Periimplantite e a importância do especialista em periodontia na manutenção dos tecidos / Periimplantitis and the importance of the periodontic specialist in tissue maintenance

Introdução: A peri-implantite é uma condição patológica associada a placa que ocorre nos tecidos de suporte ao redor de implantes dentários. Se caracteriza pela presença de sinais clínicos proveniente de inflamação na mucosa periimplantar conhecido como mucosite e subsequente perda progressiva do osso de suporte denominado como periimplatite. Objetivo: Classificar os principais sinais e sintomas clínicos da doença periimplantar a fim de estabelecer um diagnóstico, apresentar quais fatores devem ser avaliados durante o planejamento e manutenções de implantes dentários, os fatores de risco locais e sistêmicos, o tratamento e a importância do implantodontista com o periodontista realizar planejamento correto visando um prognostico favorável. Metodologia: Revisão de literatura foi realizada no PubMed, buscando artigos dos anos de 2010 a 2021. Resultado: Os estudos mostraram que o acúmulo de placa bacteriana nos implantes resultará no desenvolvimento de mucosite e podendo posteriormente se estabelecer a peri-implantite. Uma história de doença periodontal, tabagismo e falta de terapia de suporte devem ser considerados como indicadores de risco para o desenvolvimento de peri-implantite. Conclusão: É de suma importância o trabalho simultâneo do implantodontista com o periodontista com o intuito de se obter um bom planejamento e consequentemente reduzir danos a curto e longo prazo nos tecidos periimplantares. O sucesso do tratamento de doenças periimplantares está na prevenção, envolvendo reforço de higiene oral e manutenções periódicas(AU)

Introduction: A peri-implantitis is a plaqueassociated pathological condition that occurs in the supporting tissues around dental implants. If indifferent to the presence of proven clinical signs of inflammation in the peri-implant mucosa known as mucosite and subsequent progressive loss of supporting bone termed as peri-implatite. Objective: To classify the main signs and clinical signs of peri-implant disease an objective to establish a diagnosis, present the factors to be adopted during the planning and maintenance of dental implants, the local and systemic risk factors, the treatment and the importance of the implantodontist with the periodontist carrying out correct planning, a favorable prognosis. Methodology: A literature review was performed in PubMed, looking for articles from 2010 to 2021. Results: Advanced studies show that the accumulation of bacterial plaque in implants will result in the development of mucositis and may subsequently establish peri-implantitis. A history of periodontal disease, smoking and lack of supportive therapy should be considered as risk indicators for the development of peri-implantitis. Conclusion: The simultaneous work of the implantodontist with the periodontist is of paramount importance in order to obtain a good planning and consequently reduce short and long-term damage to the peri-implant tissues. The successful treatment of peri-implant diseases lies in prevention, involving reinforcement of oral hygiene and periodic maintenance(AU)

Receptor-Type Protein-Tyrosine Phosphatase ζ and Colony Stimulating Factor-1 Receptor in the Intestine: Cellular Expression and Cytokine- and Chemokine Responses by Interleukin-34 and Colony Stimulating Factor-1.

Differential intestinal expression of the macrophage growth factors colony stimulating factor-1 (CSF-1), interleukin (IL)-34, and their shared CSF-1 receptor (CSF-1R) in inflammatory bowel disease (IBD) has been shown. Diverse expression between CSF-1 and IL-34, suggest that IL-34 may signal via an alternate receptor. Receptor-type protein-tyrosine phosphatase ζ (PTPRZ1, RPTP-ζ), an additional IL-34 receptor, was recently identified. Here, we aimed to assess PTPRZ1 expression in IBD and non-IBD intestinal biopsies. Further, we aimed to investigate cellular PTPRZ1 and CSF-1R expression, and cytokine- and chemokine responses by IL-34 and CSF-1. The expression of PTPRZ1 was higher in non-IBD colon compared to ileum. PTPRZ1 expression was not altered with inflammation in IBD, however, correlated to IL34, CSF1, and CSF1R. The expression patterns of PTPRZ1 and CSF-1R differed in peripheral blood mononuclear cells (PBMCs), monocytes, macrophages, and intestinal epithelial cell line. PBMCs and monocytes of the same donors responded differently to IL-34 and CSF-1 with altered expression of tumor-necrosis factor α (TNF-α), IL-1ß, interferon γ (IFN-γ), IL-13, IL-8, and monocyte chemotactic protein-1 (MCP-1) levels. This study shows that PTPRZ1 was expressed in bowel tissue. Furthermore, CSF-1R protein was detected in an intestinal epithelial cell line and donor dependently in primary PBMCs, monocytes, and macrophages, and first hints also suggest an expression in these cells for PTPRZ1, which may mediate IL-34 and CSF-1 actions.

