Bones and Joints

Normal Structure of Bones

 Depends on
 Interaction
of bones with muscles
 Hormonal regulation of calcium and phosphate
metabolism
 Homeostasis of bone formation and bone resorption
 Osteoclasts vs. osteoblasts
Functions of Bones
 Movement of limbs, via mechanical support of
muscles
 Protection of the internal organs
 Ribs, skull
 House bone marrow cells
 Medullary canal
 Storage of calcium and phosphate salts
Facts to know about Bones
 Bones are living tissues
 Constantly change, based on stress (pressure and
tension)
 Hypertrophy, deconditioning
 Bones are not affected by autoimmune diseases
 Joints are affected by autoimmune diseases
 Rheumatoid arthritis
Joints
 Form the junction between 2 bones
 Provide skeletal support
 Provide firmness to the skeleton
 Provide ability for movement to occur
Pathology
Sprain
 Injury to the ligamentous structures around a joint
 Classified depending on amount of tissue damage
 First, second, third degree
Dislocations
 Complete loss of joint integrity with loss of anatomic
relationships
 Often significant ligamentous damage occurs
 Subluxation: partial disruption of anatomic
relationship within the joint
Heterotropic Ossification
 Bone formation in muscle and other soft tissue areas
 Occurs mostly after trauma
 Symptoms:
 May be asymptomatic
 Pain and loss of motion

 Edema, warmth, erythema, tenderness

 PT:
 Gentle PROM- no forcible manipulation
Osteogenesis Imperfecta
 “defective bone formation”
 Related to gene mutations encoding collagen type I
 Collagen type I
 Widespread in the body
 Thin skin, defective heart valves
 Affects bones and connective tissue
 Clinical presentation depends on severity of disease
Osteogenesis Imperfecta
“This newborn has short
extremities due to
multiple intrauterine
fractures. Multiple rib
fractures were present
also. This is the
neonatal lethal type of
OI.”

http://www.brown.edu/Courses/Digital_Path/systemic_path/bone/ogi1.html
Osteomyelitis
 Inflammation of the bones caused by an infectious
organism
 In children, infection occurs via the circulatory system
 Bacteria enters the metaphysis through arteries
supplying nutrients to the bone
 Metaphysis very porous, so the infection spreads easily
and multiplies rapidly→ forms pus → spreads to the
to adjacent portions of the epiphysis
Osteomyelitis
 Pus filled cavities form → body attempts to wall off
infection by producing reactive bone
 Bone deformities result, increasing predisposition to
fractures
 Fractures heal poorly because of pus in the area

 In adults… usually result of puncture wound into

bone or respiratory/urinary tract infection
 Osteomyelitis

http://graphics8.nytimes.com/images/2007/08/01/health/adam/9712.jpg http://podiatry.files.wordpress.com/2007/03/fig1staphsimosteo.jpg
Osteomyelitis
 Clinical Manifestations
 Vary between adults and children
 Pain

 Fever

 Local manifestations: edema, erythema, tenderness

Osteomyelitis
 Risk factors:
 Chronic illness
 Surgical procedure to bone

 Open fracture

 Implanted orthopedic device

 Treatment
 Antibiotics

 Surgical drainage of pus

 Surgical repair of defect
 Osteoporosis
 Characterized by reduction of total bone mass density (BMD)and
microdamage to bone structure that results in susceptibility to
fractures

http://content.revolutionhealth.com/contentimages/images-image_popup-w7_osteoporosis.jpg http://www.healthline.com/images/staywell/37381.jpg
Osteoporosis
 Most common metabolic bone disease
 Osteoporosis is a major public health threat for an
estimated 44 million Americans
 Primarily a disease of older age
 But…can occur at any age

 80% are ♀

Adopted from: http://www.nof.org/osteoporosis/diseasefacts.htm

Osteoporosis
 Risk Factors
 Gender

 Race

 Family history
 Age

 Low body weight

 Early menopause

 Low physical activity levels

 Calcium and Vit D intake

 alcohol, smoking, caffeine

Osteoporosis
 Severity depends on:
 Initial bone mass
 Bone mass peaks at ages 25-35
 Then bone resorption > bone formation
 Process accelerated after menopause
 Body size
 Dietand lifestyle (intake of Vit D and calcium, ETOH,
smoking)
 Hormones (estrogen)

