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Oral malodorous compound causes caspase-8 and -9 mediated programmed cell death in osteoblasts
Journal of Periodontal Research
|November 19, 2011
Summary
Hydrogen sulfide (H2S) causes osteoblast apoptosis, a key factor in periodontal disease. This study reveals H2S triggers cell death via p53, mitochondrial pathways, and caspase-8 activation.
Area of Science:
- Oral biology
- Cell biology
- Biochemistry
Background:
- Hydrogen sulfide (H2S) is a volatile sulfur compound linked to oral malodor and periodontal disease.
- The specific impact of H2S on alveolar bone cells (osteoblasts) and its underlying mechanisms remain largely unknown.
Purpose of the Study:
- To investigate the apoptotic effects of H2S on osteoblasts.
- To elucidate the molecular pathways involved in H2S-induced osteoblast apoptosis.
Main Methods:
- Murine calvaria osteoblasts were exposed to H2S and analyzed for apoptosis using flow cytometry and ELISA.
- Mitochondrial function, cytochrome c release, caspase activity, p53, BAX/Bcl-2 expression, and DNA fragmentation were assessed.
Main Results:
- H2S exposure significantly increased osteoblast apoptosis in a time-dependent manner.
- Key apoptotic indicators including mitochondrial depolarization, cytochrome c release, p53 activation, caspase-3, -8, -9 activity, and DNA fragmentation were elevated.
- BAX gene expression was upregulated, while Bcl-2 was downregulated, suggesting intrinsic pathway involvement.
Conclusions:
- H2S induces apoptosis in osteoblasts at concentrations found in gingival crevicular fluid.
- The primary molecular mechanisms involve the p53 pathway, mitochondrial disruption, and caspase-8 activation, contributing to periodontal disease pathogenesis.
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