acid-phosphatase and Ameloblastoma

Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) released from the ameloblastoma, as in bone metastases of cancer cells. However, the clinical features of ameloblastoma, including its growth rate and patterns of invasion, are quite different from those of bone metastasis of cancer cells, suggesting that different underlying mechanisms are involved. Therefore, in the present study, we examined the possible mechanisms underlying the invasive expansion of ameloblastoma in the jaw bone. Expression levels of RANKL assessed by western blotting were markedly lower in ameloblastoma (AM-1) cells than in highly metastatic oral squamous cell carcinoma (HSC-3) cells. Experiments coculturing mouse macrophages (RAW264.7) with AM-1 demonstrated low osteoclastogenic activity, as assessed by tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cell formation, probably because of low release of RANKL, whereas cocultures of RAW264.7 with HSC-3 cells exhibited very high osteoclastogenic activity. Thus, RANKL release from AM-1 appeared to be too low to generate osteoclasts. However, AM-1 cultured directly on calcium phosphate-coated plates formed resorption pits, and this was inhibited by application of bafilomycin A1. Furthermore, vacuolar-type H+-ATPase (V-ATPase) and H+/Cl- exchange transporter 7 (CLC-7) were detected on the surface of AM-1 cells by plasma membrane biotinylation and immunofluorescence analysis. Immunohistochemical analysis of clinical samples of ameloblastoma also showed plasma membrane-localized V-ATPase and CLC-7 in the epithelium of plexiform, follicular and basal cell types. The demineralization activity of AM-1 was only 1.7% of osteoclasts demineralization activity, and the growth rate was 20% of human normal skin keratinocytes and HSC-3 cells. These results suggest that the slow expansion of several typical types of ameloblastomas in jaw bone is attributable to its slow growth and low demineralization ability.

Topics: Acid Phosphatase; Ameloblastoma; Animals; Cell Line, Tumor; Cell Membrane; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; Isoenzymes; Jaw; Jaw Neoplasms; Keratinocytes; Mice; Mouth Neoplasms; Neoplasm Invasiveness; Neoplasm Metastasis; Osteoclasts; RANK Ligand; RAW 264.7 Cells; Tartrate-Resistant Acid Phosphatase; Vacuolar Proton-Translocating ATPases

Ameloblastoma, a common odontogenic tumor located in jaws, generally leads to severe damage to patient's complexion and masticatory function. To expand in jaws, ameloblastoma must have a mechanism of resorbing the surrounding bone. Our objective was to explore the bone-resorption mechanism of ameloblastoma by observing the role of Receptor activator of nuclear factor kappa B ligand (RANKL) and matrix metalloproteinase-9 (MMP-9) in the bone-resorption process.. In the study, the expression of RANKL and MMP-9 in ameloblastoma was detected using immunohistochemistry (IHC) and RT-PCR. Then, co-culture system of ameloblastoma cells and bone marrow cells from neonatal rabbit was erected to observe the potential of ameloblastoma cells to induce osteoclastogenesis. Finally, the induced osteoclasts were used for in vitro bone-resorption assay. In the co-culture system and the bone-resorption assay, the selective inhibitor of RANKL and MMP-9, osteoprotegerin (OPG) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were, respectively, used for observing the role of RANKL and MMP-9.. The expression of RANKL and MMP-9 in ameloblastoma was confirmed. Ameloblastoma cells were found to induce bone marrow cells from neonatal rabbit differentiate into osteoclasts with bone-resorption activity. In addition, OPG was found to, respectively, have markedly inhibitory effect on osteoclastogenesis (P<0.01), and slightly inhibitory action on bone resorption (P<0.05).. Ameloblastoma cells had the potential to induce osteoclastogenesis. Moreover, RANKL played an essential role in the in vitro osteoclast formation and bone resorption induced by ameloblastoma cells.

Topics: Acid Phosphatase; Ameloblastoma; Animals; Animals, Newborn; Biomarkers; Bone Marrow Cells; Bone Resorption; Calcium; Cell Count; Cell Culture Techniques; Cell Differentiation; Cells, Cultured; Coculture Techniques; Dentin; Female; Humans; Immunohistochemistry; Isoenzymes; Male; Matrix Metalloproteinase 9; Matrix Metalloproteinase Inhibitors; Osteoclasts; Osteoprotegerin; Rabbits; RANK Ligand; Reverse Transcriptase Polymerase Chain Reaction; Tartrate-Resistant Acid Phosphatase; Tissue Inhibitor of Metalloproteinase-1

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.