 Age-related changes with metabolism

Osteoporosis
 Primary  Secondary
 Etiologyunknown  Hormonal disturbances
 Accounts for most cases  Inadequate intake or
malabsorption
 Disease of elderly
 Immobilization
 ♀>♂
 Drugs (anticonvulsants,
anticoagulants)
 Tumors (hormonal lesions,
lesions that destroy the
bone directly)
Osteoporosis
 Clinical Presentation
 Symptoms can be nonspecific
 Fractures
 Head of femur, distal radius, vertebrae, hips, ribs
 In vertebrae, usually anterior wedge or compression fracture
 Vertebral fractures cause: Dowager’s hump
 Gradual height loss
 Protuberant lower abdomen

 Forward flexed posture

Osteoporosis
 Prevention
 85-90% of adult bone mass is acquired by age 18 in
girls and 20 in boys

 Tips
 Intakeof Vit. D and Calcium
 Weight bearing and strengthening exercise
 Avoid smoking and excessive alcohol

Adopted from: http://www.nof.org/osteoporosis/diseasefacts.htm

Osteoporosis
 Diagnosis:
 Bone mineral density testing
 X-rays to diagnose fractures

 Treatment:
 No cure
 Intervention to stop the progression of bone loss

 Medications

 Exercise
Osteomalacia
 “softening of the bones”
 Vitamin D deficiency or deficiency of phosphate
metabolism causes inadequate mineralization of bone
matrix
 Diagnosis difficult and delayed
 Most initially present with diffuse, generalized aching and
fatigue
 Deformities of bones common
 Bowlegs common because bones unable to carry body
weight
 Thoracic kyphosis
Paget’s Disease
 Metabolic bone disease
 Etiology
 Unknown
 Pathogenesis
 Initial stage: osteoclasts proliferate unrestrained
 Bone resorption rapid and osteoblasts cannot keep up
 Bone replaced with fibrous tissue

 Osteoblastic sclerotic phase

Paget’s Disease
 Symptoms
 Asymptomatic

 Bone pain, arthritis, deformities, fractures

 Thickened cranial bones may compress CNs →
headaches, hearing loss, dizziness
 Treatment
 Meds to inhibit bone resorption
 Goal is to induce full remission and prevent
complications of the disease
Paget’s Disease
 PT
 Symptomatic treatment
 Encourage regular exercise

 Fall prevention
Fractures
 Defect in the continuity of a bone

 Types
 Traumatic

 Stress or fatigue
 Pathologic

 insufficiency
Fractures
 Simple – single fracture line
 Complete
 Extending trough the entire thickness of the bones
 Incomplete
 Do not extend from one side to the other
 Displaced- bone has moved on either side of fracture
 Comminuted – multiple lines and fragments
 Open – skin is disrupted
 Closed – skin is not disrupted
 Complicated- infected fx
Fractures
 Healing
 Immobilization vs surgical repair
 Casting vs ORIF/THA/TKA
 Bone will begin to heal once the two side are
compressed together
 Once healing has finished, restructuring will occur once
mobilization has begun
 Depends on
 Nutritional status
 Infection
Fractures
 Medical Management
 Open reduction internal fixation (ORIF)
 Total hip or knee arthroplasty

 Casting

 Vertebral fractures: kyphoplasty, vertebroplasty

Fractures

http://www.clinicalcorrelations.org/wp-content/uploads/2007/03/800px-metacarpal_fractures.jpg
Bone Tumors
 Primary bone tumors
 Osteosarcoma (bone forming cells)
 Chondrosarcoma (cartilage cells)

 Ewing’s sarcoma (primitive mesenchymal bone marrow

cells)

 Secondary
 Metastases from breast, prostate, lung, kidneys, thyroid
Bone Tumors
 Medical Management
 Surgicalresection
 Chemotherapy

 Radiation
Osteoarthritis (OA)
 Degenerative joint disease
 Most common joint disease
 Involves the entire synovial joint
 Develops under conditions that stress the joint
surfaces
 Preferentially affects weight bearing joints
 Hips, knees, spine (vertebrae)
 Prevalence increases with age
Osteoarthritis (OA)
 Etiology
 Active disease process with joint destruction and
aberrant repair as a result of alterations in cellular
function
 Multifactorial
 Includesgenetics, nutrition, weight control, bone density,
estrogen use, local biomechanical factors, previous injury
Osteoarthritis (OA)
 Pathogenesis
 Articular cartilage
 Softens, has surface defects, irregular thinning
 Decreased ability to attenuate load
 (+) inflammation

