Contrast-enhanced multidetector computed tomography features and histogram analysis can differentiate ameloblastomas from central giant cell granulomas

BACKGROUND No qualitative or quantitative analysis of contrast-enhanced computed tomography(CT)images has been reported for the differentiation between ameloblastomas and central giant cell granulomas(CGCGs).AIM To describe differentiating multidetector CT(MDCT)features in CGCGs and ameloblastomas and to compare differences in enhancement of these lesions qualitatively and using histogram analysis.METHODS MDCT of CGCGs and ameloblastomas was retrospectively reviewed to evaluate qualitative imaging descriptors.Histogram analysis was used to compare the extent of enhancement of the soft tissue.Fisher’s exact tests and Mann–Whitney U test were used for statistical analysis(P<0.05).RESULTS Twelve CGCGs and 33 ameloblastomas were reviewed.Ameloblastomas had a predilection for the posterior mandible with none of the CGCGs involving the angle.CGCGs were multilocular(58.3%),with a mixed lytic sclerotic appearance(75%).Soft tissue component was present in 91%of CGCGs,which showed hyperenhancement(compared to surrounding muscles)in 50%of cases,while the remaining showed isoenhancement.Matrix mineralization was present in 83.3%of cases.Ameloblastomas presented as a unilocular(66.7%),lytic(60.6%)masses with solid components present in 81.8%of cases.However,the solid component showed isoenhancement in 63%.No matrix mineralization was present in 69.7%of cases.Quantitatively,the enhancement of soft tissue in CGCG was significantly higher than in ameloblastoma on histogram analysis(P<0.05),with a minimum enhancement of>49.05 HU in the tumour providing 100%sensitivity and 85%specificity in identifying a CGCG.CONCLUSION A multilocular,lytic sclerotic lesion with significant hyperenhancement in soft tissue,which spares the angle of the mandible and has matrix mineralization,should indicate prospective diagnosis of CGCG.

Molecular biomarkers of cell proliferation in ameloblastomas

Cell proliferation is a vital biological process that is important for all living organisms because of its role in growth and the maintenance of tissue homeostasis.The control of this important process differs greatly among benign and malignant neoplasms,and the evaluation of cell proliferation in neoplasms has become a common tool used by pathologists to provide useful information pertaining to diagnosis,clinical behavior,and treatment.The usefulness of information regarding cell proliferation has led to numerous studies on the value of these methods for diagnosing different types of tumors and for clinical decision making.Ameloblastomas are no exception.This review discusses the use of several classical molecular proliferation markers,including Ki-67,proliferating cell nuclear antigen,cyclin D1 and DNA topoisomeraseⅡalpha,to characterize ameloblastomas and proposes the use of new proliferation markers used previously to characterize other neoplasms.The use of these biomark-ers offers valuable opportunities to evaluate the biological behavior of this type of odontogenic tumor.

Characterization of tumors of jaw:Additive value of contrast enhancement and dual-energy computed tomography

BACKGROUND Currently,the differentiation of jaw tumors is mainly based on the lesion’s morphology rather than the enhancement characteristics,which are important in the differentiation of neoplasms across the body.There is a paucity of literature on the enhancement characteristics of jaw tumors.This is mainly because,even though computed tomography(CT)is used to evaluate these lesions,they are often imaged without intravenous contrast.This study hypothesised that the enhancement characteristics of the solid component of jaw tumors can aid in the differentiation of these lesions in addition to their morphology by dual-energy CT,therefore improving the ability to differentiate between various pathologies.AIM To evaluate the role of contrast enhancement and dual-energy quantitative parameters in CT in the differentiation of jaw tumors.METHODS Fifty-seven patients with jaw tumors underwent contrast-enhanced dual-energy CT.Morphological analysis of the tumor,including the enhancing solid component,was done,followed by quantitative analysis of iodine concentration(IC),water concentration(WC),HU,and normalized IC.The study population was divided into four subgroups based on histopathological analysis-central giant cell granuloma(CGCG),ameloblastoma,odontogenic keratocyst(OKC),and other jaw tumors.A one-way ANOVA test for parametric variables and the Kruskal-Wallis test for nonparametric variables were used.If significant differences were found,a series of independent t-tests or Mann-Whitney U tests were used.RESULTS Ameloblastoma was the most common pathology(n=20),followed by CGCG(n=11)and OKC.CGCG showed a higher mean concentration of all quantitative parameters than ameloblastomas(P<0.05).An IC threshold of 31.35×100μg/cm^(3) had the maximum sensitivity(81.8%)and specificity(65%).Between ameloblastomas and OKC,the former showed a higher mean concentration of all quantitative parameters(P<0.001),however when comparing unilocular ameloblastomas with OKCs,the latter showed significantly higher WC.Also,ameloblastoma had a higher IC and lower WC compared to“other jaw tumors”group.CONCLUSION Enhancement characteristics of solid components combined with dual-energy parameters offer a more precise way to differentiate between jaw tumors.

