peers. Appointments without discussion of alternatives or risk. The
Committees are very aware that successful appli- rights of the patient to be actively involved in
cants should have a clear moral understanding of treatment planning steadily evolved. The
what a medical career demands. The core belief Nuremberg Code of 1947, following the war tri-
is that our patients’ well-being must be the first als in which non-consensual Nazi research was
priority. Communication lies at the heart of good condemned, laid down the rights of patients to
practice and, while partly inborn, may need to be understand what was on offer, the right to choose
nurtured. We must be able to liaise with patients treatment and the right not to be harmed.
and colleagues with patience and understanding In 2005, a JBJS editorial noted: “Medicine,
and respect their need for confidentiality. Honesty law and religion are the three traditional learned
and transparency should underpin all that we do: professions. With professionalism should come
financial reward and the desire of a job for life both privilege and responsibility. As surgeons we
should be low on the list of priorities. study to achieve specialised knowledge and sup-
plement this with training and experience. Our
patients and our Governments grant us certain
privileges but expect us to be guided by ethical
This chapter is based upon the Ethics Guidelines pro- principles. We set the standards for entry, assess-
duced by the EFORT Ethics Committee (Benson MK,
Boehler N, Szendroi M, Zagra L, Puget J) in 2013. The ment, training and certification into our specialty
authis very grateful to his colleagues on the Committee and seek to ensure these standards are maintained
for their support in producing the guidelines. throughout a professional lifetime. Our patients
allow us the right, after careful explanation, to
M. K. D. Benson (*) perform operations upon them which cannot be
St Luke’s Hospital, Oxford, UK free of potential complications” [1].
e-mail: michael.benson@doctors.org.uk

184 M. K. D. Benson
Twenty-five years ago it was the exception for The sick, exhausted or depressed surgeon cannot
medical textbooks to consider ethical practice in perform well. We need to maintain our own physi-
any detail. There has been an explosion of inter- cal and mental health to practise efficiently and
est since then and no medical school curriculum strive to balance work, family and recreational
would be complete without its careful consider- pursuits appropriately [4]. We are all at risk of
ation. In its own right ethics is now a major uni- burnout, a loss of enthusiasm for work, a lack of
versity study worldwide. The excellent AAOS self-confidence and/or increasing cynicism. Each
“Code of Ethics and Professionalism for or all of these may lead to us becoming callous to
Orthopaedic Surgeons” [2] (revised in 2011) those about us. If in doubt we must seek expert
highlights the concerns we should all have for advice. We should also be aware of our colleagues
patient welfare and honourable behaviour by and support them if concerns arise.
treating orthopaedic surgeons. Nonetheless, if we have doubts about the com-
petence of a colleague or the facilities available
we should be prepared, if simple discussion fails
Innovation to resolve the problem, to pursue the matter until
the issue is settled and patients can once again be
The ethical principles we follow are not immuta- treated fairly and with skill. A recent UK report
ble: new dilemmas arise as new treatment possi- highlighted the problems which may arise when
bilities are announced. Should we leap to hospital managers strive to achieve cost savings
introduce them into our practice? Should we gain at the expense of patient care and noted: “The
financially by doing so? We should learn from the medical profession’s technical and scientific bril-
many failures of fresh, exciting but eventually liance has not been matched by its leadership or
failing innovation that sound evidence is required compassion” [5]. If we remain silent we are
that new technology is better than its predecessor potentially complicit in allowing our patients to
before we recommend it for our patients. They suffer.
increasingly have searched the media for the best
management options and are often beguiled by
premature and inaccurate advertising claims. Competence
Ethics demands that we must work within the

