Osteoporosis a musculoskeletal disorder which bones deteriorate or become brittle and fragile due to low bone mass as a result of bone
tissue loss.

 Osteoporosis occurs as a result of an imbalance between bone resorption and bone formation. Major contributing factors in the development of osteoporosis include estrogen deficiency and aging.

Classification of Osteoporosis

On the basis of etiology, osteoporosis can be classified into:

Primary Osteoporosis

Primary osteoporosis develops as a result of aging or menopause-related bone demineralization. In patients with primary osteoporosis, the bone density decreases as the age progresses. It is not merely a consequence of aging but of failure to develop optimal peak bone mass during childhood, adolescence, and young adulthood.

Secondary Osteoporosis

Secondary osteoporosis results from more severe loss of bone mass due to pathologies associated with immobilization, medications (iatrogenic), endocrine dysfunction, cancer, and chronic kidney disease.

Causes of Osteoporosis

Osteoporosis may be caused by conditions that can lead to the disturbed balance between bone formation and bone resorption.

Common causes of osteoporosis include

  •  Aging: Osteoporosis occurs at an older age, as it is believed that testosterone and estrogen are important in achieving and maintaining bone mass, so risk for osteoporosis increases with increasing age.
  • Menopause
  • Nutritional: A low calcium intake, low vitamin D intake, high phosphate intake, and inadequate calories reduce nutrients needed for bone remodeling. deficiency of calcium and vitamin D
  • Chronic renal failure
  • Immobility
  •  Hyperparathyroidism
  • Medications. Such as intake of corticosteroidsanti seizure medicationsheparin, and thyroid hormone affects calcium absorption and metabolism.
  • Chronic glucocorticoid abuse.

Common risk factors

  • Age > 50
  • Menopause (lack of estrogen)
  • Family history of fracture or osteoporosis
  • History of at least two fractures
  • Alcohol consumption
  • Smoking (inhibits activity of osteoblasts)
  • Insufficient physical activity (lack of bone remodeling)
  • Glucocorticoids (steroid-induced osteoporosis)
  • Proton pump inhibitors.

Pathophysiology of Osteoporosis

Normally, The two main cells involved in bone production pathway are osteoblasts and osteoclasts.

  • Bone resorption is caused by osteoclasts, after which new bone is deposited by osteoblasts.
  • Osteoclasts determine the final outcome of bone resorption.
  • Normal balance between osteoblast and osteoclast activities within a bone is influenced by macrophages and innate adaptive immunity. This leads to the formation of a normal bone.

In Osteoporosis,  there is a disturbance of this balance leading to increased osteoclastic activity relative to osteoblastic activity, the result is resorption, and eventual bone mass loss.

  • Reduced total bone mass. Normal homeostatic bone turnover is altered; the rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts, resulting in a reduced total bone mass.
  • Progression. The bones become porous, brittle, fragile; they fracture easily under stresses that would not break normal bone.
  •  The consequence of these changes is net loss of bone mass over time.

Role of Hormones

  • In addition to estrogen, calcium plays a significant role in bone turnover.
  • Deficiency of calcium and vitamin D leads to impaired bone deposition.
  • The parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH) increasing bone resorption in a bid to ensure adequate calcium levels in the blood.
  • The role of calcitonin, a hormone produced by the thyroid that increases bone deposition, is less clear and probably less significant

Clinical Features of Osteoporosis

  • Fractures. The first clinical manifestation of osteoporosis may be fractures, which occur most commonly as compression fractures.
  • Kyphosis. The gradual collapse of a vertebra is asymptomatic, and is called progressive kyphosis or “dowager’s hump” associated with loss of height.
  • Decreased calcitonin. Calcitonin, which inhibits bone resorption and promotes bone formation, is decreased.
  • Decreased estrogen. Estrogen, which inhibits bone breakdown, decreases with aging.
  • Increased parathyroid hormone. Parathyroid hormone increases with aging, increasing bone turnover and resorption.

