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Using a gingival epithelial tissue model, we previously showed that the periodontal pathogen Porphyromonas gingivalis specifically degraded two tight junction-associated proteins, junctional adhesion molecule 1 (JAM1) and coxsackievirus and adenovirus receptor (CXADR), which allowed the pathogen to successfully break down the gingival epithelial barrier, thus increasing epithelial permeability to LPS and PGN, which likely leads to onset of periodontal disease 10,11,12