Biofilm formation on oral implants can cause inflammation of peri-implant tissues, which endangers the long-term success of osseointegrated implants. It has been reported previously that implants revealing signs of peri-implantitis contain subgingival microbiota similar to those of natural teeth with periodontitis. The purpose of the first part of this study was an atraumatic, quantitative investigation of biofilm formation on oral implant abutments; the objective of the second part was to investigate whether Haemophilus actinomycetemcomitans and Porphyromonas gingivalis were present in the crevicular fluid around oral implants. Biofilm formation on 14 healing abutments, inserted for 14 days in 10 patients, was analysed quantitatively by use of secondary-electron and Rutherford-backscattering-detection methods. A 16S rRNA-based polymerase chain reaction detection method was used to detect the presence of H. actinomycetemcomitans and P. gingivalis in the crevicular fluid. For this investigation, samples of sulcus fluid were collected with sterile paper points at four measurement points per abutment. The difference between biofilm coverage of supragingival surfaces (17.5 +/- 18.3%) and subgingival surfaces (0.8 +/- 1.0%) was statistically significant (P < 0.05). By use of universal primers, bacteria were found in all the samples taken, although the two periodontal pathogens were not found in any of the samples. The absence of periodontal pathogens from the sulcus fluid during initial bacterial colonization, despite massive supragingival biofilm formation, substantiates the assumption that cellular adherence of peri-implant tissue by means of hemidesmosoma, actin filaments and microvilli reduces the risk of formation of anaerobic subgingival pockets.

ObjectivesWe here investigated whether experimental gingivitis enhances systemic markers of inflammation which are also known as surrogate markers of atherosclerotic plaque development.BackgroundGingivitis is a low-level oral infection induced by bacterial deposits with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown.Methods37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiation of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were concentrations of hsCRP, IL-6, and MCP-1, as well as adhesion capacity and oxLDL uptake of isolated blood monocytes.ResultsThe partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (34.0%, P<0.0001). This local inflammation was associated with a systemic increase in hsCRP (0.24 mg/L, P = 0.038), IL-6 (12.52 ng/L, P = 0.0002) and MCP-1 (9.10 ng/l, P = 0.124) in peripheral blood samples between baseline and day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and increased foam cell formation after oxLDL uptake (P<0.050) at day 21 of gingivitis.ConclusionsBacterial-induced gingival low-level inflammation induced a systemic increase in inflammatory markers. Dental hygiene almost completely reversed this experimental inflammatory process, suggesting that appropriate dental prophylaxis may also limit systemic markers of inflammation in subjects with natural gingivitis. International Clinical Trials Register Platform of the World Health Organization, registry number: DRKS00003366, URL: http://apps.who.int/trialsearch/Default.aspx

Clinical significance of the differences between the methods compared did not appear significant. 3D laser-scanned plaster model analysis appears to be an adequate, reliable, and time saving alternative to analogue model analysis using a calliper.

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