Oral status in patients with early rheumatoid arthritis: a prospective, case–control study
TL;DR: Increased loss of periodontal attachment and alveolar bone can be detected in patients with ERA, therefore it is proposed that the consulting rheumatologists inform the patients that they have a higher risk ofperiodontal disease.
Abstract: Objective. Patients with RA suffer from a higher risk of periodontal attachment loss and increased oral inflammation. We hypothesize that there are pathogenetic and immunological interactions between these diseases that go beyond impaired manual dexterity accompanying advanced RA. The primary objective of the present study was to determine whether a loss of alveolar bone can be detected in RA patients during the early course of the disease. Methods. In this cross-sectional, epidemiological casecontrol study, 22 patients with early RA (ERA) were compared with 22 matched healthy controls. Oral and periodontal status, clinical activity, and sociodemographic parameters were determined. Oral microbiota were analysed using real-time quantitative PCR specific for leading oral pathogens. Results. More advanced forms of periodontitis were found in ERA patients compared with controls. ERA patients had a greater number of missing teeth [ERA 5.7 (S.D. 5.0), controls 1.9 (S.D. 1.0), P = 0.002], deeper periodontal pockets [clinical attachment level: ERA 3.4 (S.D. 0.5 mm), controls 2.7 (S.D. 0.3 mm), P < 0.000], and greater bleeding on probing [ERA 18.6% (S.D. 9.0%), controls 10.5% (S.D. 5.1%), P = 0.001] despite comparable oral hygiene. Tannerella forsythia (6.77-fold, P = 0.033) subgingivally and Streptococcus anginosus (3.56-fold, P = 0.028) supragingivally were the characteristic pathogens in ERA. Conclusion. Increased loss of periodontal attachment and alveolar bone can be detected in patients with ERA, therefore we propose that the consulting rheumatologists inform the patients that they have a higher risk of periodontal disease. It would be beneficial if these patients were referred directly for intensive dental care.
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TL;DR: This review summarises the current status on the role of the microbiota in autoimmune diseases and offers novel insight into factors that initiate and drive disease progression, stratify patient risk for complications and ultimately deliver new therapeutic strategies.
Abstract: The microbiota of the human metaorganism is not a mere bystander. These microbes have coevolved with us and are pivotal to normal development and homoeostasis. Dysbiosis of the GI microbiota is associated with many disease susceptibilities, including obesity, malignancy, liver disease and GI pathology such as IBD. It is clear that there is direct and indirect crosstalk between this microbial community and host immune response. However, the precise mechanism of this microbial influence in disease pathogenesis remains elusive and is now a major research focus. There is emerging literature on the role of the microbiota in the pathogenesis of autoimmune disease, with clear and increasing evidence that changes in the microbiota are associated with some of these diseases. Examples include type 1 diabetes, coeliac disease and rheumatoid arthritis, and these contribute significantly to global morbidity and mortality. Understanding the role of the microbiota in autoimmune diseases may offer novel insight into factors that initiate and drive disease progression, stratify patient risk for complications and ultimately deliver new therapeutic strategies. This review summarises the current status on the role of the microbiota in autoimmune diseases.
173 citations
TL;DR: A significant association between RA and periodontitis is supported by the results of the systematic review and meta-analysis of studies comparing RA to healthy controls and this is not replicated when comparingRA to OA controls.
Abstract: Background: Rheumatoid arthritis (RA) and periodontitis are both chronic inflammatory disease which demonstrate similarities in terms of mechanism, histopathology and demography. An association between these conditions has been demonstrated previously but has been called into question more recently. Methods: The published databases MEDLINE, EMBASE and PsycINFO were searched using search terms related to RA and periodontitis. Articles were selected if they included data on the number of people with RA diagnosed with periodontitis (or periodontal disease parameters) compared to a control comparison group. Review articles, case reports, animal model studies, non-English language and articles with unavailable abstracts were excluded. Data was extracted, critically appraised using the Downs and Black tool and a random effect Mantel-Haenszel meta-analysis was performed. Results: 21 papers met the eligibility criteria and provided data for the meta-analysis; 17 studies (including a total of 153,492 participants) comparing RA to healthy controls and 4 (including a total of 1378 participants) comparing RA to osteoarthritis (OA). There was a significantly increased risk of periodontitis in people with RA compared to healthy controls (RR: 1.13; 95% CI: 1.04, 1.23; p=0.006; N: 153,277) with a significantly raised mean probing depth, risk of bleeding on probing (BOP) and absolute value of clinical attachment loss in those with rheumatoid arthritis. When comparing RA and OA, there was no significant difference in the prevalence of periodontitis, however the risk of BOP was greater in OA than RA. Conclusion: The significant association between RA and periodontitis is supported by the results of our systematic review and meta-analysis of studies comparing RA to healthy controls. In our meta-analysis, however, this is not replicated when comparing RA to OA controls.
