Degenerative Disc Disease

Low Back Pain

Herniated Nucleus Pulposus
Cervical Spinal Stenosis
Lumbar Spinal Stenosis
Osteoporosis of Spine

WIDIYATMIKO ARIFIN PUTRO

Anatomy
The Spine
Composed of 33
vertebrae
• 7 cervical
• 12 thoracic
• 5 lumbar
• 5 sacral + 4
coccyx (fused)
Act to support the trunk
and transfer muscular
load
2
The Spinal Cord
• Elongated cylindrical mass of nerve tissue
 occupies the upper 2/3 of the vertebral
canal
• (42-45 cm)
• Conus medullaris  conical distal
• Filum terminale  1st seg. coccyx
• Ascensus medullorum
• Intumescentia cervicalis
(C 3 – Th. 2)
• Intumescentia lumbalis
(Th. 10 – L2)

3
Segments of the Spinal Cord
• Composed of 31
segments :
8 cervical
12 thoracal
5 lumbalis
5 sacralis
1 coccygeus

4
Intervertebral Disc
• nucleus pulposus
• annulus fibrosus
• hyaline cartilage
end plates

5
Facet Joints

6
7
Degenerative Disc Disease
and
Low Back Pain
 Degenerative Disc Disease (DDD)
• Unfortunately, DDD seems to be sort of a
“wastebasket term”
– While these changes are indeed “degenerative,”
this happens as we age and is not necessarily
indicative of any significant underlying pathology
or condition.

– The majority of individuals > 60 will show some

type of degenerative change(s) on lumbar
imaging.
 DDD
• Degeneration of an individual disc space
typically refers to:
1.loss of disc height,
2.loss of water content,
3.fibrosis,
4.end plate sclerosis/defects,
5.osteophyte complexes, etc.
 Degenerative Disc Disease
• The process is thought
to begin in the annulus fibrosis
with changes Normal
to the structure and chemistry of Anatomy
the
concentric layers
• Over time, these layers suffer a
loss of water content and
proteoglycan, which changes the
disc’s mechanical properties,
making it less resilient
to stress and strain
 Degenerative Disc Disease
• The process is thought
to begin in the annulus fibrosis
with changes Degenerative
to the structure and chemistry of Anatomy
the concentric layers
• Over time, these layers suffer a
loss of water content and
proteoglycan, which changes the
disc’s mechanical properties,
making it less resilient
to stress and strain
 The Aging Disc
• Thompson criteria I
– Loss of cells
– Loss of H20/  proteoglycans
–  Type II/  Type I collagen II

