View clinical trials related to Aggressive Periodontitis.
Filter by:Subjects were selected from the outpatient clinic, Department of Oral Medicine and Periodontology, Faculty of Oral and Dental Medicine, Cairo University. Ten healthy control subjects presented with clinically healthy periodontium. Ten patients who had plaque induced gingivitis. Ten patients who had generalized chronic periodontitis. Ten patients who had generalised aggressive periodontitis. Pentraxin-3 levels were evaluated in GCF and saliva of all subjects included in this study with ELISA technique.
The aim of this randomized controlled clinical trial of superiority will be to evaluate the effect of 3 g of omega-3 polyunsaturated fatty acids and 100 mg of aspirin daily supplementation over a period of 180 days as adjunct to non-surgical therapY of patients with generalized aggressive periodontitis. Probing depth, clinical attachment level, gingival index and concentration of microorganisms and cytokines at baseline, 3, and 6 12 months after the procedure will be evaluated.
The aim of this randomized controlled clinical trial of superiority will be to evaluate the effect of 3 g of omega-3 polyunsaturated fatty acids and 100 mg of aspirin daily supplementation over a period of 180 days as adjunct to surgical therapy of residual pockets from patients with generalized aggressive periodontitis. Probing depth, clinical attachment level, gingival index and concentration of microorganisms and cytokines at baseline, 3, and 6 months after the procedure will be evaluated.
The investigators planed to observe the microbiome of an aggressive periodontitis patient, during mechanical treatment, surgery(if indicated) and implant placement. The investigators designed to observe the changes after mechanical treatment.Then, the investigators will compare the sub-mucosa microbiome of implant and the subgingival community. The investigators expected a different community after treatment, and there could be similarity between implant and nature teeth.
The aim of our study is to determine the interleukin-1βeta (IL-1β), interleukin-8 (IL-8) and tumor necrosis factor-αlfa (Tnf-α) levels in gingival crevicular fluid (GCF) and clinical periodontal parameters following the treatment with Erbium,Chromium:Yttrium-Scandium-Gallium-Garnet (Er,Cr:YSGG) and diode lasers in adjunct to scaling and root planing (SRP) in patients with generalized aggressive periodontitis (GAgP). Twenty-six patients with GAgP (n=26) were enrolled in the study. The study was designed as a "split-mouth" study. In each patient, three quadrants were randomly determined as SRP-control, SRP+Er,Cr:YSGG and SRP+Diode laser. Clinical periodontal measurements were recorded at the baseline and third month after the treatment. Cytokines levels in GCF were determined by enzyme-linked immunosorbent assay (ELISA).
Approaches and objectives related to the treatment of patients with aggressive periodontitis are not markedly different compared patients with the chronic form. However, the large bone loss related to young age in this aggressive form, justify a well-founded strategy, intending to further stabilization of disease progression. For this, should make use of regenerative therapies in the advanced stages of treatment. Noteworthy is the use of proteins derived from the enamel matrix (EMD) in patients with chronic periodontitis, but there is little evidence about the effects of this material in aggressive periodontitis. Thus, the present study aims to evaluate the use of EMD in patients with aggressive periodontitis, comparing them to individuals with chronic periodontitis. Will then be selected 45 subjects, among patients with generalized chronic periodontitis (GCP) and generalized aggressive periodontitis (GAP), with one or more intra-bony defects in radiographic examination, with a minimum size of 4 mm deep and 2 mm horizontal, associated with a probing depth (PD) ≥6mm, to be treated according to the groups: GAP+OFD (n = 15) GAP patients which will receive open flap debridement; GAP+OFD/EMD (n=15) GAP patients which will receive open flap debridement and application of EMD; GCP+OFD/EMD (n=15) GCP patients which will receive open flap debridement and application of EMD. Clinical evaluations will be performed at baseline, 3, 6 months and 1 year after. At baseline, 7, 15, 45 days, 3, 6 months and 1 year after will be collect samples of gingival fluid to detect bone markers by Luminex / MAGpix technology. For the periods baseline, 3, 6 months and 1 year will be collected subgingival biofilm for the detection and quantification of periodontal pathogens by real-PCR. Will still be carried x-rays on baseline, 6 months and 1 year after, and questionnaires about patient satisfaction and perception of therapy at baseline, 7 days and 6 months. To compare the parameters evaluated, ANOVA, Tukey, chi-square, Spearman and Person tests will be used (α = 5%).
The aim of this study is to assess the clinical outcomes of full-mouth ultrasonic debridement combined with clarithromycin or amoxicillin + metronidazole association for the treatment of generalized aggressive periodontitis (GAgP).
The aim of this study is to estimate GCF MCP-1 levels of healthy and Aggressive periodontitis (AgP) subjects and to compare MCP-1 levels between Localized AgP (LAgP) and Generalized AgP (GAgP) to establish its predictive value/role for distinguishing LAgP and GAgP development.
The aim of the present study is to evaluate the clinical and microbiological efficacy of moxifloxacin or amoxicillin plus metronidazole in one-stage scaling and root planing in treating generalized aggressive periodontitis. Forty five subjects will be randomly allocated to 3 treatment groups. Subgingival plaque samples will be analysed for cultivable bacteria. The primary outcome variable to determine the superiority of one treatment over the others would be differences between groups for means CAL changes at 6 months post-treatment. Secondary outcome variables include differences between therapies for the mean changes in the mean levels of PD and the proportion of BOP.
The inflammatory response involves many players from the immune response, including B lymphocytes. These cells are responsible for the synthesis of immunoglobulins in response to the presence of an antigen. They are characteristic of chronic inflammation. There are several subsets of B cells characterized by specific membrane markers. Once activated, these cells express many factors contributing to tissue destruction seen in periodontitis and particularly in osteoclastogenesis (receptor activator of nuclear factor kappa-B ligand, tumor necrosis factor, interleukin-6, macrophage inflammatory protein-1α and Monocyte Chemoattractant Protein-3). During the establishment of a periodontal disease, an important inflammatory infiltrate is observed in the gum. This infiltrate is characterized by the presence of many B lymphocytes. B cell subsets in the blood and the gum of patients with periodontitis have been little studied. However, the number of autoreactive B cells (cluster of differentiation (CD)19+, CD5+) has been reported to be higher in the blood of patients with periodontal disease. In the gum, the rate of B and T cells increases with the level of inflammation and is correlated with the severity of the inflammatory process. Activation of B cells is a prerequisite for the progression of gingivitis to periodontitis. B cell distribution could then be an indicator of disease progression, but also allow to study the response to treatment. The aim of this pilot study is to characterize B cell subsets in the blood and the gum of patients with periodontitis, according to disease activity. Analysis of B cells in the blood could highlight the association of a particular subpopulation with aggressive periodontal disease and evidence a particular biological profile of the host response. The investigators also wish to observe the evolution of this phenotype following an unconventional surgical therapy. This study would better understand the pathogenesis of periodontal disease and refine the diagnosis, prognosis and treatment of periodontitis, and thus participate in the development of personalized medicine. Biological monitoring of therapeutic effects may be initiated and allow more effectively prevent recurrence.