Abstract
Receptor activator of nuclear factor-κB (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.
| Original language | English |
|---|---|
| Pages (from-to) | 987-998 |
| Number of pages | 12 |
| Journal | American Journal of Pathology |
| Volume | 169 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jan 1 2006 |
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All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
Cite this
B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease. / Kawai, Toshihisa; Matsuyama, Takashi; Hosokawa, Yoshitaka; Makihira, Seicho; Seki, Makoto; Karimbux, Nadeem Y.; Goncalves, Reginaldo B.; Valverde, Paloma; Dibart, Serge; Li, Yi Ping; Miranda, Leticia A.; Ernst, Cory W.O.; Izumi, Yuichi; Taubman, Martin A.
In: American Journal of Pathology, Vol. 169, No. 3, 01.01.2006, p. 987-998.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease
AU - Kawai, Toshihisa
AU - Matsuyama, Takashi
AU - Hosokawa, Yoshitaka
AU - Makihira, Seicho
AU - Seki, Makoto
AU - Karimbux, Nadeem Y.
AU - Goncalves, Reginaldo B.
AU - Valverde, Paloma
AU - Dibart, Serge
AU - Li, Yi Ping
AU - Miranda, Leticia A.
AU - Ernst, Cory W.O.
AU - Izumi, Yuichi
AU - Taubman, Martin A.
PY - 2006/1/1
Y1 - 2006/1/1
N2 - Receptor activator of nuclear factor-κB (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.
AB - Receptor activator of nuclear factor-κB (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.
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U2 - 10.2353/ajpath.2006.060180
DO - 10.2353/ajpath.2006.060180
M3 - Article
VL - 169
SP - 987
EP - 998
JO - American Journal of Pathology
JF - American Journal of Pathology
SN - 0002-9440
IS - 3
ER -