169 citations
TL;DR: Dysbiosis was detected in the gut and oral microbiomes of RA patients, but it was partially restored after treatment, and functional changes of microbiota and molecular mimicry of human antigens in RA individuals were found.
120 citations
Cites background from "Oral status in patients with early ..."
...Subgingival Tannerella forsythia and supragingival Streptococcus anginosus were two characteristic pathogenic bacteria in early RA [61]....
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TL;DR: The majority of the articles have confirmed that there is a correlation between PD and RA, since both disorders have characteristics in common and result from an imbalance in the immunoinflammatory response.
Abstract: Periodontitis (PD) and rheumatoid arthritis (RA) are immunoinflammatory diseases where leukocyte infiltration and inflammatory mediators induce alveolar bone loss, synovitis, and joint destruction, respectively. Thus, we reviewed the relationship between both diseases considering epidemiological aspects, mechanical periodontal treatment, inflammatory mediators, oral microbiota, and antibodies, using the keywords "periodontitis" and "rheumatoid arthritis" in PubMed database between January 2012 and March 2015, resulting in 162 articles. After critical reading based on titles and abstracts and following the inclusion and exclusion criteria, 26 articles were included. In the articles, women over 40 years old, smokers and nonsmokers, mainly constituted the analyzed groups. Eight studies broached the epidemiological relationship with PD and RA. Four trials demonstrated that the periodontal treatment influenced the severity of RA and periodontal clinical parameters. Nine studies were related with bacteria influence in the pathogenesis of RA and the presence of citrullinated proteins, autoantibodies, or rheumatoid factor in patients with PD and RA. Five studies investigated the presence of mediators of inflammation in PD and RA. In summary, the majority of the articles have confirmed that there is a correlation between PD and RA, since both disorders have characteristics in common and result from an imbalance in the immunoinflammatory response.
110 citations
Cites background from "Oral status in patients with early ..."
...In the remainder of the studies, the most frequently reported treatment for rheumatoid arthritis included disease-modifying antirheumatic drugs (methotrexate, sulfasalazine, and leflunomide) [38, 39, 42, 43, 46, 51, 54, 56, 57, 59], biologic therapy (anti-TNF-α) [34, 38, 39, 42, 59], corticosteroids (prednisolone) [38, 42, 43, 46, 51, 54, 56, 59], and/or nonsteroidal anti-inflammatory drugs [43, 46–48, 51, 54, 57]....
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...Among the selected trials, eight studies broached the epidemiological and clinical relationship of patients with PD and RA [38, 41, 44, 45, 49, 54, 56, 59], indicating a higher prevalence of PD in patients with RA, which have worse periodontal parameters....
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TL;DR: The role of the gut microbiota in shaping local and systemic immune responses and how disturbances in the host–microorganism interplay can potentially affect the development and progression of rheumatic diseases are reviewed.
Abstract: The human gut harbours a tremendously diverse and abundant microbial community that correlates with, and even modulates, many health-related processes. The mucosal interfaces are particularly active sites of microorganism-host interplay. Growing insight into the characteristic composition and functionality of the mucosal microbiota has revealed that the microbiota is involved in mucosal barrier integrity and immune function. This involvement affects proinflammatory and anti-inflammatory processes not only at the epithelial level, but also at remote sites such as the joints. Here, we review the role of the gut microbiota in shaping local and systemic immune responses and how disturbances in the host-microorganism interplay can potentially affect the development and progression of rheumatic diseases. Increasing our understanding of how to promote host-microorganism homeostasis could therefore reveal novel strategies for the prevention or alleviation of rheumatic disease.
110 citations
References
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Medical University of Vienna1, Boston University2, Arthritis Research UK3, Johns Hopkins University4, University of California, San Francisco5, Charité6, University of Toronto7, National Jewish Health8, Harvard University9, University of Paris10, University of Leeds11, Catholic University of the Sacred Heart12, Erasmus University Rotterdam13, University of Colorado Denver14, Leiden University15, University of California, San Diego16, University of Massachusetts Medical School17, University of Michigan18, University of Washington19, McGill University20, University of Pittsburgh21, Ministry of Health (New Zealand)22, New York University23, University of Manchester24, University of Amsterdam25
TL;DR: This new classification system redefines the current paradigm of RA by focusing on features at earlier stages of disease that are associated with persistent and/or erosive disease, rather than defining the disease by its late-stage features.
