| pubmed-article:11792558 | pubmed:abstractText | There is increasing interest in the degree to which bone remodeling, particularly in cortical bone, is "targeted" at fatigue microdamage. The theory that microdamage initiates remodeling in close proximity to microcracks, thereby removing them, and that this accounts for a significant fraction of the overall remodeling activity, has been gaining acceptance. However, the association between the initial, resorptive stage of remodeling and microcracks in histologic sections of cortical bone is far from complete; indeed, the great majority of resorption spaces are not spatially associated with microcracks. This observation has maintained support for the older concept that most remodeling occurs primarily for such metabolic purposes as calcium homeostasis. To gain further insight regarding the degree to which microdamage governs remodeling, this study presents a mathematical analysis based on the unorthodox hypothesis that all cortical bone remodeling is initiated by, and in close proximity to, microcracks. Equations are derived showing that, because remodeling basic multicellular units (BMUs) travel several millimeters beyond their point of initiation, the relative numbers of resorption spaces and microcracks found in close spatial proximity or isolated from one another are consistent with the hypothesis. The results also predict the degree to which the spatial association between resorption spaces and microcracks should exceed that due to chance alone. There are as yet very limited experimental data suitable for testing this model, but the existing data closely correspond to the model's predictions. | lld:pubmed |
