orthopedic rotation

1. Balqees Majali

2. ..Osteoporosis is a systemic skeletal disease
characterized by decreased bone density and a
deterioration in bone quality
(microarchitectural changes), leading to
compromised bone strength and an enhanced
risk of fractures that are not due to significant
trauma.

3.  The operational definition of osteoporosis :
World Health Organization cutoffs used in the diagnosis of
osteoporosis (BMD at the hip)
Normal bone T-score > − 1 SD
Osteopenia T-score between − 1 and − 2.5 SD
Osteoporosis T-score < − 2.5 SD
Established (severe
osteoporosis)
T-score < − 2.5 SD + fragility fracture

4. Osteoporosis types
Primary
Juvenile Senile postmenopausal
Secondary
rheumatic gastrointestinal
hematologic
al
endocrine

5. osteoporosis in children is defined on the basis
of a history of one or multiple vertebral
fragility fractures OR the presence of both:
 a clinically significant fracture history in the
absence of local disease or high-energy
trauma
 as well as a BMD Z-score ≤ − 2.0 SD at the
lumbar spine and/or the total body less head
(TBLH) adjusted for age, gender, and body
size

6. This condition includes a group of heritable disorders
characterized by low bone density and skeletal fragility
Skeletal involvement in patients with IJO is the result of
impaired osteoblast activity and mainly affects cancellous bone
Impaired activation of Wnt–β-catenin signaling was
demonstrated in autosomal dominant IJO with heterozygous
mutations in WNT1

7. Symptomatic postmenopausal osteoporosis is an
exaggerated form of the physiological bone depletion that
normally accompanies ageing and loss of gonadal activity.
Two overlapping phases have been recognized:
* early postmenopausal syndrome characterized by rapid bone loss due
predominantly to increased osteoclastic resorption (high-turnover
osteoporosis)
* and a less well-defined syndrome which emerges in elderly people and is due
to a gradual slow-down in osteoblastic activity and the increasing effects of
dietary insufficiencies, chronic ill health and reduced mobility (low-turnover
osteoporosis).
Around the menopause, and for the next 10 years,
bone loss normally accelerates to about 3% per year
compared with 0.3% during the preceding two decades

8.  Caucasoid (white) or Asiatic ethnicity
 Family history of osteoporosis
 History of anorexia nervosa and/or amenorrhoea
 Low peak bone mass in the third decade
 Early onset of menopause
 Unusually slim or emaciated build
 Oophorectomy
 Early hysterectomy
 Nutritional insufficiency
 Chronic lack of exercise
 Cigarette smoking
 Alcohol abuse

9. Back pain
History of previous
colles fracture
Compression
fractures of the
vertebral bodies
Fracture of ankle or
femoral neck
Increased thoracic
kyphosis
• DEXA may show significantly reduced
bone density in the vertebral bodies or
femoral neck.

10. (a) This woman noticed that she was becoming more and more round
shouldered; she also had chronic backache and her x-ray (b) shows obvious
compression fractures of T12 and L1. Six years after this x-ray was obtained,
she fell in her kitchen and sustained the fracture shown in (c).
A B C

11.  Primary osteoporosis in men accounts for about
40% of all cases . Secondary osteoporosis ensues
from several conditions (i.e., hypogonadism,
alcoholism, multiple myeloma,
hyperparathyroidism, malabsorption, and use of
corticosteroids), and is the most common type of
male osteoporosis
 Special consideration should be given to
osteoporosis associated with androgen
deprivation therapy for prostate cancer, a
common disease in men, because such treatment
is accompanied by significant bone loss and an
increased risk of fragility fractures . Therefore,
the exclusion of underlying pathological
conditions in male osteoporosis is mandatory

12. According to the ISCD Positions , bone
densitometry is required to confirm a diagnosis
of osteoporosis in men over 70 years or those
with a history of fragility fractures
BMD measurement using DEXA is justified for
male subjects at any age in the presence of a
risk factor for low bone mass, such as low
body weight, high-risk medication use, or a
disease or condition associated with bone
loss
Treatment is much the same
as for postmenopausal
osteoporosis

13.  In individuals with osteoporosis, a fracture
can be caused by even a minor fall or during
routine activities, such as twisting and
bending. Typically, significant back pain
along the spine is experienced after a fracture
happens.

