The cells and matrix comprising skeletal tissue form a specialized architecture uniquely adapted for weight bearing, motion and marrow development. Bone also serves as a mineral reservoir for the organism and is, by necessity, highly responsive to complicated endocrine signals responsible for maintaining and modifying mineral homeostasis. In addition, the complex bone matrix may serve as a growth factor repository and thereby operate to influence haematopoietic events and contribute to the regenerative properties of bone. Bone modeling during development and remodeling throughout life are dependent upon factors that regulate the number and activity of both bone-forming osteoblasts and bone-resorbing multinucleated osteoclasts. Deciphering the biochemical and molecular mechanisms that govern bone cell precursor recruitment, differentiation and activity is, therefore, important for understanding both normal and pathological processes in bone. The osteoclast is believed to degrade bone matrix by releasing hydrolytic enzymes, superoxide radicals and protons into what can best be described as an extracellular phagolysosome. There are many unanswered questions about the exact developmental relationship between osteoclasts, osteoclast precursors and other cells of the mononuclear-phagocyte family. The research in our group focuses on: identifying and characterizing unique osteoclast plasma membrane proteins to better understanding how the specialized bone-resorbing ability of this cell is accomplished and regulated; identifying factors derived from the bone environment that influence osteoclast development and determining how these signals may be modified during development and aging; examining the functional and regulatory role of free radicals in bone remodeling; and, examining how osteoclast-derived chemokines and matrix degradation products influence bone-forming osteoblasts.Cell, development, molecular biology, and biochemistry of bone cell interactions; role of chemokines in normal or pathological bone processes; mechanisms of nitric oxide regulation and action in osteoclasts; interactions  between vascular and bone cells in skeletal physiology, inflammation, and osteoporosis; cellular mechanisms associated with elevated bone loss in  osteogenesis imperfecta. 

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