Periostin, an extracellular matrix protein functioning as an important structural mediator and adhesion molecule, has been shown to be an important regulator of connective tissue integrity. This study aimed to evaluate the levels of periostin in chronic periodontitis (CP) and aggressive periodontitis (AgP) compared to non-periodontitis (NP). Individuals were submitted to gingival crevicular fluid (GCF) and saliva sampling. Periodontal examination consisted of plaque index (PI), gingival index (GI), probing depth (PD), bleeding on probing (BOP), and clinical attachment level (CAL) measurements. Assays for periostin were performed by an enzyme-linked immunosorbent assay. Periodontitis patients presented more severe clinical indices compared to the NP group (p < 0.001). The mean GCF level of periostin was lowest in the AgP group as compared to the other groups and was lower in the CP group as compared to the NP group (p < 0.001). Increased levels of periostin were observed in the saliva of patients with AgP as compared to the CP and NP groups (p < 0.05). There was a negative relationship between GCF periostin levels and clinical parameters (p < 0.01), whereas a positive correlation was observed between salivary periostin levels and full-mouth GI and CAL scores (p < 0.01). To our knowledge, this is the first report investigating periostin levels in GCF and saliva in aggressive periodontitis. The results suggest that subjects with CP and AgP exhibit a different periostin profile. Periostin in GCF may have a protective role against periodontal disease. Furthermore, salivary periostin concentrations may have a promising diagnostic potential for the aggressive forms of periodontal disease.

IL-35 could have an important role in suppressing periodontal inflammation and maintaining periodontal health. Additional studies are required to evaluate its role in periodontal diseases.

The purpose of this clinical study is to comparatively investigate the interleukin-33 (IL-33) levels in gingival crevicular fluid (GCF), saliva and plasma of patients with periodontal disease as well as periodontally healthy subjects and the association between these levels and clinical parameters. GCF, saliva and plasma samples were collected from systemically healthy, non-smoker chronic periodontitis patients (CP group, n = 20), gingivitis patients (G group, n = 20) and periodontally healthy control groups (H group, n = 20). Full-mouth clinical periodontal parameters were also recorded. IL-33 levels were determined by ELISA. The total amount of GCF IL-33 was greater in the G and CP groups compared to the H group (p < 0.05). The GCF IL-33 concentration was significantly lower in the CP group than in the H and G groups (p < 0.001). Salivary or plasma IL-33 levels were similar in the study groups. The total amount of GCF IL-33 was positively correlated with the GI, PI and BOP (%) (p < 0.05). Considering the present findings, the increase in total amounts of GCF IL-33 may have a role in the pathogenesis of periodontal disease.

No abstract

IL-37 was expressed in all biofluids. According to our findings, the total amount of IL-37 in gingival crevicular fluid, or salivary or plasma concentrations of IL-37, may not be useful diagnostic markers to differentiate periodontal disease and the periodontally healthy condition. The difference in gingival crevicular fluid IL-37 concentration between the study groups may be a result of the variation in gingival crevicular fluid volume, as suggested by the negative correlation between gingival crevicular fluid volume and gingival crevicular fluid IL-37 concentration. In the light of our findings, it seems that IL-37 is not involved in periodontal disease. Further comprehensive studies may clarify this issue more clearly.