osteoporosis i will talk about : definition &epidemiology& risk factor&psychopathology &classification & diagnosis&treatment &complication & prevention.

1. Osteoporosis
BY: Nader Amer al-
assadi
Student at Taiz university

2. Outlines
1- Definition
2- Epidemiology
3- Risk factor
4-Pathophysiology
5-Classification
6- Osteoporosis Clinical Presentation.
7-Diagnosis
8-Treatment
9-Comblication
10-Prevention

3. what is Osteoporosis?
is a chronic, progressive disease of multifactorial etiology and it is
the most common bone Metabolic disease in humans.
Characterized by:
◦ Low bone mass
◦ Microarchitectural deterioration
◦ Compromised bone strength
◦ Increased risk for fracture
◦ “Silent disease” until complicated by fractures

4. Epidemiology
incidence
Globally, osteoporosis is by far the most common metabolic bone disease, estimated to
affect over 200 million people worldwide.
1.5 million osteoporotic fractures occur each year:
700,000 are vertebral fractures
300,000 are hip fractures
200,000 are wrist fracture
demographics
-The risk for osteoporosis increases with age as BMD declines. Senile osteoporosis is most
common in persons aged 70 years or older.
-Secondary osteoporosis, however, can occur in persons of any age.
-male: female ratio is 1:4 postmenopausal woman
-Men have a higher prevalence of secondary osteoporosis, with an estimated 45-60% of cases
being a consequence of hypogonadism, alcoholism, or glucocorticoid excess.
-Osteoporosis can occur in persons of all races and ethnicities. In general, however, whites
(especially of northern European descent) and Asians are at increased risk .

5. (NOF) has
categorized the risk factors into two
categories: nonmodifiable and
modifiable:
Nonmodifiable risk factors include the following:
- Personal history of fracture as an adult
- History of fracture in a first-degree relative
- White race
- Advanced age
- Female sex
- Dementia
- Poor health or fragility
16 September 2021

6. Cont…
Potentially modifiable risk factors include the following:
- Current cigarette smoking
- Low body weight (< 127 lb)
- Estrogen deficiency such as that caused by early menopause (age <
45 years) or - - bilateral ovariectomy and prolonged premenopausal
amenorrhea (>1 year)
- Low lifelong calcium intake
- Alcoholism
- Impaired eyesight despite adequate correction
- Recurrent falls
- Inadequate physical activity
- Poor health or frailty
16 September 2021

7. Risk Factors
Major
History of fracture as an adult
Fragility fracture in first degree
relative
Caucasian/Asian
postmenopausal woman
Low body weight
Current smoking
Use of oral corticosteroids >
3mo.
Additional
Estrogen deficiency at early age
(< 45 YO)
Poor health/frailty
Recent falls
Low calcium intake (lifelong)
Low physical activity
> 2 alcoholic drinks per day

8. Medical Conditions Associated with Increased
Risk of Osteoporosis
COPD
Cushing’s syndrome
Eating disorders
Hyperparathyroidism
Hypophosphatasia
IBS
RA, other autoimmune
connective tissue disorders
Insulin dependent diabetes
Multiple sclerosis
Multiple myeloma
Stroke (CVA)
Thyrotoxicosis
Vitamin D deficiency
Liver diseases
Not an inclusive list

9. Drugs Associated with
Reduced Bone Mass
Aluminum
Anticonvulsants
Cytotoxic drugs
Glucocorticosteroids
(oral/high dose inhaled)
Immunosuppresants
Gonadotropin-releasing
hormone (e.g. Lupron)
Lithium
Heparin (chronic use)
Supraphysiologic thyroxine
doses
Aromatase inhibitors
Depo-Provera
Not an inclusive list

10. A potentially useful mnemonic for osteoporotic risk factors
is OSTEOPOROSIS, as follows:
LOw calcium intake
Seizure meds (anticonvulsants)
Thin build
Ethanol intake
HypOgonadism
Previous fracture
ThyrOid excess
Race(white, Asian)
Other relatives with osteoporosis
Steroids
Inactivity
Smoking

12. Pathophysiology
It is increasingly being recognized that
multiple pathogenetic mechanisms interact in
the development of the osteoporotic state.
Understanding the pathogenesis of
osteoporosis starts with knowing how bone
formation and remodeling occur.

