title: Inhibition of experimental bone resorption and osteoclast formation and survival by 2-aminoethanesulphonic acid.
abstract: It is known that bone resorption is mediated by osteoclasts, and lipopolysaccharide (LPS) and inflammatory mediators such as interleukin-1 (IL-1) and prostaglandin E2 (PGE2) induce osteoclast differentiation from haemopoietic cells, 2-aminoethanesulphonic acid, which is known as taurine, is an important nutrient and is added to most synthetic human infant milk formulas. In this study, it was found that 2-aminoethanesulphonic acid inhibits the stimulation of bone resorption mediated by LPS of the periodontopathic microorganism Actinobacillus actinomycetemcomitans Y4 in organ cultures of newborn mouse calvaria. The effect of 2-aminoethanesulphonic acid on the development and survival of osteoclast-like multinucleated cells produced in a mouse bone-marrow culture system was also examined. 2-aminoethanesulphonic acid (100 microg/ml) suppressed the formation of these osteoclast-like cells in the presence of LPS of A. actinomycetemcomitans Y4, IL-1alpha or PGE2 in mouse marrow cultures. On the other hand, 2-aminoethanesulphonic acid did not inhibit 1alpha, 25-dihydroxyvitamin D3-mediated osteoclast differentiation. Although IL-1alpha elongated the survival of the osteoclast-like cells, 2-aminoethanesulphonic acid blocked the supportive effect of IL-1alpha on osteoclast survival. 2-aminoethanesulphonic acid showed no effect on the growth of mouse osteoblasts. Finally, it was found that 2-aminoethanesulphonic acid inhibited alveolar bone resorption in experimental periodontitis in hamsters. These results suggest that 2-aminoethanesulphonic acid is an effective agent in preventing inflammatory bone resorption in periodontal diseases.
authors.affiliation: Department of Oral Science, National Institute of Infectious Diseases, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Koide
authors.forename: N
authors.initials: N
authors.lastname: Okahashi
authors.forename: R
authors.initials: R
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Kazuno
authors.forename: K
authors.initials: K
authors.lastname: Shibasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Yamazaki
authors.forename: K
authors.initials: K
authors.lastname: Kaneko
authors.forename: N
authors.initials: N
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Ohguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Ishihara
authors.forename: T
authors.initials: T
authors.lastname: Noguchi
authors.forename: T
authors.initials: T
authors.lastname: Nishihara
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans; D016301:Alveolar Bone Loss / Q000517:prevention & control; D000818:Animals; D001854:Bone Marrow Cells; D001862:Bone Resorption / Q000473:pathology / Q000517:prevention & control*; D002117:Calcitriol / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D006224:Cricetinae; D046508:Culture Techniques; D015232:Dinoprostone / Q000502:physiology; D005260:Female; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D007375:Interleukin-1 / Q000502:physiology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008647:Mesocricetus; D051379:Mice; D010006:Osteoblasts / Q000187:drug effects; D010010:Osteoclasts / Q000166:cytology / Q000187:drug effects*; D010518:Periodontitis / Q000150:complications; D012886:Skull; D013654:Taurine / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D002120:Calcium Channel Agonists; D018836:Inflammation Mediators; D007375:Interleukin-1; D008070:Lipopolysaccharides; D013654:Taurine; D002117:Calcitriol; D015232:Dinoprostone