Age-related nontraumatic fractures are a major public health problem. Even though lower bone mass is the most commonly implicated variable for the age-related increase in fracture incidence, studies show that the resistance of bone material against fracture (toughness) diminishes with age. The mechanisms for the age-related loss of toughness are, however, unknown and may involve alterations in the quality of the bone material. The review of literature presented here identifies changes in the quality of bone material at ultrastructural, lamellar, osteonal, and tissue levels as plausible contributors to the biomechanical changes in aging human bone. The changes in bone quality at these multiple levels of organization result in a systematic breakdown of the mechanical and biological mechanisms that provide bone with its resistance against fracture. Animal studies conducted to date suggest that, similar to bone mass, bone quality may be partially regulated by genetics.
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