Understanding Patients limits of our competence. We must recognise our
and Ourselves own boundaries and seek more expert opinion
when we are in doubt. This is a sign of strength,
All doctors must recognise that patients may not of weakness, and patients appreciate our hon-
have very different preconceptions and under- esty when we recommend another opinion. This
standing of what treatment is available. We learn recognition of our own limitations may clash
to not only identify their disease problems but with ambition. There is nothing wrong with this
also understand how their psychological and in itself and indeed it is essential if we are to
social background may affect decision-making make progress in the science of medicine and in
[3]. The ethical doctor considers this with care. our own careers. It should, however, be with the
We neglect our ethical responsibilities if, when support of others and not at their expense. It
offering advice, we fail to see the complexity of ought to be tempered by altruism. We must
our patients’ needs. acknowledge the contribution of others—work-
If we are to serve our patients well we must ing in teams is almost always better than doing so
work out a proper work/life balance for ourselves. in isolation.
21 Ethics 185
The Real World ourselves from the problem. Honesty is key. A

simple explanation of the problem without mini-
Against the background of our desire to treat mising it should lay the foundation for close per-
patients to the best of our ability lie the financial sonal supervision of the proposed management
restrictions on service which our governments of the problem. This should happen promptly as
often have to impose. It is inevitable that this will anxiety and anger grow exponentially after the
lead to conflicts of interest. Nowhere is this more event. Proper explanation and an apology if indi-
difficult than in the beginning and end of life cated will always be appreciated. Even the hardi-
sagas that beset us. While these are outside the est of us is distressed when a patient is harmed
scope of this chapter the moral dilemmas which and it is our fault and the patient should be aware
we face each day may affect our ability to deliver of our concern. We must of course learn from any
timely and best care to our orthopaedic patients. mistakes and enter fully into a root-cause analy-
sis of the problem and any litigation which might
follow.
Maintaining Skills
It is of course essential that we keep up to date by ur Responsibility for Teaching,

