Osteoporosis by Dr Zeinah Keen

Osteoporosis is the most common metabolic bone disease in Australia and can result in devastating physical, psychosocial, and economic consequences. It is often overlooked and undertreated, however, in large part because it is clinically silent before manifesting as fracture. It has been most frequently recognised in elderly white women, although it does occur in both sexes, all races, and all age groups.

Bone is continually remodelled throughout our lives in response to microtrauma. Bone remodelling 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.
Dense cortical bone and spongy trabecular or cancellous bone differ in their architecture but are similar in molecular composition. Both types of bone have an extracellular matrix with mineralized and nonmineralized components. The composition and architecture of the extracellular matrix is what imparts mechanical properties to bone. Bone strength is determined by collagenous proteins (tensile strength) and mineralized osteoid (compressive strength). The greater the concentration of calcium, the greater the compressive strength. In adults, approximately 25% of trabecular bone is resorbed and replaced each year, compared with only 3% of cortical bone.
Bone mass peaks around the third decade of life and slowly decreases afterward. A failure to attain optimal bone strength by this point is one factor that contributes to osteoporosis, which explains why some young postmenopausal women have low bone mineral density (BMD) and why some others have osteoporosis. Therefore, nutrition and physical activity are important during growth and development. Nevertheless, hereditary factors play the principal role in determining an individual’s peak bone strength. In fact, genetics account for up to 80% of the variance in peak bone mass between individuals.
The primary causes of Osteoporosis are oestrogen deficiency, ageing, calcium and vitamin D deficiency. Secondary factors can be related to underlying disease or deficiency or drugs, particularly steroids.

Signs and Symptoms

Osteoporosis generally does not become clinically apparent until a fracture occurs. Fractures can occur anywhere but typically are in the vertebrae, hips, wrists and pelvis. Pain is sharp, nagging, dull and exacerbated by movement.

Diagnosis is based on clinical symptoms, a thorough case history and physical and radiographic examination. Physical examination would elicit pain on palpation and percussion, loss of height and restricted range of movement. X-rays can show if an osteoporotic fracture has occurred.
Bone mineral density (BMD) measurement is recommended in the following patients;

• Women age 65 years and older and men age 70 years and older, regardless of clinical risk factors.
• Postmenopausal women and men above age 50–69, based on risk factor profile.
• Postmenopausal women and men age 50 and older who have had an adult-age fracture, to diagnose and determine the degree of osteoporosis.

Dual-energy X-ray absorptiometry (DXA) is currently the criterion standard for the evaluation of BMD. Peripheral DXA is used to measure BMD at the wrist.

Lifestyle modification for prevention of osteoporotic fractures includes the following;
• Increasing weight-bearing and muscle-strengthening exercise.
• Ensuring optimum calcium and vitamin D intake as an adjunct to active antifracture therapy.
• Smoking cessation.
• Moderate alcohol consumption.
• Education around risk factors.
• Medications are advisable in postmenopausal women and men over the age of 70 if there is a history of Osteoporotic fractures and low bone mass.
• Surgery is occasionally indicated for painful osteoporotic vertebral compression fractures.

Useful Resources fracture spine

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