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Aim: To evaluate effects of probiotic Lactobacillus reuteri (L. reuteri) lozenges as an S/RSD adjunct on site‐level changes at molars with deep pockets. Materials and methods: 447 molar sites with pockets ≥ 5 mm from a previous randomized clinical trial of adjunctive L. reuteri lozenges for 28 days were analyzed. Multilevel mixed‐effect models (MLM) were constructed to analyze site‐level outcomes "change in CAL" and "pocket closure" (residual PPD < 5 mm) in placebo and probiotic groups at 90 and 180 days. Possible patient‐, tooth‐, and site‐level predictors were analyzed as fixed‐effects. Results: Estimated change in CAL in probiotic (90 day: 0.87 mm, 180 day: 0.68 mm) was greater than placebo treated molar sites (90 day: 0.73 mm, 180 day: 0.66 mm) and the relative risk (RR) of pocket closure in the probiotic group (90 day: 1.7, 180 day: 1.6) was higher as compared to placebo. Furcation involvement and BOP at site predicted significantly worse treatment outcomes. Conclusion: As compared to S/RSD with placebo, a 28‐day course of adjunctive probiotic L. reuteri lozenges improved CAL change at molar sites with ≥ 5 mm deep pockets and conferred a higher probability of shallow residual pocket depth. Presence of furcation‐involvement and bleeding on probing worsened treatment outcomes. [ABSTRACT FROM AUTHOR]

Background: The production of chemokines by tissue resident cells during inflammation is considered one of the main mechanisms involved in the formation of inflammatory infiltrates. Fibroblasts are the main resident cell type in gingival and periodontal ligament tissues, and their ability to produce chemokine stromal cell-derived factor 1 alpha (SDF-1α) and its receptor CXCR4 under stimulation by gram negative bacteria, Porphyromonas gingivalis, commonly found in periodontal infections was investigated. Methods: Western blots were used to assess SDF-1α and CXCR4 protein expression levels in human gingival fibroblast cells (HGF-1) induced by Lipopolysaccharide (LPS) from P. gingivalis in the presence or absence of LY294002, a highly selective inhibitor of PI-3K/Akt. RT-PCR and quantitative Real-time PCR was performed using gingival mRNAs from periodontitis patients. Immunohistochemistry was performed to analyze the expression and subcellular localization of SDF-1α and CXCR4, together with NF-κβ phosphorylation, in specimens from patients with periodontitis and in an experimental rat periodontitis model. Results: We found that P. gingivalis LPS up-regulated SDF-1α and CXCR4 protein levels and elevated phosphorylation of the SDF-1α-responsive NF-κβ and Akt at 24 h in HGF-1 cells. SDF-1α and CXCR4 mRNA and protein expression levels were high in all patients with periodontitis. In the P. gingivalis-induced rat experimental periodontitis model, SDF-1α and CXCR4 immunoreactivity was higher in gingival and periodontal ligament tissues compared to the control. Conclusion: Our data showed that PI-3K/Akt is an upstream participant in the P. gingivalis LPS-mediated induction of SDF-1 α. Taken together, these results suggest that the chemokine SDF-1α and its receptor CXCR4 contribute to P. gingivalis-induced periodontal inflammation. [ABSTRACT FROM AUTHOR]