View clinical trials related to Periodontitis.
Filter by:Periodontitis is a chronic inflammatory disease of the tooth supporting structures induced by a dysbiosis in the oral and subgingival microenvironment of susceptible patients. The long-term swallowing of high doses of periodontal pathogenic microorganisms could induce a dysbiosis of the intestinal microbiota, favouring the establishment of an 'inflamed' microbiome in terms of composition and/or function. The present project is aimed at a better understanding of the etiopathogenetic correlation between periodontitis and intestinal dysbiosis, and aims to explore the hypothesis that periodontal treatment may influence the multi-omics profile on the oral-gut-systemic axis. 70 patients affected by stage III-IV periodontitis will be recruited, and treated by means of full-mouth scaling and root planing. Salivary, subgingival plaque, plasma and stool samples, together with a complete periodontal charting and a food diary will be collected and compared at baseline and after treatment. Age, gender and BMI-matched healthy individuals will be recruited as controls.
The goal of this clinical trial is to compare the efficacy of Noisome as carrier of minocycline hydrochloride gel to minocycline hydrochloride in Stage II or Stage III Periodontitis . The main questions it aims to answer are: - Is the Noisome carrier of minocycline hydrochloride has an effect in comparing to minocycline hydrochloride in Stage II or Stage III Periodontitis? - what is the release profile of of minocycline hydrochloride noisome gel and minocycline hydrochloride gel? Participants will be asked to maintain oral hygiene after application of treatment Researchers will compare the effect of noisome as a carrier of locally delivered minocycline hydrochloride gel to minocycline hydrochloride gel in stage II or stage III periodontitis patients as an adjunct to non-surgical periodontal treatment] to see if Plaque Index (PI) , Gingival index,Clinical attachment level (CAL) &Periodontal Pocket Depth decreased or not.
Inflammatory bowel disease (IBD) is a chronic and recurrent inflammatory disease of the gastrointestinal tract characterised by complex interactions between genetic susceptibility, environmental factors, microbiota and host immune response. It has two main forms, Crohn's disease (CD) and Ulcerative colitis (UC). The main mechanism of IBD pathogenesis is dysregulated host immune response to commensal microbiota and disruption of the balance of pro- and anti-inflammatory cytokines in genetically predisposed individuals. Periodontitis is a multifactorial inflammatory disease associated with dental biofilm resulting in the loss of periodontal supporting tissues and subsequently teeth. Although the occurrence of the disease depends on multifactorial factors, bacterial plaque is the primary etiological factor and various bacterial species found in plaque are responsible for initiating and maintaining the inflammatory and immune response in periodontal disease. Periodontal diseases are known to contribute to many systemic diseases/conditions or systemic disorders are known to affect periodontal disease. Although the relationship between IBD and periodontitis is based on the potential link between oral and intestinal microbiomes and host immunoinflammatory response, the pathological interactions between the two diseases have not yet been determined. From this point of view, the aim of our study was to investigate the effect of periodontal status on serum, saliva and gingival biomarkers (TIM-3, TNF-α, IL-6 and IL-17) in patients with IBD and to evaluate the relationship between these values and periodontal clinical parameters. This is the first study to examine TIM-3 levels in saliva, serum and gingival samples in patients with IBD and periodontitis with IBD.
