Postmenopausal Osteoporosis

Postmenopausal Osteoporosis

Osteoporosis simply means “porous bones”. It is a disease if the bones that leads to an increased risk of fracture. Bones are highly metabolically active tissue with remodelling continuing throughout life. This remodelling process involves a delicate balance between bone resorption by osteoblasts and bone formation by osteoblasts. An imbalance, in which more resorption than formation occurs, leads to net loss of bone per remodelling cycle. This imbalance causes osteoporosis.

Osteoporosis is defined by the World Health Organization (WHO) as bone mineral density (BMD) that is 2.5 standard deviations or more below the mean peak bone mass (average of young, healthy adults) as measured by dual energy x-ray absorptiometry scan (DEXA scan). The term establised osteoporosis includes the presence of a fragility fracture. The disease may be classified as primary type 1, primary type 2, or secondary. The form of osteoporosis most common in woman after menopause is referred to as primary type 1 or postmenopausal osteoporosis. Primary type 2 is age related while secondary is due to disease (eg: chronic renal disease, thyroid disorders) or medications (eg: sterod induced osteoporosis).

Oestrogen, Peak Bone Mass and Osteoporosis

Menopause is characterised by the loss of oestrogen production by the ovaries. This may occur through natural means or following the surgical removal of both ovaries. This loss of oestrogens accelerates bone loss for a period ranging from five to eight years. In terms of bone remodelling, the lack of oestrogen enhances the ability of osteoclasts to absorb bone (hence, more bone is lost) while reducing osteoblast activities (hence, less bone is produced). If the peak bone mass of the person is high, it may take a while before bone is lost to reach the point of being osteoporotic.

If peak bone mass is low, then postmenopausal osteoporosis takes place earlier. Peak bone mass is reached during the fourth decade of life. Bone loss commences after that and is universal. Over their lifetimes, woman lose about 35% of their cortical bone and 50% of trabecular bone.

Peak bone mass is affected by genetics (may be related to vitamin D receptors, oestrogen receptors, collagen type 1, interleukin 6 or transforming growth factor changes), hormonal, nutritional and mechanical factors (eg weight bearing exercises). Other than oestrogen deficiency, the rate of bone loss is also affected by family history, low body weight, race, physical inactivity, low calcium intake, cigarette smoking, excessive alcohol consumption, drugs and diseases.

Postmenopausal osteoporosis should no longer be an accepted process of ageing. It is both preventable and treatable. Management strategies for postmenopausal women involve identifying those at risk for fracture, followed by instituting measures that focus on reducing modifiable risk factors through dietary and lifestyle changes, and if indicated, pharmacological therapy. Doctors must proactively prevent and treat osteoporosis in their daily practice.

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