O
attending relevant meetings, liaising with col- Training and Research
leagues and reading current research and review
literature. It is best practice to keep careful Teachers and trainers in orthopaedics must ensure
records of our involvement in continuing educa- that future surgeons develop the requisite knowl-
tion and to audit our practice to help in the regu- edge and ethical standards needed to look after
latory competence assessments now demanded patients with skill and compassion. Our students,
of us. Wherever possible medical reports should trainees, colleagues and patients learn in part by
be recorded contemporaneously. We should take the examples we set. Our manners and behaviour
part in relevant local and national databases [6, should inform and guide them in their futures.
7]. We should be certain that drugs and treatment Our aim should be to encourage continuing edu-
are prescribed only when the patient’s health has cation: we do not simply instruct and train but
been properly assessed and then offer effective should stimulate interest and enquiry while
treatment based on the best available evidence. remembering that our patients’ interests always
When a cure is not possible we must do all we come first. These principles apply just as much in
can to alleviate pain and distress. In all our deal- research projects as in clinical practice.
ings with patients we should be as impartial as We should remember that, even if criticism is
possible: we should not for example be influ- justified, it is not acceptable to humiliate any col-
enced by status or religious or ethnic league or trainee in front of a patient, nurse or
considerations. colleague. This belittles both surgeon and recipi-
ent. If censure is necessary it should be confiden-
tial with a thoughtful explanation of how the
Complications matter may be resolved.
Experienced doctors must support junior col-
Inevitably complications will follow some of our leagues practically as well as theoretically: it is
care and it is vitally important that we recognise unacceptable to leave them unsupervised or
our responsibilities for them. Patients are upset unsupported in managing cases with which they
and angry when things go wrong. Our worst have no familiarity. It is equally inappropriate for
response is to blame someone else and distance junior doctors to undertake such cases without
186 M. K. D. Benson
seeking support. Our patients should understand treatment advice on economic reasons, particu-
that surgeons work best in teams. While we larly if these are for personal or institutional gain.
should all understand this, team unity does not Furthermore, gifts should not be solicited as they
equate to delegation of responsibility in such a might tempt the unethical surgeon to expedite
way that no one accepts leadership. treatment, assure the patient of his/her personal
involvement or improve accommodation in hos-
pital. In addition, given today’s limited resources
Informed Consent and irrespective of whether treatment is public or
private, we should not advise expensive treat-
Informed consent is mandatory in everyday clini- ments or devices of no proven benefit. It may be
cal practice. While it has medico-legal implica- difficult to separate personal interest from our
tions, more importantly it demands our ethical treatment options: some doctors have industry
concern [8]. It is insufficient to delegate the task and research links which might tempt them to
to a junior colleague with no experience of a pro- skew any advice given. It is a temptation we
cedure. It must be carefully and fully explained in should all resist [11].
understandable terms to the patient or responsi-
ble person. The risks, alternatives, advantages
and disadvantages should be discussed and time Research
given for questions to be asked. Critically, the
consent form should be witnessed by a surgeon Research should increase and develop our under-
fully conversant with the procedure [9]. Lemaire standing of disease and its management with the
et al. [8] remind us that our patients may fail to aim of improving patient outcomes. It must be
understand the issues and forget much of the guided by principle. All research including retro-
information provided. What they do remember is spective should be considered by the Institution’s
how the information was given: this should Ethical Committee. We should encourage ethical
remind us of the importance of establishing rap- committees to review progress in these studies to
port. As Brenner et al. [10] point out, an under- ensure that they remain focused, safe and rele-
standing alliance between patient and doctor vant as the parameters may change subtly as time
generates improved healthcare outcomes and passes. Where possible, laboratory experiments
minimises the risk of later litigation. Potential are preferable to animal or human ones. The ethi-
conflicts of interest, such as research, industry cal, institutional and government guidelines
grants, financial or other rewards for the doctor or which guide behaviour vary in Europe but some
institution, should be discussed openly and core ideals are common to all. Patients must be
honestly. fully informed about the objectives, risks and
potential benefits of the study and given time to
reflect before agreeing [12]. A senior investigator
Financial Rewards should outline the study to the patient and be sure
that it is properly understood.
Doctors’ fees, when payable for private practice, To counteract the many potential ethical pit-
should reflect the time and complexity of the pro- falls in research, honesty and integrity are essen-
cedure. Patients should know that they will not be tial. The sponsorship necessary for research may
abandoned if they run out of money as a result of come from our own institutions, charities, gov-
unforeseen circumstances. The patient in both ernments or industry. If individual or institutional
privately and publicly funded systems should benefit flows from the research project the patient
base treatment decisions on need and not on should be made fully aware of it [11]. Poor results
finance. It would be deeply unethical to base any should not be excluded on any pretence. Plagiary
21 Ethics 187
should be avoided with proper acknowledgement who offer peer review for medical journals must
paid to sources. No individuals’ names should be be aware of possible fraud and be prepared to
added to a research paper unless they have con- question scientific papers if there is doubt [13].
tributed significantly. Equally, all those who con-
tribute significantly should be included. Study
participants should be advised of its progress and Conflicts of Interest
outcomes.
When a surgeon has collaborated in develop- As the options for spreading information increase
ing a new instrument or technique it is reasonable we should be aware that conflicts of interest
for him/her to be financially rewarded. It is less should always be declared in every medium. It is
honourable for a surgeon to be paid simply for perhaps inevitable that conflicts arise when the
using a prosthesis and allowing his/her name to ambition of the individual vies with ethical obli-
be used for publicity purposes. No surgeon gation. The pharmaceutical and manufacturing
