Aim: Interleukin-17 (IL-17) is a proinflammatory cytokine that plays an important role in inflammation and tissue destruction in periodontal disease. This study aimed to assess the level of IL-17 in gingival crevicular fluid (GCF) of patients with chronic periodontitis (CP) and healthy controls. Materials and methods:This case-control study was performed on 30 patients with CP (53% males, 47% females, mean age of 37.2 ± 5.95 years) and 30 healthy controls (53% males, 47% females, mean age of 30.63 ± 5.22 years). The GCF was collected using paper points. A paper point was inserted into the pocket and remained there for 30 seconds. It was then placed in a sterile tube containing 300 µL of phosphate buffered saline and stored at -70° C. Level of IL-17 was measured using enzyme-linked immune sorbent assay (ELISA). The level of IL-17 was compared between the two groups using independent sample t-test at 0.05 level of significance. Results:The mean GCF level of IL-17 was 53.46 pg/L in CP patients and 38.1 pg/L in healthy controls. This difference was statistically significant (p = 0.025). Conclusion:The CP patients had significantly higher GCF level of IL-17 compared to healthy controls. Clinical significance:The finding of this study highlight the role of IL-17 in the pathogenesis of periodontal disease. Within the limitations of the present study, it may be suggested that measurement of GCF level of IL-17 can serve as a bioindicator of periodontal destruction and gingival inflammation.

Aim: Periodontitis is an inflammatory disease causing destruction of tooth-supporting structures. It is often caused by gram-negative microorganisms such as Porphyromonas gingivalis (P. gingivalis ). Common treatments for periodontitis are often nonspecific and include mechanical plaque removal and surgery. This study aimed to assess the amount of bone loss and antibody titer against P. gingivalis in rats. Materials and methods: This in vitro experimental study was conducted on 66 Surrey rats free of black pigmented pathogens, which were randomly divided into six groups of 11. Groups I and II were vaccinated with formalin-killed whole-cell (FKWC) P. gingivalis with incomplete Freund's adjuvant as the vaccine carrier, and groups III and IV were vaccinated with incomplete Freund's adjuvant and PG buffer. Groups V and VI were considered as positive and negative controls, respectively. Three weeks later, they were vaccinated with a booster dose. At 28 days, groups I, III, and V were inoculated with viable P. gingivalis (ATCC 33277) four times at 48-hour intervals for induction of periodontitis. One week after booster dose administration and two weeks after oral inoculation of bacteria, serum and saliva samples were obtained for assessment of antibody titer. Ten weeks after final bacterial inoculation, the serum and saliva samples were obtained to assess antibody titer, and subgingival plaque samples were obtained from the maxillary second molar site to assess the bacterial count. The rats were then sacrificed to assess bone loss. Results: Serum and saliva antibody titers in groups I and II were significantly different from those in other groups one week after booster dose and two and 10 weeks after oral inoculation of bacteria (p < 0.001). In terms of bone loss and bacterial count in the subgingival plaque, group I was not significantly different from the negative control group and groups II, IV, and VI (p > 0.99), but had a significant difference with the positive control (group V) and group III (p < 0.001). Conclusion:This study showed successful immunization against P. gingivalis , which increased serum IgG and saliva IgA titers, limited the colonization of P. gingivalis in subgingival plaque, and restricted the alveolar bone loss.

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Background and Aim: This study aimed to assess the antibody titer against Porphyromonas gingivalis (P. gingivalis) in rats with experimentally induced periodontitis. Materials and Methods: Thirty-three Surrey rats were randomly divided into three groups (n=11). Group 1 was vaccinated with formalin-killed whole cell (FKWC) P. gingivalis with incomplete Freund's adjuvant as vaccine carrier and orally inoculated with viable P. gingivalis (ATCC 33277). Group 2 was vaccinated with incomplete Freund's adjuvant and PG buffer and orally inoculated with viable P. gingivalis (positive control). Group 3 was vaccinated as group 2 without inoculation (negative control). Two weeks later, they were vaccinated with a booster dose. One week later, serum and saliva samples were obtained to assess antibody titer. Oral inoculation of bacteria was then done four times every 48 hours. Two weeks later, serum, saliva and subgingival plaque samples were obtained from the maxillary second molar area for assessment of P. gingivalis count in the subgingival plaque. Data were analyzed using Mann-Whitney U test and Wilcoxon signed-rank tests. Results: Serum and salivary antibody titers against P. gingivalis in group 1 one week after booster dose and two weeks after oral inoculation of bacteria were significantly different from those in other groups (P<0.05). Groups 1 and 3 were not significantly different in terms of bacterial count in subgingival plaque (P=1.000) but the difference between groups 1 and 2 was significant (P<0.001). Conclusion: Vaccination with FKWC P. gingivalis increased serum IgG and salivary IgA and limited the colonization of P. gingivalis in subgingival plaque of rats.