O efeito adjunto de uma suplementação alimentar à base de ômega-3 no tratamento da periodontite: um estudo clínico e imunológico / The adjunctive effects of Omega-3 dietary supplementation in the treatment of periodontitis: a clinical and immunological study

O objetivo foi avaliar se a suplementação com ômega (ω)-3 no tratamento não cirúrgico da periodontite melhora os resultados clínicos e imunológicos. Avaliar os níveis séricos dos ω-3 e ω-6 na doença periodontal, investigar se o tratamento periodontal associado ou não a suplementação com ω-3 afeta os níveis séricos destes. Assim como avaliar a expressão de um painel de citocinas relacionadas a osteoclatogênese no fluido gengival (FG) de sítios dos pacientes com gengivite e periodontite, adicionalmente relacionar estas citocinas a densidade óptica do osso alveolar destes sítios. Por fim, investigar se as terapias propostas neste estudo afetam os parâmetros clínicos periodontais, a densidade óptica do osso alveolar e a expressão das citocinas no FG. Para isso foi realizado um ensaio clínico piloto, randomizado, duplo-cego, controlado-placebo, com vinte e um pacientes com periodontite e dezesseis com gengivite. Estes foram investigados para os níveis séricos dos ácidos graxos poli-insaturados de cadeia longa (AGPI-CL), ácido eicosapentaenóico (EPA), ácido docosahexaenóico (DHA), ácidos docosapentaenóico (DPA), o ácido araquidônico (AA) usando cromatografia gasosa. O FG dos sítios controle-gengivite, controle-periodontite e destruído de pacientes com periodontite foi avaliado para Receptor ativador do fator nuclear kappa-B ligante (RANK-L), osteoprotegerina (OPG), a osteocalcina (OC), fator de necrose tumoral (TNF)-α, interferon (IFN)-γ, interleucina (IL) -1ß, IL-4, IL-6 e IL-10, utilizando imunoensaio multiplex. Pacientes com periodontite foram subagrupados em grupos com e sem Síndrome Metabólica para avaliação dos AGPI-CL. Sítios dos pacientes com periodontite foram subagrupados em sítios sem e com considerável desmineralização ópticas baseado na avaliação da densidade óptica alveolar representada pelos valores de pixels das radiografias intraorais digitais para avaliação das citocinas no FG. Pacientes com periodontite foram randomizados em raspagem e alisamento radicular mais suplementação com ω-3 (RAR+ω-3) ou placebo (RAR+placebo), e foram reavaliados depois de quatro meses para AGPI-CL no soro, citocinas no FG e densidade alveolar óptica. Os níveis significativamente maiores dos AGPI-CLs foram observados em pacientes com periodontite em comparação com gengivite. A profundidade de bolsa mostrou uma correlação positiva significativa com DHA, DPA e AA. Após RAR+ω-3, DPA, AA, AA/EPA e AA/DHA reduziram significativamente, e depois da RAR+placebo todos os níveis dos AGPI-CLs reduziram significativamente. Os níveis das citocinas, IFN-γ, IL-4, IL-10, RANK-L e OC, no FG de sítios controle-gengivite foram menores comparados aos sítios controle-periodontite e destruído. O mesmo resultado foi observado para os níveis da IL-1ß, IL-6 e OPG em comparação com sítios destruídos. Pacientes com periodontite apresentaram níveis mais baixos de IL-1ß e OPG em sítios controle-periodontite comparado aos destruídos. Após RAR+ω-3, o nível da IL-4 aumentou e os níveis de OC, IFN-γ e IL-10 diminuíram. Não houve diferenças significativas entre os grupos experimentais para a densidade alveolar óptica e parâmetros. Em conclusão, os níveis séricos dos AGPI-CLs são afetados pela gravidade de doença periodontal e diferem com a presença da síndrome metabólica. Citocinas relacionadas a osteoclatogênese no FG refletem a gravidade periodontal e diferem com densidade óptica alveolar alterada. A suplementação com ω-3 não melhora clinica ou imunologicamente o resultado do tratamento periodontal.

