Odontogenic lesions in opercula of permanent molars delayed in eruption

Opercula of permanent first and second molars delayed in eruption were investigated histologically to detect possible causes of eruption failure. The material comprised operation specimens from exposure of 74 non-erupted molars in 63 young individuals (34 boys, 29 girls). Eighteen of the 74 specimens (or 24.3%) were diagnosed as "classical" odontogenic tumors belonging to the following entities: ameloblastic fibroma (seven), ameloblastic fibrodentinoma (six), ameloblastic fibro-odontoma (four) and complex odontoma (one). Twenty-two specimens (or 29.7%) showed a hitherto unrecognized odontogenic lesion of hamartomatous character, termed odontogenic giant cell fibromatosis (OGCF). Thus, 54.1% of the specimens could be diagnosed as odontogenic tumors or hamartomas. Histomorphologic changes could not be detected in the remaining 34 specimens (45.9%). Odontogenic tumors were associated with unerupted first molars much more frequently than with second molars (ratio 8:1). The OGCF had a strong association with unerupted mandibular molars. Further, opercula of mandibular first molars frequently revealed odontogenic lesions whereas tissue overlying the crown of unerupted maxillary second molars often was reported as normal operculum.     

Ameloblastic sarcoma of the mandible

Malignant ameloblastic odontogenic tumors have traditionally been classified as either ameloblastic fibrosarcomas, dentinosarcomas or odontosarcomas. This separation is based on the presence of either dentine or dentine and enamel in some lesions. To date, 28 cases of ameloblastic fibrosarcoma, one case of ameloblastic dentinosarcoma, and seven cases of ameloblastic odontosarcoma have been reported in the literature. An additional case of ameloblastic dentinosarcoma is reported in this paper together with a critical review of the clinicopathologic features of previously reported cases of malignant ameloblastic neoplasms. The presence of dental matrix material is not specific and is found in a wide variety of odontogenic tumors in variable amounts. This study supports the concept that the presence of dental matrix material does not alter the basic biologic characteristics of these neoplasms. Accordingly, to simplify a confusing nomenclature, we suggest that malignant tumors of this type be referred to collectively as ameloblastic sarcomas.     

Peripheral ameloblastic fibroma of the maxilla: report of a case and review of the literature

Peripheral odontogenic lesions are considered to be rare within the classification of odontogenic tumors. Also referred to as extraosseous or soft tissue odontogenic tumors, peripheral odontogenic tumors share the same histopathologic characteristics of their central or intraosseous counterparts. Ameloblastic fibroma is a rare odontogenic tumor that arises from both odontogenic epithelium and connective tissue. Only 2 cases of peripheral ameloblastic fibroma have been reported in the English-language literature, one of which did not show the classic features of an ameloblastic fibroma. In this report, we describe a rare case of a peripheral ameloblastic fibroma in the maxilla of a 3-year-old girl.     

Frequency of odontogenic cysts and tumors: a systematic review

A systematic review of the literature from 1993 to 2011 was undertaken examining frequency data of the most common odontogenic cysts and tumors. Seven inclusion criteria were met for the paper to be incorporated. In the preliminary search 5231 papers were identified, of these 26 papers met the inclusion criteria. There were 18 297 odontogenic cysts reported. Of these there were 9982 (54.6%) radicular cysts, 3772 (20.6%) dentigerous cysts and 2145 (11.7%) keratocystic odontogenic tumors. With the reclassification of keratocystic odontogenic tumor in 2005 as an odontogenic tumor, there were 8129 odontogenic tumors reported with 3001 (36.9%) ameloblastomas, 1163 (14.3%) keratocystic odontogenic tumors, 533 (6.5%) odontogenic myxomas, 337 (4.1%) adenomatoid odontogenic tumors and 127 (1.6%) ameloblastic fibromas. This systematic review found that odontogenic cysts are 2.25 times more frequent than odontogenic tumors. The most frequent odontogenic cyst and tumor were the radicular cyst and ameloblastoma respectively.     

