A single application of hydrogen sulphide induces a transient osteoclast differentiation with RANKL expression in the rat model.
OBJECTIVE
Oral malodor is mainly attributed to volatile sulphur compounds (VSCs) such as hydrogen sulphide (H(2)S), methyl mercaptan and dimethyl sulphide. VSC accelerate periodontal soft tissue destruction. However, there is little information about the potential role of H(2)S in alveolar bone loss. The purpose of this animal study was to examine the effects of sodium hydrogen sulphide (NaHS), H(2)S donor drug, on osteoclast differentiation in rat periodontal tissue.


METHODS
Twenty-four male Wistar rats (8 weeks old) were divided into four groups: a control group and three experimental groups, which were examined at 3h, 1 day, and 3 days after topical application of 3microl NaHS (lM in physiological saline) into the gingival sulcus of rat first molar. Expression of tumour necrosis factor (TNF)-alpha, RANKL, NF-kappaB 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-kappaB mRNA was observed at 3h after NaHS application.


CONCLUSIONS
H(2)S application caused a transient increase of osteoclast differentiation with up-regulation of RANKL expression in osteoblasts. H(2)S, which is primarily responsible for halitosis, may also contribute to alveolar bone resorption through RANKL expression.
Irie
Koichiro
K
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8525, Japan.
Ekuni
Daisuke
D
Yamamoto
Tatsuo
T
Morita
Manabu
M
Yaegaki
Ken
K
Ii
Hisataka
H
Imai
Toshio
T
D000135:Acid Phosphatase / Q000032:analysis; D000287:Administration, Topical; D000539:Alveolar Process / Q000187:drug effects / Q000473:pathology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D002454:Cell Differentiation / Q000187:drug effects; D003238:Connective Tissue / Q000187:drug effects / Q000473:pathology; D004195:Disease Models, Animal; D004846:Epithelial Attachment / Q000187:drug effects / Q000473:pathology; D005110:Extracellular Space / Q000187:drug effects; D005881:Gingiva / Q000187:drug effects / Q000473:pathology; D006862:Hydrogen Sulfide / Q000008:administration & dosage / Q000494:pharmacology*; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D016328:NF-kappa B / Q000032:analysis; D010010:Osteoclasts / Q000187:drug effects*; D010513:Periodontal Ligament / Q000187:drug effects / Q000473:pathology; D010519:Periodontium / Q000187:drug effects* / Q000473:pathology; D053245:RANK Ligand / Q000032:analysis*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides / Q000008:administration & dosage / Q000494:pharmacology; D000071681:Tartrate-Resistant Acid Phosphatase; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D015854:Up-Regulation
D015415:Biomarkers; D007527:Isoenzymes; D016328:NF-kappa B; D053245:RANK Ligand; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; C025451:sodium bisulfide; D006862:Hydrogen Sulfide