下颌骨巨大成釉细胞瘤

成釉细胞瘤是来源于牙源性上皮的良性肿瘤,但具有局部侵袭性,且少数有恶变可能,属于＂临界瘤＂范畴。巨大成釉细胞瘤目前临床上已罕见,现就我科收治的2例下颌骨巨大成釉细胞瘤报道如下。 1临床资料例1,患者男,47岁,因下颌渐进性增大15年伴生长迅速4年入院。患者于1995年发现颏部一核桃大小包块,曾于2003年就诊,因经济原因未行治疗,2006年起肿块生长迅速,并在颏部出现瘘管伴脓血溢出,于2010年1月再次就诊。查体：下颌体部可见一大小约20 cm×14 cm×12 cm椭圆形巨大肿块,颏部见瘘管伴脓性分泌物溢出,质硬,下颌牙列缺失（图1A）。

Recurrence and cancerization of ameloblastoma: multivariate analysis of 87 recurrent craniofacial ameloblastoma to assess risk factors associated with early recurrence and secondary ameloblastic carcinoma

Objective: The recurrence and progression of ameloblastoma are unpredictable. Therefore, we examined the influence of clinical factors on recurrence time and analyzed the clinical factors associated with early recurrence and cancerization. We then developed a staging system to predict early recurrence and cancerization. Methods: All of the primary craniofacial ameloblastoma patients treated in Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine were recorded. There were 87 recurrent cases used to create a staging system and tested in a Cox regression analysis for risk factors associated with early recurrence or cancerization following surgery. Results: There were 890 craniofacial ameloblastoma patients, and 72 cases had recurrence. There were also 15 cases with cancerous recurrence. The overall recurrence rate was 9.78%, and the cancer rate was 1.69%. The primary cases were classified into the following 3 stages based on clinicopathological features: stage I, the maximum tumor diameter <= 6 cm; stage II, the maximum diameter of tumor >6 cm or tumor invasion to the maxilla sinus/orbital floor/soft tissue; and stage III, tumor invasion of the skull base or metastasis into regional lymph nodes. When the method of surgery was controlled by partial correlation, the staging had significance with recurrence time (P=0.004). The Cox analysis showed the tumor stage was correlated with recurrence time (P=0.027) and cancerization time (P=0.002). However, the surgical method did not influence the recurrence time when adjusted for cofounding variables. Conclusions: Tumor larger than 6 cm and invasion to soft tissues or adjacent anatomical structures are associated with early recurrence. This staging system can be used to predict the risk factors of early recurrence and cancerization in ameloblastoma patients.

Current concepts in ameloblastoma-targeted therapies in B-raf proto-oncogene serine/threonine kinase V600E mutation: Systematic review