Transformation of ameloblastic fibroma to fibrosarcoma.

The direct transformation of an ameloblastic fibroma into a fibrosarcoma in a 16-year-old Caucasian male is reported. Although no ameloblastic epithelium was found in the recurrent tumor, the odontogenic origin of the fibrosarcoma was evident. The ameloblastic fibrosarcoma and the fibrosarcoma of identical odontogenic origin represent an entity which should be distinguished from conventional fibrosarcoma as these tumors demonstrate different clinical behaviors.     

A review of 318 odontogenic tumors in Kaduna, Nigeria.

PURPOSE: To analyze 318 odontogenic tumors seen at a tertiary oral care center in Kaduna, Nigeria for comparison with findings in previous Nigerian and world records. MATERIALS AND METHODS: A retrospective survey of odontogenic tumors based on the classification of Kramer et al was undertaken at the Maxillofacial Unit, Ahmadu Bello University Teaching Hospital, Kaduna, Nigeria, from all histopathologically proven cases of tumors and tumor-like lesions of the oral and perioral structures. Data were retrieved from case notes, radiographs, histopathology results, and follow-up records. Information collected were used to complete a questionnaire and subjected to analysis. RESULTS: There were 990 tumor and tumor-like lesions of the oral and perioral structures, of which 318 were odontogenic tumors (32%). Twelve histopathologic types of odontogenic tumors were found with more benign (n=314; 99%) than malignant (n=4; 1%). Ameloblastoma made up 233 (73%) of the tumors, followed by odontogenic myxoma (n=38; 12%), ameloblastic fibroma (n=9; 3%), and the adenomatoid odontogenic tumor (2%). Three cases of calcifying odontogenic cyst were co-existent with ameloblastoma (2) and ameloblastic fibro-odontoma (1). Among 275 surgically treated odontogenic tumors, enucleation was performed in 64 cases (23%), dentoalveolar segment resection with preservation of lower border of the mandible (n=33; 12%), segmental resection (n=168; 61%), and composite resection (n=9; 3%); 1 case was deemed inoperable. At least 8 cases of ameloblastoma (13%) recurred out of 60 followed up. CONCLUSION: Ameloblastoma is a fairly common tumor of Nigerian Africans accounting for 73% of odontogenic tumors and 24% of all tumors and tumor-like lesions of the oral and perioral structures. Various forms of resection are practiced to eradicate the tumor in view of the late presentation in our environment. Patients in Nigeria do not often return for follow-up reviews. A minimum of 5 years of follow-up reviews are necessary after treatment of ameloblastoma.     

Immunohistochemical detection of phosphorylated Akt, PI3K, and PTEN in ameloblastic tumors

OBJECTIVE: To evaluate roles of the Akt signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated Akt (pAkt), PI3K, and PTEN was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: 11 tooth germs, 40 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with antibodies against pAkt, PI3K, and PTEN. RESULTS: Immunoreactivity for pAkt, PI3K, and PTEN was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and ameloblastic tumors. The levels of immunoreactivity for pAkt and PI3K were slightly higher in ameloblastic tumors than in tooth germs. Plexiform ameloblastomas showed significantly higher expression of PI3K than follicular ameloblastomas, and PI3K immunoreactivity in ameloblastomas without cellular variation was significantly higher than that in acanthomatous ameloblastomas. The level of PTEN immunoreactivity was significantly lower in ameloblastomas than in tooth germs. CONCLUSION: Expression of pAkt, PI3K, and PTEN in tooth germs and ameloblastic tumors suggests that these signaling molecules regulate cell survival and growth in normal and neoplastic odontogenic tissues by mediating growth factor signals. Increased expression of pAkt and PI3K and decreased expression of PTEN in ameloblastic tumors may participate in oncogenesis of odontogenic epithelium by activating the Akt signaling pathway.     

