歯周炎におけるケモカインの発現および発現制御に関する研究

Periodontal disease, a chronic inflammatory disease of the attachment structures of the teeth, is one of the most significant causes of tooth loss in adults and the most prevalent form of bone pathology in humans, besides being a modifying factor of an individual's systemic health. The bacterial biofilm attached to the surface of the tooth, close to the periodontal tissues, is the etiologic factor for this disease. Inflammatory and immune responses, initiated by periodontopathogens, are thought to protect the host against infection; however, the persistence of a local chronic host response may alter the protective roles of inflammatory cells and produce deleterious effects in these tissues. In fact, the development of periodontal diseases seems to be related to the progression of the inflammatory cell infiltrate into the deeper periodontal tissues. In this situation, chemokines, found in both gingival tissue and crevicular fluid, are thought to play important roles in the immunopathogenesis of periodontal diseases. Recently, we have reported that an intense expression of chemokines, including fractalkine, CCL20 and CXCL16, in periodontal diseased tissues can be observed. In periodontal connective tissues, fractalkine can drive the migration of NK cells. CCL20 is a chemoattractant of memory-type T cells and immature dendritic cells, and CXCL16 can attract Th1-type lymphocytes and NKT cells. These chemokines might be involved in the initiation and progression of periodontal disease.