should be persuaded to use an appliance against industries have been made very aware of the pit-
his/her better judgment. Once again patients must falls which may accompany inappropriate links
be fully informed of any payment from a third with surgeons and, for example, the Eucomed
party which may influence their management. If Code of Ethical Business Practice [14] now very
later follow-up shows that early good results can- clearly defines how the necessary close links
not be replicated these findings should be reported should be forged.
in the scientific literature and the manufacturer Our relationships with industry should be
should take prompt reparative action. open, honest and transparent. Each depends
The concept of intellectual property is straight- heavily on the other and close liaison is essential.
forward: most research institutions are well Orthopaedic surgeons should preserve their inde-
aware of the rules which govern it and the patents pendence and no agreement with industry should
which may be needed. We must take care not to be reached if it interferes with the surgeon’s sur-
claim another’s ideas as our own. There have gical and prescribing practices.
sadly been many examples of ethical misconduct It is appropriate for industry to sponsor pro-
in scientific research and we all share responsi- motional product meetings, training and educa-
bility to report them. The US Public Health tion and to cover the reasonable costs of those
Service (PHS) and the National Science attending. It should be made clear that these are
Foundation (NSF) include, under the umbrella of promotional meetings. Orthopaedic instructors at
“scientific misconduct”, plagiarism, deception, such meetings may be paid a fee in addition. Any
falsification and/or fabrication of data together recompense should be declared. No uninvolved
with “other practices that seriously deviate from accompanying person should be eligible for any
those that are commonly accepted within the sci- expenses.
entific community for proposing, conducting or Industrial support for orthopaedic surgeons to
reporting research”. Reputations and livelihoods attend local, national and international confer-
are lost when results are fabricated or deliber- ences is fine provided that it complies with hospi-
ately misinterpreted. We should, however, distin- tal, local and national guidelines. The support
guish between honest error and deliberate fraud may include financial, scientific, technical and
and recognise that there may be differences in the organisational assistance. It is essential that sup-
analysis and interpretation of data [4]. port is reasonable: it should cover standard rather
Although we know that research must be hon- than luxury fares and accommodation. Such sup-
est, unbiased and rigorous, fraudulent publication port should be open and declared and its accep-
remains a risk as surgeons are tempted to present tance may differ between countries. Financial
their own results favourably. Editors and those recompense for meeting attendance is more criti-
188 M. K. D. Benson
cal in countries where surgeons are less well address. We must maintain our patients’ confi-
rewarded for their activities. It is important to dentiality, follow ethical guidelines and report
remember that junior trainees are often in greater unprofessional and/or dishonest advertising [17].
need of support than their seniors. It should not be forgotten that publicity may
Consultant advisors to industry should be either benefit or harm career prospects as social
selected on the basis of their expertise and not sites allow both positive and negative commen-
just by the volume or value of their practice. Any tary [18]. Information should be kept up to date.
collaboration should be open and transparent. Once again honesty, integrity and a clear aspira-
Remuneration should reflect the surgeon’s contri- tion to improve our patients’ health should be the
bution and not the value of the product. driving forces behind any information we
Our collective and individual consciences publish.
need to be nurtured. We should be very aware
when our actions are not solely in the best inter-
ests of our patients. Our dealings must always be Conclusion
seen to be “reasonable”. If we maintain our own
ethical principles we will pass on to the next gen- The summary which follows is taken from the
eration of surgeons ideals every bit as important article on Orthopaedic Ethics co-written with
as their surgical skills. members of the EFORT Ethics Committee [19].
“As orthopaedic surgeons we should continue to
treat our patients with honesty, compassion, skill
Advertising and care. Our aims should always be to ‘cure and
to care’ [20]. If we rely solely on technique and
While many surgeons are disconcerted by adver- neglect our ethics of service we become a trade
tisements which promote the skills of a particular and not a profession [21]. The therapeutic alliance
surgeon, institute or technique, there are surpris- between doctor and patient should be based on
ingly few official restrictions in place. Gillon understanding, confidence and co-operation and
[15], in his 1989 editorial, drew attention to the form the platform for successful treatment [22].
long-standing disapproval of self-promotion, but We have a long tradition of earning the respect
recognised that patients have the right to choose of our patients and colleagues and must ensure that
both their surgeon and their treatment and unless we continue to deserve the trust they place in us”.
they have access to accurate information they are
unable to make an informed decision.
National associations recognise that advertis- References
ing is now inevitable but stress that we should not
deceive the public. Surgeons may use any form of 1. Benson MK, Bourne R, Hanley E Jr, Harrison J,
Jodoin A, Nicol R, van Wyk L, Weinstein S. Ethics
public communication, including newspapers, in orthopaedic surgery. J Bone Joint Surg Br.
magazines, telephone directories, radio, televi- 2005;87(11):1449–51.
sion, direct mail or social media. However, the 2. American Academy of Orthopedic Surgeons & the
communication must not contain misleading American Association of Orthopedic Surgeons:
Code of Ethics and Professionalism for Orthopedic
statements or make false claims particularly Surgeons (Adopted October 1988. Revised: 1991,
about the author’s institution or precedence over 1995, 2001, 2002, 2004, 2005, 2009, 2011).
his/her peers. It is now recognised that surgeons 3. Gadamer HG. In: Grieco S, Lingiardi V, editors. Dove
and institutions need to publicise their skills and si nasconde la salute. Milano: Cortina; 1994.
4. Ariyan S. Of mice and men. Honesty and integrity in
expertise in the public interest [16]. Nonetheless medicine. Ann Surg. 1994;220(6):745–50.
the freedom to advertise presents both opportu- 5. Halligan A. The Francis report: what you permit, you
nity and risk and there are challenges we should promote. J R Soc Med. 2013;106(4):116–7.
21 Ethics 189
6. Capelli O, Riccomi S, Scarpa M, Magrini N, Rovatti 14. Eucomed Code of Ethical Business Practice at http://
E, Cacciapuoti I, Brambilla A. Clinical audit in pri- www.eucomed.org/key-themes/ethics, 2008.
mary care: from evidence to practice. In: Capelli O, 15. Gillon R. Advertising and medical ethics. J Med