Immunohistochemical detection of insulin-like growth factors, platelet-derived growth factor, and their receptors in ameloblastic tumors

BACKGROUND: To evaluate the roles of growth factors in oncogenesis and cytodifferentiation of odontogenic tumors, expression of insulin-like growth factors (IGFs), platelet-derived growth factor (PDGF), and their receptors was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 47 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against IGF-I, IGF-II, IGF-I receptor (IGF-IR), PDGF A-chain, PDGF B-chain, PDGF alpha-receptor, and PDGF beta-receptor. RESULTS: Immunohistochemical reactivity for IGFs, PDGF chains, and their receptors was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and in benign and malignant ameloblastic tumors. The expression levels of IGF-II and PDGF chains were significantly higher in ameloblastic tumors than in tooth germs. Malignant ameloblastic tumors showed higher reactivity for PDGF chains than benign ameloblastomas and higher reactivity for platelet-derived growth factor receptors than tooth germs. The expression levels of PDGF chains were significantly higher in follicular ameloblastomas than in plexiform ameloblastomas. Desmoplastic ameloblastomas showed higher expression of IGFs and IGF-IR when compared with other ameloblastoma subtypes. CONCLUSION: Expression of IGFs, PDGF, and their receptors in tooth germs and ameloblastic tumors suggests that these growth factor signals contribute to cell proliferation or survival in both normal and neoplastic odontogenic tissues. Expression of these molecules in odontogenic tissues possibly affects interactions with the bone microenvironment during tooth development and intraosseous progression of ameloblastic tumors. Altered expression of the ligands and receptors in ameloblastic tumors may be involved in oncogenesis, malignant potential, and tumor cell differentiation.     

Hybrid odontogenic tumor of calcifying odontogenic cyst and ameloblastic fibroma

Odontogenic tumors composed of 2 distinct types of lesions are unusual. We report an odontogenic tumor that was composed of calcifying odontogenic cyst and ameloblastic fibroma that occurred in the right posterior maxilla of a 22-year-old Korean woman. The tumor had a cystic component with an ameloblastic epithelial lining and conglomerates of so-called ghost cells, and there were deposits of dentinoid material adjacent to the cyst. These are features characteristic of calcifying odontogenic cyst. Enamel organ-like epithelial islands were observed within a dental papilla-like stroma of the cyst wall. Additionally, a solid portion of the tumor had characteristic features of ameloblastic fibroma, i.e., a myxoid cellular stroma with numerous elongated islands of ameloblastic epithelium. Ghost cell masses were found in the area of ameloblastic fibroma as well. The distribution of the ghost cells suggests that this is a hybrid lesion rather than a collision tumor.     

Immunohistochemical detection and distribution of enamelysin (MMP-20) in human odontogenic tumors

Enamelysin is a tooth-specific protease that was initially isolated from porcine enamel organ and subsequently from human odontoblasts. Since this protease is thought to play important roles in tooth development, the evaluation of enamelysin in odontogenic tumors may aid our understanding of the histogenesis and cell differentiation of such lesions. A monoclonal antibody (203-1C7) was generated against synthesized human enamelysin oligopeptide and was used to assess the immunolocalization of enamelysin in healthy developing tooth germs and various types of odontogenic lesions. In tooth germs, enamelysin expression was detected only in the secretory enamel. Thus, 203-1C7 may serve as an enamel-specific marker in the late stage of enamel matrix development and calcification. In odontogenic lesions, strong enamelysin staining was demonstrated in the immature enamel matrix of ameloblastic fibro-odontomas and odontomas. Furthermore, enamelysin was also detected in globular amyloid masses and calcified foci in calcifying epithelial odontogenic tumors, hyaline droplets, small and large mineralized areas in adenomatoid odontogenic tumors, and a portion of ghost cells in calcifying odontogenic cysts. Positive reactivity was also observed in selected tumor cells in some of these tumors. No intracellular staining for enamelysin was detected in ameloblastomas or the ameloblastic portion of ameloblastic fibro-odontomas. Also, enamelysin was not detected in dentin, dysplastic dentinoid hyaline matrices, and cementum that were present within the tumors examined. Thus, taken together, our results suggest that the enamelysin-specific monoclonal antibody (203-1C7) may be utilized as a marker of early enamel development and that enamelysin may be involved in the pathogenesis of specific odontogenic tumors.     