– Annular fissures
– Mechanical incompetence
– Bony changes III

IV

V V
 Degenerative Disease:
Facet Arthritis
• Changes in disc structure
and function can lead to
changes in the articular
facets, especially
hypertrophy (overgrowth),
resulting from the
redirection of compressive
loads from the anterior and
middle columns to
the posterior elements
 Degenerative Disease:
Facet Arthritis
• Facet Injections
– Anesthetic effect
– Relief may last for several
months or only a few weeks,
or a few days
Degenerative Disease: Osteophytes
• There may also be
hypertrophy of the
vertebral bodies adjacent to
the degenerating disc; these
bony overgrowths are
known as osteophytes
(or bone spurs)
 Degenerative Disc Disease
• Symptoms
– Low back pain and/or
buttocks pain
– If leg pain also exists, there is
likely an additional cause, eg,
HNP, stenosis, etc
– DDD is not usually the sole
diagnosis
 Degenerative Disc Disease:
Discogenic Pain
• Discogenic pain is pain
originating from the disc
itself; an internally
disrupted disc may result in
disc material causing
chemical irritation of nerve
fibers
 Degenerative Disc Disease
• Diagnosis
– Patient examination
– Xray
– MRI
– CT, in some cases, to rule out
other diagnosis
– Discography
• Nonoperative care
– Rest for acute, low back pain
– NSAID medication
– Physical therapy
• Exercise/walking
• Low-impact aerobics
• Trunk strengthening
 Degenerative Disc Disease
• Surgical care
– Failure of nonoperative treatment
• Minimum of 6 weeks
– Fusion
• Removal of disc and replacement with bone graft, or a
cage-filled bone graft, or a bone graft substitute
– Anterior approach
– Posterior approach
– Combined approach
– Arthroplasty
• Articulating disc replacement
 Low Back Pain (LBP)
• LBP is extremely common
• ~85% of LBP is idiopathic
• Most patients with LBP improve on their own
in time
– Physical therapy and pain meds (even
nonprescription such as NSAIDs) are appropriate
mainstays of initial treatment.
 Taking a history in a pt. with LBP
• Evaluation of patients with LBP should be
geared towards identification of those
patients with a potentially serious underlying
etiology.
– Cancer
– Infection – osteomyelitis, abscess, etc.
– Fracture
– Cauda Equina Syndrome
 Things that should raise a “red flag”
• Previous dx of cancer, unexplained weight loss
• Immunosuppression, dx of steroid use, dx of
IV drug abuse, Dx of skin/other infection(s)
• Dx of recent falls or trauma (including surgery)
• Bladder dysfunction or fecal incontinence,
“saddle anesthesia”, leg weakness
• Pain that doesn’t improve with rest;
• failure to improve after 4 weeks conservative
management
 Other things to check with LBP
• Social factors are important to ask about.
– Employment status
– Any pending litigation?
• Vitals can give clues (fever with infection, etc).
• Routine labs are usually sufficient.
• Good physical exam should pick up
neurological compromise, if present.
• Palpation of the spine looking for tenderness,
etc., also important (trauma, infection).
 Radiography
• Currently, radiographic imaging is not
recommended for patients with no “red flags”
on history and physical if they have had
symptoms less than 4 weeks duration.
• If red flags present, or persistent symptoms
beyond 4 weeks, radiographic evaluation is
recommended.
– Then referral as/if appropriate.
Herniated Nucleus Pulposus
 Concept
• Intervertebral discs can be thought of,
conceptually, kind of like a “jelly donut.” The
outside is the annulus fibrosus, and the inside
“jelly” is the more watery nucleus pulposus.
– Intervertebral discs act as shock absorbers
between the vertebral bodies.

– Just like jelly donuts have a “weak spot” where

the jelly squirts out if you squeeze them, the
annulus of discs is weak posteriorly where the
nucleus pulposus can herniate through, causing
symptoms.
 Presentation
• The classic presentation of Herniated Nucleus
Pulposus (HNP), both for cervical and lumbar
spine, is radiculopathy.
– The disc herniation impinges upon a nerve root,
causing characteristic pain.
– Thoracic disc hernations are much, much rarer.
 Lumbar HNP
• “Sciatica” is the classic radiculopathy of
lumbar HNP, though the exact presentation
depends upon the nerve root(s) involved.
• Motor weakness can occur, which again is
representative of the nerve root(s) involved.
– L4 – quadriceps (knee extension)
– L5 – tibialis anterior (foot dorsiflexion)
– S1 – gastrocnemius (foot plantar flexion)
– Lower Motor Neuron signs
 Lumbar HNP
• 90% of herniated discs are paracentral (slightly
off to one side) and affect the nerve root that
corresponds to the lower vertebral level.