13. remodeling
Bone undergoes both radial and longitudinal growth and is continually
remodeled throughout our lives in response to microtrauma. Bone remodeling
renews bone strength and mineral, preventing the accumulation of damaged
bone.
Bone remodeling occurs at discrete sites within the skeleton and proceeds in
an orderly fashion, and bone resorption is always followed by bone formation,
a phenomenon referred to as coupling.

16. Alterations in bone formation and resorption
Osteoporosis is multifactorial with an interplay of genetic, intrinsic,
exogenous, and lifestyle factors.The hallmark of osteoporosis is a
reduction in skeletal mass caused by an imbalance between bone
resorption and bone formation.

17. Estrogen deficiency leads to increased expression of RANKL by osteoblasts and decreased
release of OPG increased RANKL results in recruitment of higher numbers of
preosteoclasts as well as increased activity, vigor, and lifespan of mature osteoclasts.
Alterations in bone formation and resorption
Estrogen deficiency

19. Calcium and vitamin D deficiency
Calcium, vitamin D, and PTH help maintain bone homeostasis.
Insufficient dietary calcium or impaired intestinal absorption of calcium
due to aging or disease can lead to secondary hyperparathyroidism.
PTH is secreted in response to low serum calcium levels. It increases
calcium resorption from bone decreases renal calcium excretion, and
increases renal production of 1,25-dihydroxyvitamin D (1,25[OH]2 D)—
an active hormonal form of vitamin D that optimizes calcium and
phosphorus absorption, inhibits PTH synthesis, and plays a minor role
in bone resorption.

20. Classification of osteoporosis:
Primary osteoporosis
Secondary osteoporosis

21. Type of Primary Osteoporosis Characteristics
Juvenile osteoporosis
Usually occurs in children or young
adults of both sexes
Normal gonadal function
Age of onset: usually 8-14 years
Hallmark characteristic: abrupt bone
pain and/or a fracture following trauma.
Idiopathic osteoporosis
Postmenopausal osteoporosis
(type I osteoporosis)
Occurs in women with estrogen
deficiency
Characterized by a phase of accelerated
bone loss, primarily from trabecular
bone Fractures of the distal forearm and
vertebral bodies common.
Age-associated or senile
osteoporosis (type II osteoporosis)
Occurs in women and men as BMD
gradually declines with aging
Represents bone loss associated with
aging Fractures occur in cortical and
trabecular bone Wrist, vertebral, and hip
fractures often seen
primary osteoporosis

22. Secondary osteoporosis
Secondary osteoporosis occurs when an underlying disease, deficiency, or drug
causes osteoporosis
Cause Examples
Genetic/congenital
Renal hypercalciuria – one of the most important secondary causes
of osteoporosis; can be treated with thiazide diuretics
Cystic fibrosis
Ehlers-Danlos syndrome
Glycogen storage disease
Gaucher disease
Marfan syndrome
Menkes steely hair syndrome
Riley-Day syndrome
Osteogenesis imperfecta
Hemochromatosis
Homocystinuria
Idiopathic hypercalciuria
Hypogonadal states
Hypogonadal
states
Androgen insensitivity
Anorexia nervosa/bulimia nervosa
Female athlete triad
Hyperprolactinemia
Panhypopituitarism
Premature menopause
Turner syndrome
Klinefelter syndrom

23. endocrine
disorders
Cushing syndrome
Diabetes mellitus
Acromegaly
Adrenal insufficiency
Estrogen deficiency
Growth hormone deficiency
Hypercortisolism
Hyperparathyroidism
Hyperthyroidism
Hypogonadism
Hypophosphatasia
Pregnancy
Porphyria
Prolactinoma
Deficiency states
and malabsorption
syndromes
Alcoholism
Anorexia nervosa
Calcium deficiency
Magnesium deficiency
Protein deficiency
Vitamin D deficiency [56, 57]
Bariatric surgery
Celiac disease
Cystic fibrosis
Gastrectomy
Malnutrition
Parenteral nutrition
Chronic liver disease

