Biological and Psychosocial Mechanisms Underlying Oral Inflammation and Disease

项目总结/摘要 在美国，近一半的成年人患有牙周病，他们的身体、心理和经济状况都受到影响。 这些条件的负担沉重地落在非白人和低收入美国人身上。口腔健康 差异持续存在，与几种系统性健康状况的差异并行，包括2型糖尿病（T2D） - 是美国的主要死因之一T2D和牙周病（PD）具有良好的特征， 与共同的风险因素和炎症机制的相互关系导致两者的风险增加 条件最近的证据表明，未解决的口腔炎症支付的发病关键作用， PD和T2D的进展。然而，是什么原因加剧了一些人的口腔炎症， 而不是其他人仍然难以捉摸。本研究主要探讨口腔环境敏感性与心理社会敏感性的关系。 炎症过程是PD和T2D风险差异的关键驱动因素。该项目的总体目标是 确定口腔炎症的各种来源和心理社会风险因素在调解关系中的作用 将种族、民族和SES与PD和T2D风险联系起来。中心假设是暴露于个体（例如， 慢性应激）和结构（例如，社会心理压力和逆境会增加口腔 炎症通过几种机制，这反过来又会增加PD和T2D的风险。该项目进一步 检查这些心理社会因素对口腔炎症的下游后果是否部分 解释PD和T2D风险与种族、民族和SES相关的差异。为了解决这些假设， 一项关于口腔炎症和疾病风险的生物学和心理社会因素的纵向研究将 与我们的临床合作伙伴在350名成年人的多元化社区样本中进行。生物学， 将在基线和两年后进行心理社会和临床评估， 检查三个特定目的：1）检查导致口腔炎症的各种生物过程， 他们与当前和未来PD风险/严重程度的关联; 2）检查心理社会压力之间的关联 和结构逆境与当前和未来的口腔炎症;和3）检查口腔炎症之间的关系， 炎症和当前和未来的T2D风险。通过这个项目的完成，共同的，可修改的生物 以及导致口腔炎症和PD和T2D风险差异的心理社会机制将被 阐明。这项研究的结果可以帮助识别新的，创新的预防，筛查和干预 PD和T2D的策略，如果在疾病早期开始干预，这两种疾病都是可逆的 课程（例如，在牙龈炎和前驱糖尿病发作时）。这些研究结果也将为一个综合的 了解美国的健康差异，并帮助推进公共卫生和临床干预措施， 通过针对多个领域的卫生基础因素，最大限度地提高效率和影响。

PROJECT SUMMARY/ABSTRACT Periodontal diseases affect nearly half of all adults in the US, and the physical, psychological, and financial burdens of these conditions fall disproportionally on non-white and lower-income Americans. Oral health disparities persist in parallel with disparities in several systemic health conditions, including type 2 diabetes (T2D) - one of the leading causes of death in the US. T2D and periodontal disease (PD) have well-characterized reciprocal relations with shared risk factors and inflammatory mechanisms driving increased risk for both conditions. Recent evidence suggests that unresolved oral inflammation pays a key role in the onset and progression of both PD and T2D. However, what causes exacerbated oral inflammation in some individuals and not others remains elusive. This study focuses on the psychosocial and environmental sensitivity of oral inflammatory processes as a key driver of disparities in PD and T2D risk. This project’s overall objective is to determine the role of various sources of oral inflammation and psychosocial risk factors in mediating relations linking race, ethnicity, and SES with PD and T2D risk. The central hypothesis is that exposure to individual (e.g., chronic stress) and structural (e.g., pollution) psychosocial stressors and adversities can increase oral inflammation via several mechanisms, which can, in turn, increase PD and T2D risk. This project further examines whether the downstream consequences of these psychosocial factors on oral inflammation partially explain disparities in PD and T2D risk associated with race, ethnicity, and SES. To address these hypotheses, a longitudinal study of the biologic and psychosocial factors underlying oral inflammation and disease risk will be conducted with our clinical partners in a diverse, community-based sample of 350 adults. Biologic, psychosocial, and clinical assessments will be conducted at baseline and two years later to allow for the examination of three specific aims:1) examine various biologic processes contributing to oral inflammation and their associations with current and future PD risk/severity; 2) examine associations between psychosocial stress and structural adversities and current and future oral inflammation; and 3) examine relations between oral inflammation and current and future T2D risk. Through completion of this project, common, modifiable biologic and psychosocial mechanisms contributing to oral inflammation and disparities in PD and T2D risk will be elucidated. Findings from this study could help identity new, innovative prevention, screening, and intervention strategies for PD and T2D, both of which are reversable conditions if intervention is initiated early in the disease course (e.g., at the onset of gingivitis and prediabetes). These findings will also inform an integrated understanding of health disparities in the US and help advance public health and clinical interventions that maximize efficiency and impact by targeting factors underpinning health across multiple domains.