– Example: a typical L4/5 disc herniation would

cause symptoms referrable to the L5 nerve root.
 Lumbar HNP – when to operate
• The natural history of herniated discs is to
resolve over time.
• If conservative management can adequately
treat a patient’s pain, this is the preferred
course of action.
• If conservative management fails to
adequately control pain, surgery can be
performed (often times on an outpatient
basis).
 Cervical HNP
• Classic presentation is to “wake up with it.”
Usually no identifiable factor.
– Causes painful limitation of neck motion and
symptoms corresponding to the affected nerve
root(s)
• The majority of cervical herniated discs will
catch the nerve root corresponding to the
lower vertebral level.
– Ex: A C6/7 disc herniation will impinge upon the
C7 root.
 Cervical HNP
• Just as is the case with Lumbar HNP,
conservative therapy is the mainstay of
treatment.
• Surgery indicated for those that don’t improve
with conservative management, or with
new/progressive neurologic deficit.
Cervical Spinal Stenosis
 Cervical Spinal Stenosis (CSS)
• Stenosis – a constriction or narrowing of a
duct or passage.
– Cervical spinal stenosis, thus, is narrowing of the
spinal canal (within which lies the cervical spinal
cord).
• This narrowing can be from any of a multitude of
causes. Usually, though, this is referring to more
chronic types of processes, rather than acute or sudden
ones.
 CSS – when it causes problems…
• Radiculopathy – from nerve root compression.
– The term “radiculopathy” refers to disease of the
nerve roots; LMN signs, pain/parasethesias.
• Myelopathy – from spinal cord compression.
– The term “myelopathy” refers to pathological
changes of the spinal cord itself.
• Pain and sensory changes in the back of the
head, neck, and shoulders.
 CSS - Myelopathy
• The goal here is to avoid missing patients who
are myelopathic, because once stenosis has
evolved to the point that it is compressing
(and causing damage to) the spinal cord, the
progression of symptoms may be
variable…but it is going to progress.
 CSS myelopathy - History
• Some patients attribute weakness to “getting
old,” and because they aren’t having neck pain
(many myelopathic patients don’t), they don’t
realize there’s a problem that needs
addressing.
– Ask about fine motor movements, like buttoning
buttons, tying shoes, signing checks, handwriting
changes, using utensils, etc. “Clumsiness” with
fine motor skills is common.
 CSS myelopathy - Physical Exam
• Hyperactive reflexes are the most common
physical exam finding in myelopathy.
– Remember the difference between Upper Motor
Neuron and Lower Motor Neuron signs.
– Remember symmetry – a Hoffman’s on one side, if
not on the other, should raise a red flag.
– Remember that a Babinski reflex, if present, is
ALWAYS abnormal.
• T2 weighted MRI, sagittal view;
This patient has multilevel
degenerative changes of the
cervical spine. The bottom two
arrows show mild stenosis with
CSF (white, fluid signal) still
flowing around the cord.
However, the top arrow is
pointing to the C3/4 level where
there is severe cervical spinal
stenosis, no CSF around the cord
(compression), and signal
change within the spinal cord
itself (indicating damage).
 Surgery
• The goal of surgery is to halt the progression
of myelopathy through adequate
decompression of the area(s) of stenosis.
• Once patients are clinically myelopathic,
complete return of function and/or remission
of symptoms almost never occurs.
– This is why they need to be identified early!
Lumbar Spinal Stenosis
 Lumbar Spinal Stenosis (LSS)
• Just as we discussed with Cervical Spinal
Stenosis, “Lumbar Spinal Stenosis” can occur
secondary to anything which narrows the
lumbar spinal canal
 Lumbar Spinal Stenosis
• Remember that the Spinal Cord ends at the
Conus Medullaris, which is typically located at
the L1/2 interspace in adults.
– L1/2 is the lumbar level least likely to be affected
by Lumbar Spinal Stenosis.

• Thus, Lumbar Spinal Stenosis doesn’t cause

myelopathy; when it affects the motor system,
lower motor neuron signs are what you’ll find.
 LSS - presentation
• The “classic” presentation of Lumbar Spinal
Stenosis is Neurogenic Claudication (NC), or
“pseudoclaudication.” (~60% sensitivity, but
>90% specificity).

– Gradually progressive back, thigh, buttock, and/or

leg pain that is relieved by rest and/or,
characteristically, a change in posture; usually
through flexion at the hips (sitting or squatting,
etc.).
 Neurogenic Claudication
• Neurogenic Claudication is thought to arise
from compression of, irritation to, or ischemia
of the lumbosacral nerve roots.

• This is in contrast to Vascular Claudication

(VC), which is secondary to insufficiency of
vascular supply to meet demand of muscles
(pain is ischemic, but from muscles).
• “Anthropoid posture”
(walking bent-over as
though they’re pushing
a shopping cart) is
common in NC, and
pain may be
reproduced with
lumbar extension.
• Vascular Lab Studies
may help differentiate
between NC and VC
– Ankle-Brachial Index
(ABI)
– Ultrasound

Table 14-18 adapted from Greenberg’s

Handbook of Neurosurgery, 6th ed.
 Management
• Unless there is severe neurological deficit,
conservative medical management is usually tried
prior to pursuing surgery.
– Pain meds, epidural steroid injections, etc.