24. Inflammatory
diseases
Inflammatory bowel disease/Crohn disease
Ankylosing spondylitis
Rheumatoid arthritis
Systemic lupus erythematosus
Hematologic and
neoplastic
disorders
Hemochromatosis
Hemophilia
Leukemia
Lymphoma
Multiple myeloma
Sickle cell anemia
Systemic mastocytosis
Thalassemia
Metastatic disease
Medications
Anticonvulsants
Antipsychotic drugs
Antiretroviral drugs
Aromatase inhibitors
Chemotherapeutic/transplant drugs: cyclosporine, tacrolimus,
platinum compounds, cyclophosphamide, ifosfamide, high-dose
methotrexate [58]
Furosemide
Glucocorticoids and corticotropin [59] : prednisone (≥5 mg/day for ≥3
mo) [60]
Heparin (long term)
Hormonal/endocrine therapies: gonadotropin-releasing hormone
(GnRH) agonists, luteinizing hormone-releasing hormone (

25. Osteoporosis Clinical Presentation
History:
Keep in mind that osteoporosis occurs in many people who have few or no risk factors for this
condition. Often, patients who have not sustained a fracture do not report symptoms that
would alert the clinician to suspect a diagnosis of osteoporosis; thus, this disease is a "silent
thief" that generally does not become clinically apparent until a fracture occurs.
So the history should focus in:
- Age (> 50 years), sex (female), and race (white or Asian)
- Family history of osteoporosis, particularly maternal history of fractures.
- Reproductive factors, especially regarding early menopause and estrogen replacement
therapy.
- ypogonadal states: men with hypogonadism secondary to any genetic or other conditions
are at higher risk.
16 September 2021

26. Cont…
- Smoking: smokers are at higher risk
- Alcohol consumption
- Low levels of physical activity: immobility increases the risk [65] ; spinal
cord injury and stroke cause physical impairment and are common causes
of immobility.
- Strenuous exercise that results in amenorrhea (such as that which occurs
in marathon runners)
- Calcium and vitamin D intake
- History of low-trauma "fragility" fracture in patients aged 40 years or
older.
-Coexisting medical conditions associated with bone
loss:hyperparathyroidism, hypogonadism, leukemia, rheumatoid arthritis,
celiac disease, and Cushing syndrome.
- Medications associated with bone loss: examples are glucocorticoids,
cyclosporine,anticonvulsant.
16 September 2021 by nader al_ assadi

27. Physical Examination
Patients with suspected osteoporosis should undergo a
comprehensive physical examination.
•The physical examination should begin with an inspection of the patient. Height
measurement with a stadiometer at each visit may be useful.
• Examination of active and passive range of motion (ROM) assists in determining
whether spine, hip, wrist, or other osseous pathology may be present.
•Athorough neurologic examination is essential to rule out spinal cord and/or
peripheral nerve compromise.
•Sign of fracture (eg:Patients with vertebral compression fractures may have point
tenderness over the involved vertebrae and demonstrate a thoracic kyphosis with
an exaggerated cervical lordosis.
•signs of collagen defects : Patients with osteoporosis may have physical findings
consistent with subtle collagen defects. These include a short fifth digit,
hyperlaxity, hearing loss.
•Balance difficulties :Patients with osteoporosis are known to have decreased
balance, possibly secondary to differences in balance control strategies and sway
amplitude. Patients may have difficulty performing tandem gait and performing
single limb stance. Poor balance may be noted particularly in patients with severe
kyphosis resulting from vertebral compression fractures because their altered
center of gravity makes ambulation with a stable base of support difficult for them.