 Joint
space narrowing
 Subchondral bone changes
 Sclerosis
 Osteophytes
Osteoarthritis (OA)
 Signs and symptoms
 Jointpain (gradual onset, unilateral usually)
 Decreased strength and ROM

 Increased pain with weight bearing and activity

 Swelling localized to the joint

 Morning stiffness
 Lasts ~30 minutes
 Crepitus

 Locking of joint
Osteoarthritis (OA)
 Treatment Goals
 Decrease pain
 Improve function

 Slow disease progression

Osteoarthritis (OA)

http://myhealth.ucsd.edu/library/healthguide/en-us/images/media/medical/hw/h9991217.jpg
Osteoarthritis (OA)
 Treatment
 Medications  Supplements
 Analgesics  Chondroitinsulfate
 Topical analgesics  Glucosamine
 NSAIDs
 Cox-2 inhibitors
 Injectable
glucocorticoids
 Viscosupplements

Adapted from: http://www.arthritis.org/disease-center.php?disease_id=32&df=treatments

Osteoarthritis (OA)
 Treatment
 PT/OT

 Weight loss

Adapted from: http://www.arthritis.org/disease-center.php?disease_id=32&df=treatments

Osteoarthritis (OA)
 Treatment
 Surgical management
 Arthroscopy
 Joint replacement
 Unicompartmental
 Total

Adapted from: http://www.arthritis.org/disease-center.php?disease_id=32&df=treatments

Degenerative Disk Disease (DDD)
 Common musculoskeletal disease
 Peak in 40-50 y/o
 Etiology
 Age related changes
 Genetic inheritance

 Inadequate metabolite transport

 Repetitive external mechanical loading

Degenerative Disk Disease (DDD)
 Pathogenesis
 Same synovial process as in OA
 Intervertebral disks lose volume, shape and structure
Degenerative Disk Disease (DDD)
 Pathogenesis
 Intervertebral disk looses height with age
 Declinein arterial supply to the periphery of the disk and
impaired nutrient delivery
 Affects cellular function
 Reduced cellular waste removal and increased lactic acid
concentration
 Low pH compromises cellular metabolism
 Leads to cell death

 Repetitive external mechanical loading

 Leads to fatigue failure of the matrix
Degenerative Disk Disease (DDD)
 Associated conditions
 Spinal stenosis
 Spinal canal narrows
 Degenerative spondylolisthesis
 Anterior slippage of one vertebrae on another
 ***both cause compression of the spinal cord
 Further compromised if osteophytes are present
Degenerative Disk Disease (DDD)
 Clinical features
 Some may not have any…but if they do…
 Both cause
 Low back pain
 Lower extremity pain and parasthesias
 Lower extremity weakness
Degenerative Disk Disease (DDD)
 Clinical Features (cont.)
 Stenosis
 Neurogenicclaudication
 Symptoms improve with flexion
 Degenerative Disk Disease (DDD)

http://www.backpain-
http://services.epnet.com/GetImage.aspx/getImage.aspx?Im guide.com/Chapter_Fig_folders/Ch06_Path_Folder/Ch06_Buttons/06-
ageIID=7290 5%20AF%20Spondylolisthesis.jpg
Degenerative Disk Disease (DDD)
 Treatment
 Meds

 Lifestylechanges
 Aerobic conditioning

 Physical therapy

 Surgery
 Laminectomy
 Diskectomy
 Fusion
 Epidural
Rheumatoid Arthritis (RA)
 Affects 1% of world population
 2-3x more common in women

 Unknown etiology
 Chronic, systemic inflammatory disease
 Genetic and familial predisposition

 Environmental triggers

 Joint inflammation consequence of massive infiltration

of immune cells into synovial fluid
Rheumatoid Arthritis (RA)
 Pathogenesis
 Primarily involves the synovial joints
 Begins as synovitis
 Leads to exudation of fluid and inflammatory cells