14. Risk factors for low BMD and fragility/low-energy fractures: levels of
evidence are also shown (level 1: evidence from RCTs or metanalyses of
RCTs; level 2: evidence from prospective cohort studies or poor-quality
RCTs; level 3: evidence from case–control studies or retrospective
cohort studies)
Risk factor For BMD For fracture
BMD 1 1
age 1 1
Fragility fractures after 40 years of age 2 1
Family history of fragility fractures 2 2
Chronic corticosteroid therapy 1 1
Premature menopause (< 45 years) 1 2
Weight 1 2
Reduced calcium intake 1 1
Reduced physical activity 2 2
smoking 2 1
alcohol 2 3
Risk factors for falls - 1

15. BMD The BMD depends on peak bone mass and bone loss related to menopause
and aging, and is influenced by genetic and nutritional factors, life habits,
coexisting diseases, and other pharmacologic therapies
age For both genders, fracture risk is significantly dependent on age, and fracture
risk approximately doubles with each decade. Advancing age contributes to
fracture risk independently of BMD.
Previous
fractures
previous fracture, regardless of location, increases the risk of new fractures
.The risk also depends on the number of previous fractures.
Although a previous fracture is often related to a low BMD, the risk of new
fractures is an independent risk factor.
Family
history
A positive history of osteoporotic fractures is regarded as the most reliable
prognostic indicator of a genetic risk of osteoporotic fractures
Comorbidity Several pathological disorders are associated with an increased fracture risk.
In many of these conditions, the risk is mediated by the reduction in BMD
Medical
treatments
glucocorticoid therapy is the most common cause of secondary osteoporosis,
mostly due to factors independent of BMD
Other drugs, such as adjuvant hormone blocking therapy
Immobility causing a reduction in BMD due to increased bone resorption, is a moderate
risk factor for fragility fractures
Smoking is an independent moderate risk factor for vertebral fractures and peripheral
fractures in both sexes

16.  Decreased bone density can be appreciated by decreased
cortical thickness and loss of bony trabeculae in the early
stages in radiography. Bones like the vertebra, long
bones (proximal femur), calcaneum and tubular bones
are usually looked at for evidence of osteoporosis
 Plain radiograph:
• pencilling of vertebrae
• loss of cortical bone (picture frame vertebra) and trabecular bone (ghost
vertebra)
• compression fractures and vertebra plana
• loss of trabeculae in proximal femur area, which is explained by Singh's
index (and can also be seen in the calcaneum)
• in tubular bones (especially metacarpals), there will be thinning of the
cortex
• cortical thickness <25% of the whole thickness of metacarpal signifies
osteoporosis (normally 25-33%)

22. 1) History :
Assessment of risk factors
2) Physical examination:
assessment of patient posture, which looks for
increased kyphosis of the thoracic spine, a
protruded abdomen, and a loss of body height,
which may be ascribed to the presence of one
or more vertebral deformities

23. 3) Conventional X-ray :
of the thoracic and lumbar spine is useful for
detecting prevalent vertebral fractures
4)BMD:
measurements are important as they can be
used to better estimate the individual fracture
risk, differentiate between mild and severe forms
of bone loss, and select the appropriate
treatment follow-up
5) Laboratory tests:
mandatory to exclude the main forms of
secondary osteoporosis and for mineral
metabolism assessment

24.  conventional X-ray of the thoracic and
lumbar spine for the detection of
osteoporotic vertebral fractures
 dual-energy X-ray absorptiometry (DEXA)
 quantitative computed tomography (QCT) .
 Bone quantitative ultrasonography (QUS)
measures other parameters of the bone (i.e.,
elasticity and stiffness) that appear to be
related to mechanical strength

25.  A morphometric analysis is required in order to quantify
abnormal variations in vertebral shape.
A semiquantitative method (SQ) that measures the
anterior, middle, or posterior heights of the dorsal and
lumbar vertebral bodies in lateral projection via
conventional radiography (MRX) or with DEXA (vertebral
fracture assessment, VFA) is usually employed. If one of
these three heights decreases by more than 20%, the
fracture is morphometrically documented
 Indicated in :
1) Acute back pain that worsens while standing and/or
does not improve for several days in a person at high
risk for a fragility fracture.
1) Unexplained chronic back pain in a patient with a
history of a prevalent fragility fracture
1) A height reduction of more than 4 cm compared to
the maximum height reached by the subject or > 2
cm from the last control

26.  The gold standard for quantitative assessment of
bone mineral status in adults is DEXA, performed
at the lumbar spine (L1–L4) and hip
 It accurately and precisely measures bone
density, which is the best predictor of the risk of
osteoporotic fracture
 The parameters obtained are bone mineral
content (BMC) in grams, area in cm2, and BMD in
g/cm2
 BMD measurements at the lumbar spine, femoral
neck, total hip, and distal third of the radius have
been demonstrated to predict fragility fractures

27. The T-score shows the bone density compared with that of a young
adult (at the age of 35 years) of the same gender. The Z-score is
calculated in the same way, but the comparison is made with someone
of the same age, gender, race, height, and weight.

