徳島大学 教育・研究者情報データベース(EDB)

1. The Forsyth Institute, Department of Immunology
2. 徳島大学.大学院ヘルスバイオサイエンス研究部.発達予防医歯学部門.健康長寿歯科学講座(2004年4月1日〜)
3. 広島大学.歯学部附属病院
4. 三菱ウェルファーマ 株式会社

1. 河井 敬久([The Forsyth Institute, Department of Immunology])

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2. (英) Matsuyama Takashi

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3. 細川 義隆([徳島大学.病院.診療科.歯科.むし歯科(第一保存科)])

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4. 牧平 清超([広島大学.歯学部附属病院])

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5. 関 誠([三菱ウェルファーマ 株式会社])

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6. (英) Nadeem Karimbux

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7. (英) Reginaldo B. Goncalves

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8. (英) Paloma Valverde

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9. (英) Serge Dibart

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10. (英) Yi-Ping Li

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11. (英) Leticia A. Miranda

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12. (英) Cory W.O. Ernst

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13. (英) Yuichi Izumi

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14. Taubman Martin([The Forsyth Institute, Department of Immunology])

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(英) B and T Lymphocytes Are the Primary Sources of RANKL in the Bone Resorptive Lesion of Periodontal Disease

(英) Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.

1. (英) B-Lymphocytes
2. (英) Bone Resorption
3. (英) Carrier Proteins
4. (英) Cell Differentiation
5. (英) Cells, Cultured
6. (英) Gene Expression Regulation
7. (英) Gingiva
8. (英) Glycoproteins
9. (英) Humans
10. (英) Lymphocyte Activation
11. (英) Membrane Glycoproteins
12. (英) Microscopy, Confocal
13. (英) Osteoclasts
14. (英) Osteoprotegerin
15. (英) Periodontitis
16. (英) RANK Ligand
17. (英) Receptor Activator of Nuclear Factor-kappa B
18. (英) Receptors, Cytoplasmic and Nuclear
19. (英) Receptors, Tumor Necrosis Factor
20. (英) T-Lymphocytes

1. (英) Article.Affiliation: Department of Immunology, The Forsyth Institute, 140 The Fenway, Boston, MA 02115, USA.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, N.I.H., Extramural

4. (英) OtherID: PMC1698808