The association between rheumatoid arthritis and periodontal disease

被引:172
作者
Detert, Jacqueline [1 ]
Pischon, Nicole [2 ]
Burmester, Gerd R. [1 ]
Buttgereit, Frank [1 ]
机构
[1] Charite, Dept Rheumatol & Clin Immunol, D-10117 Berlin, Germany
[2] Charite, Dept Periodontol, D-13353 Berlin, Germany
关键词
PORPHYROMONAS-GINGIVALIS; ORAL BACTERIA; SYNOVIAL-FLUID; HLA DR4; ANTIBODIES; SMOKING; CELLS; PURIFICATION; ADHESION; TISSUE;
D O I
10.1186/ar3106
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic, plaque-associated inflammation of the gingiva and the periodontium are among the most common oral diseases. Periodontitis (PD) is characterized by the inflammatory destruction of the periodontal attachment and alveolar bone, and its clinical appearance can be influenced by congenital as well as acquired factors. The existence of a rheumatic or other inflammatory systemic disease may promote PD in both its emergence and progress. However, there is evidence that PD maintains systemic diseases. Nevertheless, many mechanisms in the pathogenesis have not yet been examined sufficiently, so that a final explanatory model is still under discussion, and we hereby present arguments in favor of this. In this review, we also discuss in detail the fact that oral bacterial infections and inflammation seem to be linked directly to the etiopathogenesis of rheumatoid arthritis (RA). There are findings that support the hypothesis that oral infections play a role in RA pathogenesis. Of special importance are the impact of periodontal pathogens, such as Porphyromonas gingivalis on citrullination, and the association of PD in RA patients with seropositivity toward rheumatoid factor and the anti-cyclic citrullinated peptide antibody.
引用
收藏
页数:7
相关论文
共 61 条
[41]   THE ROLE OF INFLAMMATORY MEDIATORS IN THE PATHOGENESIS OF PERIODONTAL-DISEASE [J].
PAGE, RC .
JOURNAL OF PERIODONTAL RESEARCH, 1991, 26 (03) :230-242
[42]  
Pischon N, 2008, J PERIODONTOL, V79, P979, DOI [10.1902/jop.2008.070501, 10.1902/jop.2008.070501 ]
[43]   Effects of Porphyromonas gingivalis on cell cycle progression and apoptosis of primary human chondrocytes [J].
Pischon, N. ;
Roehner, E. ;
Hocke, A. ;
N'Guessan, P. ;
Mueller, H. C. ;
Matziolis, G. ;
Kanitz, V. ;
Purucker, P. ;
Kleber, B-M ;
Bernimoulin, P. ;
Burmester, G. ;
Buttgereit, F. ;
Detert, J. .
ANNALS OF THE RHEUMATIC DISEASES, 2009, 68 (12) :1902-1907
[44]   Role of bacterial proteinases in matrix destruction and modulation of host responses [J].
Potempa, J ;
Banbula, A ;
Travis, J .
PERIODONTOLOGY 2000, 2000, 24 :153-192
[45]   Protection of rats from adjuvant arthritis by immunization with naked DNA encoding for mycobacterial heat shock protein 65 [J].
Ragno, S ;
Colston, MJ ;
Lowrie, DB ;
Winrow, VR ;
Blake, DR ;
Tascon, R .
ARTHRITIS AND RHEUMATISM, 1997, 40 (02) :277-283
[46]   LOCAL ANTI-TYPE-II COLLAGEN ANTIBODY-PRODUCTION IN RHEUMATOID-ARTHRITIS SYNOVIAL-FLUID - EVIDENCE FOR AN HLA-DRL-RESTRICTED IGG RESPONSE [J].
RONNELID, J ;
LYSHOLM, J ;
ENGSTROMLAURENT, A ;
KLARESKOG, L ;
HEYMAN, B .
ARTHRITIS AND RHEUMATISM, 1994, 37 (07) :1023-1029
[47]   Hypothesis: The humoral immune response to oral bacteria provides a stimulus for the development of rheumatoid arthritis [J].
Rosenstein, ED ;
Greenwald, RA ;
Kushner, LJ ;
Weissmann, G .
INFLAMMATION, 2004, 28 (06) :311-318
[48]   Periodontitis, A True Infection [J].
Saini, Rajiv ;
Marawar, P. P. ;
Shete, Sujata ;
Saini, Santosh .
JOURNAL OF GLOBAL INFECTIOUS DISEASES, 2009, 1 (02) :149-+
[49]   HUMAN-IMMUNOGLOBULIN G (IGG) FC-RECEPTOR-IIA (CD32) POLYMORPHISM AND IGG2-MEDIATED BACTERIAL PHAGOCYTOSIS BY NEUTROPHILS [J].
SANDERS, LAM ;
FELDMAN, RG ;
VOORHORSTOGINK, MM ;
DEHAAS, M ;
RIJKERS, GT ;
CAPEL, PJA ;
ZEGERS, BJM ;
VANDEWINKEL, JGJ .
INFECTION AND IMMUNITY, 1995, 63 (01) :73-81
[50]  
Schellekens GA, 2000, ARTHRITIS RHEUM-US, V43, P155, DOI 10.1002/1529-0131(200001)43:1<155::AID-ANR20>3.0.CO