1. Identification of RANKL in osteolytic lesions of the facial skeleton.
- Author
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Tay JY, Bay BH, Yeo JF, Harris M, Meghji S, and Dheen ST
- Subjects
- Acid Phosphatase metabolism, Dentigerous Cyst metabolism, Facial Bones metabolism, Facial Bones pathology, Humans, Immunohistochemistry, In Situ Hybridization, Isoenzymes metabolism, Osteoprotegerin, Radicular Cyst metabolism, Receptors, Calcitonin metabolism, Receptors, Tumor Necrosis Factor, Signal Transduction, Tartrate-Resistant Acid Phosphatase, Ameloblastoma metabolism, Glycoproteins metabolism, Jaw Neoplasms metabolism, Odontogenic Cysts metabolism, Osteolysis metabolism, Receptors, Cytoplasmic and Nuclear metabolism
- Abstract
RANKL (receptor activator of nuclear factor kappaB 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.
- Published
- 2004
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