Trabecular bone architecture in the pathogenesis and prevention of fracture

Abstract

Rapid loss of trabecular bone (as after menopause) occurs by complete removal of some structural elements, leaving those that remain more widely separated and less well connected. The most likely cellular mechanism is an increase in the number of resorption cavities deep enough to lead to focal perforation of trabecular plates, either as a non-specific consequence of increased remodeling activation, or as a specific consequence (direct or indirect) of estrogen deficiency. Disruption of the connections between structural elements produces a disproportionate loss of strength, for which the increased thickness of the remaining trabeculae can only partly compensate. Consequently, the most biomechanically significant component of trabecular bone loss occurs rapidly and irreversibly. This emphasizes the importance of prevention, but no treatment except estrogen replacement is of proven efficacy in preventing estrogen-dependent bone loss. For adequate repair of structural damage after it has been allowed to occur, adding bone to existing surfaces may be insufficient, and it may be necessary to devise some means of forming new bone directly in the bone marrow cavity in order to re-establish normal connectivity.