The role of adenosine to regulate osteoimmunology in inflammatory bone destruction

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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.