Effect of technetium-99 conjugated with methylene diphosphonate (99 Tc-MDP) on OPG/RANKL/RANK system in vitro.

BACKGROUND: RANKL and RANK play an important role in jaw resorption during the development of the ameloblastomas. Therefore, the aim of this study was to explore the effect of 99 Tc-MDP on OPG/RANKL/RANK system on RAW264.7 and MC3T3-E1 cell lines in vitro and provide the theoretical basis for the clinical treatment of the jaw ameloblastoma. METHODS: Different concentrations of 99 Tc-MDP were used to treat RAW264.7 and MC3T3-E1 cell lines. The cell proliferative inhibition rate was analyzed by CCK-8. Cell apoptosis and cell cycle were detected by flow cytometry. Western blot was used to detect the expression of OPG, RANKL, and RANK. RESULTS: Treatment of RAW264.7 cell lines with different concentrations of 99 Tc-MDP had inhibitory effects and decreased the expression of RANK protein. The cell proliferation of 99 Tc-MDP on MC3T3-E1 cell lines was stronger at 48 hours than at 24 hours except for 100 µg/mL concentration group. Compared with the concentration of 0.01 µg/mL, the treatment of MC3T3-E1 cells with 100 µg/mL 99 Tc-MDP showed that the cell proliferative effect decreased at 24 hours and 48 hours (P < 0.05). After treatment with 0.01 µg/mL 99 Tc-MDP, the expression of OPG in MC3T3-E1 cells was significantly increased (P < 0.05). Compared with 0.01 µg/mL, the expression of RANKL was decreased after treatment with 100 µg/mL 99 Tc-MDP (P < 0.05). CONCLUSION: 99 Tc-MDP can induce apoptosis of RAW264.7 cells and inhibit the expression of RANK protein. The effect of 0.01 µg/mL of low concentration of 99 Tc-MDP can promote the proliferation of MC3T3-E1 cells and increase the expression of OPG and RANKL protein. 99 Tc-MDP may have adjuvant therapeutic effects on the treatment of jaw ameloblastoma.

Ameloblastoma: a clinical review and trends in management.

Ameloblastoma is a rare odontogenic neoplasm of the mandible and maxilla, with multiple histologic variants, and high recurrence rates if improperly treated. The current mainstay of treatment is wide local excision with appropriate margins and immediate reconstruction. Here we review the ameloblastoma literature, using the available evidence to highlight the change in management over the past several decades. In addition, we explore the recent molecular characterization of these tumors which may point towards new potential avenues of personalized treatment.

Regulation of IL-6 and IL-8 production by reciprocal cell-to-cell interactions between tumor cells and stromal fibroblasts through IL-1α in ameloblastoma.

Ameloblastoma is an odontogenic benign tumor that occurs in the jawbone, which invades bone and reoccurs locally. This tumor is treated by wide surgical excision and causes various problems, including changes in facial countenance and mastication disorders. Ameloblastomas have abundant tumor stroma, including fibroblasts and immune cells. Although cell-to-cell interactions are considered to be involved in the pathogenesis of many diseases, intercellular communications in ameloblastoma have not been fully investigated. In this study, we examined interactions between tumor cells and stromal fibroblasts via soluble factors in ameloblastoma. We used a human ameloblastoma cell line (AM-3 ameloblastoma cells), human fibroblasts (HFF-2 fibroblasts), and primary-cultured fibroblasts from human ameloblastoma tissues, and analyzed the effect of ameloblastoma-associated cell-to-cell communications on gene expression, cytokine secretion, cellular motility and proliferation. AM-3 ameloblastoma cells secreted higher levels of interleukin (IL)-1α than HFF-2 fibroblasts. Treatment with conditioned medium from AM-3 ameloblastoma cells upregulated gene expression and secretion of IL-6 and IL-8 of HFF-2 fibroblasts and primary-cultured fibroblast cells from ameloblastoma tissues. The AM3-stimulated production of IL-6 and IL-8 in fibroblasts was neutralized by pretreatment of AM-3 cells with anti-IL-1α antibody and IL-1 receptor antagonist. Reciprocally, cellular motility of AM-3 ameloblastoma cells was stimulated by HFF-2 fibroblasts in IL-6 and IL-8 dependent manner. In conclusion, ameloblastoma cells and stromal fibroblasts behave interactively via these cytokines to create a microenvironment that leads to the extension of ameloblastomas.

