Background Chronic inflammation is believed to be a major mechanism underlying the pathophysiology of type 2 diabetes. Periodontitis is a cause of systemic inflammation. We aimed to assess the effects of periodontal treatment on glycaemic control in people with type 2 diabetes. Methods In this 12 month, single-centre, parallel-group, investigator-masked, randomised trial, we recruited patients with type 2 diabetes, moderate-to-severe periodontitis, and at least 15 teeth from four local hospitals and 15 medical or dental practices in the UK. We randomly assigned patients (1:1) using a computer-generated table to receive intensive periodontal treatment (IPT; whole mouth subgingival scaling, surgical periodontal therapy [if the participants showed good oral hygiene practice; otherwise dental cleaning again], and supportive periodontal therapy every 3 months until completion of the study) or control periodontal treatment (CPT; supra-gingival scaling and polishing at the same timepoints as in the IPT group). Treatment allocation included a process of minimisation in terms of diabetes onset, smoking status, sex, and periodontitis severity. Allocation to treatment was concealed in an opaque envelope and revealed to the clinician on the day of first treatment. With the exception of dental staff who performed the treatment and clinical examinations, all study investigators were masked to group allocation. The primary outcome was between-group difference in HbA,, at 12 months in the intention-to-treat population. This study is registered with the ISRCTN registry, number ISRCTN83229304.

Background: Rate of progression of periodontitis has been used to inform the design

Within the limitations of the research, the data show that mean annual attachment level change varies considerably both within and between populations. Overall, the evidence does not support or refute the differentiation between forms of periodontal diseases based upon progression of attachment level change.

Degree III furcation involvements were surgically created at four first molars in each of three monkeys. Following 6 weeks of healing, full-thickness flaps were elevated. Following 24% EDTA gel conditioning, the defects were treated with one of the following: (1) enamel matrix proteins (EMD), (2) guided tissue regeneration (GTR) or (3) a combination EMD and GTR. The control defects did not receive any treatment. After 5 months of healing, the animals were sacrificed. Three 8 μm thick histological central sections, 100 μm apart, were used for histomorphometric analysis in six zones of each tooth either within the furcation area or on the pristine external surface of the root. In all specimens, new cementum with inserting collagen fibres was formed. Following GTR or GTR + EMD, cementum was formed up to and including the furcation fornix indicating complete regeneration on the defect periphery. Periodontal ligament fibres were less in all four modalities compared to pristine tissues. In the teeth treated with GTR and GTR + EMD a higher volume of bone and periodontal ligament tissues was observed compared to EMD. After 5 months of healing, regenerated tissues presented quantitative differences from the pristine tissues. In the two modalities where GTR alone or combined with EMD was used, the regenerated tissues differed in quantity from the EMD-treated sites.

OBJECTIVEShortened leukocyte telomere length (LTL) and diagnosis of periodontitis are associated with an increased risk of complications and mortality in diabetes. This study investigated the association between LTL, endotoxemia, and severity of periodontitis in a large cohort of people with diabetes. RESEARCH DESIGN AND METHODSSix hundred thirty individuals (371 with type 2 and 259 with type 1 diabetes) were recruited from the University College Hospital in London, U.K. During a baseline visit, blood was collected for standard biochemical tests and DNA extraction, while a dental examination was performed to determine diagnosis and extent of periodontitis. LTL was measured by real-time PCR, and endotoxemia was assessed by the limulus amoebocyte lysate method. RESULTSTwo hundred fifty-five individuals were diagnosed with gingivitis, 327 with periodontitis (114 with moderate and 213 with severe disease), and 48 with edentulous. Diagnosis of periodontitis was associated with shorter LTL (P = 0.04). A negative association between LTL and endotoxemia was found in the severe periodontitis and type 2 diabetes groups (P = 0.01 for both). Shorter LTL was associated with increased extent of periodontitis (P = 0.01) and increased insulin resistance (homeostatic model assessment). Multiple adjustments for biochemical, anthropometric, and medication-use variables did not affect the results. CONCLUSIONSLTL is associated with endotoxemia and diagnosis of periodontitis in people with diabetes. LTL shortening might represent a novel biological pathway accounting for previous epidemiological data that documented higher prevalence of diabetes and its complications in people with periodontitis and vice versa.