29. Diagnosis
lap
25 hydroxyvitamin D level
- low 25 hydroxy cholecalciferol levels (25 hydroxy vit D) in patients sustaining low energy.
IMAGE
Radiographs
indications
• suspicion of fracture
• loss of height
• pain in thoracic or lumbar spine
• recommended views
• lateral spine radiograph
• AP pelvis or hip
• findings
• thinned cortices
• loss of trabecular bone
• kyphosis
• codfish vertebra

30. codfish vertebra

31. Radiographic findings can suggest the presence of osteopenia, or bone loss, but
cannot be used to diagnose osteoporosis. Osteopenia is suggested by a cortical width
that is less than the medullary width. Radiographs may also show fractures.
Plain radiography is not as accurate as BMD testing. Because osteoporosis
predominantly affects trabecular bone rather than cortical bone, radiography does
not reveal osteoporotic changes until they affect the cortical bone. Cortical bone is
not affected by osteoporosis until more than 30% of bone loss has occurred.
Approximately 30-80% of bone mineral must be lost before radiographic lucency
becomes apparent on radiographs. Thus, plain radiography is an insensitive tool for
diagnosing osteoporosis.
1-Plain x ray

35. 2dual-energy x-ray absorptiometry (DXA

36. dual-energy x-ray absorptiometry (DXA

38. The 2020 update of the American Association of Clinical
Endocrinologists (AACE) guidelines provides the following
criteria for the diagnosis of osteoporosis in postmenopausal
women :
1- T-score -2.5 or below in the lumbar spine,
femoral neck, total proximal femur, or 1/3 radius.
2- Low-trauma spine or hip fracture (regardless of
BMD)
3- T-score between -1.0 and -2.5 and a fragility
fracture of proximal humerus, pelvis, or distal
forearm.
4- T-score between -1.0 and -2.5and high
FRAX(Fracture Risk Assessment Tool )

39. Quantitative Computed
Tomography
QCT scanning of the spine is the most sensitive method for
diagnosing osteoporosis, because it measures trabecular
bone within the vertebral bon.
1- QCT is a very sensitive technique when repeated
measurements are needed to detect small changes in
BMD,
2- modern three-dimensional (3D) QCT acquisition has a
scan time less than 10 seconds for the lumbar spine or
proximal femur.
3- and there is no interference by osteophytes.

40. Single-photon emission computed
tomography (SPECT)
represents a tomographic (CT-like) bone imaging
technique that offer:
1- better image contrast
2- more accurate lesion localization than planar bone
scanning.
3- PECT scanning is helpful when accurate localization of
skeletal lesions within large and/or anatomically complex
bony structures is required.(no bone overlap)

41. Quantitative Ultrasonography
Quantitative ultrasonography (QUS) of the calcaneus is a low-cost
portable screening tool. It has the advantage of not involving
radiation, but it is not as accurate as other imaging methods.
Ultrasonography cannot be used for monitoring skeletal changes over
time, nor can it be used to monitor the response to treatment,
because of its lack of precision.

42. Magnetic Resonance Imaging
These osteoporotic fractures demonstrate characteristic changes in
the bone marrow that distinguish them from other uninvolved parts of
the skeleton and the adjacent vertebra.

43. Bone Scanning
one scans assesses the function and tissue metabolism of organs by
using a radionuclide (technetium-99m [99m Tc]) that emits radiation in
proportion to its attachment to a target structure.
This technique detects an increase in osteoblastic activity (as seen in
compression fractures.

44. Bone Biopsy and Histologic Features.
Bone biopsy can help to exclude underlying pathologic conditions,
such as mastocytosis, that may be responsible for presumed
osteoporotic fracture. Typically, iliac crest biopsy is performed either
in the minor procedure suite or in the operating room.
Histologic examination of osteoporotic bone may reveal generalized
thinning of trabeculae and irregular perforation of trabeculae,
reflecting unbalanced osteoclast-mediated bone resorption.

45. Non operative treatment
lifestyle modification & vitamins
pharmacologic treatment
Treatment

46. Regular Weight-Bearing Exercise
Defined as those in which bones and muscles work
against gravity as feet and legs bear the body’s weight
-Include walking, stair climbing, dancing, tennis, yoga.
-Improve agility, strength, balance.
-May increase bone density modestly, reduce fall risk,
enhance muscle strength, improve balance.

47. Avoidance of Tobacco and Alcohol
Tobacco products detrimental to skeleton, overall health
.NOF National Osteoporosis Foundation (strongly
encourages tobacco cessation programs as osteoporosis
intervention) .