Topics: Acid Phosphatase; Ameloblastoma; Dentigerous Cyst; Facial Bones; Glycoproteins; Humans; Immunohistochemistry; In Situ Hybridization; Isoenzymes; Jaw Neoplasms; Odontogenic Cysts; Osteolysis; Osteoprotegerin; Radicular Cyst; Receptors, Calcitonin; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Signal Transduction; Tartrate-Resistant Acid Phosphatase

Four cases of granular-cell ameloblastoma were studied by light and electron microscopy, histochemistry and electron enzyme histochemistry. Microscopically, granular cells commonly occurred in a follicular pattern, but, in one case, they were in a plexiform pattern. The high activity of acid phosphatase and electron microscopic features revealed that the cytoplasmic granularity was ascribed to the high content of lysosomes. It was speculated that granular-cell ameloblastoma occurs due to the altered dysfunction of tumor cells, and the age factor is related to the pathogenesis of this tumor.

Topics: Acid Phosphatase; Aged; Alkaline Phosphatase; Ameloblastoma; Glucuronidase; Humans; Male; Mandibular Neoplasms; Microscopy, Electron; Middle Aged; Naphthols

Jaw ameloblastomas produce most frequently (62%) multilocular translucences. An unilocular translucence was observed in 28% of the cases. In both forms, secondary cysts were present. This radiomorphologic finding is of pathognomonic value. Conchiform or finger-shaped translucences were seen in 10% of the cases. Such radiographic changes were observed in ameloblastomas arising from the oral mucosa. The border of the radiolucent area was always sharply defined and had a lobulate or wreathed form. The ameloblastoma spreads in an expansive or invasive way. The bone destruction is in all probability caused by the acid phosphatase activity of the tumour. Bone transformation occurs simultaneously with bone destruction and might be regarded as a morphologic sign of the defence mechanism.

Topics: Acid Phosphatase; Ameloblastoma; Bone Regeneration; Bone Resorption; Humans; Jaw Neoplasms; Mouth Neoplasms; Neoplasm Invasiveness; Radiography

Topics: Acid Phosphatase; Adenoma, Chromophobe; Ameloblastoma; Astrocytoma; Biopsy; Brain; Brain Neoplasms; Cell Differentiation; Cerebellar Neoplasms; Cerebellum; Choroid Neoplasms; Choroid Plexus; Ependyma; Ependymoma; Esterases; Ganglia; Ganglioneuroma; Hemangiosarcoma; Histocytochemistry; Humans; Medulla Oblongata; Medulloblastoma; Meninges; Meningioma; Neuroectodermal Tumors, Primitive, Peripheral; Neuroma; Neurons; Oligodendroglioma; Pituitary Gland; Pituitary Neoplasms; Sarcoma

Topics: Acid Phosphatase; Alkaline Phosphatase; Ameloblastoma; Aminopeptidases; Esterases; Glucuronidase; Histocytochemistry; Humans; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adult; Alkaline Phosphatase; Ameloblastoma; Enzymes; Female; Histocytochemistry; Humans; Odontogenic Tumors; Oxidoreductases; Tooth Germ

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Alkaline Phosphatase; Ameloblastoma; Child; Craniopharyngioma; Cysts; Dihydrolipoamide Dehydrogenase; Electron Transport Complex IV; Epithelium; Esterases; Female; Histocytochemistry; Humans; Jaw Neoplasms; Leucyl Aminopeptidase; Male; Oxidoreductases; Skin Neoplasms

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Ameloblastoma; Electron Transport Complex IV; Female; Histocytochemistry; Humans; Male; Microscopy, Electron; Periodontium; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenofibroma; Alkaline Phosphatase; Ameloblastoma; Aminopeptidases; Animals; Breast Neoplasms; Carcinoma, Squamous Cell; Female; Glucosephosphate Dehydrogenase; Glucuronidase; Histocytochemistry; Humans; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Mice; Mouth Neoplasms; Sarcoma, Experimental; Skin Neoplasms; Succinate Dehydrogenase; Tumor Virus Infections

Topics: Acid Phosphatase; Alkaline Phosphatase; Ameloblastoma; Aminopeptidases; Dihydrolipoamide Dehydrogenase; Electron Transport Complex II; Esterases; Galactosidases; Glucuronidase; Histocytochemistry; L-Lactate Dehydrogenase; Research; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenoma; Alkaline Phosphatase; Ameloblastoma; Arthritis; Bone Cysts; Bone Neoplasms; Chondrosarcoma; Fibroma; Fibrous Dysplasia of Bone; Geriatrics; Giant Cell Tumors; Humans; Neoplasm Metastasis; Osteitis Fibrosa Cystica; Osteoma; Osteosarcoma; Prognosis; Radiography; Sarcoma, Ewing; Tuberculosis; Tuberculosis, Osteoarticular