View clinical trials related to Periodontal Disease.
Filter by:Porphyromonas gingivalis is one of the major bacteria involved in the formation and progression of chronic periodontitis. Pathogens invading the gingiva face the host's innate immune system at first and later on the acquired immune system which includes secreted antibodies and specialized cells. Although both the arms of the immune system are coordinated to overcome the infection, there are several known mechanisms which help pathogens as Porphyromonas gingivalis evade immunity. As a result, inflammatory mediators secreted by immune cells cause tissue damage and lead the inflammation process towards chronicity instead of clearing the pathogen. Up till recently most of the studies focused on the role of macrophages, dendritic cells and lymphocytes at the response to periodontal pathogenic bacteria while the role of fibroblasts (the most abundant cell in the connective tissue) was less examined. Fibroblasts are spindle shaped cells which have the ability to produce extra cellular matrix and respond to growth factors and cytokines. They are able to affect cells in the infected tissue and contribute to immune response efficiency. As known in the case of lymphocytes, fibroblasts also vary in subtypes, each differs in phenotype, immune interactions, extra cellular matrix production and destruction, migration abilities and so on. Two main fibroblasts subtypes in the oral cavity originate in the gingival tissue and the periodontal ligament anchoring teeth to the surrounding alveolar bone. Amongst the differences between the two are collagen production ability and receptors profile over the cell surface. Considering all that, the investigators aim to obtain and use periodontal ligament and gingival tissues removed anyways during common dental procedures in order to extract the different fibroblasts subtypes residing there and compare their response to Porphyromonas gingivalis.
The objective of this study is to evaluate Photodynamic Therapy (PDT) as adjunct on non surgical periodontal therapy in patients with type 2 diabetes. A total of 40 individuals will be selected and divided in two groups. On the treatment stage, the control group (Group C) will receive standard non surgical periodontal treatment. The Test Group (Group T) will be treated with PDT as an adjunct to non surgical periodontal treatment. The treatment will be repeated 4 times in two weeks, followed by dental prophylaxis every 15 days until accomplish 3 months. The follow-up will be done for 6 months. The clinical parameters measured will be: plaque index, pocket depth, bleeding on probing, relative clinical insertion level and suppuration. In addition, the evaluation of crevicular fluid volume and the levels of IL-1, TNF-α, subgingival microbiota by the hybridization DNA-DNA Checkerboard technique. The investigators expect to find identical or better results for the test group.
To establish Oraqix is safe when used on adolescent volunteers.
Peri-implantitis is an infectious disease that resides in the mucosa surrounding dental implants and also affects the supporting bone. Because the number of implants placed in everyday clinical practice is continuously increasing, it is reasonable to anticipate an increasing prevalence of peri-implantitis. However, from the literature there is very little reliable evidence suggesting which could be the most effective interventions for treating peri-implantitis. The primary objective of this controlled clinical study is to evaluate the microbiological effect of decontamination of the implant surface during the surgical treatment of peri-implantitis using a chlorhexidine or placebo solution. The secondary objectives are to assess both the clinical and the microbiological effectiveness of treatment of peri-implantitis. It is hypothesized that rinsing of the implant surface using a 0.12% chlorhexidine solution does not lead to better microbiological and clinical results compared to rinsing with a placebo solution. The present study is a double-blind, placebo-controlled, randomized clinical trial. Adult patients with at least one endosseous implant in the oral cavity with clinical and radiographical signs of peri-implantitis will be included in this study. Implants with peri-implantitis lesions will be surgically exposed, followed by mechanical cleansing using curettes and gauzes and cotton pellets soaked in saline followed by either 1 minute of rinsing with a placebo solution (saline with appearance of chlorhexidine) (control group) or 1 minute of chemical cleansing using 0,12% chlorhexidine + cetylpyridinium chloride (CPC) without alcohol (Perio-aid®) (test group). After 1 minute of saline rinsing the gingival flap will be returned slightly apical (in order to reduce pockets) and will be firmly sutured. For both groups the surgery is followed by 2 weeks of mouthrinses with 0,12% chlorhexidine + Cetylpyridinium Chloride (CPC) without alcohol (Perio-aid®) two times daily during 30 seconds. The main study parameter is the microbial composition of the biofilm on the dental implant surface. Secondary study parameters are bleeding on probing, probing pocket depth, suppuration on probing, microbiological composition of the peri-implant sulcus, radiographic marginal bone level on standardized intraoral radiographs, presence of plaque, presence of calculus, marginal soft tissue recession implant failure, complications and adverse events.