This study provides prevalence data for NUG in the British Armed Forces and description of its treatment and associated risk factors. Oral hygiene and smoking must be addressed in patients with NUG and prescribing protocols should be carefully followed.

Background Periodontal intrabony defects are usually treated surgically with the aim of increasing attachment and bone levels and reducing risk of progression. However, recent studies have suggested that a minimally invasive non-surgical therapy (MINST) leads to considerable clinical and radiographic defect depth reductions in intrabony defects. The aim of this study is to compare the efficacy of a modified MINST approach with a surgical approach (modified minimally invasive surgical therapy, M-MIST) for the treatment of intrabony defects. Methods This is a parallel-group, single-centre, examiner-blind non-inferiority randomised controlled trial with a sample size of 66 patients. Inclusion criteria are age 25–70, diagnosis of periodontitis stage III or IV (grades A to C), presence of ≥ 1 ‘intrabony defect’ with probing pocket depth (PPD) > 5 mm and intrabony defect depth ≥ 3 mm. Smokers and patients who received previous periodontal treatment to the study site within the last 12 months will be excluded. Patients will be randomly assigned to either the modified MINST or the M-MIST protocol and will be assessed up to 15 months following initial therapy. The primary outcome of the study is radiographic intrabony defect depth change at 15 months follow-up. Secondary outcomes are PPD and clinical attachment level change, inflammatory markers and growth factors in gingival crevicular fluid, bacterial detection, gingival inflammation and healing (as measured by geometric thermal camera imaging in a subset of 10 test and 10 control patients) and patient-reported outcomes. Discussion This study will produce evidence about the clinical efficacy and potential applicability of a modified MINST protocol for the treatment of periodontal intrabony defects, as a less invasive alternative to the use of surgical procedures. Trial registration ClinicalTrials.gov, NCT03797807 . Registered on 9 January 2019.

Objectives: The purpose of this systematic review was to evaluate the available evidence in the literature in regards to the subgingival microbial population of chronic periodontitis in subjects with Type 2 Diabetes Mellitus (T2DM+PD) compared to non-diabetic subjects (NDM+PD). Materials and Methods: A literature search was conducted at Ovid MEDLINE and EMBASE database from 1980 to 2016, supplemented by hand searching as needed. Studies presenting with at least one of the primary outcomes (presence of any subgingival microorganisms, proportion and/or the amount of any subgingival plaque bacteria in T2DM+PD versus NDM+PD) were included. Screening, data extraction and quality assessment were conducted independently and in duplicate. Results: From 611 citations, 19 full-text papers were screened and 11 articles were included for critical appraisal by both reviewers. Some evidence of a difference in the microbial profile between chronic PD subjects with and without T2DM was identified. The strength of evidence is strongest in Tannerella forthysia (T.forsythia) which was reported to be less frequent in the diabetic (T2DM+PD) group in five of the studies, followed by a weaker strength of evidence for other periodontal pathogens such as Porphyromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), which were also found less frequent in the diabetic (T2DM+PD) group. Conclusion: Only few studies have compared T2DM+PD with NDM+PD. It is therefore, strongly recommended that further studies which include four distinct groups of participants (NDM+PD, T2DM+PD, NDM+NPD, T2DM+NPD) instead of using intra-subject comparisons between healthy and diseased sites of the same subjects. Clinical Relevance: Differences in bacterial populations of T2DM+PD in comparison to NDM+PD subjects may indicate the need of different protocols for the treatment of the diabetic patients with periodontal disease.