ABSTRACT
Vários fatores biológicos têm sido estudados como biomarcadores da condição periodontal. O óxido nítrico (NO) faz parte de uma família de radicais livres envolvidos com a homeostasia, resposta imunológica, atividade cardiovascular e neurotransmissão. O NO pode ser produzido pelo organismo humano via óxido nítrico sintase (NOS) dependente ou via NOS independente. No mecanismo NOS independente a produção de NO envolve um ciclo entero-salivar de redução do nitrato (NO3-) em nitrito (NO2-) e a sua subsequente conversão em NO. Os estímulos inflamatórios presentes na doença periodontal também são capazes de induzir a formação de NO e há relatos na literatura de que o mesmo possa atuar interferindo na progressão da periodontite. No osso, assim como em outros tecidos, a produção de NO pode ser estimulada por lipopolisacarídeos (LPS) bacterianos. Nesse mecanismo tem sido sugerida uma importante participação das bactérias bucais. O objetivo deste trabalho foi avaliar por meio de revisão da literatura a relação do óxido nítrico, nitrato e nitrito com a condição periodontal e se procedimentos terapêuticos periodontais podem interferir com esses fatores. O óxido nítrico é um importante mediador de várias atividades biológicas. Os níveis de NO2- parecem estar aumentados na periodontite, comparativamente à gengivite e saúde gengival. Apesar da produção de NO ter um papel primário bactericida, é provável que essa produção em altas concentrações resulte em danos aos tecidos periodontais do hospedeiro. Nas lesões periodontais quantidades consideráveis de NO são geradas principalmente por macrófagos, neutrófilos polimorfonucleares, linfócitos e fibroblastos induzidos pelas citocinas e por LPS. A oferta dietética de NO3- influencia a síntese de NO e a produção de NO2-. Não está completamente elucidada a real influência do tratamento periodontal sobre os níveis de NO2.(AU)
Several biological factors have been studied as biomarkers of periodontal condition. Nitric oxide (NO) is part of a family of free radicals related to homeostasis, immunological response, cardiovascular activity, and neurotransmission. NO can be produced by human body via nitric oxide synthase (NOS) dependent or an pathway independent of NOS. In the independent pathway NO production involves an enterosalivary cycle by which nitrate (NO3-) is reduced to nitrite (NO2-) followed by its subsequent conversion to NO. The inflammatory stimuli present in periodontal disease are also able to induce the formation of NO and there are reports in the literature that the same may act by interfering on the progression of periodontitis. In bone, like other tissues, NOproduction may be stimulated by lipopolysaccharide (LPS) from bacteria. In this mechanism it has been suggested an important role of oral bacteria. The aim of this study was to evaluate through a literature review the relationship between NO, NO3- and NO2- and periodontal condition. Also whether periodontal therapeutic procedures can interfere in NO, NO3- and NO2- or not. NO is an important mediator in various biological activities. NO2- levels seem to be high in periodontitis when compared to gingivitis and gingival health. Although NOproduction has a bactericidal primary role, probably in high concentrations its production results in damage to host periodontal tissues. In periodontal lesions greater amounts of NO are generated primarily by macrophages, polymorphonuclear neutrophils, lymphocytes and fibroblasts and induced by cytokines and LPS. NO3-from diet influences the synthesis and production of NO and NO2-. It is not completely understood the real influence of periodontal treatment on the levels of NO2- (AU)
Subject(s)
Periodontitis , Inflammation , Nitric OxideABSTRACT
aim of this study was to evaluate the efficacy of periodontal scaling and oral hygiene instruction for patients with mild chronic periodontitis and rheumatoid arthritis through clinical periodontal parameters and laboratory tests for CRP (C- reactive protein) and ESR (erythrocyte sedimentation rate). Twelve individuals with rheumatoid arthritis and 12 healthy individuals were evaluated, with a mean age of 45.38 and 46.75 respectively, all female and with mild, chronic periodontitis. The participants were evaluated clinically and periapical radiographs were taken (T1), after which periodontal treatment was instituted. After ninety days (T2), new clinical and laboratory data were obtained. Probing depth, bleeding index, and plaque indexes were observed in both groups, and the results demonstrated reductions but no statistical differences. Laboratory tests for CRP and ESR produced higher values for the rheumatoid arthritis group with T1- T2 reductions on the average, but the values were still higher than in the health group. We conclude that periodontal therapy in patients with rheumatoid arthritis and mild chronic periodontitis showed a improvement in the periodontal clinical parameters and laboratory tests that were evaluated.
ABSTRACT
The purpose of this study was to evaluate the presence of A. actinomycetemcomitans, P. gingivalis, P. intermedia, E. corrodens and F. nucleatum in 30 subjects with chronic periodontitis treated by scaling and root planing (SRP) plus minocycline (test group) during 12 months with regular trimester maintenance care. Additionally, we evaluated whether the beneficial effects of the therapy on the microbial flora persisted for 24 months. The test group (n = 15) and the control group [SRP plus placebo (n = 15)] were randomly assigned. After SRP, subjects received minocycline or placebo at the baseline, and at 3, 6, and 9 months at all sites with a periodontal pocket depth (PD) of >or= 6 mm. Moreover, two homologous teeth, initially PD >or= 6 mm, were clinically and microbially monitored by PCR at the baseline, and at 3, 6, 9, 12 and 24 months. Differences in mean PD values between groups were analyzed by Student's t-test (P < 0.05). The results for bacterial frequencies showed no significant differences between groups (Fisher's Exact test, P < 0.05) or between time-points (Friedman test, P < 0.05). We failed to detect any differences between groups related to the presence of target pathogens for 12 months. The effects of both therapies on the microbial flora did not persist for 24 months. The group without supportive periodontal therapy showed an improvement in the pattern of pathogens with either of the therapies.
