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Accessing the Cytotoxicity and Cell Response to Biomaterials
Published on: July 8, 2021
Oral malodorous compound inhibits osteoblast proliferation
Toshio Imai1, Hisataka Ii, Ken Yaegaki
1Department of Oral Health, School of Life Dentistry at Tokyo, Nippon Dental University, Tokyo, Japan. imai-109@tky.ndu.ac.jp
Journal of Periodontology
|December 8, 2009
Summary
Hydrogen sulfide (H2S) significantly inhibits osteoblast proliferation by affecting the mitogen-activated protein kinase (MAPK) pathway. This study reveals H2S
Area of Science:
- Oral biology
- Cell signaling
- Periodontal disease mechanisms
Background:
- Oral malodorous compounds like hydrogen sulfide (H2S) are linked to periodontitis.
- Volatile sulfur compounds (VSCs) exhibit toxicity to periodontal tissues, impacting collagen, extracellular matrix, and inducing apoptosis.
- H2S toxicity is comparable to cyanate, highlighting its potential role in oral pathology.
Purpose of the Study:
- To investigate the impact of H2S on osteoblast proliferation.
- To elucidate the role of the mitogen-activated protein kinase (MAPK) signaling pathway in H2S-induced effects on osteoblasts.
Main Methods:
- Osteoblasts (human NHOst and murine MC3T3-E1) were exposed to varying concentrations of H2S.
- Cell proliferation was quantified using [3H]thymidine incorporation assays.
- Mitogen-activated protein kinase (MAPK) pathway activation (ERK1/2 and p38 phosphorylation) was assessed via Western blot analysis in NHOst.
Main Results:
- H2S exposure significantly reduced osteoblast proliferation in a dose-dependent manner, with a 79% decrease at 100 ng/ml.
- H2S treatment transiently increased ERK1/2 and p38 phosphorylation, indicating MAPK pathway activation.
- Inhibition of MAPK/ERK kinase (MEK) or p38 blocked H2S-induced activation of these signaling molecules.
Conclusions:
- Hydrogen sulfide (H2S) demonstrably inhibits human osteoblastic cell proliferation.
- The MAPK signaling pathway mediates the inhibitory effects of H2S on osteoblast proliferation.
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