Active clinical trials for "Periodontitis"

Today, to understand pathogenic mechanisms involved in periodontitis remains a challenge to identify biomarkers or therapeutic targets to improve prevention and screening, as well as the effectiveness of periodontitis treatments. The aim is to characterize, in vivo, specific molecular markers reflecting the activity of the pathology, which could lead to improve the knowledge of the pathogenesis of periodontitis; determine target molecules involved in tissue destruction; determine molecular profiles of patients at local and systemic risk; determine therapeutic targets For this purpose, biological samples will be collected (plaque, saliva, crevicular fluid) from patients with periodontitis stage 3 or 4 versus patients with a healthy periodontium. Biological samples will be collected before and all along the periodontal treatment. Gingiva explants collection will be sampling within the surgical procedures (if they are needed). The primary objective is to investigate tissue and cellular expression of molecular markers associated with periodontal destruction during periodontitis in relation to periodontal infection and systemic changes in host response. A characterization of the cytokines in gingival fluid and unstimulated saliva (Luminex® technique) of patients with periodontitis versus without periodontitis will be done. The secondary objective is to study the influence of periodontitis on systemic pathologies via serum analysis of molecules and bacteria involved in periodontal destruction. Immunofluorescence evaluation of protein expression and distribution (inflammatory mediators, inflammatory pathway signaling proteins) in gingival explants, characterization of proteases (MMP) present in gingival fluid and unstimulated saliva (Luminex® technique) and microbiological analysis of the subgingival biofilm (by quantitative PCR).

Although of low prevalence, aggressive periodontitis is a rapid destructive form of periodontal disease that initiates at a young age, leading to premature loss of first molars and incisors. Little is known on the mechanisms of this disease. It is imperative to understand mechanisms of disease to establish proper treatment. We have established a controlled study in a comparable population presenting similar aggressive disease characteristics to evaluate the mechanisms of this disease. It is the goal of this study to determine immunological and microbiological mechanisms responsible for the rapid tissue destruction in children with localized aggressive periodontitis and how traditional periodontal intervention affects these mechanisms. Important knowledge gained with this proposal will aid in defining specific treatment approaches to better control disease progression and prevent disease initiation in susceptible individuals.

This study aimed at exploring the effect of nonsurgical periodontal treatment on galectin 1 and 3 GCF levels in patients having gingivitis, periodontitis stage III compared to periodontally healthy individuals and if galectin-1 and -3 could serve as diagnostic markers and/or therapeutic targets for periodontitis, in addition to revealing their possible role in the periodontal disease. 45 systemically healthy participants were enrolled in this investigation, equally subdivided into three groups of 15 patients each: gingivitis, periodontitis (stage III) and control group with healthy gingiva. Probing depth, clinical attachment level, gingival and plaque index were registered. GCF levels of galectin-1 and -3 were evaluated in all included groups (before and after non-surgical treatment for periodontitis group) using enzyme linked immune-sorbent assay (ELISA) kit.

Objectives: Primary: To determine the efficacy of periodontal treatment on mental health outcomes in patients with major depression and periodontitis. Secondary: To identify the effect of periodontal treatment on oral, periodontal, and fecal metagenomic microbiomes, and on systemic levels of inflammation (bacterial, viral, and fungal) and their impact on mental health outcomes. Material and method: A 6-month pilot randomized controlled clinical trial is designed. The study will be conducted in patients with moderate or severe DM (Patient Health Questionnaire-9 [PHQ-9] index of 9 or higher) and stage III-IV periodontitis who will be assigned to two different interventions: Test group: standard periodontal treatment consisting of two sessions of supragingival and subgingival debridement (steps 1 and 2) under local anesthesia. Control group: periodontal treatment consisting of two sessions of supragingival debridement (step 1) under local anesthesia. The study will consist of 6 visits: Screening visit (v0) Baseline visit (v1): In the mental health center: patients will receive a structured clinical interview for the DSM-IV (SCID) and the patient will fill out a series of specific scales on a study-specific electronic device [Beck Depression Inventory (BDI); UCLA Loneliness Scale, Center for Epidemiologic Studies Depression scale [CES-D]; Childhood Trauma Questionnaire short form (CTQ-SF); The World Health Organization Quality of Life questionnaire (WHOQOL); Hamilton scale (HAM-D17); Global Assessment of Functioning (GAF) Scale]. At the UCM School of Dentistry: patients will receive a complete periodontal examination (clinical and radiographic). A subgingival microbiological sample, a saliva sample and a blood sample will also be taken. At the participant's home: the stool samples will be deposited by the participants at home in the specific collection vial. Intervention visits (v2-3): Two periodontal treatment sessions (test or control) will be carried out one week apart. Re-evaluation visit (v4): Six weeks after treatment, all periodontal clinical variables will be recorded. Follow-up visits at 3 and 6 months: after periodontal treatment, all the variables recorded at the baseline visit will be taken Statistical analysis: Periodontal treatment (test/control) will be considered as the independent variable and the Hamilton scale (HAM-D17) will be considered the primary response variable. The rest of the variables will be considered as secondary variables. A crude bivariate analysis of comparison of means or proportions will be carried out depending on the nature of the variable. In addition, crude and adjusted regression models will be performed.

