Department of Periodontics and Department of Oral Medicine, University of Washington, Seattle, WA, USA; Oral Health Sciences, University of Kristianstad, Kristianstad, Sweden; and Department of Periodontology, University of Bern, Bern, Switzerland.
J Oral Microbiol. 2012;4. doi: 10.3402/jom.v4i0.11829. Epub 2012 Feb 13.
An association between oral disease/periodontitis and rheumatoid arthritis (RA) has been considered since the early 1820s. The early treatment was tooth eradication. Epidemiological studies suggest that the prevalence of RA and periodontitis may be similar and about 5% of the population are aged 50 years or older. RA is considered as an autoimmune disease whereas periodontitis has an infectious etiology with a complex inflammatory response. Both diseases are chronic and may present with bursts of disease activity. Association studies have suggested odds ratios of having RA and periodontitis varying from 1.8:1 (95% CI: 1.0-3.2, NS) to 8:1 (95% CI: 2.9-22.1, p<0.001). Genetic factors are driving the host responses in both RA and periodontitis. Tumor necrosis factor-α, a proinflammatory cytokine, regulates a cascade of inflammatory events in both RA and periodontitis. Porphyromonas gingivalis is a common pathogen in periodontal infection. P. gingivalis has also been identified in synovial fluid. The specific abilities of P. gingivalis to citrullinate host peptides by proteolytic cleavage at Arg-X peptide bonds by arginine gingipains can induce autoimmune responses in RA through development of anticyclic citrullinated peptide antibodies. In addition, P. gingivalis carries heat shock proteins (HSPs) that may also trigger autoimmune responses in subjects with RA. Data suggest that periodontal therapies combined with routine RA treatments further improve RA status.
Periodontal infection (P. gingivalis) carries a unique risk for development of autoimmune antibodies associated with RA. Patients with RA have either lost many teeth or usually have severe periodontitis. Additional research, both in regards to basic mechanisms as well as clinical studies, are necessary before it can be said that there are causative links between RA and periodontitis. Cross-disciplinary research in well-defined populations should be performed to further enhance knowledge and develop clinical strategies how to coordinate therapy and risk assessments of RA and periodontitis.
自从 19 世纪 20 年代以来，人们就已经认识到口腔疾病/牙周炎与类风湿关节炎（RA）之间存在关联。早期的治疗方法是拔牙。流行病学研究表明，RA 和牙周炎的患病率可能相似，约有 5%的人口年龄在 50 岁或以上。RA 被认为是一种自身免疫性疾病，而牙周炎则具有感染病因，伴有复杂的炎症反应。两种疾病都是慢性的，可能会出现疾病活动的爆发。关联研究表明，RA 和牙周炎并存的几率比从 1.8:1（95%可信区间：1.0-3.2，无统计学意义）到 8:1（95%可信区间：2.9-22.1，p<0.001）不等。遗传因素是导致 RA 和牙周炎宿主反应的原因。肿瘤坏死因子-α（TNF-α），一种促炎细胞因子，调节 RA 和牙周炎中炎症事件的级联反应。牙龈卟啉单胞菌是牙周感染的常见病原体。也在滑液中发现了 P. gingivalis。牙龈卟啉单胞菌通过精氨酸牙龈蛋白酶在 Arg-X 肽键处的蛋白水解切割使宿主肽瓜氨酸化的特殊能力可以通过产生抗环瓜氨酸肽抗体在 RA 中诱导自身免疫反应。此外，P. gingivalis 携带热休克蛋白（HSPs），这也可能在 RA 患者中引发自身免疫反应。数据表明，牙周治疗与常规 RA 治疗相结合可进一步改善 RA 状况。
牙周感染（牙龈卟啉单胞菌）会增加与 RA 相关的自身抗体的产生风险。RA 患者要么已经失去了许多牙齿，要么通常患有严重的牙周炎。在能够确定 RA 和牙周炎之间存在因果关系之前，还需要进行更多的基础机制和临床研究。应在明确界定的人群中进行跨学科研究，以进一步增强知识，并制定如何协调 RA 和牙周炎的治疗和风险评估的临床策略。
