Osteoporoses: a rationale for further definitions?

Abstract

Bone's biologic mechanisms adapt it to meet the needs of its mechanical usage and muscle strength. Modeling by drifts can increase bone strength and "mass," BMU-based remodeling can conserve or reduce them, and neither can do the other's work. Under increasing forces on bone, modeling increases bone strength and "mass" and remodeling maintains the extra bone. In disuse, modeling turns OFF and remodeling reduces bone strength and "mass" to cause osteopenia. Osteopenia increases bone fragility as does bone microdamage, and they can coexist. Too little bone for one's mechanical usage and muscle strength can cause spontaneous fractures and/or bone pain. The bone-loss and tissue-dynamic patterns in acute and chronic disuse strongly copy the patterns in developing and established osteopenias in known medical conditions. Such things suggest that at least three osteoporosis variants can occur: (1) in physiologic osteopenias, bone strength and "mass" would decrease to correspond to reduced muscle strength and physical activity so that spontaneous fractures and bone pain would not occur. An intrinsic bone disorder would not cause this osteopenia, and fractures would only follow injuries, usually of extremity bones. (2) In "true osteoporosis," bone strength and "mass" could not meet the needs of muscle strength and physical activities, so that spontaneous fractures and/or bone pain would occur, mainly in the spine. An intrinsic bone disorder would cause this affection. Of course, injuries could fracture extremity bones too. (3) Features of (1) and (2) could combine variably in "combination states." These proposals have implications for the diagnosis, management, and study of the osteoporoses.