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Aim: This randomized clinical study was designed to evaluate the effect of probiotic intervention using lactobacilli on the periodontal condition of volunteers without severe periodontitis., Material and Methods: Freeze-dried Lactobacillus salivarius WB21 (WB21)-containing tablets or a placebo were given to volunteers in a double-blind randomized study. A total of 66 volunteers were finally enrolled and randomly assigned to receive tablets containing WB21 (6.7 x 10(8) CFU) with xylitol or xylitol alone (placebo) three times a day for 8 weeks. Periodontal clinical parameters and whole saliva samples were obtained at baseline (BL), 4 weeks, and the end of the interventional period (8 weeks). Salivary lactoferrin (Lf) levels were measured by enzyme-linked immunosorbent assay. Lactobacilli in saliva and plaque samples was detected by semi-quantitative RT-PCR using 16S rRNA primers., Results: Periodontal clinical parameters were improved in both groups after an 8-week intervention. Current smokers in the test group showed a significantly greater improvement of plaque index and probing pocket depth from BL when compared with those in the placebo group. Salivary Lf level was also significantly decreased in the test group smokers., Conclusion: Our results indicate that probiotics could be useful in the improvement/maintenance of oral health in subjects at a high risk of periodontal disease.

Human leukocyte elastase, a neutrophil serine protease, is considered to be a potential immunoregulatory protease. Since the PDGF receptor (PDGFR) on periodontal ligament (PDL) cells is a crucial element for various functions, such as wound healing in periodontal tissue, we investigated the effect of elastase on the expression of PDGFR on PDL cells by flow cytometry and Western blotting. We found that PDGFR-alpha disappeared with an increasing dose of elastase, and PDGFR-beta was degraded into several fragments. Elastase degraded both receptors on fixed cells, indicating that the degradation resulted from direct proteolysis on the cell surface. Elastase also then disturbed the phosphorylation of ERK1/2, JNK/SARK, and p38, triggered by PDGF-AA and PDGF-BB, suggesting that elastase inhibited PDGFR-dependent cell activation in PDL cells. These results suggest that elastase may modulate the PDGF-mediated activity of PDL cells during periodontal wound healing.