Osteoporosis must be viewed as a pathological condition which affects the entire skeleton and is characterized by a low bone mass in combination with microarchitectural changes particularly of cancellous bone, both adding to the fragility of bone at distinct sites of the axial as well as the perpendicular skeleton. The two major determinants of bone mass and mineral density in later life in both sexes, i.e., (i) the extent of the peak bone mass in early adulthood as well as (ii) the rate of involutional bone loss thereafter, both are governed by a complex interaction of genetic, age-related, hormonal, nutritional, environmental and life style factors in the regulation of systemic calcium and phosphate homeostasis and, equally important, of local bone remodeling processes. Osteoporosis results from an imbalance of bone resorption (osteoclast activity) and bone formation (osteoblast activity). Based on pathophysiological concepts, effective strategies for prevention and treatment of osteoporosis can be designed. Thus, modification of nutritional (calcium and/or vitamin D deficiency), endocrine (estrogen deficiency) and life style factors (physical activity) are important principles not only for prevention of osteoporotic bone loss but also for treatment of the overt disease which can be aided by a variety of drugs that either inhibit bone resorption or increase bone formation.
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