Because periodontal pathogens, such as Porphyromonas gingivalis, are gram-negative bacteria, they contain LPS on their cell surfaces. It is said that periodontal disease is caused by LPS or that removing LPS via tooth brushing improves periodontal disease, but this is incorrect. A persistent perception of LPS as an endotoxin combined with the fact that periodontal pathogens have LPS gives rise to such misunderstanding. LPS seen in periodontal pathogens has a slightly different structure from that of other gram-negative bacteria and it exceptionally binds to a different receptor, TLR2. Binding to TLR2 means to cause the same reaction as Lactobacillus peptidoglycan or mushroom ß-glucan, rather than LPS (*1). Thus, the problem does not lie in the fact that periodontal pathogens have LPS, but lie in the fact that periodontal pathogens are alive and proliferate, actively dissolving the gingiva and lysing tissues to induce inflammation.
(*1) Signaling by toll-like receptor 2 and 4 agonists results in differential gene expression in murine macrophages, Infection and Immunity 69 (3): 1477-1482 (2001)
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