981 resultados para Periodontal Pathogens


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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.

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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.

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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.

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Alveolar bone loss associated with periodontal diseases is the result of osteoclastogenesis induced by bacterial pathogens. The mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) is a critical negative regulator of immune response as a key phosphatase capable of dephosphorylating activated MAPKs. In this study, rat macrophages transduced with recombinant adenovirus (Ad.)MKP-1 specifically dephosphorylated activated MAPKs induced by lipopolysaccharide (LPS) compared with control cells. Bone marrow macrophages from MKP-1 knockout (KO) mice exhibited higher interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, and select chemokine compared with wild-type (WT) mice when stimulated by LPS. In addition, bone marrow cultures from MKP-1 KO mice exhibited significantly more osteoclastogenesis induced by LPS than when compared with WT mice. Importantly, MKP-1 gene transfer in bone marrow cells of MKP-1 KO mice significantly decreased IL-6, IL-10, TNF-α and chemokine levels, and formed fewer osteoclasts induced by LPS than compared with control group of cells. Furthermore, MKP-1 gene transfer in an experimental periodontal disease model attenuated bone resorption induced by LPS. Histological analysis confirmed that periodontal tissues transduced with Ad. MKP-1 exhibited less infiltrated inflammatory cells, less osteoclasts and less IL-6 than compared with rats of control groups. These studies indicate that MKP-1 is a key therapeutic target to control of inflammation-induced bone loss.

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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.

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

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

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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.

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This study analyzes the clot stabilization on root surfaces of teeth impregnated with cotinine and nicotine and the influence of the scaling in the adhesion of blood components, observing the influence of new exposition to nicotine and/or cotinine after scaling. Fifteen human teeth extracted due to periodontal disease of non-smokers patients were selected and manually scaled. Four dentin blocks were obtained from each tooth (n = 60). Samples received blood application or reimpregnation with nicotine and/or cotinine, depending on the groups. Group 1: PBS immersion + root scaling + blood; group 2: nicotine + root scaling + blood; group 3: nicotine + root scaling + nicotine reapplication + blood; group 4: cotinine + root scaling + blood; group 5: cotinine + root scaling + cotinine reapplication+ blood; group 6: nicotine and cotinine + root scaling + nicotine and cotinine + blood. Samples were kept in 2 ml of each substance for 24 hours. Each group received a blood drop and was analyzed by SEM. The higher amount of blood components was present in teeth exposed to cotinine and the groups submitted to scaling and blood application in comparison with groups that received reapplication of toxic substances after scaling. The greater toxic effect on root dentin surface was after the exposure to nicotine and cotinine. Results suggest that periodontal healing may be delayed in smokers due to the direct inhibition of clot stabilization on the root surface when nicotine and cotinine are present concomitantly.

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The aim of this paper was to search though a revision of the literature the cares before, during and after the orthodontic treatment in patients with a periodontal disease. The literature shows that the orthodontical treatment in healthy patients brings no risk to the periodontium, although the presence of an active periodontal disease counter indicates the dental movement. Thus, it is extremely important to execute a correct diagnosis of any periodontal alteration and treat them before the beginning of the orthodontical treatment. Besides, during the whole orthodontical treatment is also important to have a periodontal control with periodic reevaluations and at the end of the orthodontical treatment, a new oral hygiene orientation may be needed to finally establish the follow-up of the patient according to the risk of periodontal disease.

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Nitric oxide (NO) is a free radical with participation in almost all physiologic host processes; however, in high concentrations it may damage the tissues. Its immunoregulatory action is present in the inflammation and in auto-immune mechanisms, being intensively studied in the medical area. Recently, some studies have also reported that NO could play a role as etiopathogenic factor of the periodontal disease, which shows inflammatory and multifactorial course. Due to beneficial or damage effects of NO, according to its concentrations, some studies have been focused in the evaluation of inhibitor of NO-Synthase (NOS) as therapeutic agents in inflammatory processes. In this context, the aim of this study was to report the role of NO and NOS inhibition in the periodontal disease modulation process. In conclusion, it could be suggested that NO seems to play an essential role in evolution of inflammatory periodontal disease, and that the NOS inhibition may be considered as a promising therapeutic in modulation of inflammatory process.

