Although RA pathomechanisms remains incompletely understood, periodontitis and RA share pathogenic features : genetic and environmental influences, chronic inflammatory disease, immunoregulatory imbalance, bacterial factors, persistence of antigen/peptide and clinical factors (conjunctive and hard tissues destruction). Several hypothesis can be evocated : Gram negative bacterial systemic spreading, inflammatory transmitter substance systemic spreading (IL1, IL6, IL17, PGE2), systemic spreading of bacterial degradation products (LPS for example). Currently Porphyromonas gingivalis (PG) might be a susceptibility factor to RA because PG has an enzyme, the peptidylarginine deiminase leading to auto antibodies creation and RA increasing. As periodontitis, RA is chronic disease with a cyclic increase evolution, needing a complex pluridisciplinary treatment approach. Recent studies have reported an increased prevalence of RA patients with periodontal disease. Others studies show that periodontal treatment induces a significant decrease of the sedimentation rate and of the DAS28. Periodontitis is suspected to be an independent, aggravating factor in patients with RA (given the definition from NIH : an aggravating factor is something that makes a condition worse). So periodontal treatment cannot be considered as a RA treatment per se. But it is hypothesised that treating periodontitis in RA patients showing signs of periodontitis could result in improvement in RA disease activity. To date the role of periodontitis as an aggravating factor in these patients remains unclear, and only RCT designs can reasonably be used to test this causal hypothesis. There still remains some RA patients who have persistent symptoms and frequent exacerbations despite specialist care and continuous treatment, so results of treating aggravating factors are needed. As the majority of patients will benefit from a systematic evaluation and treatment of aggravating factors, the periodontal treatment strategy need to be tested. The aim of this randomised controlled trial is to assess the effectiveness of periodontal treatment for rheumatoid arthritis patients. To assess the effectiveness of periodontal treatment to reduce the severity of rheumatoid arthritis (RA), in patients suffering from both periodontitis and rheumatoid arthritis. The hypothesis is that periodontal treatment reduce the severity of rheumatoid arthritis.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
22
* Mechanical debridement (scaling, root planning, subgingival curettage) * Antimicrobial therapy (systematically administered: amoxicillin or clindamycin). * Antiseptic mouthrinses, gel or dentifrice * Oral hygiene instructions (to educate and motivate patients to control the accumulation of plaque and calculus)
CHU de Bordeaux
Bordeaux, France
Pôle Odontologie Hôpital Purpan - Pavillon Rayer
Toulouse, France
Evaluation of parodontitis therapeutic care as assessed by variation in DAS28 score
Time frame: Day 15 and day 90
Evaluation of parodontitis therapeutic care as assessed by variation in ACR 20 score
Time frame: Day 15 and day 90
Evaluation of parodontitis therapeutic care as assessed by variation in HAQ score
Time frame: Day 15 and day 90
Evaluation of parodontitis therapeutic care as assessed by variation in GOHAI score
Time frame: Day 15 and day 90
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