BACKGROUND Ameloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies.Different signaling pathways that participate in the progression of these tumors have been identified.B-raf proto-oncogene serine/threonine kinase(BRAF)is a protein involved in the behavior of ameloblastomas,and it is related to many cell mechanisms.BRAF gene mutations have been identified in ameloblastomas,of which the BRAF V600E(valine substituted by glutamic acid at amino acid 600)mutation has been the most common and can be present concomitantly with other mutations that may be involved in its behavior.Targeted therapies have been used as an alternative in the case of resistance or contraindications to conventional treatments.AIM To document the presence of BRAF V600E and additional mutations,their behavior,and targeted therapies in these tumors.METHODS An electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE,Cochrane,EMBASE,and SpringerLink using the terms“ameloblastomas”,“BRAF V600E”,“additional mutations”,and“targeted therapies”.Ameloblastomas were classified according to WHO guidelines.Inclusion criteria were articles in English,published not more than 10 years ago,and studies with laboratory works related to BRAF V600E.Articles were evaluated by two independent reviewers and retrieved for full-text evaluation.The EBLIP Critical Appraisal Checklist was used to evaluate the quality of the eligible studies.Descriptive statistical analysis was performed.RESULTS Two independent reviewers,with a substantial concordance indicated by a kappa coefficient of k=0.76,evaluated a total of 19 articles that were included in this study.The analysis registered 521 conventional ameloblastomas(AM),81 unicystic ameloblastomas(UA),13 ameloblastic carcinomas(AC),three metastatic ameloblastomas(MA),and six peripheral ameloblastomas(PA),of which the histopathological type,anatomic location,laboratory tests,expression of BRAF mutation,and additional mutations were registered.The BRAF V600E mutation was found in 297 AM(57%),63 UA(77.7%),3 AC(23%),1 MA(50%),and 5 PA(83.3%).Follicular type predominated with a total of 116 cases(40%),followed by plexiform type with 63 cases(22.1%).Furthermore,both types presented additional mutations,in which alterations in JAK3 P132T,SMARCB1,PIK3CA,CTNNB1,SMO,and BRAF G606E genes were found.Four case reports were found with targeted therapy to BRAF V600E.CONCLUSION The identification of BRAF V600E and additional mutations as an aid in targeted therapies has been a breakthrough in alternative treatments of ameloblastomas where surgical treatments are contraindicated.

BRAF inhibitor:a novel therapy for ameloblastoma in mandible

Ameloblastoma is a benign but locally aggressive odontogenic neoplasm that accounts for 10% of all tumors arising in the mandible and maxilla (1). Eighty percent of ameloblastomas arise in the mandible, and they are usually found in young adults. It frequently recurs if not adequately

EXPRESSION AND SIGNIFICANCE OF bcl-2 FAMILY IN AMELOBLASTONA

Objective： To study the expression of bcl-2 and bax in human ameloblastoma （AB）, and investigate the role of apoptosis in genesis and development of AB and the relation of apoptosis with the clinic biological characteristics of AB. Methods： BCL-2 and BAX proteins were detected in 75 cases of AB （primary AB 31 cases, recurrent AB 37 cases, malignant AB 7 cases） by S-P method. Oral normal mucosa （NOM） and Odontogenic kerotosyst （OKC） were used as controls. Bcl-2 and bax mRNA in 20 cases of AB, 12 cases of OKC were detected by in situ hybridization. Results： The positive ratio of BCL-2 protein was 88.0% （66/75） in AB, 74.3% （26/35） in OKC and 44.4% （4/9） in NOM, respectively （P〈0.001）. BCL-2 protein was expressed in peripheral cells and a few scattered stellate-shape cells in AB. The positive ratio of BAX protein was 74.7% （56/75）in AB, 65.7%（23/35）in OKC and 77.8%（7/9） in NOM, respectively （P〈0.001）. BAX protein was expressed in peripheral cells and stellate-shape cells with similar intensity. BCL-2 expression increased in recurrent and AB canceration（P〈0.01）, while for BAX expression, the positive ratio was higher in recurrent AB, but lower than that of malignant AB. A moderate negative correlation between BCL-2 and BAX protein was found （rk=-0.331, P〈0.001）. Conclusion： AB has much more apoptosis-inhibiting protein than apoptosis- accelarating protein. Apoptosis plays an important role in genesis, development of AB. The fashion and intensity of bcl-2 and bax expression were different in various tissues and in benign or malignant AB.

Desmoplastic Ameloblastoma —A Case Report

The desmoplastic ameloblastoma (DA) is a rare variant of the conventional ameloblastoma. It accounts for only 4% to 13% of all ameloblastomas. Desmoplastic ameloblastoma (DA) was included in the World Health Organization Classification of Head and Neck Tumors (WHO-2005) as a variant of ameloblastoma with specific clinical, imaging and histological features. The desmoplastic variant of ameloblastoma usually appears in the anterior and premolar regions as a mixed radiolucent and radiopaque lesion, sometimes resembling a benign fibro-osseous lesion [1]. Ameloblastoma is a locally aggressive tumor that may cause recurrence and in rare cases, malignant transformation with repeated postsurgical recurrences [2] [3]. In this paper we present a case of a 47-year-old female with swelling in the left upper jaw, bopsy of which turned out to be desmoplastic ameloblastoma.