Periodontitis is a common chronic inflammatory disease characterised by the destruction of the soft and hard tissues supporting the tooth, including alveolar bone, periodontal ligament and cementum. Periodontitis has been associated with different host characteristics such as diabetes or neutrophil disorders and environmental factors such as smoking, alcohol consumption and stress. On the other hand, periodontal bacterial infection triggers a systemic immune response that is associated with an increased risk of different disorders such as bacterial pneumonia, cardiovascular disease and autoimmune diseases. Rheumatoid arthritis (RA) is a severe chronic autoimmune disease of unknown etiology, characterised by symmetrical, erosive synovitis of the joints, sometimes with multisystem organ involvement, joint destruction and excessive bone loss. Although the etiology of RA is unknown, it is thought to occur in individuals with genetic predisposition as a result of exposure to various environmental factors. RA and periodontitis are chronic destructive inflammatory diseases with common genetic and environmental risk factors, pathogenesis mechanisms and complex multifactorial pathological processes. Several studies suggest that periodontitis, a common inflammatory disease of the periodontium surrounding the teeth and triggered by bacteria in the mouth, is associated with RA and may initiate and worsen inflammation in RA. Non-surgical periodontal treatment (COPT), which is considered the gold standard in the treatment of periodontitis with hand instruments and ultrasonic instruments, has been shown to provide significant improvements in the clinical outcomes of periodontitis patients with RA. COPT is performed to stop the progression of periodontal diseases. Considering the studies supporting the bidirectional relationship between periodontitis and RA, it is thought that COPT may affect the clinical and biochemical values of RA. Based on these points, the aim of our study was to investigate the relationship between serum and salivary ANGPTL-4, MMP-13, TNF-α and IL-6 levels and periodontal disease in individuals with RA and to evaluate the effects of COPT on RA disease severity in vivo.
Pulpitis is the pulpal inflammation in response to irritants which are either microbial, chemical, or physical (mechanical and thermal) in origin. Clinically, pulpitis is termed as reversible or irreversible, whereas histologically, it is described as acute, chronic or hyperplastic . Pulpitis is considered reversible when the pulp can heal following conservative management . For such cases, a coronal pulpotomy is considered as a definitive treatment option having 78% to 90% of success rate . In irreversible pulpitis (IP), the pulp is not capable of healing, thus it is treated traditionally complete pulpectomy.
The goal of this observational study is to investigate the ability of Periodontists, Clinicians with Expertise in Periodontics and General Dental Practitioners to diagnose periodontitis using the 2017 AAP / EFP World Workshop classification of periodontal diseases. The purpose of this study is to conduct a online survey in order to: 1. investigate Italian dentists' knowledge on the new classification of periodontal diseases. 2. evaluate the reliability of the diagnosis between different examiners in classifying periodontitis; 3. evaluate the accuracy of the use of grading in the diagnosis of periodontitis; 4. evaluate diagnostic accuracy of staging application in classifying periodontitis.
Apical lesions usually present clinically as a chronic infection, remaining as asymptomatic apical periodontitis(AAP). Because the balance among inflammation and bacteria is a dynamic process, AAP may undergo an acute exacerbation and become symptomatic, presenting as symptomatic apical periodontitis or acute abscess, or it may evolve from the acute to the chronic stage. Identification of specific biomarker could help in establishing more accurate diagnosis. Biological marker serves as a parameter that is indicative of underlying physiology and health of the tissue. It is measurable as well as quantifiable. The aim of this study: To assess the level of potential biomarkers in asymptomatic and symptomatic apical Periodontitis, and to determine the prediction potential of the same biomarkers for the outcome of endodontic treatment after 1year recall…
Periodontitis is a destructive disease that follows untreated gingivitis and is characterized by gingival inflammation, clinical attachment loss, alveolar bone loss and periodontal pocket formation, increased tooth mobility and tooth loss. Although the primary etiological factor is microbial dental plaque, the host response plays an important role in the transition from periodontal health to disease. Smoking is a major risk factor for periodontitis and affects the formation and severity of the disease and healing after periodontal treatment by changing the host response to plaque. Proinflammatory and antiinflammatory cytokines have an important role in the pathogenesis of periodontal disease. Among these cytokines, interleukin (IL)-1β, IL-10 and currently IL-39 have been associated with periodontal disease. Further studies with post-treatment longitudinal evaluation are needed to elucidate the functions of IL-39 and its possible role in the pathogenesis of periodontal diseases. In this study, it was aimed to investigate the effects of non-surgical periodontal treatment on salivary and gingival crevicular fluid (GCF) IL-39, IL-1β and IL-10 levels in smokers and non-smokers with Stage 3 Grade B periodontitis and periodontally healthy individuals, both smokers and non-smokers. To the best of our knowledge, there is no study investigating the effects of non-surgical periodontal treatment and smoking on IL-39. 50 individuals with periodontitis and 50 periodontally healthy individuals (total 100 individuals) will be included in our study, and these two groups will be divided into two sub-groups as smokers and non-smokers. Clinical measurements (Plaque index, probing depth, gingival recession, clinical attachment level, bleeding on probing), saliva and GCF samples will be taken from all individuals at the beginning of the study. Non-surgical periodontal treatment will be performed in individuals with periodontitis. Saliva and GCF samples will be collected before treatment. The clinical measurements, saliva and GCF collection will be repeated 12 weeks after the treatment. The saliva and GCF levels of IL-39, IL-1β and IL-10 will be analyzed by ELISA. Cotinine levels will be examined to evaluate the effects of smoking before and after treatment in periodontal health and periodontitis. With this study, we aimed to develop IL-39 diagnostic kits for the diagnosis of periodontal diseases, detection of disease activity, follow-up of response to treatment and healing.
