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J Dent Res 83(4): 349-353, 2004
© 2004 International and American Associations for Dental Research


RESEARCH REPORT
Biological

Identification of RANKL in Osteolytic Lesions of the Facial Skeleton

J.Y.Y. Tay1,*, B.H. Bay2, J.F Yeo3, M. Harris4, S. Meghji5, and S.T. Dheen2

1 Dept. of Oral and Maxillofacial Surgery, National Dental Centre, 5 Second Hospital Avenue, S168938, Singapore;
2 Dept. of Anatomy, National University of Singapore;
3 Dept. of Oral and Maxillofacial Surgery, National University of Singapore;
4 Dept. of Oral and Maxillofacial Surgery, St Bartholomew’s and the Royal London School of Medicine and Dentistry, United Kingdom; and
5 Eastman Institute of Oral Science, UK;

* corresponding author, juliet_tay{at}yahoo.com

RANKL (receptor activator of nuclear factor {kappa}B ligand) promotes osteoclast differentiation, stimulates osteoclast activity, and prolongs osteoclast survival and adherence to bone. Abnormalities of the RANKL/RANK/osteoprotegerin system have been implicated in a range of diseases, including osteoporosis. To date, no work has been done in osteolytic lesions of the facial skeleton. In this study, specimens of ameloblastomas, dentigerous cysts, odontogenic keratocysts, and radicular cysts were subjected to immunohistochemical analysis for RANKL and tartrate-resistant acid phosphatase (TRAP). Immunofluorescence staining for TRAP was visualized under confocal microscopy. All specimens demonstrated distinct positive immunoreactivity to RANKL and TRAP. The TRAP-positive cells also stained with in situ hybridization for human calcitonin receptor, a definitive marker for osteoclasts. Mononuclear pre-osteoclasts were observed to migrate from blood to the connective tissue stroma and multinucleate toward the bone surface. It can be concluded that RANKL plays a role in bone resorption in osteolytic lesions of the facial skeleton.

KEY WORDS: RANKL • immunohistochemistry • confocal microscopy • osteoclast • bone resorption







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