title: Aging and strength of bone as a structural material.
abstract: There is a general, age-related reduction in the material strength and stiffness of bone in both men and women. Between the ages of 35 and 70, cortical bone strength in bending is diminished by about 15-20%, and cancellous bone strength in compression is reduced about 50%. In addition, bone becomes increasingly brittle and fractures with less energy. It is hypothesized that this tendency is driven by the need for remodeling to repair fatigue damage, and the fact that most osteonal and endotrabecular remodeling events fail to replace all the bone that they remove. Each remodeling event also introduces cement line interfaces, which although affording protection against fatigue failure, weaken bone for monotonic loading. Remodeling also affects collagen fiber orientation, mineralization, and the amount of unrepaired fatigue damage, which are additional determinants of bone strength and stiffness. Mechanical factors apparently inhibit age-related bone loss where stresses are higher by reducing remodeling rates and/or the deficit at each remodeling site. They may also stimulate modeling responses, primarily in the form of periosteal bone formation, which, in men more than women, alter bone size and shape to effectively compensate for loss of material strength. Suggested directions for future research include elucidation of the relationships between (1) histologically observable microcracks and bone fragility, (2) remodeling and the repair of fatigue damage, and (3) estrogen and other hormones and mechanically adaptive responses.
authors.affiliation: Orthopaedic Research Laboratory, University of California, Davis 95616.
authors.forename: B
authors.initials: B
authors.lastname: Martin
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000473:pathology / Q000502:physiology*; D015519:Bone Density / Q000502:physiology*; D016723:Bone Remodeling; D001842:Bone and Bones / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D050723:Fractures, Bone / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D013314:Stress, Mechanical