49. Avoidance of Tobacco and Alcohol
Excessive alcohol
intake also
detrimental to
bone health and
requires
treatment.

50. Adequate Intake of Calcium/Vitamin D
Adequate intakes of dietary calcium and vitamin D,
including supplements if necessary
◦ Elemental calcium per day at least 1200 -1500 mg.
◦ Vitamin D3 per day 800 -1000 international units (IU).
Vitamin D3 (cholecalciferol) plays major role in Ca
absorption Controlled clinical trials have demonstrated
the combination reduces fracture risk Inexpensive, well-
tolerated.

51. Calcium/D Product Selection
Product (% elemental
Ca)
Elemental
Calcium
(mg)
Vitamin
D (units)
Comments
Calcium carbonate
(40)
-Tums Ultra
-Caltrate 600 Plus
-Oscal Plus D
-Viactiv Chews
400
600
500
500
200
125
100
Requires acidic environment for dissolution and
disintegration. Best to take with meals.
Greater risk for constipation with carbonate
form.
Calcium citrate (24)
-Citracal Plus D
- Citracal Petites with
VitD
315
200
200
200
Take without regard to meals. Serving size
usually equals 2 capsules so label can be
misleading to patients.
Vitamin D
-Multivitamin (D3)
-Vitamin D
120-450 400
100-400

52. Vitamin D and Fall Risk
In addition to its effect on BMD, may contribute to reduction in fracture risk
◦ Improved muscle function(o+R+c)
◦ Reduction in risk for falls
Vitamin D deficiency prevalent in older adult population
◦ Inadequate sun exposure, use of sunscreen
◦ Homebound, institutionalized
◦ Maintain 25-hydroxyvitamin D3 at least > 40 ng/mL
◦ Treatment: 50,000 IU vitD weekly x 6-8 weeks, then assess need for chronic
monthly therapy

53. Pharmacological treatment

54. Who Should Be Treated?
NOF Recommendations – 2008
Initiate therapy to reduce fractures in
postmenopausal women/men > 50 with:
1. BMD T-scores < -2.5 at hip or spine
2. Prior vertebral or hip fracture
3. Low bone mass (T-scores -1.0 to -2.5 at hip or spine) when:
– 10-year probability of hip fracture is > 3%
– 10-year probability of major osteoporosis-related fracture is > 20%
– Based on US-adapted WHO algorithm
www.nof.org

55. FDA-Approved Drugs for Osteoporosis
Bisphosphonates
◦ Alendronate, Alendronate plus
D (Fosamax®
, Fosamax Plus D®
)
◦ Risedronate, Risedronate with
Calcium (Actonel®
)
◦ Ibandronate (Boniva®
)
Selective Estrogen Receptor
Modulators (SERMs)
◦ Raloxifene (Evista®
)
Calcitonin (Miacalcin®
,
Fortical®
, Calcimar®
)
Parathyroid Hormone [PTH
(1-34), teriparatide]
◦ Forteo®
Estrogen/Hormone Therapy
(ET/HT)
◦ Premarin®
, Estrace®
, Prempro®

56. Bisphosphonates – Antiresorptive Agents
Agents FDA-approved for:
◦ Prevention and treatment of osteoporosis in postmenopausal women
◦ Treatment to increase bone mass in men with osteoporosis
◦ Treatment of glucocorticoid-induced osteoporosis in men and women
receiving glucocorticoids
◦ Treatment of Paget’s disease of bone in men and women
Mechanism: inhibits bone resorption by attaching to bony surfaces
undergoing active resorption and inhibiting action of osteoclasts
◦ Leads to increases in bone density and reduced fracture risk

57. Bisphosphonates
Very well tolerated in patients who adhere to proper
administration techniques
Proper patient counseling for correct administration is
KEY to reduce risk of adverse effects and increase
tolerability
Place in Therapy: should be considered first-line for
prevention/treatment of osteoporosis in patients with
no contraindications.

