The application of this model can only be recommended for short (

The aim of this study was to compare the short-term performance of a session of single photodynamic therapy (PDT) and of a conventional ultrasonic debridement (UST) in persistent pockets of maintenance patients. In a prospective, randomized, controlled, single-blind clinical study, patients with chronic periodontitis with at least two persistent pockets (>4 mm) were enrolled. They were treated either with UST (n = 29) or PDT (n = 25). Clinical and microbiological examinations were performed at baseline and after 3 months. For UST, the mean probing depth was reduced from 5.3 to 4.5 mm (p = <0.001) and for PDT from 5.3 to 4.7 mm (p < 0.001) with no difference between the two treatment modalities. Microbial counts were significantly reduced about 30% to 40% immediately after debridement but returned to baseline values a 3 months irrespective of treatment. PDT is not superior to conventional mechanical treatment of persistent pockets, but it may be a meaningful therapeutic alternative; the clinical effects were too minor to draw a definitive conclusion.

In the present study, a 1.5% dexibuprofen mouth rinse had no effect on gingivitis whereas an anti-plaque effect was demonstrated.

Stroke is accompanied by a strong inflammatory reaction in the brain. Periodontal disease is a chronic local infection which causes a systemic low grade inflammation. We hypothesized that a mild systemic inflammatory reaction as caused by periodontal disease prior to stroke onset, may exert a neuroprotective effect in a rat model of focal ischemia. To test this hypothesis, marginal periodontitis was induced by ligatures on the second maxillary molars in BB/LL Wistar rats for 3 weeks. Two weeks after periodontitis initiation, focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery. After a survival time of 7 days after ischemia, rats were killed and bone loss was determined on the buccal and palatinal surfaces of the defleshed jaw. In addition, markers of systemic inflammation were determined in a different group of laboratory animals at 14 days after the onset of periodontitis. The infarct size and markers of the inflammatory reaction in the brain were determined by immunohistochemistry. We found: (i) rats with ligatures exhibited significantly more periodontal bone loss than the control rats; (ii) the development of periodontitis was associated with an elevated gene expression for several markers of systemic inflammation (interleukin-10, transforming growth factor beta 1, tumor necrosis factor alpha, interleukin-1beta and interferon gamma; (iii) rats with periodontitis and a mild systemic inflammation had a significantly reduced infarct volume and a significant reduction in the number of brain macrophages in the infarcted area. In conclusion we found that mild systemic inflammation elicited prior to stroke onset may have a neuroprotective effect in rats by reducing the infarct volume and tissue destruction by brain macrophages.