Bioengineering the ameloblastoma tumour to study its effect on bone nodule formation.

Ameloblastoma is a benign, epithelial cancer of the jawbone, which causes bone resorption and disfigurement to patients affected. The interaction of ameloblastoma with its tumour stroma drives invasion and progression. We used stiff collagen matrices to engineer active bone forming stroma, to probe the interaction of ameloblastoma with its native tumour bone microenvironment. This bone-stroma was assessed by nano-CT, transmission electron microscopy (TEM), Raman spectroscopy and gene analysis. Furthermore, we investigated gene correlation between bone forming 3D bone stroma and ameloblastoma introduced 3D bone stroma. Ameloblastoma cells increased expression of MMP-2 and -9 and RANK temporally in 3D compared to 2D. Our 3D biomimetic model formed bone nodules of an average surface area of 0.1 mm2 and average height of 92.37 [Formula: see text] 7.96 µm over 21 days. We demonstrate a woven bone phenotype with distinct mineral and matrix components and increased expression of bone formation genes in our engineered bone. Introducing ameloblastoma to the bone stroma, completely inhibited bone formation, in a spatially specific manner. Multivariate gene analysis showed that ameloblastoma cells downregulate bone formation genes such as RUNX2. Through the development of a comprehensive bone stroma, we show that an ameloblastoma tumour mass prevents osteoblasts from forming new bone nodules and severely restricted the growth of existing bone nodules. We have identified potential pathways for this inhibition. More critically, we present novel findings on the interaction of stromal osteoblasts with ameloblastoma.

Ameloblastomas Exhibit Stem Cell Potential, Possess Neurotrophic Properties, and Establish Connections with Trigeminal Neurons.

Ameloblastomas are locally invasive and aggressive odontogenic tumors treated via surgical resection, which results in facial deformity and significant morbidity. Few studies have addressed the cellular and molecular events of ameloblastoma onset and progression, thus hampering the development of non-invasive therapeutic approaches. Tumorigenesis is driven by a plethora of factors, among which innervation has been long neglected. Recent findings have shown that innervation directly promotes tumor progression. On this basis, we investigated the molecular characteristics and neurotrophic properties of human ameloblastomas. Our results showed that ameloblastomas express dental epithelial stem cell markers, as well as components of the Notch signaling pathway, indicating persistence of stemness. We demonstrated that ameloblastomas express classical stem cell markers, exhibit stem cell potential, and form spheres. These tumors express also molecules of the Notch signaling pathway, fundamental for stem cells and their fate. Additionally, we showed that ameloblastomas express the neurotrophic factors NGF and BDNF, as well as their receptors TRKA, TRKB, and P75/NGFR, which are responsible for their innervation by trigeminal axons in vivo. In vitro studies using microfluidic devices showed that ameloblastoma cells attract and form connections with these nerves. Innervation of ameloblastomas might play a key role in the onset of this malignancy and might represent a promising target for non-invasive pharmacological interventions.

Midkine expression correlating with growth activity and tooth morphogenesis in odontogenic tumors.

