Journal
ARCHIVES OF ORAL BIOLOGY
Volume 54, Issue 8, Pages 723-729Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.archoralbio.2009.05.006
Keywords
Hydrogen sulphide; Osteoclast; RANKL; Periodontal disease
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology, Tokyo, Japan [20390538001, 21792149]
- Grants-in-Aid for Scientific Research [21792149] Funding Source: KAKEN
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Objective: Oral malodor is mainly attributed to volatile sulphur compounds (VSCs) such as hydrogen sulphide (H2S), methyl mercaptan and dimethyl sulphide. VSC accelerate periodontal soft tissue destruction. However, there is little information about the potential role of H2S in alveolar bone loss. The purpose of this animal study was to examine the effects of sodium hydrogen sulphide (NaHS), H2S donor drug, on osteoclast differentiation in rat periodontal tissue. Design: Twenty-four male Wistar rats (8 weeks old) were divided into four groups: a control group and three experimental groups, which were examined at 3 h, 1 day, and 3 days after topical application of 3 mu l NaHS (l M in physiological saline) into the gingival sulcus of rat first molar. Expression of tumour necrosis factor (TNF)-alpha, RANKL, NF-kappa B and tartrate-resistant acid phosphatase (TRAP) was evaluated in the periodontal tissue. Results: Three hours after NaHS application, TNF-alpha expression increased in the periodontal ligament. The numbers of RANKL-positive osteoblasts and TRAP-positive osteoclasts significantly increased progressively with time and reached a maximum level after 1 day. Significant up-regulation of RANKL and NF-kappa B mRNA was observed at 3 h after NaHS application. Conclusions: H2S application caused a transient increase of osteoclast differentiation with up-regulation of RANKL expression in osteoblasts. H2S, which is primarily responsible for halitosis, may also contribute to alveolar bone resorption through RANKL expression. (C) 2009 Elsevier Ltd. All rights reserved.
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