Calretinin Expression in Unicystic Ameloblastoma and Odontogenic Cysts

Background: Unicystic ameloblastoma arises from similar tissues as the odontogenic cysts. It may also arise from the epithelial lining of these cysts. Furthermore, the epithelial lining of unicystic ameloblastoma is variable and may be almost completely nondescript, which may lead to diagnostic confusion with odontogenic cysts. Calretinin is a calcium-binding protein that has been suggested to be a specific immunohistochemical marker for ameloblastic tissues. The aim of this study was to investigate the usefulness of calretinin in the differentiating unicystic ameloblastoma from odontogenic keratocyst, dentigerous cyst and radicular cyst of the jaws. Materials and Methods: Formalin-fixed, paraffin embedded tissue blocks of 23 unicystic ameloblastomas, 6 odontogenic keratocysts, 8 dentigerous cysts and 10 radicular cysts were utilized. Five micrometer thick sections were made from the tissue blocks and mounted on silanized glass slides. Immunohistochemical staining was done using a 1:100 dilution of mouse monoclonal anti-calretinin primary antibodies (Abcam, SA;Clone 1F5H1) and incubating overnight at 4&deg;C. The staining reaction was visualised using diaminobenzidine substrate solution. Stained tissue sections were evaluated for the presence, distribution, and intensity of staining of the immunoreactive cells. Data analysis was done using SPSS version 23. Statistical tests employed were Chi square test and Kruskal-Wallis test. The level of significance was set at 95% (p-value Results: Calretinin expression was seen in 14 (60.9%) cases of unicystic ameloblastoma, 3 (50.0%) cases of odontogenic keratocyst and a lone (12.5%) case of dentigerous cyst. None of the 10 cases of radicular cyst showed positive expression of calretinin. Staining in unicystic ameloblastoma was mostly localized to the superficial layers, whereas in odontogenic keratocyst it involved all layers of the epithelial lining. There was significant association between lesion type and the immunohistochemical expression of calretinin (p = 0.003). There were also significant differences in calretinin immunoreactivity of unicystic ameloblastoma compared to dentigerous cyst and radicular cyst. Conclusion: The findings of this study suggest that calretinin expression could help differentiate unicystic ameloblastoma from dentigerous cyst and radicular cyst, but not from odontogenic keratocyst.

Maxillary Ameloblastoma, Epidemiological Aspects and Treatment at the Yalgado Ouedraogo University Hospital (Burkina Faso)

Purpose: To report any epidemiological, anatomo-clinical and therapeutic aspects of maxillary ameloblastoma at the Yalgado Ouedraogo University Hospital (CHU-YO). Materials and Method: This was a descriptive and retrospective study covering the period ranging from January 1, 2010 to December 31, 2016. All patients received in the stomatology department for maxillary ameloblastoma with histological confirmation were included in the study. Consultation registers were used as the basis for data collection. Results: In our study, 50 cases were reported, i.e. an incidence of 7.14 cases per year. The mean age was 30.16 years with a sex ratio of 0.56. Housewives were the most affected and the average time to consultation was 2.5 years. The site of the tumor was in the majority of cases the mandible 82%, with swelling as the main reason for consultation. X-rays showed a predominance of monogeodic images in 56% of the cases. Conservative surgery was performed in 56% of the cases. Conclusion: Ameloblastoma is common in our area, characterized by delayed consultation. Strengthening of the technical facilities and awareness campaigns for the populations for early consultation are required.

Soft Tissue Recurrence with a Mucocele of an Intraosseous Ameloblastoma

Ameloblastoma is an odontogenic tumor of high frequency and usually occurs as an intraosseous growth. Ameloblastomas frequently recur, sometimes undergoing malignant transformation. These tumors are usually characterized as being multilocular, of the follicular type histopathologically, and invading strongly at the border region of the tumor. More than 10% p53-positive tumor cells give a prognostic indication for a tendency to recur. A recurrent ameloblastoma usually occurs in the intraosseous region near the site of the original lesion. In very rare cases, a recurrent tumor proliferates distantly from the original site in the soft tissue only. We report a rare case of recurrent ameloblastoma in the buccal mucosa with a mucocele that originated from the small salivary glands after the extirpation of an intraosseous (mandibular) ameloblastoma. We also performed a p53 immunohistochemical study of this recurrent tumor.