editor. Primary care at a glance—hot topics and new Ethics. 1989;15(2):59–60.
insights. London: IntechOpen Limited; 2012, ISBN: 16. Gholami-Kordkheili F, Wild V, Strech D. The impact
978-953-51-0539-8. of social media on medical professionalism: a system-
7. National Institute for Clinical Excellence. Principles for atic qualitative review of challenges and opportuni-
Best Practice in Clinical Audit. Radcliffe Medical Press, ties. J Med Internet Res. 2013;15(8):e184.
Abingdon, UK. Qual Saf Health Care 2002; 11:392. 17. Ferguson AH. The evolution of confidentiality in

8. Lemaire R. Informed consent—a contemporary the United Kingdom and the West. Virtual Mentor.
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9. Singh S, Mayahi R. Consent in orthopaedic surgery. 18. Timimi FK. Medicine, morality and health care social
Ann R Coll Surg Engl. 2004;86(5):339–41. media. BMC Med. 2012;10:83.
10. Brenner LH, Brenner AT, Horowitz D. Beyond
19. Benson MK, Boehler N, Szendroi M, Zagra L, Puget
informed consent: educating the patient. Clin Orthop J. Ethical orthopaedics for EFORT. Eur Orthop
Relat Res. 2009;467(2):348–51. Traumatol. 2014;5(1):1–8.
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of industrial funding of orthopaedic research. J Bone etiche dell’impresa scientifico-tecnologica. Milano:
Joint Surg Br. 2005;87(11):1452–3. Rusconi Ed; 1992.
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sent for total hip arthroplasty: does a written infor- profession. J Med Ethics. 1985;11(2):72–8.
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Orthopaedic Study Guide Series

More information about this series at http://www.springer.com/series/13489

ISSN 2520-1115 ISSN 2520-1123 (electronic)

Library of Congress Control Number: 2018966999

© Springer Nature Switzerland AG 2019

Knowledge expands exponentially and it has been increasingly difficult for

Philadelphia, PA, USA John D. Kelly IV

Part I Musculoskeletal System Anatomy

Part II Musculoskeletal System Physiology

6 Bone Tissue Physiology�������������������������������������������������������������������� 53

Part III Musculoskeletal System Pathology

10 Metabolic Bone Diseases������������������������������������������������������������������ 73

11 Orthopaedic-Related Issues with Genetic Disorders�������������������� 83

Todd J. Albert Hospital for Special Surgery, New York, NY, USA

John D. Kelly IV Department of Orthopedic Surgery, University of

Case Examples ion with complete resolution of his pain by

© Springer Nature Switzerland AG 2019 3

Main Topics • Chondrification and ossification occur

Lumbar Spine Sacroiliac Spine

Anatomy fibrocartilaginous pubic symphysis and resists

G. Pereira (*) · J. D. Kelly IV

© Springer Nature Switzerland AG 2019 9

Portals • Requires disruption of the abductor

 nterolateral Approach (Watson

• Pelvic ring is composed of the sacrum and the • Tile classification

 ecent Developments in Pelvis/Hip

hip arthroscopy using pre- and postopera- (C) Infection

(A) Femoral head To emulate native anatomy how should the

A 68-year-old man with crippling osteoarthritis Review Questions

(C) The anterior complex ligamentous structures (E) Posterior approach

What approach requires release of the short (A) Femoral nerve

Osseous [1–5] –– Acromion

© Springer Nature Switzerland AG 2019 17

• Creates cavity compression and 50% of the

Muscles • Shoulder internal rotators are stronger than the

Muscles of the shoulder

Neurovascular Supplies motor to subscapularis and teres

–– Anterior –– Space for olecranon process in full

Ligamentous Stability • Provides stability to valgus stress:

