View clinical trials related to Periodontal Diseases.
Filter by:Primary Objective: To identify changes in systemic markers of inflammation following periodontal treatment, comparing two standard treatment modalities (hands scaling and ultrasonic scaling) Secondary Objectives: To investigate bacteraemia, composition and function of oral bacteria, treatment outcomes following periodontal treatment, patient and operator preferences, and treatment time comparing hand scaling and ultrasonic scaling.
Chlorhexidine is considered as gold standard for its antiplaque and antigingivitis efficacy till date but it has got many side effects. So it is need of the hour that investigators will find some substitute having similar antiplque and antigingivitis efficay but have less or no adverse effects. so in this study investigators planned to do "Comparative evaluation of antiplaque and antigingivitis efficacy of ocimum sanctum (tulsi) extract mouthrinse with 0.12% chlorhexidine mouthrinse.
Visfatin is an adipokine that plays an important role in immune functions as a growth factor, enzyme, and proinflammatory mediator. The investigators aimed to determine the levels of visfatin, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in gingival crevicular fluid (GCF) in both obese/non-obese patients, with/without generalized chronic periodontitis (GCP). Patients were categorized as obese (O) (n=31) or non-obese (nO) (n=19). Groups were divided into four subgroups according to periodontal conditions: (1) periodontally healthy without obesity (nO-Ctrl); (2) GCP without obesity (nO-CP); (3) periodontally healthy with obesity (O-Ctrl); and (4) GCP with obesity (O-CP). Demographic variables and anthropometric and laboratory data were recorded. Periodontal measurements were recorded at baseline and 3rd months after either non-surgical periodontal treatment or calorie restricted diet therapy. At the same time GCF samples were taken from patients to analyze TNF-alpha, IL-6, and visfatin levels.
This study investigates the differences between subjects with and without periodontitis in: the prevalence of (pre)diabetes mellitus, the risk of atherosclerotic cardiovascular disease, the prevalence of metabolic syndrome and the risk of obstructive sleep apnea syndrome.
The purpose of this study is to determine of local application of commericially-available, FDA-approved preparation of simvastatin is effective in increasing clinical attachment levels (primary outcome), as well as alveolar bone (secondary outcome) compared to standard mechanical therapy in patients on periodontal maintenance therapy (PMT). Subjects undergoing PMT at the UNMC College of Dentistry clinics will be recruited to participate in the randomized one-year clinical trial based on the following eligibility criteria: 1) diagnosis of chronic advanced periodontitis (generalized or localized), 2) participating in regular PMT visits (3-6) month intervals), 3) no systemic diseases or medication which significantly impact periodontal inflammation or bone turnover (e.g. steroids, bisphosphonates, > 325 mg aspirin/day and in good general health, 4) one experimental quadrant of the mouth with an inflamed 6-9 mm interproximal posterior periodontal pocket with history of bleeding on probing (BOP), 5) willingness to sign consent form. Subjects will be divided into two groups for additional therapy in a 6-9 mm interproximal periodontal pocket at baseline: 1) local anesthesia and mini-flap reflection with subgingival mechanical debridement plus application of the simvastatin-methylcellulose gel or 2) local anesthesia and mini-flap reflection with subgingival mechanical debridement plus application of methylcellulose gel alone. Samples/measurement will be obtained at the designated experimental site at baseline, 2 weeks, 6 and 12 months during PMT: 1) digital radiographs (baseline and 12 months only; bone height measurements), 2) presence of explorer-detectable supragingival plaque, 3) 30-second gingival crevicular fluid (GCF) sample (markers of inflammation, bone turnover), 4) recession from the cemento-enamel junction, 5) probing pocket depth and bleeding on probing (BOP). Following the 12-month visit, the research-specific intervention and measurements in the experiment quadrant will be removed from routine PMT.
This study aimed to investigate the effects of diode laser (DL) in addition to non-surgical periodontal treatment on periodontal parameters, systemic inflammatory response, and serum hemoglobin A1c (HbA1c) level in patients with uncontrolled type 2 diabetes mellitus (T2DM) and chronic periodontitis.
The aim of this study was to evaluate the effect of obesity and exercise on periodontal and biochemical parameters [serum, saliva and gingival crevicular fluid (GCF) adipokines (interleukin-1β, tumor necrosis factor-α, leptin, resistin and adiponectin)].
Despite significant improvement in treating periodontal disease (PD) and the identification of multiple risk factors, little is known about the specific contribution of genetics to PD pathogenesis. Several genomewide association studies (GWAS) of PD have been published, but only one reported locus has reached the threshold for genome-wide significance. Epidemiological studies and biological experiments established associations and suggested common pathogenetic pathways between PD and cardiovascular disease (CVD), diabetes (DM), and osteoporosis. The overall objective is to identify genetic loci for PD as a first step toward a better understanding of PD pathogenesis. In a preliminary study in the Women's Genome Health Study (WGHS), new-onset cases of PD were associated with a family history of myocardial infarction (MI). Further preliminary analyses presented shared phenotypic variation of PD/CVD, PD/DM, or PD/osteoporosis that could be accounted by the whole-genome genetic matrices. Several variants from the GWAS catalog of bone density and family history of MI were found correlated with PD in the WGHS. Based on these findings and the literature, the central hypothesis is that there are common pathogenetic links between PD and these other diseases and that GWAS using the comorbidity case definitions will help identify potential common loci.
The purpose of the study was to evaluate, from a microbiological point of view, microbiota around teeth and implants in the same patient affected by periodontal disease and peri-implant disease, all compared with a healthy tooth. From the identification of particular bacterial species in the examined sites, it is intended to be traced back to the identification of a clear etiopathogenic process, which may shed light on the similarities and differences between the two diseases. In recognition of these mechanisms, the investigators think to develop new therapeutic strategies for the future.
Recent studies have shown that the systemic inflammation caused by periodontal disease (PD) can determine important changes in the coronary arteries, favoring atherosclerosis progression and development of acute coronary syndromes (ACS). The aim of ATHERODENT study is to assess the interrelation between PD, inflammation and progression of coronary atherosclerosis in patients with ACS. Material and methods: This case-control observational study will enroll 100 patients (group 1 - ACS and associated PD, and group 2 -ACS and no PD), in whom the following data will be collected: (1) demographic and clinical data, (2) cardiovascular risk factors, (3) full characterization of PD markers, (4) systemic inflammatory biomarkers, (5) imaging biomarkers derived from transthoracic echocardiography, computed tomography, coronary angiography, optical coherence tomography and intravascular ultrasound, and (6) assessment of the presence of specific oral bacteria in samples of coronary plaques collected by coronary atherectomy, which will be performed during percutaneous revascularization interventions, when indicated in selected cases, in the atherectomy sub-study. The follow-up will be performed at 1, 3, 6, 12, 15, 18 and 24 months. The primary endpoint of the study will be represented by the rate of major adverse cardiovascular events (MACE rates) in PD vs non-PD patients and in correlation with: (1) the level of systemic inflammation triggered by PD and/or by ACS at baseline; (2) the vulnerability degree of atheromatous plaques in the coronary tree (culprit and non-culprit lesions); and (3) the presence and burden of oral bacteria in atheromatous plaques. Secondary endpoints will be represented by: (1) the rate of progression of vulnerability degree of non-culprit coronary plaques; (2) the rate of progression of atheromatous burden and calcium scoring of the coronary tree; and (3) the rate of occurrence of left ventricular remodeling and postinfarction heart failure.