IADR Abstract Archives
Activation of pSTAT3 on and CD45+ cells in Human Gingival Tissues
Objectives: Periodontitis is a chronic inflammatory disease in which the locally deployed immune response against a dysbiotic subgingival microbiome results in alveolar bone resorption and tooth loss. The transcription factor signal transducer and activator of transcription 3 (STAT3) integrates and transduces the signaling of multiple pro-inflammatory cytokines associated with periodontitis. STAT3 is also crucial for Th17 cell differentiation, a critical CD4+ T cell subset in periodontitis immunopathogenesis. Despite the importance of this protein, there is a gap in our knowledge regarding which cell type activates STAT3 (pSAT3) in human periodontal tissues. Hence, this study aimed to evaluate the STAT3 activation on hematopoietic (CD45+) cells in gingival tissues from healthy and periodontitis subjects.
Methods: After clinical evaluation, diagnosis, selection, and consent, a standardized gingival tissue sample was obtained from each volunteer. Gingival tissues were fixed, included in paraffin, and activation of STAT3 and immune cells was evaluated via immunofluorescence using an anti-pSTAT3 and anti-CD45 antibody. Immuno-positive cells were counted in 20 tissues (10 healthy and 10 periodontitis) using the Image J software. Data are shown in mean ± SEM. P-values of <0.05 were considered statistically significant.
Results: Total percentages of pSTAT3 and CD45 immune-positive cells were significantly higher in the periodontitis tissues than compared with the healthy gingival tissues (54,1± 28,4% pSTAT3 and 59,3 ± 36,9%CD45). pSTAT3 was highly detected in the epithelium of periodontitis tissues and distributed within the basal layer cells.
Conclusions: Immune cells and STAT3 transcription factor were more activated in gingival tissues obtained from subjects with periodontitis than healthy. Furthermore, STAT3 activation was higher and more widely distributed in basal layer cells of epithelium.
Methods: After clinical evaluation, diagnosis, selection, and consent, a standardized gingival tissue sample was obtained from each volunteer. Gingival tissues were fixed, included in paraffin, and activation of STAT3 and immune cells was evaluated via immunofluorescence using an anti-pSTAT3 and anti-CD45 antibody. Immuno-positive cells were counted in 20 tissues (10 healthy and 10 periodontitis) using the Image J software. Data are shown in mean ± SEM. P-values of <0.05 were considered statistically significant.
Results: Total percentages of pSTAT3 and CD45 immune-positive cells were significantly higher in the periodontitis tissues than compared with the healthy gingival tissues (54,1± 28,4% pSTAT3 and 59,3 ± 36,9%CD45). pSTAT3 was highly detected in the epithelium of periodontitis tissues and distributed within the basal layer cells.
Conclusions: Immune cells and STAT3 transcription factor were more activated in gingival tissues obtained from subjects with periodontitis than healthy. Furthermore, STAT3 activation was higher and more widely distributed in basal layer cells of epithelium.