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 Anatomy
chemistry of the
concentric layers
Over time, these layers
suffer a loss of water
content and proteoglycan,
which changes the discs
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 Anatomy
chemistry of the concentric
layers
Over time, these layers
suffer a loss of water
content and proteoglycan,
which changes the discs
mechanical properties,
making it less resilient
to stress and strain
 The Aging Disc
Thompson criteria I
Loss of cells
Loss of H20/
proteoglycans II
Type II/ Type I
collagen
Annular fissures
III
Mechanical
incompetence
Bony changes
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 doesnt 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
 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 patients 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 dont
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.

 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 variablebut it is going to
progress.
 CSS myelopathy - History
Some patients attribute weakness to
getting old, and because they
arent having neck pain (many
myelopathic patients dont), they
dont realize theres 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 Hoffmans 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 doesnt

cause myelopathy; when it affects the
motor system, lower motor neuron signs
are what youll 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 theyre
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 Greenbergs
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 dse characterised
by:
Low bone mass
Micro-achitectural breakdown of
bone tissue
 silent killer
Preventable dse
Devastating physical, psychosocial
and economical consequence
Increasingly becoming a global
problem-most common metabolic
bone dse afflicting approx. 200m
worldwide.
 WHO DEFINITION:
DEFINITION BMD MEASUREMENT T-SCORE

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

BMD for young adult
women
OSTEOPAENIA BMD 1-2.5 SD below T-Score btn -1 and -2.5
the mean for young
adult women
OSTEOPOROSIS BMD >2.5 SD below T-Score <-2.5
mean for young adult
women
SEVERE BMD >2.5 SD below T-Score <-2.5 with
OSTEOPOROSIS mean for young adult fragility fractures
women in a patient
who has already
experienced >1
fractures
 This definition applies to postmenopausal
women and men >50yrs
T-Score= patients BMD
BMD of control subjects who
are at their peak BMD
Z-Score=patients 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-
osteoclastsdifferentiation and
prolonged survival of osteoclasts via
IL-1,IL-6,TNF.
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 TGF
 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) Cadeficiency
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
hyperPTHproduction 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 theres 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
healingcumulatively leads to
weakening of cancellous bony
structure
 Osteoporosis Vs
Osteomalacia
Normal human skeleton60% 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 7 th
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, ehlers danlos, gauchers,
marfans sx,osteogenesis
imperfecta, hypoPO4
ENDOCRINOPATHIES Cushings sx, DM,adrenal insuff.,
prolactinomas, hyperthyroidism,
hyper-PTH, Hypogonadism,
panhypopituitarism, klinefelters,
turners sx
DEFICIENCY STATES Ca2+, Mg2+, Vit. D def, protein
def., celiac dse, 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/m 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>50Y % ESTIMATED % ESTIMATED
RS) TO HAVE TO HAVE LOW
OSTEOPOROSI BONE MASS
S
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
progressesdifficulty with balance,
back pains, resp. compromise, risk of
pneumonia

QOL

Presence of a # at one vertebral

level5-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
 Complications:
Chronic pain
morbidity and mortality
QOL
Prolonged immobility
Severe kyphosis
Spinal deformitiesdowagers
humploss of 1-2 of height by 7 th
decade of life
Loss of self-esteemdepression
 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
Pagets 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
 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 Ca,mg,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>1 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
(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
angiogenesisvascular 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 AlendronateBMD 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