Ki-67 immunohistochemical expression in mandibular ameloblastoma: A prognostic indicator for local recurrence

Objective: This study used Ki-67 to evaluate the proliferative activity of ameloblastoma in an attempt to provide a scientific basis for any differences in the biologic behaviour that exists between the different types of ameloblastoma and correlate the results with the recurrence rate. Study design: We assessed Ki-67 expression by immunohistochemistry in 32 cases of mandibular ameloblastoma. Formalin-fixed, paraffinembedded blocks were sectioned and used for Haematoxylin & Eosin (H&E) staining. H&E slides were used to re-evaluate the histological types of the ameloblastoma. Immunohistochemical analysis for Ki-67 with a labelled streptavidin-biotin-peroxidase complex technique was performed on tumour sections using Monoclonal Mouse Anti-Human Ki-67 Antigen (clones MIB1, code M7240, Dako Corporation). Lymph nodes (lymphoma) were used as positive control for Ki-67. Results: The specimens comprised 18 cases of Follicular ameloblastoma, 7 cases of Cystic ameloblastoma, 4 cases of plexiform ameloblastoma, and 3 cases of Acanthotic ameloblastoma. The results showed that cellular proliferative activity varied within the ameloblastoma types. There was no statistically significant difference in the Ki-67 Acanthotic, cystic and follicular types of ameloblastoma, while plexiform type showed statistically significantly higher levels than the other 3 types. The mean Ki-67 labelling index of plexiform ameloblastoma ranged from 13 to 30 with a mean of 19.75. The mean values of Ki-67 were statistically significantly higher in recurrent than?non-recurrent cases. Conclusion: The significant expression of Ki-67 could provide useful prognostic markers for proliferative activity and good prognostic indicators for recurrence rate of mandibular ameloblastoma.

Recurrent ameloblastoma in the anterior skull base: Report of 3 cases

Recurrent ameloblastoma is common following inadequate excision but rarely presents in the anterior skull base. We presented 3 patients with recurrent ameloblastoma in the anterior skull base including the frontotemporal fossa and the pterygomaxillary fossa that occurred following multiple enucleations, segmental mandibulectomy, or partial maxillectomy for ameloblastoma in the jaws. Attenborough approach was used in the exposure of the frontotemporal fossa. Attenborough plus Barbosa approach was used in the exposure of the pterygomaxillary fossa. The patients were treated by radical dissection. Microscopy confirmed that the histopathologic pattern of one case was fixed follicular and plexiform, two cases were follicular. All patients healed without serious complications. The local recurrences of the patients following the operations were found in 3 to 4 years. The present study showed that the tumors in the regions had a greater recurrence potential even when treated with radical dissection, and the original tumors were the high-risk follicular pattern.

Hybrid ameloblastoma in a nigerian: Report of a case and review of literature

Background: Hybrid Ameloblastoma is a rare type of ameloblastoma that is presently receiving attention in some quarters. Altogether, less than 30 cases have been reported in the scientific literature, thus calling for the need to report more cases in order to add to the body of knowledge on this lesion. This case report is aimed to add to the number of cases that are building up in the scientific literature. Materials and Methods: A 50-year-old female presented with a 3-year history of an anterior mandibular swelling extending from the body of the mandible on the right to the body of the mandible on the left. Orthopantomograph of the lesion revealed a mixed radiolucent and radiopaque lesion that extended from the distal region of the right mandibular second premolar to distal region of the left mandibular second molar. Segmental mandibulectomy with immediate replacement with reconstruction was undertaken. Results: Specimen which was subjected to histopathologic examination reported a diagnosis of Keratinizing Follicular Ameloblastoma and Desmoplastic Ameloblastoma with Osteoplasia, consistent with a diagnosis of Hybrid Ameloblastoma. There has been no sign of recurrence 7 months after a regular follow-up and the patient is planned for a long term follow-up. Conclusion: Besides histological details that combine both conventional ameloblastoma and desmoplastic ameloblastoma, the present case of hybrid ameloblastoma bears similar clinical features as well as treatment modalities to that of conventional solid multicystic ameloblastoma.

