Reduction in bone mass has long dominated the thinking about and approach to the problem of osteoporosis. A now large body of evidence indicates that bone mass is not adequate to explain satisfactorily either the skeletal fragility of osteoporosis or the effects of bone active agents. By contrast, bone remodeling activity seems to provide a better explanation of both. It is suggested that current syntheses in the field are shifting to this conclusion. In attempting to make sense out of how a process designed by evolution to sustain bone strength could instead be contributing to weakness, I suggest: (1) prevailing bone remodeling levels are substantially higher than are optimal for maintenance of bone strength; (2) this high level has discernible environmental causes; and (3) such high remodeling is a major source - perhaps the major source - of osteoporotic bony fragility. Within this context, reduced bone mass, rather than the primary cause of fracture, is seen as a factor that predisposes individuals to the harmful effects of excessive remodeling.
All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism