Methotrexate promotes recovery of arthritis-induced alveolar bone loss and modifies the composition of the oral-gut microbiota.

OBJECTIVES: The impact of rheumatoid arthritis (RA) on the shaping of the oral and gut microbiome raises the question of whether and how RA treatment modifies microbial communities. We examined changes in the oral and gut microbiota in a mouse model of antigen-induced arthritis (AIA) treated or not with methotrexate (MTX). METHODS: Maxillae and stools were evaluated by the MiSeq platform of the V4 region of the 16S rRNA gene. Alveolar bone parameters were analysed by micro-computed tomography. Moreover, arthritis-induced changes in hyperalgesia and oedema were assessed, along with the impact on periodontal bone health. RESULTS: Microbial communities in MTX-treated AIA mice revealed distinct clusters compared to the control and AIA groups. Overall, MTX impacted the richness and variability of microorganisms in the oral-gut axis microbiome at the phylum level. Regarding the oral microbiome, while in the control group the most dominant phylum was Firmicutes, in the AIA group there was a shift towards the predominance of Campilobacteriota and Bacteroidetes associated with the disease. MTX treatment led to greater dominance of the health-associated phylum Proteobacteria. In the gut microbiome, AIA induction resulted in increased abundance of the Verrucomicrobiota phylum, and MTX treatment restored its levels compared to control. Importantly, the MTX-treated AIA animals had significantly less periodontal bone loss, as well as decreased hyperalgesia and joint oedema compared to the AIA animals. CONCLUSION: Data suggest the benefit of MTX treatment in protecting alveolar bone, in addition to providing new insights on the drug-microbiome interaction in the course of RA.

Are neutrophil extracellular traps the link for the cross-talk between periodontitis and rheumatoid arthritis physiopathology?

OBJECTIVES: Neutrophil extracellular traps (NETs) play a role in the pathogenesis of periodontitis and rheumatoid arthritis (RA). However, it remains poorly understood whether NETs participate in the cross-talk between periodontitis and RA. Herein, we investigated the production of NETs in individuals with periodontitis and RA and its association with clinical parameters. The impact of periodontal therapy on RA and NET release was also assessed. METHODS: The concentration of NETs and cytokines was determined in the saliva and plasma of individuals with early RA (n = 24), established RA (n = 64) and individuals without RA (n = 76). The influence of periodontitis on the production of NETs and cytokines was also evaluated. RESULTS: Individuals with early RA had a higher concentration of NETs in saliva and plasma than individuals with established RA or without RA. Periodontitis resulted in an increase in the concentration of NETs of groups of individuals without RA and with early RA. The proportion of individuals with high concentrations of IL-6, IL-10 and GM-CSF was higher among individuals with periodontitis than among individuals without periodontitis. The concentrations of TNF-α, IL-6, IL-17/IL-25 and IL-28A were particularly high in individuals with early RA. Worse periodontal clinical parameters, RA onset and RA activity were significantly associated with circulating NETs. Periodontal therapy was associated with a reduction in the concentration of NETs and inflammatory cytokines and amelioration in periodontitis and RA. CONCLUSION: This study reveals that NETs are a possible link between periodontitis and RA, with periodontal therapy resulting in a dramatic switch in circulating NET levels.

Osteocytes play an important role in experimental periodontitis in healthy and diabetic mice through expression of RANKL.

AIM: Periodontitis results from bacteria-induced inflammation. A key cytokine, RANKL, is produced by a number of cell types. The cellular source of RANKL critical for periodontitis has not been established. METHODS: We induced periodontal bone loss by oral inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in both normoglycaemic and streptozotocin-induced type 1 diabetic mice. Experimental transgenic mice had osteocyte-specific deletion of floxed receptor activator of nuclear factor kappa-B ligand (RANKL) mediated by DMP-1-driven Cre recombinase. Outcomes were assessed by micro-CT, histomorphometric analysis, immunofluorescent analysis of RANKL and tartrate-resistant acid phosphatase staining for osteoclasts and osteoclast activity. RESULTS: Oral infection stimulated RANKL expression in osteocytes of wild-type mice, which was increased by diabetes and blocked in transgenic mice. Infected wild-type mice had significant bone loss and increased osteoclast numbers and activity, which were further enhanced by diabetes. No bone loss or increase in osteoclastogenesis or activity was detected in transgenic mice with RANKL deletion in osteocytes that were normoglycaemic or diabetic. CONCLUSIONS: This study demonstrates for the first time the essential role of osteocytes in bacteria-induced periodontal bone loss and in diabetes-enhanced periodontitis.

Arthritis-induced alveolar bone loss is associated with changes in the composition of oral microbiota.

Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory disorders that cause bone loss. PD tends to be more prevalent and severe in RA patients. Previous experimental studies demonstrated that RA triggers alveolar bone loss similarly to PD. The aim of this study was to investigate if arthritis-induced alveolar bone loss is associated with modification in the oral microbiota. Checkerboard DNA-DNA hybridization was employed to analyze forty oral bacterial species in 3 groups of C57BL/6 mice: control (n = 12; without any challenge); Y4 (n = 8; received oral inoculation of Aggregatibacter Actinomycetemcomitans strain FDC Y4) and AIA group (n = 12; chronic antigen-induced arthritis). The results showed that AIA and Y4 group exhibited similar patterns of bone loss. The AIA group exhibited higher counts of most bacterial species analyzed with predominance of Gram-negative species similarly to infection-induced PD. Prevotella nigrescens and Treponema denticola were detected only in the Y4 group whereas Campylobacter showae, Streptococcus mitis and Streptococcus oralis were only found in the AIA group. Counts of Parvimonas micra, Selenomonas Noxia and Veillonella parvula were greater in the AIA group whereas Actinomyces viscosus and Neisseira mucosa were in large proportion in Y4 group. In conclusion, AIA is associated with changes in the composition of the oral microbiota, which might account for the alveolar bone loss observed in AIA mice.

Brain-derived neurotrophic factor in chronic periodontitis.

Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family. Outside the nervous system, BDNF has been shown to be expressed in various nonneural tissues, such as periodontal ligament, dental pulp, and odontoblasts. Although a role for BDNF in periodontal regeneration has been suggested, a function for BDNF in periodontal disease has not yet been studied. The aim of this study was to analyze the BDNF levels in periodontal tissues of patients with chronic periodontitis (CP) and periodontally healthy controls (HC). All subjects were genotyped for the rs4923463 and rs6265 BDNF polymorphisms. Periodontal tissues were collected for ELISA, myeloperoxidase (MPO), and microscopic analysis from 28 CP patients and 29 HC subjects. BDNF levels were increased in CP patients compared to HC subjects. A negative correlation was observed when analyzing concentration of BDNF and IL-10 in inflamed periodontium. No differences in frequencies of BDNF genotypes between CP and HC subjects were observed. However, BDNF genotype GG was associated with increased levels of BDNF, TNF-α, and CXCL10 in CP patients. In conclusion, BDNF seems to be associated with periodontal disease process, but the specific role of BDNF still needs to be clarified.

The oral microbiota and gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is one of the most frequent endocrine conditions during pregnancy. GDM is linked to adverse pregnancy outcomes and has implications for maternal health. Studies have demonstrated the link between pathogenic periodontal bacteria, glycemic control, and the risk of diabetes. The objective of the current study is to perform a mini-review of the available literature on the potential changes in the oral microbiota of women with GDM. The review was conducted by two independent reviewers (LLF and JDC). Indexed electronic databases (PubMed/Medline, Cochrane Library, Web of Science, and Scopus) were searched, including articles published in English and Portuguese. A manual search was also performed to identify related articles. The oral microbial community of pregnant women with GDM is unique from that of healthy pregnant women. The majority of the alterations found in the oral microbiota of women with GDM point to a pro-inflammatory environment with high levels of bacteria associated with periodontitis (Prevotella, Treponema, anaerobic bacteria) and a depletion of bacteria associated with periodontal health maintenance (Firmicutes, Streptococcus, Leptotrichia). More well-designed studies differentiating between pregnant women with good oral health and those with periodontitis are needed to ascertain which differences are due to GDM or periodontitis.

Methotrexate and Non-Surgical Periodontal Treatment Change the Oral-Gut Microbiota in Rheumatoid Arthritis: A Prospective Cohort Study.

This study evaluated the changes in the composition of oral-gut microbiota in patients with rheumatoid arthritis (RA) caused by methotrexate (MTX) and non-surgical periodontal treatment (NSPT). Assessments were performed at baseline (T0), 6 months after MTX treatment (T1), and 45 days after NSPT (T2). The composition of the oral and gut microbiota was assessed by amplifying the V4 region of the 16S gene from subgingival plaques and stools. The results of the analysis of continuous variables were presented descriptively and non-parametric tests and Spearman's correlation were adopted. A total of 37 patients (27 with periodontitis) were evaluated at T0; 32 patients (24 with periodontitis) at T1; and 28 patients (17 with periodontitis) at T2. MTX tended to reduce the alpha diversity of the oral-gut microbiota, while NSPT appeared to increase the number of different species of oral microbiota. MTX and NSPT influenced beta diversity in the oral microbiota. The relative abundance of oral microbiota was directly influenced by periodontal status. MTX did not affect the periodontal condition but modified the correlations that varied from weak to moderate (p < 0.05) between clinical parameters and the microbiota. MTX and NSPT directly affected the composition and richness of the oral-gut microbiota. However, MTX did not influence periodontal parameters.

Association between polymorphisms in interleukin-17A and -17F genes and chronic periodontal disease.

OBJECTIVE: Interleukin-17 (IL-17) is a cytokine that induces neutrophil recruitment and the release of inflammatory mediators in several inflammatory conditions; nevertheless, the involvement of IL-17 gene polymorphisms in chronic periodontitis (CP) has not been addressed yet. Our aim was to evaluate the association between periodontal status and the polymorphisms IL-17A G197A and IL-17F C7488T in subjects with CP along with their impact on levels of inflammatory mediators. MATERIAL AND METHODS: Genomic DNA was obtained from 30 CP patients and 30 healthy controls (HCs). IL-17A G197A and IL-17F C7488T polymorphisms were determined using PCR-RFLP. Serum and periodontal tissues were collected and processed for ELISA, myeloperoxidase (MPO), and/or microscopic analysis. RESULTS: The frequencies of genotypes in the CP group were significantly different from those of HC. Odds ratio indicated that increased risks for CP were associated with the -197A allele, not with the -7488T allele. In addition, the -197A allele was correlated with worse clinical parameters, higher MPO activity, and increased expression of inflammatory mediators (IL-17A and IL-8) than the other genotypes. CONCLUSIONS: These results indicate that the IL-17A -197A allele is associated with increased risk for CP, likely because this genotype relates to the enhanced inflammation in periodontal tissues.

A controversial role for IL-12 in immune response and bone resorption at apical periodontal sites.

Periapical lesions are inflammatory conditions of tooth periapical tissues, triggered by dental pulp infection and characterized by exudation of immune cells to the affected tissues and production of inflammatory mediators such as cytokines. The inflammatory periapical reaction is mainly driven by Th1, Th2, and Th17 responses, and such polarization may modulate progression of the disease and expression of bone proresorptive cytokines. IL-12 is a potent inducer of IFN-γ production, which stimulates Th1 effector cells. Many evidences have shown a positive correlation between the bone resorptive cytokine IL-1ß and the production of IL-12 and IFN-γ. Furthermore, IL-12 may have a potential role in the release of bone resorptive mediators and blockade of Th2 cytokines, affecting the progression of periapical bone loss. Nevertheless, IL-12 and IFN-γ have also been described as suppressors of osteoclast differentiation and activation, favoring bone maintenance. This paper focuses on the controversial roles of IL-12 in periapical lesions.

Composite-derived monomers affect cell viability and cytokine expression in human leukocytes stimulated with Porphyromonas gingivalis.

OBJECTIVES: Dental composites release unreacted resin monomers into the oral environment, even after polymerization. Periodontal cells are, therefore, exposed to substances that potentially elicit the immune inflammatory response. The underlying molecular mechanisms associated with the interaction between resin monomers and human immune cells found in the gingival crevicular fluid are not fully understood yet. This study investigated the ability of bisphenol A-glycidyl methacrylate (BISGMA), urethane dimethacrylate (UDMA) and triethylene glycol dimethacrylate (TEGDMA) to induce apoptosis and cytokine release by human leukocytes stimulated with a periodontal pathogen. METHODOLOGY: Peripheral blood mononuclear cells (PBMC) from 16 healthy individuals were included in this study. To determine the toxicity, the PBMC were incubated for 20 hours, with monomers, for the analysis of cell viability using MTT assay. To evaluate cell death in the populations of monocytes and lymphocytes, they were exposed to sub-lethal doses of each monomer and of heat-inactivated Porphyromonas gingivalis (P. gingivalis) for 5 hours. Secretions of IL-1ß, IL-6, IL-10 and TNF-α were determined by ELISA after 20 hours. RESULTS: UDMA and TEGDMA induced apoptosis after a short-time exposure. Bacterial challenge induced significant production of IL-1ß and TNF-α (p<0.05). TEGDMA reduced the bacterial-induced release of IL-1ß and TNF-α, whereas UDMA reduced IL-1ß release (p<0.05). These monomers did not affect IL-10 and IL-6 secretion. BISGMA did not significantly interfere in cytokine release. CONCLUSIONS: These results show that resin monomers are toxic to PBMC in a dose-dependent manner, and may influence the local immune inflammatory response and tissue damage mechanisms via regulation of bacterial-induced IL-1ß and TNF-α secretion by PBMC.

Oral health-related quality of life among individuals with rheumatoid arthritis.

OBJECTIVE: To evaluate the oral health-related quality of life (OHRQoL) of individuals with rheumatoid arthritis (RA) in comparison with individuals with no RA. METHOD: A cross-sectional study was carried out with 112 individuals distributed into two groups. Group 1 (G1) consisted of 42 RA individuals and group 2 (G2) consisted of 70 individuals without RA. Participants' OHRQoL was assessed by means of the long form of the Oral Health Impact Profile (OHIP). The OHIP has 49 questions distributed across seven domains: functional limitation, physical pain, psychological discomfort, physical disability, psychological disability, social disability, and handicap. The overall score ranges between 0 and 196. A higher score denotes a greater negative impact on OHRQoL. All participants underwent oral examination for the evaluation of clinical variables. Sociodemographic and oral behavior variables were also collected. Data analysis included descriptive statistics, Mann-Whitney test, and regression analysis. RESULTS: Individuals in G1 presented higher OHIP overall score (p = 0.006) than G2 individuals. G1 individuals also presented higher scores in the functional limitation (p = 0.003) and the physical disability (p = 0.005) domains than G2 individuals. Individuals with RA (p = 0.044), individuals who brushed their teeth less often (p = 0.019), and those with a higher number of decayed, missing, and filled teeth (DMFT) (p = 0.038) presented a significantly higher OHIP-49 overall score (more negative perception of their OHRQoL) than individuals without RA, individuals who brushed their teeth more often, and those with a lower DMFT. CONCLUSION: RA individuals had a more negative perception of their OHRQoL compared with individuals with no RA.

Oral microbial dysbiosis linked to worsened periodontal condition in rheumatoid arthritis patients.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint inflammation. Individuals with RA have a higher risk of periodontitis and periodontitis has been linked to RA through the production of enzymes by periodontal pathogens that citrullinate proteins. This linkage is supported by findings that periodontitis is associated with increased RA severity and treatment of periodontitis can improve the symptoms of RA. The possible mechanism for this association is through dysbiosis of the oral microbiota triggered by RA-induced systemic inflammation. We examined the RA status of subjects by measuring the number of tender and swollen joints, anti-citrullinated protein antibody and rheumatoid factor. Periodontal disease status and salivary cytokine levels were measured, and dental plaque analyzed by 16S rRNA high throughput sequencing. RA patients had a higher bacterial load, a more diverse microbiota, an increase in bacterial species associated with periodontal disease, more clinical attachment loss, and increased production of inflammatory mediators including IL-17, IL-2, TNF, and IFN-γ. Furthermore, changes in the oral microbiota were linked to worse RA conditions. Our study provides new insights into the bi-directional relationship between periodontitis and RA and suggest that monitoring the periodontal health of RA patients is particularly important.

Influence of periodontal treatment on rheumatoid arthritis: a systematic review and meta-analysis.

OBJECTIVE: To evaluate the influence of periodontal treatment on rheumatoid arthritis activity. METHODS: MEDLINE/PUBMED, The Cochrane Library, Clinical Trials, SciELO and LILACS were searched for studies published until December 2014. Included articles were: prospective studies; including patients older than 18 years, diagnosed with periodontitis and rheumatoid arthritis submitted to non-surgical periodontal treatment; with a control group receiving no periodontal treatment; with outcomes including at least one marker of rheumatoid arthritis activity. Methodological quality of the studies was assessed using PEDro scale. Quantitative data were pooled in statistical meta-analysis using Review Manager 5. RESULTS: Four articles were included. Non-surgical periodontal treatment was associated with a significant reduction of DAS28 (OR: -1.18; 95% CI: -1.43, -0.93; p<0.00001). Erythrocyte sedimentation rate, C-reactive protein, patient's assessment of rheumatoid activity using visual analogical scale, tender and swollen joint counts showed a trend toward reduction (not statistically significant). CONCLUSIONS: The reduction of DAS 28 in patients with rheumatoid arthritis after periodontal treatment suggests that the improvement of periodontal condition is beneficial to these patients. Further randomized controlled clinical trials are necessary to confirm this finding.

Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity.

Diabetes is a risk factor for periodontitis, an inflammatory bone disorder and the greatest cause of tooth loss in adults. Diabetes has a significant impact on the gut microbiota; however, studies in the oral cavity have been inconclusive. By 16S rRNA sequencing, we show here that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic. Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption. Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pathogenic. Our findings provide a mechanistic basis to better understand how diabetes can increase the risk and severity of tooth loss.

Is chronic periodontitis premature in systemic lupus erythematosus patients?

The aim of this study was to compare the frequency and severity of chronic periodontitis (CP) in systemic lupus erythematosus (SLE) patients with individuals without rheumatic diseases. Seventy-five patients with SLE were compared to 75 individuals without rheumatic diseases (control group) matched for age, educational level, and income. The activity of SLE was assessed with the Systemic Lupus Erythematosus Disease Activity Index 2000. Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index for Systemic Lupus Erythematosus evaluated SLE-related damage. Dental evaluation included measuring plaque index and parameters of periodontal disease (probing depth, clinical attachment level, and bleeding on probing). Fifty-one (68 %) SLE patients and 42 (56 %) control individuals had CP (p = 0.13). Periodontal status was similar in both groups. Considering only individuals with CP, SLE patients were younger than controls (40.7 ± 9.8 versus 46.14 ± 12.5 years of age, p = 0.02). CP was not associated with activity or therapeutics in SLE patients. Severity of periodontal parameters was similar in SLE patients and control subjects; however, CP occurred earlier in SLE patients.

Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status.

BACKGROUND: Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to affect the subgingival microbiota and clinical periodontal status. However, this relationship has not been examined in subjects with systemic lupus erythematosus (SLE). The objective of our study was to investigate the influence of SLE on the subgingival microbiota and its connection with periodontal disease and SLE activity. METHODS: We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing. RESULTS: SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis. CONCLUSIONS: SLE is associated with differences in the composition of the microbiota, independently of periodontal status.

Influence of periodontal treatment on rheumatoid arthritis: a systematic review and meta-analysis. / Influência do tratamento periodontal na artrite reumatoide: revisão sistemática e metanálise.

OBJECTIVE: To evaluate the influence of periodontal treatment on rheumatoid arthritis activity. METHODS: MEDLINE/PUBMED, The Cochrane Library, Clinical Trials, SciELO and LILACS were searched for studies published until December 2014. Included articles were: prospective studies; including patients older than 18 years, diagnosed with periodontitis and rheumatoid arthritis submitted to non-surgical periodontal treatment; with a control group receiving no periodontal treatment; with outcomes including at least one marker of rheumatoid arthritis activity. Methodological quality of the studies was assessed using PEDro scale. Quantitative data were pooled in statistical meta-analysis using Review Manager 5. RESULTS: Four articles were included. Non-surgical periodontal treatment was associated with a significant reduction of DAS28 (OR: -1.18; 95% CI: -1.43, -0.93; p <0.00001). Erythrocyte sedimentation rate, C-reactive protein, patient's assessment of rheumatoid activity using visual analogical scale, tender and swollen joint counts showed a trend towards reduction (not statistically significant). CONCLUSIONS: The reduction of DAS 28 in patients with rheumatoid arthritis after periodontal treatment suggests that the improvement of periodontal condition is beneficial to these patients. Further randomized controlled clinical trials are necessary to confirm this finding.

Is there an association between systemic lupus erythematosus and periodontal disease?

