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Published on: December 3, 2020
Pocket epithelium in the pathological setting for HMGB1 release
N Ebe1, M Hara-Yokoyama, K Iwasaki
1Section of Periodontology, Department of Hard Tissue Engineering, Biochemistry, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo, Tokyo 113-8549, Japan.
Journal of Dental Research
|December 15, 2010
Summary
Periodontal disease elevates High-mobility group box-1 (HMGB1) protein levels. Bacterial metabolites in periodontal pockets trigger HMGB1 release from gingival epithelial cells, contributing to inflammation.
Area of Science:
- Oral biology
- Immunology
Background:
- High-mobility group box-1 (HMGB1) protein functions as a nuclear transcription factor and an extracellular pro-inflammatory cytokine.
- Elevated HMGB1 levels are observed in gingival crevicular fluid of periodontal patients.
Purpose of the Study:
- To investigate the role of the periodontal pocket environment in the release of HMGB1.
- To determine if periodontopathic bacteria or their metabolites can induce HMGB1 release from gingival epithelial cells.
Main Methods:
- Immunohistochemical staining of inflamed gingival tissues to localize HMGB1.
- Treatment of a human gingival epithelial cell line with butyric acid, a bacterial metabolite.
Main Results:
- HMGB1 was found to translocate from the nucleus to the cytoplasm in the pocket epithelium of inflamed gingiva.
- Butyric acid induced passive release of HMGB1 via necrosis in gingival epithelial cells.
Conclusions:
- The periodontal pocket epithelium exhibits unique pathological changes leading to HMGB1 release.
- Bacterial metabolites, such as butyric acid, can induce HMGB1 release from gingival epithelial cells, potentially exacerbating periodontal disease.
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