Atlas of pathophysiology, 2 Edition

Part II - Disorders

Musculoskeletal disorders

Osteoporosis

Osteoporosis is a metabolic bone disorder in which the rate of bone resorption accelerates while the rate of bone formation slows, causing a loss of bone mass. Bones affected by this disease lose calcium and phosphate salts and become porous, brittle, and abnormally vulnerable to fractures. Osteoporosis may be primary or secondary to an underlying disease, such as Cushing's syndrome or hyperthyroidism. It primarily affects the weight-bearing vertebrae. Only when the condition is advanced or severe, as in secondary disease, do similar changes occur in the skull, ribs, and long bones. Often, the femoral heads and pelvic acetabula are selectively affected.

Age Alert

Primary osteoporosis is often called senile or postmenopausal osteoporosis because it most commonly develops in postmenopausal women.

Causes

Primary osteoporosis

·   Unknown

·   Contributing factors:

§  Mild but prolonged negative calcium balance

§  Declining gonadal and adrenal function

§  Relative or progressive estrogen deficiency

§  Sedentary lifestyle

·   Smoking

Secondary osteoporosis

·   Prolonged therapy with corticosteroids, heparin, anticonvulsants

·   Total immobilization or disuse of a bone (as in hemiplegia)

·   Alcoholism, malnutrition, malabsorption, scurvy

·   Lactose intolerance

·   Endocrine disorders such as hyperthyroidism, hyperparathyroidism, Cushing's syndrome, diabetes mellitus

·   Osteogenesis imperfecta

·   Sudeck's atrophy (localized to hands and feet)

Pathophysiology

In normal bone, the rates of bone formation and resorption are constant; replacement follows resorption immediately, and the amount of bone replaced equals the amount of bone resorbed. The endocrine system maintains plasma and bone calcium and phosphate balance. Estrogen also supports normal bone metabolism by stimulating osteoblastic activity and limiting the osteoclastic-stimulating effects of parathyroid hormones. Osteoporosis develops when new bone formation falls behind resorption. For example, heparin promotes bone resorption by inhibiting collagen synthesis or enhancing collagen breakdown. Elevated levels of cortisone, either endogenous or exogenous, inhibit GI absorption of calcium.

Clinical Tip

When the rate of bone resorption exceeds that of bone formation, the bone becomes less dense. Men have approximately 30% greater bone mass than women, which may explain why osteoporosis develops later in men.

Signs and symptoms

·   Typically, asymptomatic until a fracture occurs

·   Spontaneous fractures or those involving minimal trauma to vertebrae, distal radius, or femoral neck

·   Progressive deformity—kyphosis, loss of height

·   Decreased exercise tolerance

·   Low back pain

·   Neck pain

Diagnostic test results

·   Dual energy X-ray absorptiometry test measures bone mass of the extremities, hips, and spine.

·   X-rays show typical degeneration in the lower thoracic and lumbar vertebrae (vertebral bodies may appear flattened and may look denser than normal; bone mineral loss is evident only in later stages); also reveal fractures.

·   Computed tomography scan detects spinal bone loss.

·   Laboratory studies reveal elevated parathyroid hormone.

·   Bone biopsy shows thin, porous, but otherwise normal-looking bone.

Treatment

Early prevention to control bone loss, prevent fractures, control pain

·   Limited alcohol and tobacco use

·   High-calcium diet

·   Prevention of falls

·   Early mobilization after surgery, trauma, or illness

·   Identification and treatment of risk factors

·   Physical therapy emphasizing regular, moderate weight-bearing exercise

·   Supportive devices, such as a back brace

·   Prompt, effective treatment of underlying disorder to prevent secondary osteoporosis

Pharmacotherapy

·   Estrogen; selective estrogen-receptor modulators such as raloxifene; bisphosphonates, such as alendronate and risedronate

·   Analgesics and local heat to relieve pain

·   Calcium and vitamin D supplements

·   Calcitonin

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CALCIUM METABOLISM IN OSTEOPOROSIS