Influência da infecção endodôntica e/ou periodontal associadas à diabetes na quantificação sérica da citocina pró-inflamatória IL-17 e na glicemia de ratos Wistar

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Análise hematológica por hemograma, creatinina, triglicérides e colesterol em ratos diabéticos portadores de infecção pulpar e/ou periodontal

Pós-graduação em Ciência Odontólogica - FOA

Avaliação dos efeitos da terapia fotodinâmica com hipericina-glucamina no tratamento da doen ça periodontal induzida em ratos

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Avaliação dos efeitos do laser Er,Cr:YSGG em defeitos ósseos críticos e no tratamento de doença periodontal induzida em ratos submetidos a inalção de fumaça de cigarro

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Condição periodontal, perda dentária e diferenças socioeconômicas em adultos e idosos brasileiros

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeito da atividade física na sensibilidade à insulina e no sinal insulínico em ratos com doença periodontal

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Doença periodontal em pacientes com Diabetes Mellitus: influência de polimorfismos genéticos?

Currently it is clear that there are several factors that can act as modifiers of diseases, without causing them directly, but having the potential to make these conditions to progress faster and more severe. There is a growing number of studies investigating the relationship between Diabetes Mellitus (DM) and Periodontal Disease (PD), including some studies focusing on the influence of genetic factors in this process. The aim of this study was to verify through a literature review, the influence of genetic polymorphisms in the development of PD in patients with DM. PubMed and BIREME were used as databases and the terms Periodontitis or Periodontal Disease, Polymorphism, Diabetes Mellitus were searched. After a refinement in the literature, five studies were selected and they were related to chronic PD with DM and polymorphisms in cytokine genes, especially interleukin 1 (IL1) e IL6. Polymorphisms were associated with a higher concentration of pro-inflammatory cytokines in the gingival crevicular fluid of diabetic patients when compared to non-diabetic. In conclusion, it is necessary to confirm this association with longitudinal studies that must investigate a larger number of cytokine genes in order to understand the cause-effect relationship between genetic polymorphisms, DM and PD.

Comparison between periodontal disease and a gingival carcinoma with emphasis on radiographic imaging

The majority of published papers deal mainly with prevalence, pathogenesis and treatment of squamous cell carcinoma of the gingiva (SCCG). On the other hand, little is discussed about the comparison between periodontal disease and gingival carcinoma with emphasis on radiographic imaging. In this case report we discuss the importance of the radiographic aspects in inflammatory periodontal disease and SCCG. This case report shows the importance of differentiating a localized severe periodontal disease and SCCG considering the radiographic aspects of the inflammatory bone loss and tumoral bone loss. The oral health care providers need to be familiar with the radiographic imaging of periodontal disease and SCCG.

Use of salivary biomarkers for diagnosis of periodontal disease activity: a literature review

Periodontal disease is an infectious disease characterized by the connective tissue destruction and consequent alveolar bone loss in response to plaque accumulation on the tooth surface. The clinical diagnosis of periodontal disease is based both on clinical examination involving the evaluation of probing depth and radiographic examination of alveolar bone loss but these examinations are not enough to determine the activity of the disease process. For that reason, it has been proposed to seek predictive disease markers in an attempt to assess the disease activity and so, evaluate the efficacy of the periodontal disease treatment. The aim of this review is to present recent advances in the development of proteomic, genomics and microbial biomarkers and potential clinical applications. It was concluded that periodontal treatment based on assessing the levels of salivary biomarkers emerges as a promising method in near future and will become an integral part of the evaluation of periodontal health.

Periodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesis

Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.

Improvement of an anterior infrabone defect using combined periodontal and orthodontic therapy: a 6-year follow-up case report

Extensive intraosseous lesions represent a clinical challenge for the periodontist. Sites with bone defects have been shown to be at higher risk of periodontitis progression in patients who had not received periodontal therapy. Thus, the aim of this case report was to describe a novel approach for the treatment of 1-walled intraosseous defect by combining nonsurgical periodontal therapy and orthodontic movement toward the bone defect, avoiding regenerative and surgical procedures. A 47-year-old woman underwent the proposed procedures for the treatment of her left central incisor with 9 mm probing depth and 1-walled intraosseous defect in its mesial aspect. Initially, basic periodontal therapy with scaling and root planning was accomplished. Two months later, an orthodontic treatment was planned to eliminate the intraosseous lesion and to improve the interproximal papillary area. Orthodontic root movement toward the osseous defect was performed for 13 months with light forces. After 6 years postoperative it was concluded that combined basic periodontal therapy and orthodontic movement was capable of eliminating the intraosseous defect and improve the esthetics in the interproximal papillary area between the central incisors.

Host responses induced by different animal models of periodontal disease: a literature review

Periodontitis is an infectious disease characterized by chronic inflammation of the periodontium, and it is mediated and modulated by the host immune system. In the presence of microorganisms or other antigens, immune cells (macrophages/monocytes, dendritic cells, lymphocytes, neutrophils), endothelial cells and fibroblasts secrete cytokines and trigger immune and inflammatory reactions. However, when synthesized at high levels, cytokines modify the pattern of cellular response, participating substantially in the development of chronic inflammatory pathologies, such as periodontal disease. Understanding the origin and progression of bone resorption is one of the primary goals of the field of periodontics, aiming to arrest the disease progression and to optimize future treatments. For this purpose, the development of experimental models is an important and necessary step before entering into clinical trials with new therapies. The purpose of this study is to characterize/evaluate the tissue changes induced by various models of experimental periodontitis through a literature review.

Treatment of periodontal disease with an Er,Cr:YSGG laser in rats exposed to cigarette smoke inhalation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Periodontal pathogens directly promote autoimmune experimental arthritis by inducing a TLR2- and IL-1-Driven Th17 response

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Haplotypes of susceptibility to chronic periodontitis do not influence MMP-8 levels or the outcome of non-surgical periodontal therapy

Introduction: Chronic periodontitis (CP) is a multifactorial condition, presenting immunoinflammatory reaction, in which a myriad of molecules including cytokines and matrix metalloproteinases (MMPs) interplays, making the system extremely intricate. There is scarce information regarding interconnections of biological influence among IL-4, IL-8 and MMP-8, mainly considering genetic polymorphisms, and also, whether this can influence the outcome of periodontal therapy. Previously, we reported that variants in the interleukin 4 (IL4) and interleukin 8 (IL8) genes were associated with CP in Brazilians. The aim of this study was to investigate, in individuals with different genetic backgrounds with regard to the IL4 or IL8 haplotypes, differences in the immunological levels of MMP-8 in gingival crevicular fluid (GCF) before and after non-surgical periodontal treatment. A total of 141 patients participated of this study, classified as susceptible or not to CP, according to the presence of haplotypes formed by polymorphysms in the IL4 or IL8 genes. All individuals received non-surgical periodontal therapy and follow–up continued for 45 days. The GCF samples were collected at baseline and on the 45th day. The MMP-8 levels were determined by ELISA. Results: No association was found between genetic backgrounds and MMP-8 levels in GCF or the outcome of non-surgical periodontal therapy. Conclusions: In this longitudinal clinical study, the presence of IL4 or IL8 haplotypes previously associated with CP did not influence the outcome of non-surgical periodontal therapy and the MMP-8 levels in the GCF. Additional studies are necessary to determine the mechanisms by which the IL4 or IL8 haplotypes affect individual susceptibility to CP.