The primary purpose of the study will be to look for biological biomarkers to determine which people with gum disease will have a worsening of the disease. A second objective of this study will be to look at the effects of periodontal treatment on the levels of the biomarkers that are identified.
Periodontal instrumentation aims to remove plaque and calculus from the root surface. Both manual and ultrasonic instruments have been used for such decontamination; however, establishing a healthy periodontium can result in adverse effects, such as dentin hypersensitivity. The aim of this study was to evaluate the effects of hand or ultrasonic instrumentation on dentin hypersensitivity in patients undergoing non-surgical periodontal treatment. For this controlled clinical trial of a "split mouth" design, 14 patients were selected with homologous teeth in the incisor to premolar region and probing depth ≥ 5 mm on the buccal aspect of the teeth. One side (control) was instrumented with hand instruments and the other side (test) with ultrasonic instruments. Dentin hypersensitivity was assessed in the baseline and during the follow 4 weeks after treatment, with a periodontal probe scratching the root surface and with an air jet. The patient's response was detected by a visual analog scale (VAS) of 10 cm.
The overall goal of this research is (1) to identify changes in gene expression and DNA methylation status in subjects who exhibit advanced chronic periodontal inflammation and (2) to identify microRNAs (miRNAs) and the interactive pathways associated with obesity as a modifier of periodontal infection pathogenesis.
We propose to examine a population of Native Americans who have had little or no dental care, and to determine if periodontal disease is associated with early signs of vascular dysfunction or systemic inflammation. We then propose to treat the periodontitis and re-evaluate vascular function. We will determine if gingivitis or mild/moderate periodontitis is associated with detectable vascular dysfunction. Microbial metagenomics will be correlated with vascular function.
The studies that correlate periodontal disease (PD) and diabetes mellitus (DM) suggest that individuals with poor glycemic control are at increased risk for developing infections. Despite being controlled for other important risk factors, diabetic patients are three times more likely to develop PD, and therefore, periodontitis has been proposed as the sixth complication of DM. Besides the effect of diabetes on DP, the reverse has also been studied over the past 15 years, through the idea that chronic and acute infections can directly affect the tissue resistance to insulin. Recent studies have provided evidence that controlling periodontal infection has an impact on improvement of glycemic control in diabetes mellitus patients. The vascularity of the inflamed periodontal tissue serves as a gateway to inflammatory mediators, pathogenic bacteria and their products into the bloodstream. Some researchers have suggested that periodontal treatment in type 2 diabetes mellitus (DMT2) patients, results in beneficial effect on the level of glycemic control. However, there is no conclusive evidence to support this hypothesis. This research project aims to determinate the impact of periodontal therapy on metabolic control in DMT2 individuals, and determinate the possible association between periodontal disease and DMT2. For the HbA1c outcome this clinical trial had a sample size calculation estimated at 120 patients. For the inflammatory serum markers this study had a sample size estimated at 22 individuals. Blood samples will be collected for evaluation of Hba1c and inflammatory serum markers. This data will highlight the possible role of periodontal therapy on DMT2 metabolic control.
Currently the research issue in establishing the role of periodontal disease (PD) in coronary heart disease (CHD) risk is to define the pathways that lead to cause-effect relationship between PD and CHD. There is no consensus on definition of a periodontal disease case or the threshold level that may give clear indication for this relationship. Periodontal therapy has been used in different studies with the hope that a change in periodontal disease status may modify the factors associated with CHD risk. Many of these studies, on role of periodontal therapy in the reduction of CHD associated risk-factors, were based on small study samples, and very few studies were randomized controlled trials. So a need for large prospective studies is warranted in literature.----------- A single-blind parallel-arm randomized controlled clinical trial was designed to observe the influence of periodontal treatment on serum inflammatory mediators of hsC-reactive protein, white blood cells and fibrinogen in CHD patients. Hypothesis: Periodontal therapy in CHD patients, by reducing periodontal inflammation, may decrease the host systemic inflammatory burden associated with atherogenic processes.