Abstract
Osteoclast differentiation and function is regulated by cellular signals and cytokines that also play significant roles in the immune system. There is much scope, therefore, for immune cell influence on osteoclasts and bone metabolism. Many examples of this have been identified and T cells in particular are a source of factors affecting osteoclast formation and activity, a number which have either pro-osteolytic or anti-osteolytic actions depending on the cellular and microenvironmental context. For example, IL-12 and IL-18 participate in inflammatory processes that can lead to highly destructive osteolysis, yet these cytokines potently block osteoclast formation through mediation of T cells. IL-23 participates in chronic inflammatory processes, but lack of this cytokine results in reduced bone mass in mice, pointing to an influence on physiological regulation of bone mass. Such insights suggest that therapies that target immune responses may significantly influence osteolysis. Investigations into links between the immune system and bone metabolism are thus uncovering important information about the functioning of both systems.
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