Age-related structural changes in trabecular and cortical bone: Cellular mechanisms and biomechanical consequences

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Abstract
It is proposed that there are two structurally different forms of bone loss with different rates, cellular mechanisms, and biomechanical effects. Rapid bone loss is the result of excessive depth of osteoclastic resorption cavities. This leads in trabecular bone to perforation of structural elements, increased size of marrow cavities, and discontinuity of the bone structure, and in cortical bone to subendosteal cavitation and conversion of the inner third of the cortex to a trabecularlike structure, which then undergoes the same changes as the trabecular bone originally present. These structural characteristics reduce the strength of the bones to a greater extent than the reduction in the amount of bone by itself would suggest. Slow bone loss results from incomplete refilling by osteoblasts of resorption cavities of normal or reduced size. This leads to simple thinning of residual structural elements in both trabecular and cortical bone, and reduces the strength of the bones in proportion to the reduction in the amount of bone. This concept, although derived mainly from an examination of postmenopausal bone loss, may be applicable to other osteopenic states. At the same time as bone loss is occurring on the endosteal surface, rapidly or slowly, bone is being added to the periosteal surface, but much more slowly than during growth. The cellular mechanism is the converse of that causing slow bone loss, consisting of slight overfilling of shallow resorption cavities. Slow periosteal gain serves to partly offset the structural weakness resulting from endosteal loss, but is not directly compensatory. Although less well established and of uncertain frequency and magnitude, it is likely that localized bone gain also occurs on some trabecular surfaces, especially the vertical trabecular plates in the spine that are subjected to compression. In contrast to periosteal gain, this may be a compensatory response to loss of horizontal trabeculae, but the cellular mechanism is unknown.