Muscles Inserts on posterolateral olecranon and

• Radial (posterior cord of brachial plexus) (b) Posterior approach

Due to continued pain and inability to play at

 ubscapularis Tear, Subluxation Long

A 37-year-old male presents to your clinic with a

Radial Head Fracture

38-Year-old left-hand-dominant female pre-

3 months postoperatively the patient had no

Safe Zone What is the main blood supply to the humeral

What structure is responsible for superoante-

(a) Superior glenohumeral ligament.

What artery runs with the coracoacromial

(a) Anterior humeral circumflex artery.

Compression at the suprascapular notch would

(a) Basi and meso What repair/fixation of what structure is key

11. Lieberman JR. AAOS comprehensive orthopaedic

Anatomy and Biomechanics In the knee joint, two cruciate ligaments, i.e.,

Most commonly used anterior portals:

N. K. Paschos (*) • Anterolateral.

© Springer Nature Switzerland AG 2019 31

Philadelphia, PA, USA John D. Kelly IV

Part I Musculoskeletal System Anatomy

Part II Musculoskeletal System Physiology

6 Bone Tissue Physiology�� 53

Part III Musculoskeletal System Pathology

10 Metabolic Bone Diseases�� 73

11 Orthopaedic-Related Issues with Genetic Disorders�� 83

Case Examples ion with complete resolution of his pain by

Main Topics • Chondrification and ossification occur

Lumbar Spine Sacroiliac Spine

Anatomy fibrocartilaginous pubic symphysis and resists

Portals • Requires disruption of the abductor

nterolateral Approach (Watson

ecent Developments in Pelvis/Hip

A 68-year-old man with crippling osteoarthritis Review Questions

Osseous [1–5] –– Acromion

Muscles • Shoulder internal rotators are stronger than the

Neurovascular Supplies motor to subscapularis and teres

Ligamentous Stability • Provides stability to valgus stress:

Muscles Inserts on posterolateral olecranon and

ubscapularis Tear, Subluxation Long

Radial Head Fracture

Safe Zone What is the main blood supply to the humeral

Anatomy and Biomechanics In the knee joint, two cruciate ligaments, i.e.,

Complications of knee arthroscopy are rare. Posteromedial Approach

Case Discussion • Thicker than the lateral plateau but thinner

Bony and Joint Anatomy body. The posterolateral process is larger than

2 . Surgical resection of coalition. Questions

Function Bone Composition

Osteocytes Nutrition and Metabolism

Parathyroid Hormone Aging/Degeneration

Aging in Bone Cells –– Impaired regulation of gene expression.

Introduction presence of a large extracellular matrix in which

Introduction components. The water contributes to cellular

Lubricin or superficial zone protein (SZP) is Chondrocytes

Causes of Osteoporosis in Childhood Rickets

• Angular deformities (bowleg, genu varum, Vitamin D-Resistant Rickets

Medical Treatment Radiographic findings: Similar to renal

Orthopedic Treatment Overview

Vitamin Disorders • Rare inheritable disorder, caused by defi-

Clinical Presentation Idiopathic Hyperphosphatasia

Differential diagnosis: Osteomyelitis, leuke- Growth Hormone (GH) Deficiency

Radiographic findings: Skeletal maturation Radiographic Findings

ecent and Future Developments

Case 2 weight so we can classify the SCFE as unstable

Review Questions 3. In RENAL OSTEODYSTROPHY the

Overview • According to the level of limb affection, we

Zooming In Mnemonics: ARMS DO

brosarcomas. Malignancy in patients with NF Metaphyseal Chondrodysplasia (MC)

Osteomyelitis • Secondary to a contiguous focus of infection