 Inflammation stimulates ingrowth of vessels and

proliferation of synovial cells
 Pannus develops
 Covers articular surfaces like a sheet
 Rich in inflammatory cells that secrete lytic enzymes
Rheumatoid Arthritis (RA)
 Pathogenesis (cont.)
 Cartilage is destroyed and erodes the underlying bone
 Joints become immobilized

 Undergoes osteoporosis and ankylosing

 Joint deformities result

Rheumatoid Arthritis (RA)
 Clinical Presentation
 Course unpredictable, onset insidious
 Some have acute onset of joint pain, swelling and redness

 Morning stiffness

 Chronic, symmetric inflammation of joints

 Typically small

http://www.arthritis.org/disease-center.php?disease_id=31
Rheumatoid Arthritis (RA)
 Clinical Presentation (cont.)
 Systemic symptoms
 Weakness and fatigue, malaise, low-grade fever, loss of
appetite

 Pathological lesions develop

 Rheumatoid nodules

 Chronic inflammation of internal organs

http://www.arthritis.org/disease-center.php?disease_id=31
Rheumatoid Arthritis (RA)

http://www.hopkins-arthritis.org/arthritis-info/rheumatoid-
arthritis/images/clinical/ex-artdis1.jpg
 Rheumatoid Arthritis (RA)
 Clinical Presentation
(cont.)
 Typical visible changes
include:
 ulnar deviation of the
fingers at the MCP joints
 hyperextension or
hyperflexion of the MCP
and PIP joints
 flexion contractures of the
elbows
 subluxation of the carpal
bones and toes (cocked -
up).
http://www.arthritis.org/disease-center.php?disease_id=31
 Rheumatoid Arthritis (RA)

http://z.about.com/f/p/440/graphics/images/en/17130.jpg
Rheumatoid Arthritis
 Treatment
 Goal is to reduce pain, maintain mobility, minimize
stiffness, edema and joint destruction
 Meds

 Surgery
 Synovectomy
 Total joint replacement
Gout
 “Acute, monoarticular, inflammatory arthritis”
 Characterized by hyperuricemia
 Decreasedexcretion via kidneys or
 Overproduction of uric acid

 Primarily in joints, subcutaneous tissue, and kidneys

 Great toe, ankle, instep, knee, wrist, elbow, fingers
 Occurs primarily in middle age men
Gout
 Pathogenesis
 (First symptoms occur in tarsometatarsal joints of the big
toe)
 Elevated blood uric acid levels enters the joint

 Hypersaturates the synovial fluid

 Uric crystals form and deposit in joints and periarticular

connective tissue
 Provoke acute inflammation
Gout
 Clinical Features
 Acute gout
 Cardinal signs of inflammation
 Systemic symptoms (fever, tachycardia, exhaustion,
leukocytosis)
 Chronic gout
 Lessinflammation, more bone deformities
 Painless subcutaneous deposits of uric acid (tophi)

 Deposits of urates in internal organs

Gout

http://images.suite101.com/620164_com_gout_infir.jpg
Gout
 Treatment:
 Goal is to end acute attacks and prevent recurrent
attacks
 NSAIDs
 Other meds
 Lifestyle changes
Surgical Interventions
 Total Knee Arthroplasty (TKA)

http://medicalimages.allrefer.com/large/10254.jpg http://tc.engr.wisc.edu/UER/uer01/author1/figure3.jpg
Unicompartmental Knee
Arthroplasty (UKA)

http://www.inlandortho.net/knee1.jpg
Total Hip Arthroplasty (THA)

http://www.the-health-pages.com/images/REPLACED.GIF
Open Reduction Internal Fixation
(ORIF)

http://www.emedx.com/emedx/diagnosis_information/diagnosis_information_image_files/hip_pelvis_images/subtrochanteric_hip_fracture_orif.jpg
 Other Lower Quadrant Surgeries
Hip Disarticulation Hemipelvectomy

http://www.netterimages.com/images/vpv/000/000/000/516-0550x0475.jpg http://www.netterimages.com/images/vpv/000/000/005/5528-0550x0475.jpg
Lumbar Laminectomy

http://www.eorthopod.com/images/ContentImages/spine/spine_lumbar/l
umbar_stenosis/lumbar_stenosis_surgery01.jpg