58. Bisphosphonates – Clinical
Efficacy
Controlled clinical trials indicate over 3-4 year period, alendronate ↑ bone mass
and ↓ incidence of vertebral, hip, and all non-vertebral fractures by 50%
Controlled clinical trials indicate risedronate ↑ bone mass and ↓ risk of
vertebral fractures by 40% and non-vertebral fractures by 30% over 3-year
period
Ibandronate has been shown in controlled clinical trials to ↑ BMD and reduce
the risk of vertebral fracture by 50% over 3-year period
Alendronate appears to be well tolerated and effective for at least ten years

59. Zolendronic Acid (Reclast®)
Approved for treatment of osteoporosis in postmenopausal
women in August 2007
Single 5 mg infusion given IV over > 15 minutes, once yearly
Should still supplement with calcium/vitamin D
May be ideal for those with GI contraindications to the oral
formulations.

60. SERMs – Raloxifene
FDA-approved for:
◦ Prevention and treatment of osteoporosis in postmenopausal women
Mechanism: tissue-selective activity, acts as an estrogen agonist on bone
◦ Estrogen antagonist on breast, uterus.

61. Raloxifene
Place in Therapy: considered first-line in women who
cannot tolerate bisphosphonates and have no
contraindications to therapy.
Combination therapy (usually a bisphosphonate with a
non-bisphosphonate) can provide additional small
increases in BMD when compared to monotherapy.
Impact of combination therapy on fracture rate unknown

62. Estrogen/Hormone Therapy
(ET/HT)
FDA approved for:
◦ Prevent osteoporosis
◦ Treatment of moderate/severe vasomotor symptoms of
menopause
◦ Treatment of moderate/severe symptoms of vulvar and vaginal
atrophy associated with menopause
◦ Consider topical preparations to treat vaginal symptoms rather
than oral ET/HT

63. FDA Recommendations –
ET/HT
When prescribing medications for osteoporosis,
physicians should consider all non-estrogen therapies
first.
When prescribing ET/HT, use smallest dose for shortest
amount of time to achieve treatment goals.
Prescribe ET/HT products only when benefits believed to
outweigh risks for a specific patient.

64. Calcitonin
FDA-approved for:
◦ Treatment of osteoporosis in women who are > 5 years
postmenopausal
◦ Treatment of Paget’s disease of bone.
◦ Adjunctive therapy for hypercalcemia.
Mechanism:
◦ Peptide composed of 32 amino acids which binds to
osteoclasts and inhibits bone resorption .
◦ Promotes the renal excretion of calcium, phosphate, sodium,
magnesium and potassium by decreasing tubular reabsorption.

65. Calcitonin – Clinical Efficacy
Has been shown to increase spinal bone mass and may
decrease risk of vertebral fracture .
Conflicting data on efficacy of calcitonin at sites other
than the spine.
Less effective than bisphosphonates in treatment of
osteoporosis.
Beneficial, short-term effect on acute bone pain after
osteoporotic fracture (vertebral).

66. Calcitonin
Valid option for treatment of established osteoporosis,
especially when accompanied by fracture pain
Place in therapy: because of cost, adverse effects,
inconvenience of nasal administration, recommend using
calcitonin until pain is no longer a problem and then
switching to a bisphosphonate for long-term therapy

67. Parathyroid Hormone [PTH (1-34)]
Anabolic agent
FDA-approved for:
◦ Treatment of osteoporosis in postmenopausal women at high risk for
fracture
◦ previous osteoporotic fracture, multiple risk factors for fracture, extremely low
BMD (< -2.5), or failed/intolerant to previous treatment
◦ Treatment of primary or hypogonadal osteoporosis in men at high risk of
fracture
Mechanism: recombinant formulation of endogenous
parathyroid hormone (PTH)
◦ stimulates osteoblast function, increases gastrointestinal calcium
absorption, increases renal tubular reabsorption of calcium
◦ Enhances bone turnover by initiating greater bone formation

68. Guidelines from the American Association of Clinical Endocrinologists
(AACE), updated in 2020, include the following recommendations for
choosing drugs to treat osteoporosis in postmenopausal women :
- First-line agents for most high fracture risk patients: alendronate,
risedronate, zoledronate,Denosumab.
- First-line agents for high fracture risk patients unable to use oral
therapy: abaloparatide, denosumab, romosozumab, teriparatide, and
zoledronate.
- First-line agents for spine-specific indications in select patients:
ibandronate and raloxifene
- Sequential agents: anabolic agents (eg, abaloparatide,
romosozumab, teriparatide) should be followed with a bisphosphonate
or denosumab.
Combination therapy with two or more agents has not been shown to
have a greater effect on fracture reduction than single therapy .

