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Updated: Dec 20, 2025
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
[Preliminary study on the expression and distribution of S100A8 and S100A9 in healthy and experimental periodontitis
H Y Gao1, B X Huang2, J X Hou3
1Department of Periodontology, Peking University School and Hospital of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology & Beijing Key Laboratory of Digital Stomatology, Beijing 100081, China(Gao Hongyu is working on the Department of Periodontology, Stomatological Hospital, Tianjin Medical University, Tianjin 300070, China).
Abstract:
Objective: To investigate the systemic expression profile of S100A8 and S100A9 in healthy and inflamed periodontal tissues. Methods: Experimental periodontitis models were established by ligations around the mandibular second molars of six beagle dogs for 12 weeks (ligation group). The mandibular second molars on the opposite side were kept clean (healthy control group). The expressions of S100A8 and S100A9 in healthy and inflamed periodontal tissues of six beagle dogs were examined by immunohistochemistry. The expressions of S100A8 and S100A9 in primary human gingival fibroblasts (hGF) from 3 subjects and human periodontal ligament cells (hPDLC) from 3 other subjects were detected by immunocytochemistry. Results: After the ligation for 12 weeks, the mean probing depth of ligation group [(3.86±0.14) mm] was significantly higher than that of healthy control group [(2.11±0.28) mm] (P<0.01). Results of immunohistochemistry analysis indicated that S100A8 and S100A9 could be expressed in gingival epithelial cells and might infiltrated neutrophils in the healthy periodontium. Except for the gingival epithelial cells and neutrophils, both proteins were induced and expressed in gingival fibroblasts, periodontal ligament cells, microvascular endothelial cells and bone marrow fibroblasts under inflammatory conditions. The distribution of S100A8 and S100A9 differed in the healthy oral gingival epithelium (OGE), which becomes consistent in inflamed OGE. Additionally, the expressions of S100A8 and S100A9 were confirmed in primary hGF and hPDLC. Conclusions: Periodontal inflammation might enlarge the expression scope of S100A8 and S100A9 and enrich multiple cells with expressions of S100A8 and S100A9.
