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.

The fracture of dentures is an unresolved problem. Despite increasing costs incurred by the nation on the repair of these prostheses, very little has been documented on the type of fracture encountered. This survey was carried out to determine the prevalence of type of fracture by the distribution of questionnaires to three different laboratories. Results obtained showed that 33% of the repairs carried out were due to debonded/detached teeth. Twenty-nine per cent were repairs to midline fractures, more commonly seen in upper complete dentures. The remaining 38% were other types of fractures, the majority of which constituted repairs to upper partial dentures. The latter involved detachment of acrylic resin saddles from the metal in metal based dentures and the fractures of connectors in the all-acrylic resin partial dentures.

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The present clinical trial was designed to evaluate the effects of a bioactive glass, Perioglas, in the treatment of periodontal intrabony defects. 20 patients, 23-55 years of age (44 sites), with intrabony defects completed the 1-year study. Teeth with furcation involvement were excluded. After completion of initial therapy, defects were randomly assigned to either a test or control procedure. Following flap reflection, root planing and removal of chronic inflammatory tissue in both groups, the test defects were restored with the bioactive glass particulate material. Mucoperiosteal flaps were replaced, sutured and a periodontal dressing was used. All the patients received postoperative antibiotics and analgesics and were seen at 1 week for suture removal. Follow-up was then carried out weekly and at 3 months, 6 months, 9 months and 1 year post-surgery. Plaque score, bleeding score, probing pocket depth (PPD), probing attachment level (PAL) and gingival recession were recorded at baseline, 3 months and 1 year. Standardised radiographs for computer-assisted densitometric image analysis (CADIA) were taken at baseline, immediately post-operatively and at 1 year. The CADIA data showed a significant increase (F-ratio: 15.67, p < 0.001) in radiographic density and volume between the defects treated with the Perioglas when compared to those treated with surgical debridement only. PPD and PAL showed significant improvements in both experimental and control sites, with a greater trend to improvement in the experimental sites. It was concluded that this bioactive glass is effective as an adjunct to conventional surgery in the treatment of intrabony defects.