Bone remodeling achieves three goals. First, it provides a way for the body to alter the balance of essential minerals by increasing or decreasing the concentration of these in serum. Second, it provides a mechanism for the skeleton to adapt to its mechanical environment, reducing the risk for fracture and increasing the organism’s chances for passing its genes to the next generation. Third, it provides a mechanism to repair the damage created in bone by repetitive cycles of mechanical loading. The first of these goals can be easily accomplished without site-dependent remodeling. To re-establish mineral balance, it matters little where the bone is removed or replaced, as long as mechanical integrity is not compromised, and the mineral balance is restored. The other two goals require site-dependent remodeling. It makes little sense for the remodeling system to indiscriminately increase its turnover rate at all skeletal sites in the event that a single site is damaged, nor would it be selectively or energetically advantageous to add bone tissue to sites that are already mechanically strong simply because weaker sites also need more bone tissue.

This has led some investigators9, 13, 14, 17, 20, 21 to suggest that there may be two kinds of bone remodeling: one that is stochastic, in the sense that it is not site-dependent (although it is probably not truly random); and a second that is targeted toward specific sites. The areas defined in what follows require greater research efforts to determine how these different components of the remodeling system are controlled. Questions that remain to be addressed include whether targeted remodeling does in fact occur; how much of bone’s total turnover is targeted and how much is nontargeted (stochastic); and whether these forms of remodeling are independently controlled, can respond differently to therapeutic measures, and can therefore be modulated independently of one another.