Active clinical trials for "Chronic Periodontitis"

The etiopathogenesis of periodontal disease results from complex interaction between infectious agents, mainly including bacteria, and host cellular and humoral immune responses. However it is thought that bacteria-induced pathogenesis is not sufficient alone to explain all biological and clinical features of the destructive periodontal disease. The main hypothesis is that herpesviruses, such as Epstein-Barr Virus, may participate as well by altering epithelial gingival cell biology and consequently may promote the initiation and progression of periodontitis.

The aim of this study is to investigate the systemic impact of periodontitis in patients with Metabolic Syndrome, by assessing measures of sub-clinical atherosclerosis and cardiovascular risk, microbial factors and host genetic variants, and to study the possible effect of mediators of inflammation and oxidative stress as links between the two conditions.

Generalized aggressive Periodontitis (GAgP) and chronic periodontitis (CP) are inflammatory diseases. Little is known about molecular changes and signaling cascade of host response. Inflammatory diseases are undercontrol of genetic and enviromental factors. Transcription factors are gene-specific factors that are often considered to act as a link connecting genetic and enviromental factors. The aim of this study is to investigate the gene regions that are thought to play a role in the pathogenesis of GAgP and CP, and to interpret new and reliable pathognomonic-prognostic markers in the diagnosis and treatment of these diseases with the help of expression and mutation analyzes and polymorphism studies.

The quantification of CD163 will be analysed in the subgingival plaque samples of generalized chronic periodontitis patients with and without diabetes mellitus. The demographic and the periodontal parameters were assessed and the correlated with the quantification of the CD163. The CD163 gene expression was analyzed with RT-PCR and the quantification of CD163 will be done using ELISA.

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.

50 periodontitis 50 healthy individuals serological evaluation will done to see association of 77A/G AND 11A/12A gene polymorphisms of MMP-13

The current study focuses on the localization and quantitative assessment of growth factors and cytokines related to the EMT process found in the human gingival tissue samples taken from periodontally diseased individuals compared to other samples taken from healthy individuals. Through this investigation the correlation between the severity of the disease and the amount of these factors will be studied aiming to alleviation of the high prevalence of periodontal diseases among the Egyptian population.

Quantification of NLRP3 (rs4612666) and CARD8 (rs20432111) will be analysed in the subgingival plaque and blood samples of generalized chronic periodontitis with and without coronary heart disease. The demographic and the periodontal parameters were assessed and correlated with the quantification of NLRP3 (rs4612666) and CARD8 (rs2043211) was analysed with RT-PCR

The buccal cavity is colonized by numerous microorganisms whose the number and composition could be modified with medical background (diseases and drugs) and the level of oral hygiene of the patients. Among all microorganisms identified in the periodontium, few of them are implicated in the etiopathogenesis of periodontal pathologies. To date, four major bacteria are identified for their ability to degrade periodontal tissues. Although the periodontitis is established to be the consequence of bacterial virulence and immune dysfunction, these factors fail to explain the refractory periodontitis of some patients to etiologic treatment . Others microorganisms such as protozoans could have an impact on this disease.

To assess the demographic variables, periodontal parameters and to determine the expression of Trefoil factors 2 and 3 and Adrenomedullin in unstimulated saliva samples of periodontally healthy subjects with coronary heart disease and generalised chronic periodontitis subjects with and without coronary heart disease.