Abstract
Most of the pathology associated with cholesteatoma is the result of osteoclast-mediated bone resorption in the middle ear. Cytokines, prostaglandins, nitric oxide, neurotransmitters and growth factors are associated with chronic inflammation and have been implicated in cholesteatoma-induced bone resorption. Although many different factors are known to regulate osteoclast activation, there is a final common pathway of osteoclast differentiation and resorption. Recent advances in molecular techniques and the increasing availability of genetically altered mice have provided valuable insight into the molecular mechanism of osteoclastic bone resorption. This review focuses on osteoclast biology, lessons from genetically altered mice, and their contribution to our understanding of cholesteatoma-induced bone resorption.
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