Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Porphyromonas gingivalis is strongly correlated with chronic periodontitis. Its chronic persistence in the periodontium depends on its ability to evade host immunity without inhibiting the overall inflammatory response, which is actually beneficial for this and other periodontal bacteria. Indeed, the inflammatory exudate (gingival crevicular fluid) is a source of essential nutrients, such as peptides and hemin-derived iron. In this review, I discuss how P. gingivalis can promote its adaptive fitness through instigation of subversive crosstalk signaling. These interactions involve Toll-like receptor-2, complement receptor 3, C5a anaphylatoxin receptor, and CXC-chemokine receptor 4. Their exploitation by P. gingivalis allows the pathogen to escape elimination, obtain nutrients, and collaterally inflict periodontal tissue injury.
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PMID:Immune evasion strategies of Porphyromonas gingivalis. 2216 63

Periodontitis caused by bacterial infection gradually progresses accompanied by periodontal tissue destruction. As a result, teeth lose their supporting structures, and this leads to tooth exfoliation. CXC-chemokine receptor 4 (CXCR4) is known to be expressed in lymphocytes, fibroblasts and osteoclasts in periodontal tissues, suggesting that periodontal CXCR4 signaling contributes to alveolar bone resorption in the milieu of periodontitis. However, the role of CXCR4 signaling in the pathogenesis of periodontitis has remained unknown. We established a mouse model of periodontitis by inoculation of Porphyromonas gingivalis (P.g.) into a silk ligature placed around the maxillary molar. Although there was no significant difference in the mechanical sensitivity in the periodontal tissue between P.g. treatment and sham treatment during the experimental period, mechanical allodynia in the periodontal tissue was induced after gingival injection of complete Freund's adjuvant compared with that resulting from sham and P.g. treatment alone. Moreover, CXCR4 neutralization in the periodontal tissue following P.g. treatment enhanced periodontal inflammatory cell infiltration and depressed alveolar bone resorption. These findings suggest that periodontal CXCR4 signaling in several cell types in P.g.-induced periodontal inflammation depresses alveolar bone resorption in periodontitis. CXCR4 signaling might be a target for therapeutic intervention to prevent alveolar bone resorption in periodontitis.
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PMID:CXCR4 signaling contributes to alveolar bone resorption in Porphyromonas gingivalis-induced periodontitis in mice. 2909 84