Impact of prevalence of P. gingivalis and S. cristatus in oral health disparities

牙龈卟啉单胞菌和沙门氏菌患病率的影响。口腔健康差异中的嵴 成人牙周炎在不同种族中的发病率不同， 与欧洲高加索人（EC）相比，非洲裔美国人（AA），即使当共变异如糖尿病和 其他健康和社会因素也得到了考虑。这一建议审查了两个方面的潜在作用， 口腔微生物生物膜组分（牙龈卟啉单胞菌和S. Cristatus）在这种差异。对口腔病原体P. 据报道，与没有牙周炎的受试者相比，患有牙周炎的有齿受试者的牙龈炎更高。我们 实验室是第一个报道S. cristatus和牙龈卟啉单胞菌。我们 鉴定了S. cristatus，精氨酸脱亚胺酶（ArcA），作为信号分子， P.牙龈炎的反应是抑制fimA基因的表达，fimA基因编码主要亚基 长菌毛蛋白后者是牙龈卟啉单胞菌的细菌定殖和宿主细胞侵袭所必需的。 最近，我们证明了S。cristatus确实抑制了牙龈卟啉单胞菌在小鼠口腔中的定植 减少牙周骨流失。因此，我们假设， P.牙龈炎取决于初始链球菌生物膜的性质，某些尚未确定的 牙周炎的危险因素是这些初始微生物的不同链球菌谱背后的驱动力 生物膜我们将首先比较S。冠状菌与牙龈卟啉单胞菌在口腔中的 牙周健康的AAs、EC和墨西哥裔美国人（MA）与牙周炎患者（治疗前后） 牙周治疗）。我们的目标是确定口腔癌的低患病率与 S. cristatus：与EC相比，AA或MA中的牙龈卟啉单胞菌，这可能有助于解释更高的牙龈卟啉单胞菌感染风险。 牙周炎在AA和MA。然后我们也将测试其他牙周危险因素的潜在参与 在这种差异中，以及它们在S. cristatus与牙龈卟啉单胞菌的比较。最后，我们建议 研究强化牙周健康教育是否会促进S. cristatus与P. 牙周炎患者的牙龈炎。我们预计，拟议的研究将提供重要的信息， 关于牙周炎的发病机制和在不同的牙周组织中发现的微生物生物膜的性质， 种族/民族，并将铺平道路，在未来的扩展研究，重点是发展适当的 以消除牙龈卟啉单胞菌定植为目标的干预策略。

Impact of prevalence of P. gingivalis and S. cristatus in oral health disparities Adult periodontitis is disproportionally distributed among races, and has a significantly higher incidence in African Americans (AA) compared to European Caucasians (EC), even when co-variants such as diabetes and other health and social factors have been taken into account. This proposal examines the potential role of two oral microbial biofilm components (P. gingivalis and S. cristatus) on this disparity. Titers to the oral pathogen P. gingivalis are reported to be higher in dentate subjects with, compared to those without periodontitis. Our laboratory was the first to report an intergeneric communication between S. cristatus and P. gingivalis. We identified a surface protein of S. cristatus, arginine deiminase (ArcA) that serves as a signal molecule to which P. gingivalis responds by repressing the expression of the fimA gene, which codes for the major subunit protein of long fimbriae. The latter is required for bacterial colonization of P. gingivalis and host cell invasion. Recently, we demonstrated that S. cristatus indeed inhibited colonization of P. gingivalis in the murine oral cavity and reduced periodontal bone loss in those mice tested. Therefore, we hypothesize that colonization of P. gingivalis is dependent upon the nature of the initial streptococcal biofilm, and that certain as yet unidentified risk factors of periodontitis are the driving force behind different streptococcal profiles of these initial microbial biofilms. We will first compare the prevalence of S. cristatus versus P. gingivalis in the oral cavities of periodontally healthy AAs, ECs and Mexican Americans (MA) versus those with periodontitis (before and after periodontal treatments). Our objective is to determine if there is a link between a lower prevalence ratio of oral S. cristatus:P. gingivalis in AAs, or MAs compared to ECs, which might help account for the higher risk of periodontitis in AAs and MAs. We will also then test the potential involvement of other periodontal risk factors in this disparity, and their role in the prevalence of S. cristatus versus P. gingivalis. Finally, we propose to investigate if intense education of periodontal health will promote a shift in ratio of S. cristatus versus P. gingivalis in periodontitis patients. We anticipate that the proposed studies will provide important information regarding the pathogenesis of periodontitis and the nature of the microbial biofilms found in different races/ethnics, and will pave the way for extended studies in future, focused on the development of appropriate interventional strategies targeted at eliminating of P. gingivalis colonization.