Periodontal diseases are one of the most common inflammatory diseases. Periodontitis results from products and antigens of microorganisms, which stimulates the innate immune system and local inflammatory response; characterized by gingival inflammation, attachment loss, and alveolar bone destruction. Molecules that play a role in the pathogenesis of periodontal disease can be used as biomarkers in the early diagnosis of periodontitis, in determining the rate of periodontal destruction, and in evaluating the response to periodontal treatment. CTRPs (C1q/TNF-related proteins), which are adiponectin paralogs, are involved in inflammation, lipid, and glucose metabolism, as well as physiological and pathological processes like vasodilation. CTRP-1 is a glycoprotein belonging to the CTRP family that can be detected in serum in the presence of certain antibodies. Serum CTRP-1 levels increase in type 2 diabetes, prediabetes, coronary artery diseases, congestive heart failure, and atherosclerosis. Lipopolysaccharides found in Gram-negative bacteria cell walls stimulate the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1 β, as well as indirectly increasing the production of CTRP-1. CTRP-1 is a therapeutic target in many inflammatory diseases, including periodontal diseases. However, there are no clinical studies on the role of CTRP-1 in the pathogenesis of periodontal disease. Based on these findings, the goal of our research is to examine the effects of periodontal disease on CTRP-1, IL-10, and TNF-α levels in serum and gingival crevicular fluid samples taken before and after periodontal treatment from periodontally healthy individuals and individuals with gingivitis and periodontitis, and also determine whether CTRP-1 is a potential biomarker that can be used in the diagnosis of periodontal disease. 25 patients with periodontitis, 25 with gingivitis and 25 healthy periodontals (total of 75 individuals) will be included in our study. At the beginning of the study, periodontal clinical measurements (gingival index, plaque index, probing depth, gingival recession, clinical attachment level, and bleeding on probing), serum and gingival crevicular fluid samples will be taken from all individuals. Non-surgical periodontal treatment will be applied in quadrant wise within 2 weeks to individuals with gingivitis and periodontitis. 12 weeks after treatment; the clinical measurements and the collection of serum and gingival crevicular fluid will be repeated. Biomarkers in serum and gingival crevicular fluid samples will be examined by ELISA.
Periodontitis is a bacterial inflammatory disease and antibiotic use is being empirically used as part of its treatment. However, a clinical practice guideline on periodontal treatment adjuncts published in 2015 identified weak evidence on the use of systemic antibiotics and large heterogeneity across small scale studies, suggesting that larger pragmatic clinical trials would benefit clinical decision making. This will be a prospective, randomized, placebo-controlled trial, stratified by practice and practitioner. The study will investigate the effectiveness of adjunctive antibiotics as adjunct to scaling and root planing (SRP) compared to SRP with placebo for the treatment of generalized stage II-III, grades A-C periodontitis in approximately 544 patient participants from about 34 National Dental PBRN practices. Periodontal data will be collected at baseline, re-evaluation (6 weeks), and final (12 months) study visits. Changes in periodontal clinical and patient-reported outcomes will be assessed to determine the effectiveness of SRP plus adjunctive systemic Amoxicillin / Metronidazole antibiotics (AMXM) versus SRP with Placebo.