Midkine (MK; a low molecular weight heparin-binding growth factor) is a multifunctional cytokine. MK plays a role in morphogenesis of many organs including teeth through epithelial-mesenchymal interactions. We immunohistochemically examined MK expression in various human odontogenic tumors. There was no difference in positive rate and intensity of MK between benign odontogenic tumors and their malignant counterparts. Ameloblastoma showed MK localization in the peripheral columnar cells in budding processes from the parenchyma, which frequently expressed proliferating cell nuclear antigen. MK was also preferentially expressed in keratinized cells in acanthomatous ameloblastoma and keratocystic odontogenic tumor. In odontogenic mixed tumors except for odontoma, intense immunoreactivity to MK was found in epithelial follicles, the surrounding odontogenic ectomesenchymal tissue, and the basement membrane between them. Intensity in the odontogenic ectomesenchyme decreased in relation to distance from the epithelial follicles. No expression was found in tumor cells associated with production of dental hard tissues in odontogenic mixed tumors including odontoma. These findings suggested that MK is involved in the reciprocal interaction between odontogenic epithelium and odontogenic ectomesenchymal tissue in areas without dental hard tissue formation in odontogenic mixed tumors. Coexpression of MK and proliferating cell nuclear antigen was also observed in epithelial follicles and highly cellular nodules in the ectomesenchyme of odontogenic mixed tumors. MK is considered to mediate growth activity of odontogenic tumors and cell differentiation of odontogenic mixed tumors through molecular mechanisms similar to those involved in morphogenesis of the tooth.

Expression profile of polycomb group proteins in odontogenic keratocyst and ameloblastoma.

Polycomb group (PcG) proteins are repressive chromatin modifiers required for proliferation and development. PcG proteins form two large repressive complexes, namely, Polycomb Repressive Complex 1 and 2. These proteins have been shown to drive tumorigenesis by repressing cell-type specific sets of target genes. Using immunohistochemistry, we investigated the expression patterns of five human PcG proteins, including Bmi-1, Ring1b, Mel-18, Ezh2, and Suz12, in various cellular components of odontogenic keratocysts (OKCs), ameloblastomas and, pericoronal follicles (PFs). In OKCs, expression of PcG proteins were found in the majority of cases while the expression pattern was relatively different for each PcG proteins. All PcG proteins were strongly expressed in the basal cells while some proteins showed variable expression in the parabasal and luminal cell layer of OKCs. In ameloblastomas, almost all PcG proteins showed a similar expression pattern of moderate to strong staining in the peripheral ameloblast-like cells and metaplastic squamous cells. Some of the central stellate reticulum-like cells also showed positive reaction to most PcG proteins. In PFs, most PcG proteins were intensely expressed in odontogenic epithelium lining the follicles, except Mel-18 and Suz12. The present study provides the initial evidence regarding epigenetic involvement by PcG proteins in these odontogenic lesions. Although these proteins are known to be in the same repressive group proteins, differential expression patterns of these proteins in OKCs and ameloblastomas indicates that these proteins may play different roles in pathogenesis of these odontogenic lesions.

Potential involvement of chondroitin sulfate A in the pathogenesis of ameloblastoma.

Ameloblastoma is classified as a benign odontogenic tumor characterized by locally invasive behavior and high risk of recurrence. Here, we evaluate a potential role for glycosaminoglycan, a structural component of cell membranes and extracellular matrix, in ameloblstoma pathogenesis. We subjected formalin-fixed, paraffin-embedded tissue sections of 34 cases of ameloblastoma, 10 of odontogenic keratocyst, and 17 of dentigerous cyst to immunohistochemistry using monoclonal antibodies recognizing chondroitin sulfate A (CS-A), heparan sulfate (HS), and keratan sulfate (KS). Expression levels of CS-A in epithelial component and stroma of ameloblastoma were significantly higher than those in odontogenic keratocyst and dentigerous cyst. Moreover, CS-A in ameloblastoma was more strongly expressed in stellate reticulum-like cells than in amelobast-like cells with statistical significance. On the other hand, expression levels of HS and KS in epithelial component and stroma of ameloblastoma were lower compared with CS-A. These results overall reveal that among these odontogenic lesions, CS-A is preferentially expessed in ameloblastoma, suggesting potential pathogenetic role probably in cytodifferention of tumor cells to stellate reticulum-like cells.

Osteoprotegerin (OPG) binds with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL): suppression of TRAIL-induced apoptosis in ameloblastomas.