69. Approaches to Monitoring Therapy
Always important to ask patients about adherence, encourage
continuation of therapies to reduce fracture risk
Monitoring of therapy should be considered, as up to 1/6 of
women taking effective therapies continue to lose bone, especially
if they smoke
May measure bone mineral density at a single site after one year
of therapy, but results may be misleading; usually done every 2
years
Drugs may decrease a patient’s risk for fracture even when there is
no apparent increase in BMD.

70. Complication of osteoporosis
1-vertebral compression fractures often occur with minimal stress, such as
coughing, lifting, or bending.
2- Hip fractures are the most devastating and occur most commonly at the
femoral neck and intertrochanteric regions . Hip fractures are associated with
falls. The likelihood of sustaining a hip fracture during a fall is related to the
direction of the fall. Fractures are more likely to occur in falls to the side
because less subcutaneous tissue is available to dissipate the impact.
3-Fractures can cause further complications, including chronic pain from
vertebral compression fractures and increased morbidity and mortality
secondary to vertebral compression fractures and hip fracture. They are also at
risk for the complications associated with immobility, including deep vein
thrombosis (DVT) and pressure ulcers. Respiratory compromise can occur in
patients with multiple vertebral fractures that result in severe kyphosis.
4- patients with osteoporosis develop spinal deformities and a dowager's
hump, and they may lose 1-2 inches of height by their seventh decade of life.
These patients can lose their self-esteem and are at increased risk for
depression.

72. Prevention of Osteoporosis
primary prevention of osteoporosis starts in childhood. Patients require adequate
calcium intake, vitamin D intake, and weight-bearing exercis .
beyond this, prevention of osteoporosis has two:
behavior
modification
pharmacologi
c
interventions

73. behavior modification
Patients should be counseled on :
1- smoking cessation
2- moderation(stop) of alcohol intake.
3- Regular weight-bearing exercise and back extensor strengthening
help delay bone loss.
4- sunbath 15 minute

74. pharmacologic interventions
1- calcium supplementation and
2-administration of raloxifene or
3-bisphosphonates (alendronate or risedronate).
*Bisphosphonates should be considered as first-line agents for the
prevention of osteoporosis.

76. References
1) American Association of Clinical Endocrinologists medical guidelines
for clinical practice for the prevention and treatment of
postmenopausal osteoporosis: 2020 update. Endocr Pract.
May2020; 26(Suppl 1):1-46. (2) Kelman A, Lane NE. The management of
secondary osteoporosis. Best Pract Res Clin
Rheumatol. Dec 2005;19(6):1021-37.
MEDSCape Author: Rachel Elizabeth Whitaker Elam, MD, MSc; Chief
Editor: Herbert S Diamond, MD

77. References
Actonel®
Prescribing Information (www.actonel.com)
Ann Intern Med 1990;112:352
Ann Intern Med 2006;144:753
Boniva®
Prescribing Information (www.boniva.com)
Clinical Reviews in Bone and Mineral Metabolism 2004;2(4):291
Evista®
Prescribing Information (www.evista.com)
Forteo®
Prescribing Information (www.forteo.com)
Fortical®
Prescribing Information (www.fortical.com)
Fosamax®
Prescribing Information (www.fosamax.com)

78. References
JAMA 2004;291(16):1999
J Clin Densitom 2004;7(1):1-6
J Am Acad Orthop Surg 2006;14:347
Miacalcin®
Prescribing Information (www.miacalcin.com)
Reclast®
Prescribing Information (www.reclast.com)
National Osteoporosis Foundation (http://www.nof.org)
NEJM 2003;348:1187
NEJM 2004;350(12):1189-99
Osteoporosis Int 1998;8:1

79. THANK
YOU