• If medical management is unsuccessful, surgery

for Lumbar Spinal Stenosis is aimed at removing
the bony lamina and soft tissue elements that are
contributing to the canal stenosis.
Metabolic disease of spine
Osteoporosis
 Skeletal d’se characterised by:
• Low bone mass
• Micro-achitectural breakdown of bone tissue
• “silent killer”
• Preventable d’se
• Devastating physical, psychosocial and
economical consequence
• Increasingly becoming a global problem-most
common metabolic bone d’se afflicting
approx. 200m worldwide.
 WHO DEFINITION:
DEFINITION BMD MEASUREMENT T-SCORE

NORMAL Within 1SD of mean BMD T-score >-1

for young adult women

OSTEOPAENIA BMD 1-2.5 SD below the T-Score btn -1 and -2.5

mean for young adult
women
OSTEOPOROSIS BMD >2.5 SD below mean T-Score <-2.5
for young adult women

SEVERE OSTEOPOROSIS BMD >2.5 SD below mean T-Score <-2.5 with fragility
for young adult women in a fractures
patient who has already
experienced >1 fractures
• This definition applies to postmenopausal women
and men >50yrs
• T-Score= patient’s BMD
BMD of control subjects who are at
their peak BMD
• Z-Score=patient’s BMD
BMD of patients matched for age and
sex
Z-Scores used in premenopausal women, children
and men<50yrs
 PATHOPHYSIOLOGY
• HALLMARK: reduced skeletal mass due to
imbalance btn bone resorption and formation
• Failure to build bone reserve from childhood
• Bone loss
• Aging with loss of gonadal function
• Bone loss accelerates rapidly in women during
the first years after menopause
 a) Estrogen deficiency leads to…
• ↑ expression of RANKL by osteoblasts
• ↓ release of OPG
• ↑recruitment of pre-
osteoclasts→↑differentiation and prolonged
survival of osteoclasts via IL-1,IL-6,TNFᾳ.
• T-Cells inhibit osteoblastic differentiation and
activity with premature apoptosis of osteoblasts
through cytokines e.g. IL-7
• Increased sensitization of bone to the effects
of PTH
• ↑osteoclastic apoptotic activity via
↑production of TGFᵝ
 b) Aging
• Progressive ↓ in supply of osteoblasts
• Reduced Ca2+ uptake from GIT
• Bone resorption exceeds bone formation from
3rd decade
• Women lose-30-40% of cortical bone
-50% of trabecular bone
• Men lose-15-20% of cortical bone
-25-30% of trabecular bone
 c) Ca²⁺deficiency
• →2° hyperPTH -↓ renal excretion of Ca2+
-↑ renal production of 1,25-
(OH)2-D (calcitriol)→↑ca2+ absorption from
the gut
→↑bone resorption
 d) Vit D Deficiency
• Impaired absorption of Ca2+ from gut
• Compensatory mechanism:-Leads to
hyperPTH→↑production of calcitriol from the
kidneys
• PTH and vit.D have their effect on bone being
mediated via binding to osteoblasts and
stimulating RANK/RANKL pathway
• Osteoclasts do not have receptors for Vit.D or
PTH
 Osteoporotic Fractures
• Aka Insufficiency/ fragility fractures
• Mostly from low-energy trauma/minor loads
• Vertebral bodies-1rly cancellous with
interconnected horizontal and vertical trabeculae.
• In osteoporosis there’s ↓ in both bone mass and
this internal interconnectivity(BUT preferentially
disruption is in the horizontal trabeculae)→?
Reason→?overaggresive osteoclastic resorption
 Rosen and Tenenhouse cadaveric
study:
• As many as 200-450 horizontal trabeculae
fractures per vertebral body in various stages of
healing→cumulatively leads to weakening of
cancellous bony structure
 Osteoporosis Vs Osteomalacia
• Normal human skeleton→60% mineral
40% organic material
(collagen)
• Osteoporosis-mineral: collagen ratio within
normal tho’ both are significantly ↓; bone is
porous and brittle
• Osteomalacia-mineral is reduced relative to
organic content; bone is soft.
 Classification of osteoporosis:
• Localised 1°