Osteoprotegerin (OPG) is a useful receptor in inhibiting Receptor Activator of NFkappaB Ligand (RANKL) in inducing osteoclastogenesis. Tumor Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) is a potent apoptosis-inducing ligand in ameloblastomas. Since OPG has been reported to bind to TRAIL as well, the effect of OPG in TRAIL's function in inducing apoptosis should also be investigated. To investigate on the expression of OPG in ameloblastomas, immuhistochemistry, immunofluorescence and Western blot were performed. From the immunohistochemistry results, we found that OPG was expressed in ameloblastoma tissues. Expression of OPG was clearly seen in AM-1 cells by immunofluorescence as well. Additionally, Western blot analysis confirmed OPG expression in ameloblastoma tissues and AM-1 cells. To investigate on the potential of TNFalpha, TRAIL and RANKL in inducing apoptosis, we performed an apoptosis assay. From the apoptosis assay, we found that TRAIL had the highest potential in inducing apoptosis compared to TNFalpha and RANKL. To investigate the binding of OPG with RANKL and TRAIL, we performed a binding assay. We noticed that OPG preferably bind with RANKL than TRAIL. However, at low levels of RANKL, marked binding of OPG with TRAIL was seen. As we suspected that the binding of OPG and TRAIL might cause the effect of TRAIL in inducing apoptosis in ameloblastomas, we combined the treatment of OPG and TRAIL in AM-1 cells. From the apoptosis assay, we found that under treatment of OPG, TRAIL's function in inducing apoptosis was suppressed. These data suggest that by binding with TRAIL, OPG suppressed TRAIL's function in inducing apoptosis in ameloblastomas.

Inhibition of Akt and MAPK pathways elevated potential of TNFalpha in inducing apoptosis in ameloblastoma.

Tumor necrosis factor alpha (TNFalpha) can trigger both cell survival and apoptosis. In the present study, from the flow cytometry results, we found that the prolonged-treatment of TNFalpha until 24 h, resulted apoptosis in AM-1 cells (ameloblastoma cell line). These results were confirmed by DAPI staining, which showed nuclear fragmentation feature of AM-1 cells under treatment of TNFalpha. Our further investigation using specific caspase inhibitors showed that caspase-3 played a crucial role in mediating TNFalpha-induced apoptosis in AM-1 cells. In addition, significant elevation of TNFalpha potential in inducing apoptosis was seen by applying LY294002, phosphatidylinositol-3-OH kinase (PI3K) inhibitor, or U0126, mitogen-activated extracellular-regulated kinase (MEK1/2) inhibitor, prior to the treatment of TNFalpha in AM-1 cells. These results suggested that TNFalpha induced both cell survival and apoptosis pathways in ameloblastoma and potential of TNFalpha in inducing apoptosis can be improved by inhibiting TNFalpha-induced Akt and p44/42 mitogen-activated protein kinase (MAPK) cell survival pathways.

Cisto dentígero com transformação ameloblástica / Quiste dentígero con transformación ameloblástica / Dentigerous cyst with ameloblastic transformation

Introdução: O cisto dentígero se origina pela separação do folículo que fica ao redor da coroa de um dente incluso. É o tipo mais comum de cisto odontogênico do desenvolvimento. O seu crescimento é lento, assintomático, e pode atingir grandes dimensões. Objetivo: Relatar um caso clínico cirúrgico de cisto dentígero com transformação ameloblástica, localizado na mandíbula, de paciente, gênero feminino, melanoderma, 14 anos. Caso clínico: Ao exame radiográfico apresentou área radiolúcida unilocular com margem bem definida e esclerótica envolvendo a coroa das unidades 48 e 47. Foi realizada enucleação e curetagem da lesão com exodontia destas unidades sob anestesia local em ambulatório, e aplicada a crioterapia na loja óssea. Encaminhou-se o conteúdo da lesão para exame histopatológico e o diagnóstico de cisto dentígero com transformação ameloblástica foi fechado. Comentários principais: No momento a paciente encontra-se em acompanhamento pós-operatório de 3 anos com neoformação óssea e sem recidivas(AU)