Diagnosis / Investigations

The most common test for measuring bone mineral density is;

  • Dual-energy X-ray Absorptiometry (DXA). It is a quick, painless, and noninvasive test. DXA uses low levels of x-rays as it passes a scanner over your body while you lie on a cushioned table. The test measures the BMD(bone mineral density) of your skeleton and at various sites that are prone to fracture, such as the hip and spine. Bone density measurement by DXA at the hip and spine is generally considered the most reliable way to diagnose osteoporosis.

Management of Osteoporosis


  •  To prevent further bone loss
  • To reduce your risk of bone fractures.
  •  For reduction in fracture risk with an increase in bone mass density.

Medical Management;

  1. Exercise: Exercise promotes the mineralization of bone and bone deposition particularly during growth. High impact exercise, in particular, has been shown to prevent the development of osteoporosis. However, it isn’t recommended in cases of poor nutrition, such as anorexia nervosa and celiac disease.
  2. Physical activity; Multiple studies have shown that aerobics, weight lifting, and resistance exercises can all maintain or increase BMD(bone mineral density) in postmenopausal women.
  3. Nutrition: A diet high in calcium and vitamin D prevents bone loss. Patients at risk for osteoporosis, such as persons with chronic steroid use are generally treated with vitamin D and calcium supplementation.
  4. Diet: Sufficient protein intake is necessary to maintain the function of the musculoskeletal system and to decrease the complications that occur after an osteoporotic fracture. 
  5. Smoking cessation may prevent osteoporosis. The use of tobacco products is detrimental to the skeleton as well as to overall health. 
  6. Avoiding excessive alcohol intake, or drinking only in moderation.
  7. Medications: Taking the least possible doses of certain medications associated with osteoporosis (anticonvulsants or corticosteroids).
  8. Fall prevention; by mitigating risk factors for falls are shown below:

    • Lack of assistive devices in bathrooms, by assisting with hygiene or use of hip protectors.
    • Obstacles in the walking path, Appropriate correction of visual impairment may improve mobility and reduce risk of falls.
    • Slippery conditions, by using cotton rugs and ensuring there environment is dry.

Pharmacological Management;

  • Calcium supplements with vitamin D. To ensure adequate calcium intake, a calcium supplement with vitamin D may be prescribed and taken with meals or with a beverage high in vitamin C to promote absorption, but these supplements should not be taken at the same day as bisphosphonates. • Dietary calcium 1200 ( Calcium supplement≤ 500 mg, if dietary calcium not met) mg/day and Vitamin D  800–2000 IU/day.
  • Bisphosphonates. Bisphosphonates are the first line treatment for osteoporosis. These include oral preparations of;
  1. Alendronate(70mg weekly orally.) or
  2. Risedronate(35mg weekly or 150mg monthly orally)
  3. Ibandronate(150mg monthly orally, or 3mg every 3 months through intravenous (IV) route.), or yearly intravenous infusions of
  4. Zoledronic acid ( 5mg annually through IV route.) increase bone mass and decrease bone loss by inhibiting osteoclast function.
  • Calcitonin. Calcitonin directly inhibits osteoclasts thereby reducing bone loss and increasing bone mineral density. It is used for postmenopausal women with osteoporosis. The dosing is 100units subcutaneous daily; or 200 units intranasal daily.
  • Selective estrogen receptor modulators (SERMs). SERMs such as raloxifene which is a second line treatment, reduce the risk of osteoporosis by preserving bone mineral density without estrogenic effects on the uterus. The dosing is 60mg daily orally.
  • Parathyroid hormone: Such as Teriparatide (20mcg subcutaneous daily,) and as a recombinant PTH, it stimulates osteoblasts to build bone matrix and facilitates overall calcium absorption. Abaloparatide(80mcg subcutaneous daily) can also be used.

Surgical Management;

Surgery is not the first-line treatment option, Vertebroplasty, kyphoplasty, lordoplasty, and vesselplasty are the procedures that are usually reserved for patients with either pathological or osteoporotic vertebral fractures

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