Clinical Periodontal and Microbiologic Parameters in Patients With Rheumatoid Arthritisby Dirk Ziebolz, Sven O. Pabel, Katharina Lange, Berndt Krohn-Grimberghe, Else Hornecker, Rainer F. Mausberg

Journal of Periodontology




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Omer Nuri Pamuk, Salim Donmez, Gulsum Emel Pamuk, Fulya Oz Puyan, Edward C. Keystone


Clinical Periodontal and Microbiologic

Parameters in Patients With Rheumatoid


Dirk Ziebolz,* Sven O. Pabel,* Katharina Lange,† Berndt Krohn-Grimberghe,‡ Else Hornecker,* and Rainer F. Mausberg*

Background: A limited number of studies suggest a prevalence of periodontal pathogens in patients with rheumatoid arthritis (RA); however, results are inconsistent. The aim of this study is to investigate clinical periodontal and microbiologic parameters in patients with RA.

Methods: Sixty-six patients with RA, aged 49.5 – 8.4 years, participated in the study. The periodontal classification was assessed with the periodontal screening index (PSR/PSI) allocated to the following parameters: 1) healthy; 2) gingivitis (PSR/PSI score 0 to 2, maximum one sextant score; 3) moderate periodontitis (>1 sextant PSR/PSI score 3, maximum one sextant score; or, 4) severe periodontitis (>1 sextant PSR/PSI score 4).

Pool samples were taken for microbiologic (polymerase chain reaction) analysis for the presence of 11 periodontal pathogens.

Statistical analysiswasbynon-parametricanalysisof covariance.

Results: No patients were periodontally healthy: 24 patients were classified as having gingivitis; 18 patients had moderate periodontitis; 23 patients had severe periodontitis; and one patient was toothless. For most patients, Fusobacterium nucleatum (98%), Eikenella corrodens (91%), and Parvimonasmicra (previously Peptostreptococcus micros; 88%) were above the detection threshold. Strong periodontal pathogens were less frequently detected: Aggregatibacter actinomycetemcomitans (previously

Actinobacillus actinomycetemcomitans, 16%); Porphyromonas gingivalis (58%); and Tannerella forsythia (previously T. forsythensis, 78%). Statistical analysis showed no significant influence of rheumatic factor (P = 0.33) on periodontal classification and on microbiologic parameters (P>0.05). Only smoking showed a significant influence (P = 0.0004) on the periodontal classification and in the case of E. corrodens (P = 0.02).

Conclusions: Most patients with RA in this study showed moderate-to-severe periodontitis and the presence of periodontal pathogens. No association was found between rheumatic factor on periodontal classification and microbiologic parameters. J Periodontol 2011;82:1424-1432.


Arthritis, rheumatoid; microbiology; oral health; periodontal diseases; tooth loss.

R heumatoid arthritis (RA) isachronic inflammatory disease of the joints characterized by loss of connective tissue and mineralized structures, the socalled ‘‘synovial membrane.’’1 The prevalence of the disease is 0.5% to 1%, and women are more frequently affected than men.1-3 Until now, the etiology of RA has not been unambiguously clarified. In addition to individual factors (age and sex), genetic factors (HLA-genotype), environmental factors (smoking and alcohol consumption), and bacterial infections have also been discussed as a cause.4-6 Consequently, RA shows similar etiologic factors as periodontitis, however, the two diseases differ from one another; moreover, their underlying pathogenetic mechanisms are strikingly similar.4

In recent years, there has been increasing evidence of an association between periodontitis and RA.7 This evidence suggests that patients with RA develop an increased risk of periodontitis, and show an increased tooth loss and a significantly greater clinical attachment loss (AL) than healthy individuals.8-14 However, there is currently no clear explanation as to if periodontal and rheumatic diseases occur together, and so possible causal relationships also remain unclear.7

Periodontitis is a chronic infective disease characterized by an irreversible loss of connective tissue and bone of the periodontal apparatus.15 The etiology is multifactorial and determined by a complex * Department of Preventive Dentistry, Periodontology and Cariology, University Medical

Center Goettingen, Goettingen, Germany. † Department of Medical Statistics, University Medical Center Goettingen. ‡ Rheumatology Clinic, Bad Wildungen, Germany. doi: 10.1902/jop.2011.100481

J Periodontol • October 2011 1424 interaction of inborn, acquired, and behaviorally related factors: the so-called ‘‘risk factors’’ (cigarette consumption, stress, and alcohol consumption), and genetic factors (interleukin [IL]-1 polymorphisms).15-19

However, the primary cause is the microbial colonization of the oral cavity with complex biofilms from different periodontal pathogenic bacteria.20,21 At the same time, in the subgingival plaque, various mainly Gram-negative bacteria species play a decisive role. These are organized in a complex and structured biofilm of different bacteria and can be ordered according to their pathogenicity in the pathogenesis or progression, respectively, of periodontitis to various complexes.22 In this context, particular importance has been attributed in the case of active periodontitis to the red complex with Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Treponema denticola (Td).

The more severe the oral infection with periodontal pathogenic bacteria, the greater the risk of bacteremia.23,24 Accordingly, an influence of periodontal pathogens on RA is conceivable. For example, bacterial DNA from anaerobes and high antibody titers against these bacteria has been detected in the serum and the synovial fluid of patients with RA.25-28 Also, periodontal bacteria seem to cause direct damage to joints via lipopolysaccarides and a breakdown of the extracellular cartilage matrix.29-31 In addition, an in vitro study found that Pg is able to invade primary human chondrocytes and induce cellular effects.32 Moreover, in an in vivo study, it was possible to demonstrate that dental treatment (nonsurgical periodontal treatment) results in reduced RA activity.33

The pathomechanisms and the transcription paths are currently unknown. Also, it has still not been determined which biofilm composition is present in patients with RA in conjunction with the periodontal condition. Therefore, the extent to which periodontal pathogenic bacteria can influence the pathogenesis of RA in a sustained manner is questionable, as is which factors favor the biofilm composition or are associated with RA, respectively. In this connection, it is conceivable that medication with rheumatic immunosuppressive agents influences bacterial colonization and biofilm pathogenicity and consequently could give rise to a possible potentiation of the previously mentioned cascade of effects. Likewise, the rheumatic factor and the severity of RA could be directly related to bacterial load.