• Generalised
2°
 1° Osteoporosis
(A) JUVENILE
• Children/young adults; both sexes
• 8-14 yrs
• Normal gonadal function
• Hallmark: abrupt bone pain/ fracture following
minor trauma
(B) IDIOPATHIC

a) PMO(TYPE 1)-high-turnover osteoporosis

 Women>50-65yrs
 Phase of accelerated bone loss primarily
trabecular bone
 Predorminantly increased osteoclastic activity
 Fracture vertebrae and distal forearm common
 Vertebral # occur more often in the 7th decade
of life.
b) age-related/senile osteoporosis(TYPE 2)
-Low-turnover osteoporosis
-gradual slow down in osteoblastic activity.
• Men and women >70 yrs
• Fractures in cortical and trabecular bone
• Wrist, vertebrae and hip fractures common
 2° Osteoporosis
CAUSE EXAMPLES
GENETIC/CONGENITAL Renal hypercalciuria, cystic fibrosis,
ehler’s danlos, gauchers, marfans
sx,osteogenesis imperfecta, hypoPO4²
ENDOCRINOPATHIES Cushing’s sx, DM,adrenal insuff.,
prolactinomas, hyperthyroidism, hyper-
PTH, Hypogonadism, panhypopituitarism,
klinefelter’s, turner’s sx

DEFICIENCY STATES Ca2+, Mg2+, Vit. D def, protein def., celiac

d’se, malabsorption, malnutrition,
parenteral nutrition
INFLAMMATORY CONDITIONS IBD, R.A., SLE, Ankylosing spondylitis
HAEMATOLOGICAL/ NEOPLASTIC Haemophilia,, haemochromatosis,
DISORDERS leukaemia, lymphoma, multiple myeloma,
SCD, Thalassaemia, metastases
MEDICATIONS Anticonvulsants(Rx-induced Vit D def),
antipsychotics, ARVS, Aromatase
inhibitors(Anastrozole), anticancer drugs,
Frusemide, Glucorcoticoids( PDN>5mg OD
for >3/12), longterm Heparin, Li, SSRI,
Hormonal therapies-Thyroxine, LHRH
analogues

MISCELLANEOUS Pregnancy, lactation, alcoholism,

depression, HIV/AIDS, CRD, CCF, Chronic
liver disease, amyloidosis, prolonged
immobility/disuse, Multiple sclerosis
 STAGES
• STAGE 1: loss of horizontal trabeculations
• STAGE 2: loss of vertical trabeculae
• STAGE 3: loss of both horizontal and vertical
trabeculae with resultant cavitation of the
vertebral body
 RISK FACTORS
National Osteoporosis Foundation (NOF) classifies
them into:
a) Modifiable:
 physical inactivity
 drugs, alcohol, cigarette smoking
 deficiency states
 Thin build/small stature(body wght <127lbs/
BMI<20-25 kg/m² in men),
 >10% body weight loss in men
 Androgen deprivation therapy in men
 Previous fragility fracture
 b) Non-modifiable:
• age (>50yrs)
• sex(F:M=4:1)
• race(caucasian/asian)
• genetics(+ve family history)
• amenorrhoea, late menarche, early menopause
• post-hysterectomy and oophorectomy,
• androgen/ estrogen def.
 Pneumonic=OSTEOPOROSIS
 O=lOw ca2+
 S=Seizure drugs
 T=Thin build
 E=Ethanol intake
 O=hypOgonadism
 P=Previous fracture
 0=thyrOid excess
 R=Race
 O=Other realtives with osteoporosis
 S=Steroids
 I=Inactivity
 S=Smoking
 EPIDEMIOLOGY
• 10m Americans affected(80% women)-NOF
• 34M have ↓ bone mass with ↑ risk for
osteoporosis
• 1.5m-2m osteoporotic fractures/yr (700,000
spinal #; 300,000 hip #; 200,000 wrist #)
• 1 in every 2 women and 1 in every 5 men will
eventually experience osteoporotic #
• Men have a higher prevalence of 2°
osteoporosis
 RACIAL DEMOGRAPHICS
RACE SEX(AGE>50YRS) % ESTIMATED TO % ESTIMATED TO
HAVE HAVE LOW BONE
OSTEOPOROSIS MASS