Odontogenic tumors: a review of 319 cases in a Nigerian teaching hospital

OBJECTIVE: This study sought to determine the relative frequency of odontogenic tumors in a Nigerian population and to compare these data with previous reports. STUDY DESIGN: Records of patients seen at the Lagos University Teaching Hospital between January 1980 and December 2003, with histologic diagnosis of odontogenic tumors (based on World Health Organisation classification, 1992), were analyzed. RESULTS: Odontogenic tumors constituted 9.6% of all the biopsies of oral and jaw lesions seen within the period under study. Three hundred and eight (96.6%) were intraosseous, and 11 (3.4%) were peripheral (peripheral odontogenic fibroma=7; peripheral myxoma=3; peripheral ameloblastoma=1). The mean age of patients was 29.9+/-15.6 years (range, 4-85 years). Among these cases, 96.6% of the tumors were benign and 3.4% were malignant. Ameloblastoma with predilection for the mandible was the most frequent odontogenic tumor (63%), followed by adenomatoid odontogenic tumor (AOT) (7.5%), myxoma (6.5%), calcifying epithelial odontogenic cyst (5.3%), and odontogenic fibroma (5.3%). More cases of malignant odontogenic tumors were seen than cases of calcifying epithelial odontogenic tumor and odontomas. The mean ages of patients with AOT, ameloblastic fibroma, and odontoma were significantly lower than those with ameloblastoma ( P<.05). No significant difference was found between the mean ages of patients with benign odontogenic tumors and those with malignant odontogenic tumors ( P=.058). CONCLUSIONS: Odontogenic tumors, especially ameloblastoma, are not considered rare among Nigerians, whereas odontoma, regarded as the most frequent odontogenic tumor in North and South America, is rare.     

Relative frequency of peripheral odontogenic tumors: a study of 45 new cases and comparison with studies from the literature

BACKGROUND: Peripheral (extraosseous) odontogenic tumors are rare, and reports in the literature have mainly been single case reports or a small series of cases. The aim of this study was to determine the relative frequency of peripheral (extraosseous) odontogenic tumors relative to one another and relative to their central (intraosseous) counterparts in an oral pathology biopsy service and to compare these data with information available in the literature. METHODS: The files of the Pacific Oral and Maxillofacial Pathology Laboratory of the University of the Pacific, San Francisco, CA, USA, served as the source of material for this study. Files were systematically searched for all cases of peripheral odontogenic tumors (POTs) during a 20-year-period. RESULTS: There were 91,178 cases accessed in which central and POTs were identified in 1,133 (1.24%), central tumors in 1,088 (1.2%), and peripheral tumors in 45 (0.05%). Peripheral tumors accounted for 4% of all 1133 central and POTs. Peripheral odontogenic fibroma (PODF) was the most common of the 45 POTs accounting for 51.1% (23 cases) followed by peripheral ameloblastoma (PA) 28.9% (13 cases) and peripheral calcifying cystic odontogenic tumor (PCCOT) 13.3% (six cases). Peripheral calcifying epithelial odontogenic tumor, peripheral ameloblastic fibroma, and peripheral ameloblastic carcinoma were also identified--each comprised 2.2% (one case each). PODF was more common than its central counterpart by a 1.4:1 ratio. This was the only peripheral tumor that was more common than its central counterpart. PA accounted for 9.3% of all ameloblastomas and PCCOT for 26% of all calcifying cystic odontogenic tumors. CONCLUSION: There is only scarce information in the literature on the relative frequency of POTs. Additional studies should be conducted to determine the true relative frequency. To ensure accuracy, pathologists with experience in the field of odontogenic tumors should conduct these studies. Intraosseous tumors that perforate through the bone to the gingival tissue, clinically presenting as 'peripheral tumors' should be excluded.     

