Periodontite experimental como fator de risco para potencialização dos efeitos da artrite reumatóide em ratos Wistar

Abstract

Periodontitis is a chronic multifactorial inflammatory disease that leads to the release of inflammatory mediators contributing to a systemic inflammatory response. Evidence supports the association of periodontitis with the development of systemic inflammatory diseases such as rheumatoid arthritis (RA). RA is a systemic autoimmune disease that causes chronic synovial inflammation. Studies elucidate the association of these pathologies, demonstrating that the treatment of periodontitis has a beneficial influence on RA, and that in the presence of both the clinical course is significantly accentuated. However, there are still gaps about the deleterious effects when there is an association of diseases in relation to pain, edema, and morphological impairment of synovial and periodontal tissues. In addition, we sought to analyze the repercussions of intradermal and intra-articular injections administered in isolation on periodontitis, since both injections are necessary in the experimental model of RA. Therefore, the present study evaluated whether periodontitis, by means of systemic inflammation, potentiates the deleterious effects of rheumatoid arthritis. For this purpose 51 male Wistar rats were randomized into six groups: control group (CG, n=8), rheumatoid arthritis group (RAG, n=9), periodontitis group (PG, n=9), periodontitis and rheumatoid arthritis group (PRAG, n=9), periodontitis and intra-articular group (PIAG, n=9), and periodontitis and intradermal group (PIDG, n=7). The animals were subjected to the protocols of induction of periodontitis by ligation and RA by FCA. Functional assessments on motor disability, nociceptive threshold, joint edema, and muscle strength were performed at certain periods in the experiment, resulting in a total of 9 assessments made. After 30 days the animals were euthanized and the synovial fluid of the right knee was collected for total leukocyte count, the right hemimandibles were collected for radiographic analysis, and the right knee joints and left hemimandibles were processed and photo-documented for morphological and histometric analysis, respectively. In the functional evaluations the RA group showed signs of reduction of edema and improvement of muscle strength in the last evaluations; this did not occur for the group that contained the association of pathologies, indicating that in the presence of both diseases there is a constant compromise in the inflammatory process and in muscle weakness. Moreover, in the group submitted to ligation and intra-articular injection, it was observed that most of the variables analyzed had the same repercussion as the group with periodontitis and two inoculations of FCA, suggesting that in this experimental model only periodontitis and intra-articular injection caused the necessary changes. In the leukocyte migration, there was a significant increase in the periodontitis group associated with RA; furthermore, in the morphological analysis of the synovial membrane, the group that showed intense inflammatory infiltrate, thickening of the synovial intima, fibrosis, and adipocyte disorganization was also the one with the associated diseases, demonstrating a marked impairment of synovial fluids in the presence of the two pathologies. Finally, in the radiographic and histometric analyses of the distance CEJ to ABC, the group with the greatest impairment, that is, the greatest distance between these structures, was the group that had both pathologies. Based on these findings, we conclude that periodontitis is a potentiating risk factor for the effects of rheumatoid arthritis.