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Periodontal disease is an infectious condition that results in the inflammation and gradual degradation of gum tissue and alveolar bone. Caused by plaque deposits on teeth that harden into tartar to inflame gum tissue, the condition is highly pervasive, with 15 percent of US adults over 30 years of age exhibiting destructive periodontal disease. The abundance of Treponema denticola, a spirochete, in the oral flora is strongly correlated with disease severity. T. denticola binds to Factor H (FH), a negative regulator of the complement system, through its Factor H binding protein (FhbB) to evade complement-mediated killing. The protease dentilisin, produced by T. denticola, cleaves FH for reasons that are still being studied. We hypothesize that dentilisin-dependent cleavage of FH may result in the local dysregulation of the complement immune system, leading to gum destruction. The primary goal of this research project was to identify the specific location of FH cleavage by dentilisin. Characterization of the complex interaction between T. denticola and FH may explain the molecular pathogenesis of periodontal disease.
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