Immunohistochemical detection of phosphorylated JNK, p38 MAPK, and ERK5 in ameloblastic tumors

BACKGROUND: To evaluate roles of mitogen-activated protein kinases (MAPKs) in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated JNK (p-JNK), p38 MAPK (p-p38 MAPK), and ERK5 (p-ERK5) was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Ten tooth germs, 47 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the antibodies against p-JNK, p-p38 MAPK, and p-ERK5. RESULTS: Immunoreactivity for p-JNK was detected in epithelial or neoplastic cells detached from the basement membrane in 7 tooth germs and 7 ameloblastomas, and the expression levels of p-JNK in ameloblastic tumors were significantly lower than that in tooth germs. Expression of p-p38 MAPK was found in epithelial or neoplastic cells in tooth germs and ameloblastic tumors except for two ameloblastomas, and increased expression was found in keratinizing cells of acanthomatous ameloblastomas. The expression level of p-p38 MAPK in ameloblastomas was significantly higher than the levels in tooth germs and malignant ameloblastic tumors. Immunoreactivity for p-ERK5 was found predominantly in epithelial or neoplastic cells near the basement membrane in tooth germs and ameloblastic tumors. The expression levels of p-ERK5 in ameloblastic tumors were slightly higher than that in tooth germs, and plexiform ameloblastomas showed significantly higher p-ERK5 expression than follicular ameloblastomas. CONCLUSION: Expression of p-JNK, p-p38 MAPK, and p-ERK5 in tooth germs and ameloblastic tumors suggests that these MAPK signaling pathways contribute to cell proliferation, differentiation, or apoptosis in both normal and neoplastic odontogenic tissues. Altered expression of these phosphorylated MAPKs in ameloblastic tumors may be involved in oncogenesis and tumor cell differentiation.     

成釉细胞纤维牙瘤的临床特点及治疗

成釉细胞纤维牙瘤是一种少见的牙源性肿瘤,多发生于20岁以下,男性多于女性,上下颌骨均可发生,多发生于下颌骨,生长缓慢,无自觉症状,常表现为颌面部的肿胀、牙齿迟萌。X线片常见单房改变,表现为边界清楚的囊性透射影,不易与牙源性肿瘤鉴别。组织学表现,软组织成分为牙源性上皮和胚胎性的结缔组织,类似成釉细胞纤维瘤的形态,硬组织成分为牙本质、釉质样组织,类似牙瘤。恶变可能性低,治疗方式为手术摘除,一般不易复发。该文结合我科收治的成釉细胞纤维牙瘤病例,探讨成釉细胞纤维牙瘤的临床特点及治疗与预后。     

Relative frequency of central odontogenic tumors: a study of 1,088 cases from Northern California and comparison to studies from other parts of the world.

PURPOSE: To determine the relative frequency of central odontogenic tumors in relation to all biopsy specimens and to one another in an oral pathology biopsy service and to compare the data with previous studies from different parts of the world. METHODS: Files from the Pacific Oral Pathology Laboratory of the University of the Pacific, San Francisco, CA served as a source of material for this study. Files were systematically searched for all cases of central (intraosseous) odontogenic tumors during a 20-year period. RESULTS: Central odontogenic tumors were identified in 1,088 (1.2%) cases out of the 91,178 accessed. Individually, of all odontogenic tumors, 75.9% were odontomas. The prevalence of the remaining tumors appears to be a rare occurrence. The second most common was ameloblastoma (11.7%), followed by odontogenic myxoma (2.2%). Odontomas are considered hamartomas or developmental anomalies. When excluded from the list of individual odontogenic tumors, ameloblastoma is the most common (48.5%), followed by odontogenic myxoma (9.2%), adenomatoid odontogenic tumor (7.3%), ameloblastic fibro-odontoma (7.3%), ameloblastic fibroma (6.5%), calcifying odontogenic cyst (6.5%), and odontogenic fibroma (6.1%). Each remaining tumor comprises less than 4%. CONCLUSIONS: Studies related to the relative frequency of individual odontogenic tumors from different parts of the world are difficult to compare because most studies are outdated, the list of tumors is limited, and new entities are not included. To determine the real relative frequency, further studies should be conducted, especially in Western societies, by experienced pathologists in the field of odontogenic tumors.     