Introducción: El quiste dentígero se origina por la separación del folículo que se queda alrededor de la corona de un diente no erupcionado. Es el tipo más común de quiste odontogénico de desarrollo. Su crecimiento es lento, asintomático y puede alcanzar grandes dimensiones. Objetivo: Reportar un caso quirúrgico de quiste dentígero con transformación ameloblástica. Presentación del caso: Paciente femenina de 14 años, de color de piel negra. La radiografía demostró una radiolucidez unilocular con márgenes bien definidos que envolvían la corona de los dientes 48 y 47. El tratamiento involucró una combinación de enucleación y curetaje de la lesión, exodoncia de los dientes y crioterapia para desvitalizar el hueso circundante. Se realizó el examen histopatológico, luego, se confirmó el diagnóstico de quiste dentígero con transformación ameloblástica. Conclusiones: Al momento de la redacción del reporte la paciente se encontraba en seguimiento posoperatorio de tres años con neoformación ósea y sin recidivas(AU)

Introduction: Dentigerous cysts are caused by the separation of the follicle remaining around the crown of unerupted teeth. They are the most common type of developmental odontogenic cyst. Their growth is slow and asymptomatic, and they may reach large dimensions. Objective: Report a surgical case of dentigerous cyst with ameloblastic transformation. Case presentation: A case is presented of a black female 14-year-old patient. Radiography revealed an area of unilocular radiolucency with well-defined margins enveloping the crowns of teeth 48 and 47. Treatment was a combination of enucleation and curettage of the lesion, exodontia of the teeth and cryotherapy to devitalize the surrounding bone. Eventual histopathological examination confirmed the diagnosis of dentigerous cyst with ameloblastic transformation. Conclusions: At the time when the report was written, the patient had been followed up for three years after surgery, showing bone neoformation and no recurrence of the lesion(AU)

Recurrent giant mandibular ameloblastoma in young adults.

BACKGROUND: The purpose of the study was to define the most appropriate management of the giant mandibular ameloblastoma (GMA) in young adults. METHODS: A retrospective study was performed on patients with GMA <30 years old. The data collected included initial treatment, tumor margins, reconstruction, and follow-up. Patients evaluated speech, chewing, swallowing, and facial appearance after definitive treatment. RESULTS: Thirteen patients were identified with recurrent solid/multicystic disease requiring further treatment. Definitive treatment involved segmental mandibulectomy and reconstruction with free fibular flap in all patients. Seven patients had immediate reconstruction (group A) and 6 had secondary (group B). Mandibular resection was planned at least 2 cm beyond the radiological limit, free margins were achieved in all patients, and all flaps were transplanted successfully. In group A, functional score was 13.7 ± 0.45 and facial appearance score was 4.5 ± 0.49, whereas in group B were 11.16 ± 0.37 and 3.3 ± 0.5, respectively (both p < .05). CONCLUSION: Aggressive resection of the GMA and immediate reconstruction is strongly advised. © 2015 Wiley Periodicals, Inc. Head Neck 38: E1947-E1954, 2016.

Ameloblastoma induces osteoclastogenesis: a possible role of ameloblastoma in expanding in the bone.

Ameloblastoma, a tumor located in bone, when neglected, can perforate the bone and, ultimately, spread into the soft tissues. To expand in the bone, ameloblastoma must have a mechanism of resorbing the surrounding bone. However, the mechanism for bone resorption is poorly understood. In the present study, we found that RANKL and TNFalpha were expressed and secreted by ameloblastoma cells, and was proven to induce osteoclastogenesis. Our present results also showed that phosphorylation of p38, SAPK, p44/42 and Akt were upregulated under treatment of 10xCM (concentrated conditioned media of AM-1 cells). We also noticed formation of resorption lacunae on dentin slice by 10xCM-induced osteoclast-like MNCs. These results suggested that ameloblastoma by secreting RANKL and TNFalpha could induce osteoclastogenesis.

