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Background  Chronic periodontitis is an infectious disease of the periodontium, which includes the gingival epithelium, periodontal ligament and alveolar bone. The signature clinical feature of periodontitis is resorption of alveolar bone and subsequent tooth loss. The Gram-negative oral anaerobe,  Porphyromonas gingivalis , is strongly associated with periodontitis, and it has been shown previously that  P. gingivalis  is capable of invading osteoblasts in a dose- and time-dependent manner resulting in inhibition of osteoblast differentiation and mineralization  in vitro . It is not yet clear which receptors and cytoskeletal components mediate the invasive process, nor how the signaling pathways and viability of osteoblasts are affected by bacterial internalization. This study aimed to investigate these issues using an  in vitro  model system involving the inoculation of  P. gingivalis  ATCC 33277 into primary osteoblast cultures.    Results  It was found that binding between  P. gingivalis  fimbriae and integrin α5β1 on osteoblasts, and subsequent peripheral condensation of actin, are essential for entry of  P. gingivalis  into osteoblasts. The JNK pathway was activated in invaded osteoblasts, and apoptosis was induced by repeated infections.    Conclusions  These observations indicate that  P. gingivalis  manipulates osteoblast function to promote its initial intracellular persistence by prolonging the host cell life span prior to its intercellular dissemination via host cell lysis. The identification of molecules critical to the interaction between  P. gingivalis  and osteoblasts will facilitate the development of new therapeutic strategies for the prevention of periodontal bone loss.

bmc microbiology

Integrin α5β1-fimbriae binding and actin rearrangement are essential for Porphyromonas gingivalis invasion of osteoblasts and subsequent activation of the JNK pathway