The role of adenosine to regulate osteoimmunology in inflammatory bone destruction

感染牙龈卟啉单胞菌的CD73缺陷小鼠揭示了CD73在牙周炎中的作用。与野生型小鼠相比，从CD73缺陷小鼠分离的成骨细胞分化受损。另一方面，IL-1 β在小鼠成骨细胞中降低A2A，增加A2B腺苷受体的表达。此外，CD73过表达导致RANKL表达增加，IL-1 β刺激细胞时，RANKL表达进一步增强。这些结果表明内源性腺苷参与炎症性骨破坏。

Porphyromonas gingivalis-infected CD73 deficient mice revealed the role of CD73 in periodontitis. Osteoblasts isolated from CD73 deficient mice showed impaired differentiation compared to those from wild type mice. On the other hand, IL-1 beta decreased A2A and increased A2B adenosine receptor expression in mouse osteoblasts. Moreover, CD73 overexpression resulted in increase of RANKL expression and the expression was further enhanced when the cells were stimulated with IL-1 beta. These results suggest that endogenous adenosine is involved in inflammatory bone destruction.