Objective. To study the preventive effect of Lactobacillus helveticus (L. helveticus) on periodontitis induced by Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) in rats. Methods. Eighteen 8-week-old female rats were randomly divided into three groups: Sham group, Trehalose group, and L. helveticus SBT2171 (LH2171) group. We measured the distance of the cementoenamel junction-alveolar bone crest (CEJ-ABC) to evaluate alveolar bone resorption. Hematoxylin-eosin staining was used to observe the histopathological changes of rat hemimaxillary tissues. We detected the expression of β-defensins, tumor necrosis factor-α (TNF-α), interleukin- (IL-) 1β, and IL-6 and the number of A. actinomycetemcomitans in rat gingival tissues by quantitative reverse transcriptase polymerase chain reaction. The levels of IL-1β, IL-6, and TNF-α in rat gingival tissues were also measured by enzyme-linked immunosorbent assay. Results. Compared with the Trehalose group, the distance of CEJ-ABC was prominently reduced and alveolar bone resorption was notably improved in the LH2171 group. And the infiltration of inflammatory cells in the hemimaxillary tissue decreased obviously, periodontal fibers were arranged neatly, connective tissue small blood vessels proliferated, and the number of A. actinomycetemcomitans reduced significantly in the LH2171 group. In addition, the mRNA expression and release of inflammatory factors in the gingival tissues in the LH2171 group were notably lower than those in the Trehalose group. On the 21st and 36th day, the expression of β-defensins in the gingival tissue of the LH2171 group increased significantly. Conclusion. L. helveticus improves alveolar bone resorption and increases the expression of β-defensins thereby inhibiting the number of A. actinomycetemcomitans and thus prevents periodontitis.

Background: To analyze the distribution of Porphyromonas gingivalis (P. gingivalis) kgp genotype in subgingival plaque of patients with diabetic periodontitis. The genetic polymorphism of the kgp gene in diabetic periodontitis was explored, and the correlation between different genotypes and diabetic periodontitis was obtained. Methods: Subgingival plaque samples were collected from 49 patients with periodontitis (21 with diabetes, 28 with non-diabetic periodontitis) and 11 healthy periodontal subjects. DNA was extracted, and the positive samples of P. gingivalis were screened by PCR with specific primers of 16S rRNA gene of P. gingivalis, and the fragment of kgp catalytic domain was obtained by PCR with specific primers of kgp. The genotype of kgp was determined by Mse I digestion of the catalytic domain fragment of kgp, and the experimental data were analyzed by the Pearson χ2 method. Results: Among the 11 healthy periodontal population samples collected in this study, 4 cases (36.4 %) of P. gingivalis were detected. Among 49 subgingival plaque samples of periodontitis, 47 patients (95.9 %) were detected with P. gingivalis. There was a statistical difference between the two. Among the 47 samples with P. gingivalis, the detection rate of kgp I was 57.4 %, the detection rate of kgp II was 31.9 %, and the detection rate of kgp I + II was 10.6 %. The kgp genotype was not associated with diabetes. There was no significant difference in the kgp genotypes between the two groups with different PD depths. Conclusion: P. gingivalis is associated with periodontitis. P. gingivalis kgp gene polymorphism exists in patients with diabetic periodontitis subgingival plaque.