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Periodontal Assessment in RA Study (PARAS)

RA 研究中的牙周评估 (PARAS)

基本信息

批准号：
7248818
负责人：
CLIFTON O BINGHAM
金额：
$ 7.96万
依托单位：
JOHNS HOPKINS UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-07-01 至 2010-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7248818
关键词：
Acute-Phase Proteins Adult Affect Alleles Alveolar Bone Loss American Animal Model Anti-citrullinated peptide antibody Antibiotic Therapy Antibody Formation Arthritis Atherosclerosis Bacteria Biological Bone and Cartilage Funding Cells Cerebrovascular Disorders Chronic Collagen Condition Confounding Factors (Epidemiology)Data Dental Dental Hygiene Dentistry Depth Development Diabetes Mellitus Diagnostic Dinoprostone Disease Disease Progression Disorder by Site Endopeptidases Enzymes Evaluation Event Fibroblasts Functional disorder Generations Genes Genetic Polymorphism Genetic Predisposition to Disease Gingiva Gingival Crevicular Fluid HLA-DR4 Antigen Hand Health Hemorrhage Immunologics Individual Infiltration Inflammation Inflammatory Interleukin-1 Joints Literature Maryland Matrix Metalloproteinases Measurement Newly Diagnosed Nitric Oxide Numbers Oral health Organism Outcome Pathogenesis Pathway interactions Patient Self-Report Patients Peptide Hydrolases Peptides Periodontal Diseases Periodontitis Pharmaceutical Preparations Play Population Porphyromonas gingivalis Preparation Prevalence Process Prognostic Marker Progressive Disease Relative Risks Reporting Research Personnel Research Proposals Rheumatoid Arthritis Rheumatology Risk Factors Role Salivary Sampling Serum Severities Signs and Symptoms Smoke Source Swelling Synovial Fluid Systemic disease TNF gene Testing Tissues Tooth Loss Tooth structure arthropathies bone cohort college cytokine dental surgery disability functional outcomes functional status human data illness length improved inhibitor/antagonist interest loss of function response

项目摘要

DESCRIPTION (provided by applicant): The pathogenic mechanisms of rheumatoid arthritis (RA) and periodontal disease (PD) are remarkably similar, with similar cellular events in the inflammatory focus, common profiles of cytokines, proteases, and inflammatory markers, and bone and collagen degradation. An increased prevalence of PD has been described in patients with longstanding RA, yet further exploration of this association has been limited. Many have argued that RA predisposed to the development of PD with hypothesized interactions of decreased salivary pool, poor oral hygiene from hand disability, or medication effects. The growing appreciation of Anti-CCP antibodies as diagnostic and prognostic markers for RA is significant, given that certain strains of bacteria associated with progressive periodontal disease represent a source of an enzyme producing citrullinated peptides, potentially serving to trigger the attendant antibody response seen in RA. Thus, it is possible that PD serves as a precipitant for some cases of RA or is a modifying factor of the disease. The recognition of an influence of PD on other systemic illnesses, notably diabetes and atherosclerotic disease, in which shared pathogenic mechanisms are less clear, provide additional rationale to evaluate relationships between PD and RA, diseases in which the mechanisms of disease have many similarities. It is our hypothesis that the prevalence of periodontal disease in RA patients at the onset of their arthritic disease is increased compared to matched controls without RA and that the presence and severity of PD will correlate with RA disease activity. Specific Aim 1 is to evaluate a cohort of subjects with newly diagnosed RA for periodontal health compared to control subjects without arthritis. The primary outcome measurement will be the presence of periodontal disease in RA compared to non-arthritic controls. Specific Aim 2 is to explore relationships between RA disease activity with periodontal severity. These studies represent the first comprehensive evaluation of periodontal disease in early RA and will provide important preliminary data and biological samples for further studies of disease progression, response to therapy, and to elucidate common mechanisms of pathogenesis. This study represents a collaborative effort between Rheumatology at Johns Hopkins, the Univ. Of Maryland College of Dental Surgery, and NYU College of Dentistry. The relationships developed for this study constitute a unique multi-centered interdisciplinary group of investigators and will facilitate the preparation and implementation of much broader research proposals to more clearly define the overall oral health of patients with RA.

描述（由申请人提供）：类风湿性关节炎（RA）和牙周病（PD）的致病机制非常相似，在炎症病灶中具有相似的细胞事件，细胞因子、蛋白酶和炎症标志物的共同特征，以及骨和胶原降解。在长期RA患者中，PD患病率增加，但对这种相关性的进一步探索有限。许多人认为，RA易患PD，并假设唾液池减少、手部残疾导致口腔卫生不良或药物作用的相互作用。抗CCP抗体作为RA的诊断和预后标志物的日益增长的认识是重要的，因为与进行性牙周病相关的某些细菌菌株代表了产生瓜氨酸肽的酶的来源，可能用于触发RA中所见的伴随抗体应答。因此，PD可能是某些RA病例的促发因素或疾病的修饰因子。认识到PD对其他全身性疾病的影响，特别是糖尿病和动脉粥样硬化疾病，其中共有的致病机制尚不清楚，为评价PD和RA之间的关系提供了额外的依据，这些疾病的发病机制具有许多相似之处。我们的假设是，RA患者在关节炎疾病发作时牙周病的患病率与无RA的对照组相比增加，并且PD的存在和严重程度与RA疾病活动相关。具体目标1是评估一组新诊断的RA受试者的牙周健康状况，来控制没有关节炎的受试者。主要结果测量将是牙周的存在，与非关节炎对照相比，RA中的疾病。具体目标2是探索RA疾病活动与牙周严重程度之间的关系。这些研究代表了对早期RA牙周病的首次全面评估，将为进一步研究疾病进展、治疗反应以及阐明发病机制的共同机制提供重要的初步数据和生物样本。这项研究代表了约翰霍普金斯大学流变学，马里兰州大学牙科学院和纽约大学牙科学院之间的合作努力。为这项研究建立的关系构成了一个独特的多中心跨学科研究小组，并将促进更广泛的研究提案的准备和实施，以更清楚地定义RA患者的整体口腔健康。