Abstract: Objective The 1987 American College of Rheumatology (ACR; formerly the American Rheumatism Association) classification criteria for rheumatoid arthritis (RA) have been criticised for their lack of sensitivity in early disease. This work was undertaken to develop new classification criteria for RA. Methods A joint working group from the ACR and the European League Against Rheumatism developed, in three phases, a new approach to classifying RA. The work focused on identifying, among patients newly presenting with undifferentiated inflammatory synovitis, factors that best discriminated between those who were and those who were not at high risk for persistent and/or erosive disease—this being the appropriate current paradigm underlying the disease construct ‘RA’. Results In the new criteria set, classification as ‘definite RA’ is based on the confirmed presence of synovitis in at least one joint, absence of an alternative diagnosis better explaining the synovitis, and achievement of a total score of 6 or greater (of a possible 10) from the individual scores in four domains: number and site of involved joints (range 0–5), serological abnormality (range 0–3), elevated acute-phase response (range 0–1) and symptom duration (two levels; range 0–1). Conclusion This new classification system redefines the current paradigm of RA by focusing on features at earlier stages of disease that are associated with persistent and/or erosive disease, rather than defining the disease by its late-stage features. This will refocus attention on the important need for earlier diagnosis and institution of effective disease-suppressing therapy to prevent or minimise the occurrence of the undesirable sequelae that currently comprise the paradigm underlying the disease construct ‘RA’.
5,964 citations
TL;DR: How the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics is summarized.
Abstract: Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classi- fication system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics.1 Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology.2 These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings including: 1) considerable overlap in disease categories, 2) absence of a gingival disease component, 3) inappropriate emphasis on age of onset of disease and rates of progression, and 4) inadequate or unclear classification criteria. The 1993 Europea...
4,653 citations
TL;DR: The purpose of the present investigation was to attempt to define communities using data from large numbers of plaque samples and different clustering and ordination techniques, which related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.
Abstract: It has been recognized for some time that bacterial species exist in complexes in subgingival plaque. The purpose of the present investigation was to attempt to define such communities using data from large numbers of plaque samples and different clustering and ordination techniques. Subgingival plaque samples were taken from the mesial aspect of each tooth in 185 subjects (mean age 51 +/- 16 years) with (n = 160) or without (n = 25) periodontitis. The presence and levels of 40 subgingival taxa were determined in 13,261 plaque samples using whole genomic DNA probes and checkerboard DNA-DNA hybridization. Clinical assessments were made at 6 sites per tooth at each visit. Similarities between pairs of species were computed using phi coefficients and species clustered using an averaged unweighted linkage sort. Community ordination was performed using principal components analysis and correspondence analysis. 5 major complexes were consistently observed using any of the analytical methods. One complex consisted of the tightly related group: Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. The 2nd complex consisted of a tightly related core group including members of the Fusobacterium nucleatum/periodonticum subspecies, Prevotella intermedia, Prevotella nigrescens and Peptostreptococcus micros. Species associated with this group included: Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis. The 3rd complex consisted of Streptococcus sanguis, S. oralis, S. mitis, S. gordonii and S. intermedius. The 4th complex was comprised of 3 Capnocytophaga species, Campylobacter concisus, Eikenella corrodens and Actinobacillus actinomycetemcomitans serotype a. The 5th complex consisted of Veillonella parvula and Actinomyces odontolyticus. A. actinomycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2 (A. viscosus) were outliers with little relation to each other and the 5 major complexes. The 1st complex related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.
4,143 citations
Journal Article•
TL;DR: The origin of indices for recording gingivitis and plaque is reviewed and the use of the site prevalence of a single finding is suggested, which could be used as a clinically relevant parameter for oral hygiene and gingival inflammation.
2,554 citations
TL;DR: Examination systems for oral hygiene status use either selected teeth or the highest score for a group of teeth within a segment as the basis for their scores, which are of limited value for the clinician treating an individual patient.
Abstract: A N U M B E R OF examination systems have been developed to record the oral hygiene status of an individual. Most systems use either selected teeth or the highest score for a group of teeth within a segment as the basis for their scores. When used for epidemiological studies or for evaluating the results of treatment in a study group these methods yield useful information. A numerical score, however, is of limited value for the clinician treating an individual patient. He is concerned with the locations where plaque accumulates and in the patient's progress in learning how to effectively clean these surfaces.
2,135 citations