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Osteoporosis is a disorder in which loss of bone strength leads to fragility fractures. The fundamental pathogenetic mechanisms underlying this disorder include: i) failure to achieve a skeleton of optimal strength during growth and development; ii) excessive bone resorption resulting in loss of bone mass and disruption of architecture; and iii) failure to replace lost bone due to defects in bone formation. Estrogen deficiency is known to play a critical role in the development of osteoporosis, while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute. There are multiple mechanisms underlying the regulation of bone remodeling, and these involve not only the osteoblastic and osteoclastic cell lineages but also other marrow cells, in addition to the interaction of systemic hormones, local cytokines, growth factors, and transcription factors. Polymorphisms of a large number of genes have been associated with differences in bone mass and fragility.

The process of bone remodeling or bone multicellular units (BMUs) begins with the activation of hematopoietic precursors to become osteoclasts, which normally requires an interaction with cells of the osteoblastic lineage. Because the resorption and reversal phases of bone remodeling are short and the period required for osteoblastic replacement of the bone is long, any increase in the rate of bone remodeling will result in a loss of bone mass. Moreover, the larger number of unfilled Howship lacunae and haversian canals will further weaken the bone. Excessive resorption can also result in complete loss of trabecular structures, so that there is no template for bone formation. Thus, there are multiple ways in which an increase in osteoclastic resorption can result in skeletal fragility. However, high rates of resorption are not always associated with bone loss; for example, during the pubertal growth spurt. Hence an inadequate formation response during remodeling is an essential component of the pathogenesis of osteoporosis.

The incidence of osteoporotic fractures in elderly men, just as in aged women, increases exponentially with age; the rise in men, however, is some 5–10 years later than in women. Up to 50% of male osteoporotics have no identifiable etiology; however elderly males have much higher likelihood of having an identifiable secondary cause than younger men. Therefore, clinical and laboratory evaluation of aged male osteoporotics must be thorough and should be aimed at identifying lifestyle or conditions contributing to bone loss and fragility.