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The association between platelets, angiogenesis and progression or repair of periodontal disease has been little explored and, consequently, the results are inconclusive. The pathogenic bacteria present in the periodontal pocket release endotoxins that affect the endothelial integrity and are able to induce the production of chemical mediators derived from plasma proteins and blood clotting while altering platelet function. There is great interest in the modulation of platelet activity in vascular disorders, especially cardiovascular diseases. For this reason, antiplatelet drugs, that are commonly used in the prevention of thromboembolic diseases, such as myocardial infarction, ischemic stroke and peripheral arterial disease, have been used. Aspirin is the only non-steroidal antiinflammatory agent with antiplatelet activity. In the periodontium, instead of only reduces levels of inflammatory cytokines, also significantly affects bleeding on probing, suggesting a dose-dependent modulation of periodontitis. In contrast, clopidogrel and ticlopidine are thienopyridine drugs with no known antiinflammatory action, suggesting that this benefit is related to an antiinflammatory effect indirectly correlated to their antiplatelet activity already established. In the literature there is limited information about the effect of these drugs on periodontium and periodontal disease development. Antiplatelet drugs hypothetically can change both the pathogenesis of periodontitis and subsequent periodontal tissue repair by blocking the secretion of chemical mediators which in general are important in modulating inflammation and tissue repair.

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The correct distinguishment of microorganisms involved in the periodontal disease pathogen, it is important in the understanding of its progression and adequate treatment planning. Considering this fact, some molecular methods of identification and quantification were developed and are extremely sensitive and precise in the characterization of different bacteria species. The present study aimed to realize a literature review, including studies that realized a comparative analysis between bacterial culture and real time PCR methods in the identification of pathogens. The bacterial culture method can possibly identify new microorganisms and realize antibiotics sensitivity tests. The real time PCR is a microbiologic test that identifies and quantifies bacterial species, through gene amplification of predetermined DNA fragments, with high sensitivity and specificity, and need a shorter operation time of the operator when compared to the bacterial culture method. In this way, to determine a specific diagnostic test, should be considered not only its precision in the identification of microorganisms, but the cost-benefit relationship as well.

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Gingival recession is a common deformity that affects a large number of people. This condition is frequently associated with esthetic complains and may lead to dental hypersensitivity. Thus, various surgical procedures have been proposed to provide root coverage. Since the 1950s, free and pedicle gingival grafts have been greatly used for treating gingival recession. However, after the 1985 Miller gingival recession classification, and with the development of other appropriated techniques that use subepithelial connective tissue grafts, gingival recession treatments have resulted in more predictable outcomes, especially with respect to Class I and II sites, i.e., in the absence of interproximal bone loss. This article reported the importance of aesthetical periodontal treatment in the prosthetic rehabilitation of a patient with a class I gingival recession with 3 mm of vertical extension in the superior canine. The treatment plan consisted of root coverage using subepithelial connective tissue graft (SCTG) associated with construction of new prosthesis.

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The aim of the current review was to investigate the relationship between levels of neuropeptide Substance P in periodontal disease and chronic pain. Substance P is a neuropeptide that is directly related with pain. In periodontal disease, it is expressed during the inflammatory process, and is one of the factors responsible for bone resorption. Studies have shown that Substance P levels are highest in the gingival crevicular fluid from sites with active periodontal disease and bone loss. The persistence of these substances could be sufficient to stimulate neurogenic inflammation in susceptible tissues, and cause pain. The scientific literature shows that Substance P expressed during periodontal disease can be a risk factor for patients with systemic inflammatory pathologies, such as chronic arthritis or rheumatoid arthritis. Additional research is needed to confirm the participation of this substance in the origin of some types of chronic pain.