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

牙龈假单胞菌和新冠沙门氏菌的流行对口腔健康差异的影响 成人牙周炎在不同种族之间分布不均，在 非裔美国人(AA)与欧洲高加索人(EC)相比，即使是糖尿病和 其他健康和社会因素也被考虑在内。这项提议考察了两个人的潜在作用 口腔微生物生物膜成分(牙龈假单胞菌和金黄色葡萄球菌)对这一差异的影响。口腔病原菌P. 据报道，与那些没有牙周炎的受试者相比，有齿状齿的受试者牙周炎的发生率更高。我们的 实验室是第一个报道犯罪链球菌和牙龈假单胞菌之间的属间传播的实验室。我们 鉴定了鸡冠状杆菌的一种表面蛋白，精氨酸脱亚胺酶(Arca)，它是一种信号分子，对 牙龈假单胞菌通过抑制编码主要亚单位的fimA基因的表达来做出反应。 长菌毛的蛋白质。后者是牙龈假单胞菌的细菌定植和宿主细胞入侵所必需的。 最近，我们证明了新冠沙门氏菌确实能抑制牙龈假单胞菌在小鼠口腔中的定植。 并减少受试小鼠的牙周骨丢失。因此，我们假设殖民统治 牙龈假单胞菌取决于最初的链球菌生物膜的性质，而这一点尚不确定。 牙周炎的危险因素是这些初始微生物链球菌谱不同背后的驱动力 生物膜。我们将首先比较金黄色葡萄球菌和牙龈假单胞菌在儿童口腔中的患病率。 牙周健康的AA、ECs和墨西哥裔美国人(MA)与牙周炎患者(前后)的对比 牙周治疗)。我们的目标是确定较低的口腔患病率是否与 与EC相比，AAS或MA中的牙龈假单胞菌可能有助于解释患牙周炎的更高风险 AAS和MAS中的牙周炎。然后我们还将测试其他牙周风险因素的潜在参与程度。 这种差异，以及它们在金黄色葡萄球菌和牙龈假单胞菌流行中的作用。最后，我们建议 调查强化的牙周健康教育是否会促进S.criatus与P. 牙周炎患者的牙周炎。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不同地区发现的微生物生物膜的性质 种族/伦理，并将为今后的扩展研究铺平道路，重点是发展适当的 旨在消除牙龈假单胞菌定植的干预策略。

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.