破骨細胞と関連病変

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Osteoclast is an essential bone cell that is a supporting and driving force of bone function such as remodeling of tissue and calcium metabolism. Osteoclast represents heterogeneous morphology depended on functional activity according with local tissue microenvironment. A genetic and functional disorder of osteoclast directly causes metabolic bone diseases such as osteopetrosis and osteomalasia. Otherwise, in focal non-specific bone diseases such as direct cancer invasion and inflammation, osteoclast also play an important role for development of the diseases. In the review, several examples of the microenvironment that may regulate osteoclast function in bone diseases are represented and discussed. In a case of adult type osteopetrosis, genetically malfunctioned osteoclasts recovered morphologically and functionally in the inflammatory lesion of mandibular osteomyelitis. The genetic disorder may present in a functional control pathway that cross-talking with an inflammatory signaling pathway. Another example, direct bone invasion by oral cancer induced high activation of osteoclasts in the area faced to the cancer foci. The process of osteoclastic activation in the cancer invasion site was directly reduced by irradiation therapy. Finally, in an inflammatory animal model, highly activated osteoclasts showed large and multinucleated morphology even if they detached from bone surface. The evidences suggest local tissue microenvironment of osteoclast is an essential determinant for not only osteoclastogenesis but also functional activation of mature osteoclast. While, as functional depressing mechanism, control of apoptosis in osteoclast is suspected. Further investigation for factors of microenvironment that regulate osteoclast function and morphology in bone diseases is required.
鹿児島大学の論文
2002-03-25

破骨細胞と関連病変

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