Brian T. Faddis, Ph.D.

DEPARTMENT OF Otolaryngology
Keywords: bone, osteoclast, nitric oxide, middle ear, cholesteatoma

Studies in our laboratory are geared toward understanding the mechanisms of tissue damage or injury to middle and inner ear structures. Currently, we are interested in the mechanisms modulating osteoclast activation and localized middle ear bone resorption such as that seen in cholesteatoma, chronic otitis media and otosclerosis. We are currently investigating the role of NO, specifically as a possible downstream messenger of glutamate receptor activation. It is now known that bone cells possess all the machinery required for glutamatergic activation, just as in neurons of the central nervous system. Interestingly, cultured osteoclasts derived from bone marrow of mice lacking neuronal nitric oxide synthase (NOS1) show deficits in adhesion and sealing zone formation that are similar to osteoclasts treated with the glutamate receptor antagonist MK-801. Identification of signaling pathways such as this may allow the development of non-surgical interventions for the treatment of these disorders. A variety of histological, culture and molecular techniques are used in the lab.