30. Biochemical testing in osteoporosis and associated diagnoses
Blood count Inflammatory disease or malignancy
Serum protein electrophoresis and
free kappa and lambda light chains
Multiple myeloma
ESR ↑ Differential diagnosis of inflammatory
causes of vertebral deformities
Serum calcium ↑ Primary hyperparathyroidism or other
causes of hypercalcemia
↓ e.g., secondary hyperparathyroidism,
malabsorption
Serum phosphorus ↑ Renal insufficiency grade IV
↑ Secondary renal hyperparathyroidism
↓ Malabsorption
Alkaline phosphatase ↑ Osteomalacia, Paget’s disease
Serum PTH ↑ Hyperparathyroidism
Serum creatinine Renal osteodystrophy
25-Hydroxyvitamin D3 ↑ Vitamin D intoxication
↓ Vitamin D deficiency, osteomalacia

31. Urine calcium/24 h ↓ Intestinal malabsorption
↑ Urinary stones
TSH < 0.3 mU/L endogenous or caused
by l-thyroxine medication as a risk
factor for fractures
Testosterone in men hypogonadism
Anti-tissue transglutaminase
antibodies
Celiac disease
Urinary free cortisol ↑ Adrenal hypersecretion
Bone marrow aspiration and biopsy
and undecalcified iliac crest bone
biopsy with double tetracycline
labeling
Renal failure, vitamin D-resistant
osteomalacia, mastocytosis, and
rare metabolic bone diseases
Bone resorption parameters High bone turnover as a fracture
risk

33. 1) Lifestyle and dietary measures
 A daily calcium intake of between 700 and 1200 mg should be
advised, if possible achieved through dietary intake, with use of
supplements if necessary.
 In postmenopausal women and older men (≥50 years) at increased
risk of fracture a daily dose of 800 IU cholecalciferol should be
advised.
 In postmenopausal women and older men receiving bone-protective
therapy for osteoporosis, calcium supplementation should be given if
the dietary intake is below 700 mg/day, and vitamin D
supplementation considered in those at risk of or with evidence of
vitamin D insufficiency.
 Regular weight-bearing exercise should be advised, tailored
according to the needs and abilities of the individual patient.
 Falls history should be obtained in individuals at increased risk of
fracture and further assessment and appropriate measures
undertaken in those at risk

34. 2) Pharmacological intervention
Ten year fracture probability with DEX widely available
Ten year fracture probability with limited DEXA availability

35. …Intervention thresholds for pharmacological
intervention
 The thresholds recommended for decision making
are based on probabilities of major osteoporotic and
hip fracture derived from FRAX and can be similarly
applied to men and women.
 Women with a prior fragility fracture can be
considered for treatment without the need for further
assessment, although BMD measurement may be
appropriate, particularly in younger postmenopausal
women.
 Age-dependent intervention thresholds up to 70
years and fixed thresholds thereafter provide
clinically appropriate and equitable access to
treatment.

36. In postmenopausal women:
 Alendronate or risedronate are first line treatments in
the majority of cases. In women who are intolerant of
oral bisphosphonates or in whom they are
contraindicated, intravenous bisphosphonates or
denosumab provide the most appropriate alternatives,
with raloxifene or hormone replacement therapy as
additional options. The high cost of teriparatide restricts
its use to those at very high risk, particularly for
vertebral fractures.
 Treatment review should be performed after 3 years of
zoledronic acid therapy and 5 years of oral
bisphosphonate treatment. Continuation of
bisphosphonate treatment beyond 3–5 years can
generally be recommended in individuals age ≥75 years,
those with a history of hip or vertebral fracture, those
who sustain a fracture while on treatment, and those
taking oral glucocorticoids.

37.  If treatment is discontinued, fracture risk
should be reassessed after a new fracture,
regardless of when this occurs. If no new
fracture occurs, assessment of fracture risk
should be performed again after 18 months
to 3 years.
 There is no evidence to guide decisions
beyond 10 years of treatment and
management options in such patients should
be considered on an individual basis.

38.  Alendronate and risedronate are first-line
treatments in men. Where these are
contraindicated or not tolerated, zoledronic acid
or denosumab provide the most appropriate
alternatives, with teriparatide as an additional
option.
 For estimation of fracture probability, femoral
neck BMD T-scores in men should be based on
the NHANES female reference database. When
using the online version of FRAX for the
estimation of fracture probability, femoral neck
BMD values (g/cm2) should be entered and the
manufacturer of the densitometer specified.

