IADR Abstract Archives
Histological characterization of STAT3 activation in periodontitis
Objectives: The transcription factor signal transducer and activator of transcription 3 (STAT3) integrates and transduces 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 the distribution of STAT3 in human periodontal tissues. Hence, our goal was to characterize the localization of activated STAT3 in gingival tissues from subjects with periodontitis.
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 was evaluated via immunohistochemical staining using an anti-pSTAT3 (Tyr705) antibody. Immuno-positive cells were counted in 10 representative tissue areas per sample, using the Image J software. Data are shown in mean ±SEM. P-values of <0.05 were considered statistically significant.
Results: Eighteen volunteers were initially screened, all of them diagnosed with periodontitis. Nine subjects met our inclusion criteria and were enrolled in our study. We found that 61.79 ± 2.13% of the total cells were positive for pSTAT3. Total numbers and percentages of immune-positive cells were higher in the stroma compared with the epithelium in periodontitis gingival tissues (p=0.0001 and p=0.0032, respectively). Within the epithelium, the mean expression of pSTAT3 was 55.60 ± 2.86%, located mainly in the nucleus of the basal layer cells. In the connective tissue, pSTAT3 was detected in 67.98 ± 2.90% of the cells, and the staining was homogenously located in the nucleus and cytoplasm.
Conclusions: STAT3 transcription factor is activated on tyrosine 705 in gingival tissues obtained from subjects with periodontitis. Furthermore, STAT3 activation was higher and more widely distributed in connective tissue cells compared to epithelial cells.
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 was evaluated via immunohistochemical staining using an anti-pSTAT3 (Tyr705) antibody. Immuno-positive cells were counted in 10 representative tissue areas per sample, using the Image J software. Data are shown in mean ±SEM. P-values of <0.05 were considered statistically significant.
Results: Eighteen volunteers were initially screened, all of them diagnosed with periodontitis. Nine subjects met our inclusion criteria and were enrolled in our study. We found that 61.79 ± 2.13% of the total cells were positive for pSTAT3. Total numbers and percentages of immune-positive cells were higher in the stroma compared with the epithelium in periodontitis gingival tissues (p=0.0001 and p=0.0032, respectively). Within the epithelium, the mean expression of pSTAT3 was 55.60 ± 2.86%, located mainly in the nucleus of the basal layer cells. In the connective tissue, pSTAT3 was detected in 67.98 ± 2.90% of the cells, and the staining was homogenously located in the nucleus and cytoplasm.
Conclusions: STAT3 transcription factor is activated on tyrosine 705 in gingival tissues obtained from subjects with periodontitis. Furthermore, STAT3 activation was higher and more widely distributed in connective tissue cells compared to epithelial cells.