Evaluation of circulatory and salivary levels of heat shock protein 60 in periodontal health and disease.

Background: Self‑antigens such as heat shock protein 60 (HSP 60) have recently been implicated in the periodontal disease pathogenesis. There is scant evidence regarding HSP 60 levels in circulation and saliva following periodontal disease and its possible relation to systemic inflammation. Aim of the Study: The aim was to evaluate the circulatory and salivary levels of HSP 60 in periodontal health and disease and to correlate it with high sensitivity C‑reactive protein (hs‑CRP). Materials and Methods: Forty‑five peripheral blood samples were collected from two groups of patients (periodontally healthy ‑ Group A [22 patients] and periodontal disease ‑ Group B [23 patients]). Serum, cell lysates, and saliva samples were used to detect HSP 60 levels in both groups by enzyme linked immunosorbent assay technique. Measurement of hs‑CRP was performed using an immunoturbidimetric assay. Statistical analysis was done using the student t‑test and Pearson’s correlation. Results: Circulatory HSP 60 was significantly increased in periodontal disease compared to health (P ‑ 0.038). There was a significant correlation between the totals circulating HSP 60 and hs‑CRP (P ‑ 0.052), but there was no significant correlation between the salivary HSP 60 and hs‑CRP levels in periodontal disease. Conclusion: Circulating HSP 60 levels may play a role in the systemic inflammatory state produced by periodontal disease. Salivary HSP 60 may not be used as a surrogate to determine systemic inflammation.

E-cadherin and CD1a expression in gingival epithelium in periodontal health, disease and post-treatment.

Background: Epithelial integrity is important for maintenance of periodontal health. It is not fully known if non-surgical periodontal therapy is capable of recreating the epithelial barrier in its functional state. Patients and Methods: Sixty-five patients (31 males and 34 females) were included in the study. They were divided into group A (healthy gingiva 16 patients), group B (gingivitis 17 patients), group C (periodontitis 17 patients), and group D (post-treatment 15 patients). Gingival samples were collected and immunohistochemical study was done using E-cadherin and CD1a antibody. Statistical analysis was done using analysis of variance (ANOVA), followed by Tukey-Kramer multiple comparison test for CD1a and Tukey's highly significant difference (HSD) test for E-cadherin. Result: There was a statistically significant difference (P<0.001) in the expression of E-cadherin between healthy (1.846±0.555), gingivitis (1.100±0.994), and periodontitis group (0.700±0.483). Similarly, there was a statistically significant difference (P<0.001) in the expression of CD1a between healthy (75.70±3.09), gingivitis (42.53±3.09), and periodontitis group (29.07±3.08). However, the expression of E-cadherin (1.242±0.653) and CD1a in post-treatment samples (52.18±2.90) was lower with no statistically significant difference when compared to health. Discussion: The significant reduction in E-cadherin and CD1a levels in periodontal disease when compared to health could possibly be a result of invasion by the periodontopathogens and its subsequent sequel. Although, the post-treatment samples showed significant improvement when compared to disease, the reduction in E-cadherin and CD1a levels when compared to gingival health suggests that the epithelial barrier was not yet fully established in its functional state.