NON-HISPANIC WOMEN 20 52
WHITE;ASIAN
MEN 7 35
NON-HISPANIC WOMEN 5
BLACK
MEN 4 19
HISPANIC WOMEN 10 49
MEN 3 23
• Osteoporosis-related fractures result in annual
direct expenditure of $12.2b-17.9b
• Leading cause of fractures in the elderly
• Women>50yrs have about 50% lifetime fracture
rate due to osteoporosis and about 80% of all
fractures in pple aged >50yrs.
 prognosis
• Good if bone loss is detected early
• Incase of #→ may lead to chronic pain,
disability, prolonged immobilisation, death
 Vertebral compression fractures
• 2/3 are asymptomatic and occur slowly
• Associated with ↑morbidity and mortality
• Mortality also correlates with number of
vertebral #
• Often occurs with minimal stress
• Mostly affected-middle/lower thoracic and
upper lumbar
• As posture worsens and kyphosis
progresses→difficulty with balance, back pains,
resp. compromise,↑ risk of pneumonia

• ↓ QOL

• Presence of a # at one vertebral level→5-fold ↑

risk of getting another
 CLINICAL PRESENTATIONS
• Episode of acute back pain after bending,
coughing,lifting, a fall, minor trauma
• Pain-sharp, nugging, dull; exacerbated by movt;
may radiate to the abdomen
• Progressive kyphosis with loss of height
• +/- localised pain
• Paravertebral muscle spasm exacerbated by
activity/ reduced by lying supine.
 Complications:
• Chronic pain
• ↑morbidity and mortality
• ↓ QOL
• Prolonged immobility
• Severe kyphosis
• Spinal deformities→”dowager’s hump”→loss of
1-2’ of height by 7th decade of life
• Loss of self-esteem→depression
 PHYSICAL EXAM
• Inspection
• Palpation
• Height measurement
• Active/passive ROM
• Neurological exam
• Signs esp in the elderly that may indicate
↑risk of a fall-gait problems, orthostatic
hypotn, LL weakness, cognitive impairment

• Findings of subtle collagen defects:-short 5th

digit, dentinogenesis imperfecta, hyperlaxity,
hearing loss, pes planus, bunions, blue sclera
 DDX
 Osteomalacia
 Tumors(osteolytic)
 Infections
 Osteonecrosis
 Other bone-softening metabolic disorders
 Mets
 Leukaemia/lymphoma
 Osteogenesis imperfecta
 Renal osteodystrophy
 Multiple myeloma
 Scurvy
 Paget’s disease
 Sickle cell anaemia
 Homocystinuria/homocystinaemia
 WHO-Fracture-Risk algorithm(FRAX)
• Developed to calculate 10yr probability of any
major osteoporotic # in a given patient
• Take into a/c BMD and other clinical risk fxtrs
• NOF recommends RX for patients with WHO-
10yr-probability of major osteoporosis-related #
of >20% (or >30% for hip #)
• This algorithm is useful in identifying patients
most likely to benefit from Rx.
 SCREENING
• Women >50yrs of age
• For men, not carried out routinely
US preventive Services Task Force(USPSTF)/
American College of Physicians(ACP)
recommendations:
Indications for screening in men
• Those with 10yr risk for osteoporotic # equal to
or greater than that for 65yr old women who
have no additional risk factors
 INVESTIGATIONS
i) LAB WORKUP
a) To establish baseline conditions:
-CBC
-Serum Ca²⁺,mg²⁺,po4-,Fe2+/ferritin levels
-LFTs
-TFTs
-Vit. D levels
-Cr/BUN
 b) To exclude 2° causes
• 24 hr-urinary Ca2+ levels
• PTH level
• Testosterone/gonadotropin level
• ESR/ CRP
• Urinary free cortisol levels/ dexamethasone
suppression test
• BMA
• Serum/Urinary protein electrophoresis
 ii) Biochemical markers of bone
turnover
• Reflect bone formation and resorption

• Maybe ↑in high-bone turnover states and may

also be useful in some patients for monitoring
early response to treatment
 SERUM MARKERS OF BONE
FORMATION
• Bone specific alkaline phosphatase(BSAP)
• Osteocalcin(OC)-if high, indicates a high
turnover osteoporosis
• Carboxyterminal propeptide of type 1
collagen(PICP)
• Aminoterminal propeptide of type 1
collagen(PINP)
 SERUM MARKERS OF BONE
RESORPTION
• Cross-linked C-Telopeptide of type 1
collagen(ICTP)
• Tartrate-resisitant acid phosphatase
• N-Telopeptide of collagen cross-links(NTx)
• C-telopeptide of collagen cross-links(CTx)
 URINARY MARKERS OF BONE
RESORPTION
• Hydroxyproline
• Free and total pyridinolines(Pyd)
• Free and total deoxypyridinolines(Dpd)
• NTx
• CTx
 iii) IMAGING
(a) Plain radiography
-to assess overall skeletal intergrity
-suspected #
-if patient has lost>1½” of height
• Can suggest presence of osteopaenia or bone
loss though cannot diagnose osteoporosis
• Osteoporosis predorminantly affects
trabecular bone rather than cortical bone

