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Figure 4. Bone turnover increases after menopause. Accelerated resorption (solid line) is the primary event that is soon followed by a secondary increase in bone formation (dotted line). Bone mass declines during the period of relative imbalance in bone resoprtion and formation (grey shading) and is followed by a slower progressive decrease. Antiresorptive therapy directly inhibits osteoclast action which is followed by an indirect suppression of osteoblast activity and a reciprocal increase in bone mass, though usually not to normal levels.

Figure 4. Bone turnover increases after menopause. Accelerated resorption (solid line) is the primary event that is soon followed by a secondary increase in bone formation (dotted line). Bone mass declines during the period of relative imbalance in bone resoprtion and formation (grey shading) and is followed by a slower progressive decrease. Antiresorptive therapy directly inhibits osteoclast action which is followed by an indirect suppression of osteoblast activity and a reciprocal increase in bone mass, though usually not to normal levels.

Collagen is a triple-helical molecule that undergoes extensive post-translational modifications including hydroxylation, glycosylation and covalent cross-linking. The degradation products of crosslinked collagen, which include C-telopeptide, N-telopeptide and deoxypyridinoline, may be measured in the urine as an index of osteoclast activity.

Skeletal mass accumulates rapidly during childhood, especially during the years of most rapid growth in early adolescence. Peak bone mass is achieved by age 20-25. Determinants of peak bone mass included genetics, physical activity and diet

Table 1. Secondary causes of bone loss

Genetic factors

Defects in collagen synthesis or structure Idiopathic hypercalciuria

Nutritional

Low calcium intake Vitamin D deficiency Malabsorption

Drugs

Excess glucocorticosteroids

Anticonvulsants

Heparin

Lifestyle

Immobility

Smoking

Alcohol

From PMS To PPD

From PMS To PPD

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