Periodontal disease results from the interaction between pathogenic bacteria that colonize supragingival and subgingival biofilms and the host, triggering an inflammatory response, with systemic effects leading to immune-mediated destruction of the attachment apparatus and loss of supporting alveolar bone. Immunological pathways and predisposing genetic factors common to periodontal disease and rheumatic diseases, including systemic lupus erythematosus, have been described. Case reports have suggested greater severity of periodontal disease in patients with systemic lupus erythematosus. However, studies evaluating the influence of the treatment of one disease on the clinical and laboratory manifestations of the other have yielded conflicting results.

Severe periodontal disease associated with long-term treatment with intravenous immunoglobulin.

Intravenous immunoglobulin (IVIG) is used in the treatment of neuropathy. This case report presents, for the first time, a patient with severe periodontal destruction after chronic therapy with IVIG. The patient reported having extracted his maxillary anterior teeth himself due to high mobility. Clinical examination and radiographic images show a generalized and severe periodontitis. No significant alterations in genetic or microbiological features were observed. The present case suggests that periodontal disease aggravation could be considered a new adverse effect of IVIG therapy. Postulated mechanisms are immune complexes formation, complement activation, and a direct effect in osteoclasts. In conclusion, it is important that patients that will receive IVIG treatment underwent dental evaluation.

Influence of periodontal treatment on rheumatoid arthritis: a systematic review and meta-analysis / Influência do tratamento periodontal na artrite reumatoide: revisão sistemática e metanálise

ABSTRACT Objective: To evaluate the influence of periodontal treatment on rheumatoid arthritis activity. Methods: MEDLINE/PUBMED, The Cochrane Library, Clinical Trials, SciELO and LILACS were searched for studies published until December 2014. Included articles were: prospective studies; including patients older than 18 years, diagnosed with periodontitis and rheumatoid arthritis submitted to non-surgical periodontal treatment; with a control group receiving no periodontal treatment; with outcomes including at least one marker of rheumatoid arthritis activity. Methodological quality of the studies was assessed using PEDro scale. Quantitative data were pooled in statistical meta-analysis using Review Manager 5. Results: Four articles were included. Non-surgical periodontal treatment was associated with a significant reduction of DAS28 (OR: -1.18; 95% CI: -1.43, -0.93; p < 0.00001). Erythrocyte sedimentation rate, C-reactive protein, patient's assessment of rheumatoid activity using visual analogical scale, tender and swollen joint counts showed a trend toward reduction (not statistically significant). Conclusions: The reduction of DAS 28 in patients with rheumatoid arthritis after periodontal treatment suggests that the improvement of periodontal condition is beneficial to these patients. Further randomized controlled clinical trials are necessary to confirm this finding.

RESUMO Objetivo: Avaliar a influência do tratamento periodontal sobre a atividade da doença na artrite reumatoide. Métodos: Pesquisaram-se as bases de dados Medline/PubMed, The Cochrane Library, Clinical Trials, SciELO e Lilacs em busca de estudos publicados até dezembro de 2014. Incluíram-se estudos prospectivos que avaliaram pacientes com mais de 18 anos diagnosticados com periodontite e artrite reumatoide submetidos a tratamento periodontal não cirúrgico; os estudos deveriam ter também um grupo controle não submetido a tratamento periodontal. Os resultados dos estudos deveriam contar com pelo menos um marcador da atividade da doença na artrite reumatoide. A qualidade metodológica dos estudos foi avaliada com a escala PEDro. Reuniram-se os dados quantitativos em uma metanálise estatística com o uso do Review Manager 5. Resultados: Incluíram-se quatro artigos. O tratamento periodontal não cirúrgico esteve associado a uma redução significativa no DAS-28 (OR: -1,18; IC 95%: -1,43 a -0,93; p < 0,00001). A velocidade de hemossedimentação, a proteína C-reativa, a avaliação da atividade reumatoide pela escala visual analógica e as contagens de articulações sensíveis e inchadas apresentaram uma tendência de redução (não estatisticamente significativa). Conclusões: A redução no DAS-28 em pacientes com artrite reumatoide após tratamento periodontal sugere que a melhoria na condição periodontal é benéfica a esses pacientes. São necessários mais ensaios clínicos randomizados controlados para confirmar esse achado.