Prognostic and proliferative evaluation of ameloblastoma based on radiographic boundary

Ameloblastoma is a benign odontogenic tumor with an aggressive biological behavior,and the surgical treatment frequently results in failure for the postoperative recurrence.The aim of this article was to investigate whether the proliferative ability and prognosis of ameloblastoma could be evaluated by the radiographic boundary.The ameloblastoma cases treated by the conservative therapy in our hospital between 1981 and 2001 were divided into three groups based on the nature of the radiographic borders of the lesions.The biologic behavior was evaluated by Ki-67 antibody immunohistochemically.Comparisons of prognosis and Ki-67 expression were carried out by statistic methods.There were 24 cases of well-defined edge with sclerosis（group I）,41 cases of well-defined edge without sclerosis（group II） and 32 cases of ill-defined edge（group III）.The recurrent rates were 29.2% in group I,43.9% in group II and 62.5% in group III（P,0.05）.The cells in group III expressed the highest Ki-67 level（P,0.05）.The radiographic boundary could be used as one of indicators in evaluating the proliferative ability of ameloblastoma and the patient＇s prognosis,which was consistent with Ki-67 expression.

The sequential treatment of extensive mandibular ameloblastoma

Ameloblastoma is the most frequent odontogenic tumor of the jaw. If not treated, ameloblastoma can gain an enormous size and cause severe facial disfigurement and functional impairment. Here we report two patients afflicted with extensive mandibular ameloblastoma (sized in 23 cm × 18 cm × 17 cm and 15 cm × 12 cm × 10 cm, respectively). Both the patients received the same sequential treatment including radical tumor resection, simultaneous reconstruction with fibula free flap graft, vertical distraction osteogenesis on the fibula graft, placement of endosseous dental implants, and final pros-thodontic rehabilitation. It took about 15 months to finish the entire course of treatment. And after the four-year follow-up, neither soft tissue related, nor hard tissue related problems were observed. Satisfactory facial symmetry, chewing and speech functions of the patients were restored. So this sequential treatment for extensive mandibular ameloblastoma can obtain an excellent effect by the shortest time and the lowest economical cost. Furthermore, the series also can be used to reconstruct giant mandibular defects caused by different reasons.

Hybrid Ameloblastoma in the Anterior Man-dible

Ameloblastoma—a benign epithelial odontogenic tumor-histologically occurs in different patterns, the most common of which are plexiform and follicular. “Hybrid” ameloblastoma is a variant in which areas of follicular or plexiform pattern (generally called convention alameloblastoma) coexist with areas of pronounced stromal desmoplasia (desmoplastic ameloblastoma). They most often occur in the mandibular ramus. We present a case of “hybrid” lesion—desmoplastic and conventional ameloblastoma—in the anterior mandible, focusing on its’ imaging features.

Investigation of basement membrane proteins in a case of granular cell ameloblastoma

Granular cell ameloblastoma is a rare,benign neoplasm of the odontogenic epithelium.A case of massive granular cell ameloblastoma in a 44-year-old Thai female is reported.Histopathological features displayed a follicular type of ameloblastoma with an accumulation of granular cells residing within the tumor follicles.After treatment by partial mandibulectomy,the patient showed a good prognosis without recurrence in a 2-year follow-up.To characterize the granular cells in ameloblastoma,we examined the expression of basement membrane（BM） proteins,including collagen type IV,laminins 1 and 5 and fibronectin using immunohistochemistry.Except for the granular cells,the tumor cells demonstrated a similar expression of BM proteins compared to follicular and plexiform ameloblastomas in our previous study,whereas the granular cells showed strong positivity to laminins 1 and 5 and fibronectin.The increased fibronectin expression in granular cells suggests a possibility of age-related transformation of granular cells in ameloblastoma.

Recurrent ameloblastoma of the mandible: Surgical seeding or metastasis of malignant ameloblastoma?

The controversy of surgical seeding or metastasis of a recurrent ameloblastoma is discussed in this paper, where we present a case with a history of 28 years since primary diagnosis including several tumor removals and reconstructive events. 23 years after primary diagnosis, we removed a metastasis from the neck with similar histological features as the primary tumor and the following recurrences of the mandible. We argue that the removed tumor in the neck most possibly has its origin in surgical seeding of cells during earlier resection and reconstruction and not by common ways of metastasis. The seeding of tumor cells during tumor surgery and metastasis rate of malignant ameloblastoma is discussed and the literature in this area is reviewed in the paper.