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本文引用的文献

1
Pre-existing periodontitis exacerbates experimental arthritis in a mouse model.先前存在的牙周炎会加重小鼠模型中的实验性关节炎。
J Clin Periodontol. 2011 Jun;38(6):532-41. doi: 10.1111/j.1600-051X.2011.01714.x. Epub 2011 Mar 21.
2
Impact of monocytic cells on recovery of uncultivable bacteria from atherosclerotic lesions.单核细胞对动脉粥样硬化病变中不可培养细菌恢复的影响。
J Intern Med. 2011 Sep;270(3):273-80. doi: 10.1111/j.1365-2796.2011.02373.x. Epub 2011 Apr 11.
3
What can the periodontal community learn from the pathophysiology of rheumatoid arthritis?牙周病学界能从类风湿性关节炎的病理生理学中学到什么?
J Clin Periodontol. 2011 Mar;38 Suppl 11:106-13. doi: 10.1111/j.1600-051X.2010.01669.x.
4
Prevalence and simultaneous occurrence of periodontitis and dental caries.牙周炎和龋齿的流行和同时发生。
J Clin Periodontol. 2010 Nov;37(11):962-7. doi: 10.1111/j.1600-051X.2010.01620.x. Epub 2010 Sep 7.
5
Periodontitis in RA-the citrullinated enolase connection.类风湿关节炎相关牙周炎——瓜氨酸化烯醇化酶的关联。
Nat Rev Rheumatol. 2010 Dec;6(12):727-30. doi: 10.1038/nrrheum.2010.139. Epub 2010 Sep 7.
6
A prospective study of periodontal disease and risk of rheumatoid arthritis.一项牙周病与类风湿关节炎风险的前瞻性研究。
J Rheumatol. 2010 Sep;37(9):1800-4. doi: 10.3899/jrheum.091398. Epub 2010 Jul 1.
7
Effect of Porphyromonas gingivalis-induced inflammation on the development of rheumatoid arthritis.牙龈卟啉单胞菌诱导的炎症对类风湿关节炎发展的影响。
J Clin Periodontol. 2010 May;37(5):405-11. doi: 10.1111/j.1600-051X.2010.01552.x.
8
Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and α-enolase: implications for autoimmunity in rheumatoid arthritis.牙龈卟啉单胞菌的肽基精氨酸脱亚氨酶使人类纤维蛋白原和α-烯醇化酶瓜氨酸化:对类风湿关节炎自身免疫的影响。
Arthritis Rheum. 2010 Sep;62(9):2662-72. doi: 10.1002/art.27552.
9
The environment, geo-epidemiology, and autoimmune disease: Rheumatoid arthritis.环境、地理流行病学与自身免疫性疾病:类风湿关节炎。
J Autoimmun. 2010 Aug;35(1):10-4. doi: 10.1016/j.jaut.2009.12.009. Epub 2010 Jan 18.
10
Periodontitis in systemic rheumatic diseases.系统性风湿性疾病中的牙周炎
Nat Rev Rheumatol. 2009 Apr;5(4):218-24. doi: 10.1038/nrrheum.2009.28.

牙周病、牙齿缺失与类风湿关节炎发病的相关性:来自第一届全国健康与营养调查及其随访研究的结果。

Periodontal disease, tooth loss and incident rheumatoid arthritis: results from the First National Health and Nutrition Examination Survey and its epidemiological follow-up study.

机构信息

Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.

出版信息

J Clin Periodontol. 2011 Nov;38(11):998-1006. doi: 10.1111/j.1600-051X.2011.01776.x. Epub 2011 Sep 13.

DOI:10.1111/j.1600-051X.2011.01776.x
PMID:22092471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3403745/
Abstract

AIMS

Infection may be a rheumatoid arthritis (RA) risk factor. We examined whether signs of periodontal infection were associated with RA development in the First National Health and Nutrition Examination Survey and its epidemiological follow-up study.

MATERIAL AND METHODS

In 1971-1974, 9702 men and women aged 25-74 were enrolled and surveyed longitudinally (1982, 1986, 1987, 1992). Periodontal infection was defined by baseline tooth loss or clinical evidence of periodontal disease. Baseline (n = 138) and incident (n = 433) RA cases were defined via self-report physician diagnosis, joint pain/swelling, ICD-9 codes (714.0-714.9), death certificates and/or RA hospitalization.

RESULTS

Adjusted odds ratios (ORs) (95% CI) for prevalent RA in gingivitis and periodontitis (versus healthy) were 1.09 (0.57, 2.10) and 1.85 (0.95, 3.63); incident RA ORs were 1.32 (0.85, 2.06) and 1.00 (0.68, 1.48). The ORs for prevalent RA among participants missing 5-8, 9-14, 15-31 or 32 teeth (versus 0-4 teeth) were 1.74 (1.03, 2.95), 1.82 (0.81, 4.10), 1.45 (0.62, 3.41) and 1.30 (0.48, 3.53); ORs for incident RA were 1.12 (0.77, 1.64), 1.67 (1.12, 2.48), 1.40 (0.85, 2.33) and 1.22 (0.75, 2.00). Dose-responsiveness was enhanced among never smokers. The rate of death or loss-to-follow-up after 1982 was two- to fourfold higher among participants with periodontitis or missing ≥9 teeth (versus healthy participants).

CONCLUSIONS

Although participants with periodontal disease or ≥5 missing teeth experienced higher odds of prevalent/incident RA, most ORs were non-statistically significant and lacked dose-responsiveness. Differential RA ascertainment bias complicated the interpretation of these data.

摘要

目的

感染可能是类风湿关节炎(RA)的一个风险因素。我们研究了牙周感染的迹象是否与第一国家健康和营养检查调查及其流行病学随访研究中的 RA 发展有关。

材料和方法

1971-1974 年,招募了 9702 名 25-74 岁的男性和女性,并进行了纵向调查(1982 年、1986 年、1987 年、1992 年)。牙周感染通过基线牙齿缺失或牙周病的临床证据来定义。通过自我报告的医生诊断、关节疼痛/肿胀、ICD-9 代码(714.0-714.9)、死亡证明和/或 RA 住院来确定基线(n=138)和新发(n=433)RA 病例。

结果

牙龈炎和牙周炎(与健康相比)的现患 RA 调整后比值比(OR)(95%CI)分别为 1.09(0.57,2.10)和 1.85(0.95,3.63);新发 RA OR 分别为 1.32(0.85,2.06)和 1.00(0.68,1.48)。缺失 5-8、9-14、15-31 或 32 颗牙齿的参与者中现患 RA 的 OR(与缺失 0-4 颗牙齿的参与者相比)分别为 1.74(1.03,2.95)、1.82(0.81,4.10)、1.45(0.62,3.41)和 1.30(0.48,3.53);新发 RA 的 OR 分别为 1.12(0.77,1.64)、1.67(1.12,2.48)、1.40(0.85,2.33)和 1.22(0.75,2.00)。从不吸烟者的 OR 增强了剂量反应性。与牙周健康的参与者相比,牙周炎或缺失≥9 颗牙齿的参与者在 1982 年后的死亡率或失访率高出两到四倍。

结论

尽管患有牙周病或缺失≥5 颗牙齿的参与者现患/新发 RA 的几率更高,但大多数 OR 均无统计学意义,且缺乏剂量反应性。RA 确诊的偏倚差异使这些数据的解释复杂化。