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B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease

Authors :
Toshihisa Kawai
Seicho Makihira
Cory W.O. Ernst
Serge Dibart
Yi-Ping Li
Yuichi Izumi
Makoto Seki
Yoshitaka Hosokawa
Reginaldo B. Gonçalves
Martin A. Taubman
Nadeem Y. Karimbux
Paloma Valverde
Leticia A. Miranda
Takashi Matsuyama
Source :
The American journal of pathology. 169(3)
Publication Year :
2006

Abstract

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.

Details

ISSN :
00029440
Volume :
169
Issue :
3
Database :
OpenAIRE
Journal :
The American journal of pathology
Accession number :
edsair.doi.dedup.....066d6e8a64e3ce7ee7d7077e070e113c