Evaluation of quality of life among patients after extirpation of mandibular ameloblastoma.

OBJECTIVE: To evaluate the quality of life (QOL) based on the functional, aesthetic and personal satisfaction among patients with ameloblastoma who underwent either partial or total mandibulectomy without reconstruction. DESIGN: Cross-sectional study. SETTING: The Department of Oral Surgery and Oral Pathology, School of Dentistry; Muhimbili University College of Health Sciences, Tanzania. SUBJECTS: Patients surgically treated for ameloblastoma without reconstruction. RESULTS. The postoperative problems were mostly associated with eating of solid foods, appearance and speech. All patients treated by total mandibulectomy had moderately severe problems with eating of solid foods and were dissatisfied with their appearance. CONCLUSION: The relatively small tumours resulted in a much better QOL. Public awareness programmes to avoid late referral and treatment is the most effective way to reduce the number of patients who after treatment suffer a poor QOL.

Are podoplanin and ezrin involved in the invasion process of the ameloblastomas?

The association between podoplanin and ezrin in the process of odontogenic tumors invasion has been suggested, but was not studied yet. Our purpose was to investigate the relationship between podoplanin and ezrin expressions in the odontogenic epithelium of ameloblastomas. Forty-seven ameloblastomas were analyzed by immunohistochemistry using anti-podoplanin and anti-ezrin antibodies. The expressions of both proteins were evaluated using a score method and the comparison and association between these proteins were verified, respectively, by Wilcoxon Signed-Rank test and by Spearman's rank correlation coefficient, using a statistical significance level of 0.05. The majority of tumors (87.2%) exhibited strong membranous expression of podoplanin in the peripheral cells. Cytoplasmic expression of ezrin in the peripheral cells of ameloblastomas was stronger than its membranous expression. No statistically significant correlation was observed between podoplanin and ezrin. However, there was statistically significant difference between membranous podoplanin and membranous ezrin expressions, between cytoplasmic podoplanin and membranous ezrin expressions, and between cytoplasmic podoplanin and cytoplasmic ezrin expressions. There was no statistical difference between membranous podoplanin and cytoplasmic ezrin expressions. These results suggest a synergistic role of both proteins in the process of invasion of ameloblastomas.

Dedifferentiated adamantinoma with revertant mesenchymal phenotype.

In adamantinoma of long bones, an osteofibrous dysplasia-like form with scattered epithelial elements and a classic form with abundant epithelium are distinguished. Osteofibrous dysplasia-like adamantinomas occur in children and adolescents and behave relatively benign, whereas classic adamantinomas predominate in adults and have a more aggressive clinical course. Because some osteofibrous dysplasia-like tumors have progressed to classic adamantinomas, it is hypothesized that the former is a potential precursor of the latter, showing mesenchymal-to-epithelial transformation. We report a new morphologic variant of adamantinoma in three patients with sarcomatoid transformation of the epithelial component: one in a primary tumor and two in local recurrences. One patient died of metastatic disease. Histologically, the tumors showed loss of the original characteristic epithelial differentiation with transition to fields of highly pleomorphic cells without epithelial features, high mitotic count, and deposition of osteoid and chondroid matrix. These dedifferentiated areas showed pankeratin positivity as well, although there were some changes in keratin subclass profile compared with other classic adamantinomas. This peculiar variant of long bone adamantinoma shows that in addition to mesenchymal-to-epithelial transformation in the early stage of development, progression to an aggressive subtype may be associated with epithelial-to-mesenchymal transition ("sarcomatoid dedifferentiation"), in which the epithelial immunophenotype is conserved. Thereby it may serve as an example of the plasticity of the mesenchymal phenotype. When confronted with a biopsy of a cortical tumor of the tibia showing sarcomatoid morphology and keratin positivity, adamantinoma should be included in the differential diagnosis, as its distinction has important implications for treatment and prognosis.