• Cortical bone not affected by osteoporosis

until >30% of bone loss has occurred

• 30-80% of bone mineral must be lost before

radiographic lucency becomes apparent.
(b) Densitometry
1) Dual-Energy X-Ray Absorptiometry(DXA)
-quantifies bone loss
-standard for evaluation of BMD
-not as sensitive as QCT for detecting early
trabecular bone loss, but it provides rapid
scanning times, is less costly and precise
-used to calculate BMD at the lumbar spine,
hip,prox. Femur and wrist
-data is reported as T and Z-scores
2) Single-photon Absorptiometry(SPA)

-precise and with low- radiation exposure

-relatively insensitive for detecting early-stage

osteoporosis coz it measures cortical rather
than trabecular bone.
3) Dual-Photon Absorptiometry(DPA)

-Can measure BMD in the spine and prox. Femur

-limited by poor reproducibility, prolonged
scanning times and artifacts caused by vascular
calcifications.
4) Computed Tomography

• Quantitative CT Scanning(QCT)
-assesses BMD only at the spine
-can be used in both adults and children
-is the most sensitive method for diagnosing
osteoporosis coz it measures trabecular bone
within the vertebral body.
-cf with DXA, is more expensive, poor
reproducibility, possible interference by
osteophytes, higher radiation dose
• Single-Photon Emission CT Scanning(SPECT)

-CT-Like bone imaging technique that offers

better image contrast and more accurate
lesion localisation
-increases sensitivity and specificity of bone
scanning for detection of lumbar spine lesions
by 20-50% over planar techniques
-visualise bony structures that would overlap on
planar images e.g. facet joints, pars
interarticularis, pedicles
5) U/S

• Quantitative U/S of the Calcaneus(QUS)

-The heel is the only validated skeletal site for

clinical use of QUS in osteoporosis mx.

-low cost, no radiation

-not as accurate.
6) MRI
-Useful in discriminating btn acute and chronic
fractures of the vertebrae and occult fractures
of the proximal femur.
7) Bone Scanning(99m Tc)

8) Bone biopsy and histology

 MANAGEMENT
Approach considerations
Rx is aimed at # prevention and rehabilitation.
-lifestyle modification
-pharmacotherapy
-Rx of potentially-treatable 2° causes
-surgical Mx of vertebral compression #
-rehabilitation to control pain.
 PHARMACOTHERAPY
NOF Recommendations:
Pharmacotherapy should be reserved for
postmenopausal women and men >50yrs
presenting with:
• hip/vertebral #
• T-score of -2.5 or less at the femoral neck or
spine
• low bone mass(T-score of btn -1.0 and -2.5 at
the femoral neck or spine)
• 10yr probability of a hip # of >3% or

• 10yr probability of a major osteoporosis-related

# of >20% based on FRAX

ADVISABLE THAT ALL RX SHOULD BE GIVEN WITH

CA2+ AND VITAMIN D SUPPLEMENTS
 1. BIPHOSPHONATES
• Most commonly used
• For Rx and prevention
• Oral and I.V. formulations
MOA
Binds to the hydroxyarpatite crystalls at active
bone resorption sites thereby inhibiting
osteoclastic resorption.
 S/E
• Overtime, it ↓bone turnover
• At very high levels, ↓bone strength and
resilience
• Osteonecrosis of the jaw
• Atypical femur fractures(transverse subtroch
and shaft #)
• Bone turnover markers should be monitored
and if they become significantly ↓, the
treatment holidays instituted until return to
normal levels
i. Alendronate(Fosamax)

-dose : 70mg/wk PO

-↓ fracture rate of the spine, hip and wrist by

50%

-can be combined with Vit. D(Fosamax-Plus D)

ii) Risendronate(Actonel)
-↓ vertebral fractures by 41% and non-vertebral
fractures by 39% over 3 yrs

