Remodeling of Mineralized Tissues, Part II: Control and Pathophysiology

Based on a review of literature, the bone remodeling concepts, as defined by Harold Frost, are extended to the molecular level to help explain common bone physiopathology. Remodeling of mineralized tissue is an inflammatory response to accumulated tissue damage. Inflammation activates (A) the localized cell population, which attracts circulating osteoclast precursors, and initiates foci of vascular invasion. Coordination of these cybernetic events results in formation of a cutting/filling cone (cortical bone) or a hemicutting/filling cone (trabecular bone). Damaged bone is resorbed (R) creating a self-limited resorption cavity that is then filled by bone formation (F). A genetic mechanism (RANK/RANKL/OPG) is proposed for coupling bone formation to resorption during the remodeling process. Following surgery and/or initiation of orthodontic tooth movement, a regional acceleratory response (RAP) occurs throughout the affected alveolar process. Undermining resorption during the initial stage of tooth movement is analogous to initiation of a bone remodeling cycle (A→R→F). Understanding the cell dynamics of the ARF sequence is fundamental for appreciating common remodeling disorders such as osteoporosis, Paget’s disease, hypo- and hyperparathyroidism, metastases, and external apical root resorption. Depending on the physiopathologic context, remodeling may enhance or limit the orthodontic options for management of a malocclusion.