This clinical trial aims to evaluate the clinical, biochemical and microbiological efficacy of ozone treatment as an adjunct to nonsurgical periodontal treatment (NSPT) in periodontitis patients. The main question it aims to answer is: • Is the application of gaseous ozone, as an adjunct to NSPT, to periodontal pockets in patients with periodontitis alters the clinical periodontal parameters, gingival crevicular fluid levels of inflammatory cytokines, and periodontal pathogens compared to NSPT alone? The study will be performed according to a split-mouth design, the contralateral quadrants with similar periodontal status in each patient will be randomly allocated to one of the following two different treatment modalities. Participants will be applied NSPT consisting of supra and subgingival debridement. NSPT will be applied alone in one quadrant In addition to NSPT, ozone therapy procedures were performed using a device at contralateral sites. Researchers will compare the sites with and without ozone therapy in addition to NSPT to see if ozone therapy adjunct to the NSPT affects clinical, biochemical, and microbiological changes

Periodontitis is an immune-inflammatory disease affecting the supporting structures of the teeth. It is a disease of multifactorial etiology, with microbial, genetic, environmental and host factors involved, with the release of oxygen-free radicals by the inflammatory cells. Quercetin, have shown potential antimicrobial activity, lowering of inflammatory markers, cholesterol reduction and inhibiting bone loss. However, this data has largely been obtained from in vitro and animal studies, but data from human studies are limited.

Periodontitis (gum disease) leads to the formation of gum pockets. Its treatment involves deep cleaning of the teeth, to remove soft and hard tooth deposits under the gum line. Although in the long term this leads to improvement of the gum conditions and reduced inflammation, in the hours and days post-treatment, inflammation may increase, sometimes also associated with a high temperature. A method to reduce this response has not been found yet. The goal of this multi-centre randomized controlled trial is to to test if a diet which acts to mimic periodic fasting can influence responses in the mouth and throughout the body after treatment of gum disease in patients with advanced gum disease but general health conditions. Five Spanish centres (Universidad Complutense de Madrid, Universidad Internacional de Catalunya, Universidad de Murcia, Universidad de Santiago de Compostela, Universidad de Granada) will perform the clinical part of the study, whereas the King's College of London (Guy's Hospital) will provide the analyses and processing of the data. Researchers will include 24 patients in total. The main question it aims to answer is: - Is a mimic periodic fasting (together with the classical gum treatment) effective at reducing the local and systemic inflammation provoked by the gum disease (and by the same treatment) in the short- and medium term? Although all participants will receive the necessary gum treatment (deep cleaning), researchers will randomly assign them to one of two groups. The test group will follow three cycles (the same day of the treatment, and 45- and 85 days after treatment) of 5 days each of a fasting-mimicking diet (FMD). The FMD program is a plant-based diet program designed to attain fasting-like effects while providing both macro- and micronutrients to minimize the burden of fasting and adverse effects. The FMD consists of 100% ingredients that are generally regarded as safe (GRAS) and comprises proprietary vegetable-based soups, energy bars, energy drinks, cracker snacks, olives, herbal teas, and supplements. All items to be consumed per day are individually boxed. In contrast, the control group will continue with their current diet. All patients will complete dietary diaries to estimate calorie intake during this time period. Researchers will collect blood, stool, plaque and gingival crevicular fluid samples from each patient at different time points. Besides, they will call the patients one or two times during each FMD cycle to check that everything is proceeding properly and to solve any problems or concerns they may have. In addition, a trained registered dietitian will be available during the whole study period in case participants need some support or have doubts and/or questions. If participants miss multiple visits (e.g. 2/3) will be considered as a drop-out and, if they develop a serious medical condition, they might be excluded from the study. However, independently from the participation into this study, each patient will have their gum disease regularly treated. People with periodontal disease usually have a bad dietary-habits. This investigation with its holistic approach might lead people to modify their unbalanced diet due to the possible related local and systemic benefits. In addition, cycles of 5 days might consistently raise the adherence and willingness to follow such a fasting regime.

Untreated periodontal infection may result in transient bacteremia and toxaemia which may be the cause of adverse systemic events, leading to various systemic disorders. Amongst all the systemic diseases, cardiovascular disease has been recognized as a major systemic inflammatory condition that present similarities with periodontal disease. Increased systemic biomarkers of inflammation associated with periodontal disease have been interpreted as a mechanistic link between periodontitis and cardiovascular diseases. Genetic factors are also known to play a pivotal role in influencing the inflammatory and immune response. Genetic polymorphisms are alterations in the DNA sequence found in general population. Most forms of periodontitis represent a life-long account of interactions between the genome and the environment. The previous literature has stated a strong association of genetic polymorphisms in periodontitis and coronary artery diseases. Identifying these polymorphisms can potentially lead to a better understanding of the mechanisms modulating the expression of inflammatory mediators as well as provides potential therapeutic targets in the prevention of periodontal disease. Two such novel polymorphisms have gained attention recently, namely the Dickkopf-3 and complement factor H polymorphisms. Dickkopf-3 belongs to Dickkopf family of glycoproteins. Dickkopf-3 has been mainly investigated in oncology for its role as a tumor suppressor gene and as a therapeutic target in several types of human carcinomas. Recently, Dickkopf-3 gained attention as an emerging biomarker for cardiovascular and renal diseases. Dickkopf-3 has shown to play a role in pathophysiology of arterial wall thickening and abnormality implicated in atherosclerosis. However, genetic polymorphism of Dickkopf-3 rs11544814 and complement factor H rs10737680 its protein levels have never been investigated in subgingival plaque samples of periodontitis patients with coronary artery disease specifically before and after non-surgical therapy. This may further improve our understanding of the influence of this polymorphism on the above mentioned systemic diseases.

The main objective of this study is to evaluate the effect of periodontal therapy in in subjects with a clinical diagnosis of mild to moderate AD dementia.

The aim of this prospective cohort observational study is: (i) to assess the endodontic treatment outcome in a private specialist endodontic office in Slovenia; (ii) to estimate the effect of various pre-, intra- and postoperative factors onto endodontic treatment outcome.