What can the periodontal community learn from the pathophysiology of rheumatoid arthritis?

被引：43

作者：

Culshaw, Shauna ^{[2
]}

McInnes, Iain B. ^{[1
]}

Liew, Foo Y. ^{[1
]}

机构：

[1] Univ Glasgow, Coll Med Vet & Life Sci, Inst Infect Immun & Inflammat, Glasgow Biomed Res Ctr, Glasgow G61 1BD, Lanark, Scotland

[2] Univ Glasgow, Glasgow Dent Hosp & Sch, Glasgow G61 1BD, Lanark, Scotland

来源：

JOURNAL OF CLINICAL PERIODONTOLOGY | 2011年 / 38卷

基金：

英国惠康基金; 英国医学研究理事会;

关键词：

bone destruction; host response; periodontitis; rheumatoid arthritis; ANTITUMOR NECROSIS FACTOR; DOUBLE-BLIND; T-CELL; MONOCLONAL-ANTIBODY; DESTRUCTIVE ARTHRITIS; SYNOVIAL-FLUID; BONE-MARROW; B-CELLS; THERAPY; TNF;

D O I：

10.1111/j.1600-051X.2010.01669.x

中图分类号：

R78 [口腔科学];

学科分类号：

1003 ;

摘要：

P>Aim The aim of this paper is to provide a narrative review of the aetiopathogeneis and treatments of rheumatoid arthritis (RA), focusing on aspects that may share commonality with periodontitis. Results A myriad of cell types, cytokines and pathways have been investigated in both periodontitis and RA. Chronic inflammatory diseases, including RA, psoriatic arthritis, ankylosing spondylitis and periodontitis are likely to share pathogenic mechanisms of inflammation-mediated solid tissue destruction. The aetiopathogenesis of these diseases has been extensively researched over the last several decades and advances in understanding have revolutionized arthritis therapeutics. Conclusion The rational, targeted inhibition of mediators in RA has provided clinically useful therapeutics and shed light on mechanisms underpinning disease pathogenesis. RA should be considered a prototypic disease revealing how understanding disease pathogenesis may transform therapeutic options and patient outcomes.

引用

页码：106 / 113

页数：8

共 75 条

[21] LY2439821, a Humanized Anti-Interleukin-17 Monoclonal Antibody, in the Treatment of Patients With Rheumatoid Arthritis A Phase I Randomized, Double-Blind, Placebo-Controlled, Proof-of-Concept Study [J].