Use of antidromic recording to monitor facial nerve function intraoperatively.

This report describes a technique for monitoring facial nerve activity intraoperatively utilizing antidromic nerve stimulation and sequential averaging of the evoked responses. Compound facial nerve action potentials are obtained reliably even in the presence of paralyzing doses of muscle relaxants, which render the conventional methods useless. The electrophysiological setup is straightforward, and we utilize the same sequential averaging equipment with which we monitor cortical evoked responses intraoperatively. This technique facilitates identification of the facial nerve in large cerebellopontine angle tumors with minimal mechanical trauma. Recordings from eight clinical cases are presented to illustrate the reliability and reproducibility of this technique.

Correlation of clinical and pathological features in surgically treated craniopharyngiomas.

Surgical specimens of 104 craniopharyngiomas from 93 patients were reviewed and characterized histopathologically. They were found to have either a classic adamantinous or a squamous papillary structure. The clinical features of each group were then assessed. The frequently solid (50%), always uncalcified squamous papillary tumor type was found in one-third of the adult patients (greater than or equal to 20 years) but did not occur in children. It was associated with a good functional postoperative outcome (84.6%). There have been no cases of tumor recurrence in the squamous papillary group. However, in the group with the adamantinous type of craniopharyngioma, the recurrence rate was 13% in adult patients and 9% in children. When compared to the adult adamantinous cases, the incidence of visual deficits was lower in the squamous papillary group (75% vs. 84%) but the incidence of endocrine abnormalities was higher (75% vs. 52%). Thus, the preoperative, operative, and postoperative features of the two types of craniopharyngioma were found to be distinctly different in adults and children.

The relationship of the canine acanthomatous epulis to ameloblastoma.

This paper compares the microscopic features and clinical behaviour of the acanthomatous epulis in dogs with those of ameloblastoma in human beings. The acanthomatous epulis has similar microscopic features to one histological variant of human ameloblastoma, the acanthomatous ameloblastoma. Moreover, its clinical behaviour is equivalent to that of intraosseous ameloblastoma in human beings, not of the human peripheral (extraosseous) ameloblastoma, as has been suggested. The stroma of acanthomatous epulides varies and does not always resemble periodontal ligament, a feature that in dogs has been used to distinguish them from ameloblastomas. It is concluded that the acanthomatous epulis (1) is an ameloblastoma, (2) arises from the gingival epithelium in some cases, but (3) may also arise intraosseously and then break out of bone. We recommend the term canine acanthomatous ameloblastoma as being appropriate for this lesion.

Ameloblastoma: a clinical, radiographic, and histopathologic analysis of 71 cases.

OBJECTIVES: The purpose of this study was to compare the clinical, radiologic, and histopathologic features of 71 intraosseous ameloblastomas. STUDY DESIGN: Data with respect to the patients' ages, sex, tumor locations, and surgical treatment history, as well as the radiographic findings and number of recurrences, were analyzed. The histologic types of and radiologic findings regarding tumors with higher recurrence rates were also investigated. RESULTS: The patients' ages at biopsy ranged from 11 to 70 years (mean, 30.4 years). Thirty-nine (54.9%) of the 71 subjects were males, and 32 (45.1%) were females. Sixty-two (87.3%) of the 71 ameloblastomas were located in the mandible. Swelling was the most common symptom and was experienced by 27 (38.0%) patients. Radiographically, 42 (59.2%) of the 71 tumors were unilocular with a well-demarcated border. Of the remaining 29 cases, 14 were multilocular, 2 were of soap-bubble shape, and 13 were unknown in appearance. The most common histologic pattern was plexiform, rather than follicular or acanthomatous. Sixteen cases of ameloblastoma had developed in a cyst. The overall recurrence rate was 21.1%, and the average age of the patient at recurrence was 26.4 years. CONCLUSIONS: When the diagnosis of ameloblastoma in young people remains in doubt after clinical and radiologic examination, a biopsy is necessary. Long-term follow-up at regular intervals after surgery is also recommended.