The aim was to test whether omega (ω)-3 supplementation associated to non-surgical treatment of periodontitis improves clinical and immunological results. Evaluate the serum levels of ω-3 and ω-6 in periodontal disease, hence, to investigate whether periodontal treatment with or without ω-3 supplementation affects serum levels of these. Therefore, to evaluate the expression of a panel of cytokines related to osteoclastogenesis in the gingival crevicular fluid (GCF) sites of patients with gingivitis and periodontitis, additionally relate these cytokines with optical alveolar bone density in these sites. Finally, to investigate whether the therapies proposed in this study affect the clinical periodontal parameter, the optical density of the alveolar bone and the expression of cytokines in GCF. Then was conducted a pilot clinical trial, randomized, double-blind, placebo-controlled, with twenty-one patients with periodontitis and sixteen with gingivitis. These were investigated for blood levels of long chain polyunsaturated fatty acids (LC-PUFA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), arachidonic acid (AA) using gas chromatography. The GCF of the sites of control-gingivitis, control-periodontitis and destroyed from patients periodontitis were evaluated for receptor activator of kappa-B ligand nuclear factor (RANK-L), osteoprotegerin (OPG), osteocalcin (OC), tumor necrosis factor (TNF) -α, interferon (IFN) -γ, interleukin (IL) -1ß, IL-4, IL-6 and IL-10 using multiplex immunoassay. Patients with periodontitis were subgrouped in groups with and without metabolic syndrome to evaluate the LC-PUFA. Sites of patients with periodontitis were subgrouped at sites with and without considerable optical demineralization based on the evaluation of alveolar optical density represented by the pixel values of the digital intraoral radiographs for evaluation of cytokines in GCF. Patients were randomized into the periodontal scaling and root planing more ω-3 supplementation (ω-3 SRP +) or placebo (SRP + placebo), and were assessed after four months to LC-PUFA in serum, cytokines in GCF and alveolar optical density. The significantly higher levels of LC-PUFA were observed in patients with periodontitis compared to gingivitis. The pocket depth showed a significant positive correlation with DHA, DPA and AA. After RAR + ω-3, APD, AA, AA / AA and EPA / DHA reduced significantly, and, after SRP + placebo, all levels of LC-PUFA reduced significantly. The levels of cytokines, IFN-γ, IL-4, IL-10, and OC RANK-L, from controlgingivitis sites GCF were lower compared to control-periodontitis and destroyed sites. The same result was observed for levels of IL-1ß, IL-6 and OPG compared to destroyed sites. Periodontitis patients had lower levels of IL-1ß and OPG in control-periodontitis compared to destroyed sites. After SRP + ω-3, the level of IL-4 and OC increased and levels of IFN-γ and IL-10 decreased. There were no significant differences between the experimental groups to optical density and clinical parameters. In conclusion, serum levels of LC-PUFA are affected by periodontal disease severity and differ in the presence of the metabolic syndrome. Cytokines related to osteoclastogenesis in GCF reflect the periodontal severity and differ with impaired alveolar optical density. Ω-3 supplementation does not improve clinical or immune result of non-surgical periodontal treatment.

Serum level changes of long chain-polyunsaturated fatty acids in patients undergoing periodontal therapy combined with one year of omega-3 supplementation: a pilot randomized clinical trial.

PURPOSE: We aimed to investigate the impact of nonsurgical periodontal treatment combined with one-year dietary supplementation with omega (ω)-3 on the serum levels of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and arachidonic acid (AA). METHODS: Fifteen patients with chronic generalized periodontitis were treated with scaling and root planing. The test group consisted of seven patients (43.1±6.0 years) supplemented with ω-3, consisting of EPA plus DHA, three capsules, each of 300 mg of ω-3 (180-mg EPA/120-mg DHA), for 12 months. The control group was composed of eight patients (46.1±11.6 years) that took a placebo capsule for 12 months. The periodontal examination and the serum levels of DPA, EPA, DHA, and AA were performed at baseline (T0), and 4 (T1), and 12 (T2) months after therapy. RESULTS: In the test group, AA and DPA levels had been reduced significantly at T1 (P<0.05). AA and EPA levels had been increased significantly at T2 (P<0.05). The ΔEPA was significantly higher in the test compared to the placebo group at T2-T0 (P=0.02). The AA/EPA had decreased significantly at T1 and T2 relative to baseline (P<0.05). CONCLUSIONS: Nonsurgical periodontal treatment combined with ω-3 supplementation significantly increased the EPA levels and decreased the AA/EPA ratio in serum after one year follow-up. However, no effect on the clinical outcome of periodontal therapy was observed.

Oral squamous cell carcinoma grading systems--analysis of the best survival predictor.

BACKGROUND: The TNM system has been used for decades in an attempt to predict clinical behavior and appropriate therapy for oral squamous cell carcinomas. Histopathologic classifications can be useful as an additional predictive tool. The purpose of this study was to apply four grading systems (Multiparameter Grading System, Malignancy Grading of the Deep Invasive Margins, World Health Organization grading system, and Histologic Risk Assessment) to oral squamous cell carncinomas and evaluate each system based on clinicopathologic parameters and patient survival. METHODS: The files of 53 patients diagnosed with primary oral squamous cell carcinoma at the Brazilian National Cancer Institute were evaluated. All hematoxylin and eosin-stained slides were reviewed to confirm the original diagnosis and to determine histopathologic grading. Clinicopathologic information was obtained from medical records and tumor registries. Statistical analysis was performed using Fisher's exact test or the chi-square test, the Kaplan-Meier method, and the log-rank test. RESULTS: The Multiparameter Grading System was statistically associated with pathologic staging (P = 0.02) and lymph node involvement (P = 0.0009). Differences in overall 5-year survival were significant for Histologic Risk Assessment (P = 0.015), pathologic staging (P = 0.001), lymph node status (P < 0.0001), and recurrence (P = 0.0001). Differences in cancer-specific 5-year survival were significant for Histologic Risk Assessment (P = 0.029), pathologic staging (P = 0.002), lymph node involvement (P < 0.0001), and recurrence (P < 0.0001). Poorly differentiated tumors were associated with the worst disease-free survival (P = 0.031) and recurrence (P = 0.043). CONCLUSION: Of the grading systems evaluated, Histologic Risk Assessment demonstrated the best results for survival prediction in oral squamous cell carcinoma.