41. …Osteoid throughout the skeleton is incompletely
calcified, and the bone is therefore ‘softened’
(osteomalacia).
In children there are additional effects on physeal
growth and ossification, resulting in deformities of
the endochondral skeleton (rickets).
The inadequacy may be due to defects anywhere
along the metabolic pathway for vitamin D:
nutritional lack, under-exposure to sunlight,
intestinal malabsorption, decreased 25-
hydroxylation (liver disease, anticonvulsants) and
reduced 1α-hydroxylation (renal disease,
nephrectomy, 1α-hydroxylase deficiency). The
pathological changes may also be caused by
calcium deficiency or hypophosphataemia.

42. In rickets the characteristic pathological changes
arise from the inability to calcify the intercellular
matrix in the deeper layers of the physis
The proliferative zone is as active as ever, but the
cells pile up irregularly and the entire physeal
plate increases in thickness
The zone of calcification is poorly mineralized and
bone formation is sparse in the zone of
ossification
New trabeculae are thin and weak, and with joint
loading the metaphysis becomes broad and cup
shaped.

43. Thin trabeculae lined by unusually wide uncalcified
osteoid
in severe cases the cortices also are thinner than
normal and may show signs of new or older stress
fractures
If the condition has been present for long, there may
be widespread stress deformities of the bones

44.  Vitamin D deficiency rickets, once common in
Northern Europe due to a combination of
dietary lack and under-exposure to sunlight,
is now seldom seen in its classic form. Infants
may present with tetany or convulsions.
There is failure to thrive, listlessness and
muscular flaccidity

45. Early bone changes are:
 deformity of the skull (craniotabes)
 thickening of the knees, ankles and wrists
from physeal over-growth.
 Enlargement of the costochondral junctions
(‘rickety rosary’) and lateral indentation of the
chest (Harrison’s sulcus) may also appear.
 Distal tibial bowing has been attributed to
sitting or lying cross-legged.

47.  In active rickets there is thickening and
widening of the physes, distortion of the
metaphyses and, sometimes, bowing of the
long bones. These changes often leave traces
after healing.
Before
After ttt

48. • Serum calcium and phosphate concentrations as
well as 25-HCC levels are diminished and
alkaline phosphatase is increased. Urinary
calcium excretion is diminished
Investigations
• The condition responds rapidly to vitamin D
administration in the form of calciferol 400–
1000 IU per day with calcium supplements.
After normal growth, residual deformities are
usually slight.
Treatment

49.  Osteomalacia may result from defects
anywhere along the metabolic pathway for
vitamin D:nutritional lack, under-exposure to
sunlight, intestinal malabsorption or defective
conversion to the active metabolites in the
liver or kidney.

50.  Clinical features:
Symptoms usually appear insidiously;
• bone pain, backache and muscle weakness
may be present for years before the diagnosis
is made.
• Unexplained pain in the hip or one of the
long bones may presage a stress fracture.
• Often the condition is suspected only when
the patient is admitted to hospital with a
vertebral compression fracture or an
‘insufficiency fracture’ of the femur or tibia.

51.  Suspicious features are generalized
rarefaction of bone and signs of previous
fractures of the vertebrae, ribs, pubic rami or
long bones. Almost pathognomonic is a
poorly healing stress fracture which appears
as a thin transverse band of rarefaction in the
cortex – a so-called Looser zone. There may
also be signs of secondary
hyperparathyroidism

52. (a indentation of the
acetabula producing
the trefoil or champagne
glass pelvis;
(b) Looser’s zones
(arrows) in the pubic rami
and left femoral neck
a
b

53. (c) biconcave
vertebrae; and
(d) fracture in the
mid-diaphysis of a
long bone
following low-
energy trauma (the
femoral cortices in
this case are egg-
shell thin).
c d

54. investigations
•As in rickets, serum calcium and phosphate concentrations may be
diminished and alkaline phosphatase raised. More significant are diminished
•values for 25-HCC and 1,25-DHCC. Biochemical changes are often
insignificant and biopsy may be needed for diagnosis; excessive amounts of
unmineralized osteoid can be demonstrated. Having made the diagnosis, it is
still necessary to establish the cause. Patients should be investigated for
malabsorption syndromes, liver disorders and renal disease
Treatment
•Treatment with vitamin D and calcium supplements is usually effective;
elderly people may need very large doses (up to 2000 IU per day).
•Underlying disorders of the gut, liver or kidney will need treatment as well.

55. * National institutes of health website :
1) Clinical guidelines for the prevention and treatment of
osteoporosis: summary statements and recommendations from the
Italian Society for Orthopaedics and Traumatology Published online
2017 Oct 20
2) UK clinical guideline for the prevention and treatment of
osteoporosis Published online 2017 Apr 19
* Apley concise 4th edition