-can be combined with Ca2+

iii) Ibandronate

-PO once monthly or IV 3-monthly

iv) Zolendronic Acid(Reclast)

-most potent
-↑ BMD at the spine by 4.3-5.1% and hip by 3.1-
3.5%
-↓ spine # by 70% and hip by 41%
-given IV once yearly
 2. SELECTIVE ESTROGEN RECEPTOR
MODULATORS( SERM)
• RALOXIFENE(Evista)
-↓ risk of vertebral fractures by 35%
 3. PTH
• TERIPARATIDE(human recombinant PTH)
MOA: ?stimulation of angiogenesis→vascular
endothelial stem cells differentiated to become
osteoblasts
indications
• Rx of osteoporosis where other Rx has failed or
intolerance has developed
• Finkelstein et al: combination therapy with
biphosphonates has ↓benefits

• Cosman et al: 3/12-on followed by 3/12-off

pulses of teriparatide in pts on weekly
Alendronate→BMD increased above that of
either Rx alone.
 4. CALCITONIN
MOA: ↓osteoclastic activity
-reserved for those intolerant to estrogens

-Formulations: Inj or Intranasal spray (200i.u. OD)

 5. DENOSUMAB
• Humanised monoclonal Ab against RANKL
• DOSE: 60mg SQ every 6/12
• May become 1st line of Rx for patients with
autoimmune and inflammatory disorders coz
overactivity of RANKL is a major factor in bone
loss in such pts.
 6. HRT
 Currently not recommended coz of S/E(ca
breast, MI, CVA, DVT)
i) Estrogen Derivatives-premarin, Estradiol,
Estropipate
ii) Estrogen-Progestin combinations:
-Estradiol-Levonorgesterol
-conjugated Estrogen/medroxyprogesterone
acetate
 7. OTHERS
• Vitamin-D formulations:ergocalciferol(Vit D2),
cholecalciferol(Vit D3)

• Ca2+ salts: ca-citrate, ca-carbonate

• Strontium ranelate

• Daily nitroglycerin ointment

 American association of clinical
endocrinologists
• 1st line: alendronate, risendronate, zolendronic
acid, denosumab
• 2nd line: ibandronate
• 3rd line: raloxifene
• Treatment failure: teriparatide
 SURGICAL THERAPY
• OBJECTIVE: early mobilisation and return to
normal or near normal function

• INDICATIONS: incapacitating/ persistent severe

focal back pain related to vertebral collapse
i) Anterior and posterior decompression and
stabilisation with pedicle screws, rods,
plates, cages +/- bone grafting to achieve
fusion

ii) KYPHOPLASTY
• Reduces amount of kyphosis and restores
vertebral body height
• Minimally invasive
iii) VERTEBROPLASTY

-Useful to control pain associated with vertebral #

-fuses fracture fragments into one block using
acrylic cement, preventing painful mvt of
individual fragments.
-also reduces pain by heat produced by
polymerization process as the cement hardens
-does not restore height of compressed vertebral
body
 DIETARY MEASURES
Oral Vit. D and Ca2+ supplements daily intake for
osteoporotic patients:
-Ca2+: 1200-1500mg
-Vit. D: 400-800i.u
Sources of Ca2+ : dairy products, nuts, sunflower
seeds, vegs
Vit D sources: eggs, liver, fatty fish, milk
 OTHER RX MODALITIES
• PHYSIOTHERAPY
-to strengthen back extensor muscles to
↓kyphosis
-orthotics: -Thoracolumbosacral orthotics(TLSO)
-Jewett brace
-Cruciform ant spinal hyperext(CASH)
brace
• OCCUPATIONAL THERAPY
-training in performance of activities of daily
living

• EXERCISES
-aerobic, low-impact exercise(3-5 sessions/wk
each 45-60min)
 PREVENTION OF OSTEOPOROSIS
 Starts in childhood
 Adequate ca2+/vit D intake/ weight-bearing
exercises
 2-pronged:
i) Behaviour modification-cigarette smoking
-physical inactivity
-intake of
alcohol,caffeine, animal protein
ii) Pharmacological

-regular periodic bone densitometry(every 2 yrs

for postmenopausal women)
-Longterm monitoring-DXA repeated every 2-3
yrs if baseline is normal and every 1-2yrs in
osteoporotic patients undergoing Rx.
END!
Thank you