Associação da classificação da OMS e da AHR com fatores clínico-patológicos do câncer de boca / WHO classification and HRA association with clinico pathological features of oral cancer prognostic factors

Estudos demonstram que as classificações histopatológicas auxiliam na análise do grau de malignidade do carcinoma de células escamosas (CCE) bucal. Esse trabalho estudou o perfil de 44 pacientes diagnosticados no Inca, em 1999, aplicando as classificações histopatológicas da OMS e a Avaliação Histopatológica de Risco(AHR), associando-as com fatores clínico-patológicos. A maioria dos carcinomas foi classificada como moderadamente diferenciada e de risco intermediário. A associação da OMS e da AHR com as variáveis clínico-patológicas estudadas não mostrou resultados estatisticamente significativos. Recomenda-se a aplicação das classificações utilizadas em amostra ampliada, a fim de validar os resultados apresentados.

Hiperatividade de neutrófilos na periodontite: ativação de receptores Fcy / Neutrophils´ hyperactivity in periodontitis: activation of Fcy receptors

A destruição dos tecidos periodontais está associada a liberação de enzimas proteolíticas e espécies reativas de oxigênio, predominantemente de neutrófilos ativados por receptores Fcy. O objetivo do estudo foi revisar a literatura sobre a importância do receptor Fcy na hiperativação de neutrófilos e, consequentemente, na suscetibilidade do hospedeiro a periodontite. A ativação do neutrófilo requer a ligação dos receptores Fcy por moléculas de Ig que, através de mediadores intracelulares, resulta em eventos de transdução de sinal, incluindo a transcrição de genes codificadores de citocinas, enzimas microbicidas e mobilização do citoesqueleto, levando a fagocitose, exocitose de grânulos e migração celular. Na hiperatividade do neutrófilo, suas funções estão exacerbadas. Uma explicação plausível para essa hiperatividade vem da ativação do receptor Fcy visto que os mesmos respondem de forma distinta a diferentes subclasses de IgG, dependendo: (1) de sua afinidade a estes e da atividade específica de cada categoria do receptor Fcy; (2) pela expressão do receptor Fcy pelas células; e/ou (3) da presença de polimorfismo do receptor Fcy. Sendo assim, podemos concluir que a destruição tecidual no indivíduo portador de periodontite pode estar relacionada a uma hiperatividade de neutrófilos quando ativados por IgG 1 e 2 através dos seus receptores FcαRII e III. Isto se dá principalmente nos casos de polimorfismo para FcαR II a 131, e em meio às altas concentrações de elastase, possibilitando ao FcαR maior afinidade ao ligante, independente dos patógenos periodontais Aa e Pg e do diagnóstico para periodontite ser agressiva ou crônica.

The destruction of periodontal tissue is associated with the release of proteolytic enzymes and reactive oxygenspecies, predominantly by Fcγ activated neutrophils. The aim was to review the literature about the importance of Fcy receptors in the hyperactivation of neutrophils and thus, in the susceptibility of the host in periodontitis. The activation of neutrophil requires Fcy receptor (FcγR) binding to Ig molecules that, through intracellular mediators, results in signal transduction events, including the transcription of genes for cytokines, microbicides enzymes and mobilization of the cytoskeleton, leading to phagocytosis, exocytosis of granules and cell migration. During neutrophilhyperactivity, such functions are exacerbated. A plausible explanation this hyperactivity comes from the FcγR, since they respond differently to different subclasses of IgG. It depends on: (1) its affinity to the receptors and tothe specific activity of each category of FcγR, (2) the expression of the FcγR in cells, and/or (3) polymorphisms forFcγR. Therefore, we concluded that tissue destruction in individuals with periodontitis may be related to a hyperactivity of neutrophils when activated by IgG 1 and 2 through its receptors FcγR II and III. This happens especially in cases of polymorphism for FcγR IIa 131, but also the presence of high concentrations of elastase, which allows a greatest affinity to the FcγR ligand, regardless the presence of periodontal pathogens Aa and Pg, and the specificity of the diagnostics to aggressive or chronic periodontitis.