Ameloblastic fibro-odontoma: a case report

The clinical case of an unusual ameloblastic fibro-odontoma (AFO) was reported. The patient's clinical chart as well as preoperative and postoperative radiographs and histological findings of a 20-year old man that addressed Dental Clinic at University of L'Aquila were thoroughly reviewed. The patient showed a swelling in the oral cavity and radiographic feature of a radiolucent lesion at left second premolar maxillary site. Histologic examination made diagnosis of AFO. AFO is a rare mixed odontogenic tumor with similarities to the ameloblastic fibroma (AF) and ameloblastic dentinoma. The nature and the relationships between mixed odontogenic tumours and related lesions are still controversial. Moreover is not clear if these lesions are separate pathologies or if they are different development stages of the same pathology.     

Ameloblastie fibromas and related tumors in cattle

This article concerns rare odontogenic tumors that occur predominantly in the mandibular incisor region of young cattle and which have often in the past been referred to as ameloblastomas, or as the outdated synonym, adamantinoma. Twenty-two examples from the literature and two new ones were studied. Six consisted of epithelial islands which resembled those of ameloblastoma but which were located within a cellular fibrous connective tissue that was the second component of the tumor these mixed odontogenic tumors therefore represented ameloblastic fibromas, not ameloblastomas. Eight consisted of a combination of ameloblastic fibroma and odontoma and therefore were ameloblastic fibro-odon-lomas, and one was apparently malignant (ameloblastic fibro-odontosarcoma). Excluding this last lesion, these tumors should respond well to enucleation, like their human counterparts but to confirm this hypothesis, the margins of future examples should be carefully examined to determine that they are well-demarcated, not invasive. The microscopic features of the remaining 9 tumours could not be evaluated adequately, while another 17 tumors in cattle and water buffalo reported briefly could not be studied to any extent because of insufficient information.     

Immunohistochemical detection of platelet-derived endothelial cell growth factor/thymidine phosphorylase and angiopoietins in ameloblastic tumors

BACKGROUND: To evaluate the roles of angiogenic factors in the development and progression of odontogenic tumors, expression of platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) and of angiopoietins in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 11 tooth germs, 44 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against PD-ECGF/TP and angiopoietin-1 and -2. RESULTS: Immunohistochemical reactivity for PD-ECGF/TP was detected in mesenchymal cells in tooth germs and stromal cells in ameloblastic tumors, and the level of immunoreactivity for PD-ECGF/TP was significantly higher in ameloblastomas than in tooth germs. Granular cell ameloblastomas showed PD-ECGF/TP reactivity in granular neoplastic cells as well as in stromal cells. Immunoreactivity for angiopoietin-1 and -2 was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and in benign and malignant ameloblastic tumors. Malignant ameloblastic tumors had decreased angiopoietin-1 reactivity and ameloblastic carcinomas had increased angiopoietin-2 reactivity as compared with the respective levels in tooth germs and ameloblastomas. Immunohistochemical reactivity for angiopoietin-2 was slightly higher in follicular ameloblastomas than in plexiform ameloblastomas. CONCLUSION: Expression of PD-ECGF/TP and angiopoietin-1 and -2 in tooth germs and ameloblastic tumors suggests that these angiogenic factors participate in tooth development and odontogenic tumor progression by regulating angiogenesis. Altered expression of PD-ECGF/TP and angiopoietins in ameloblastic tumors may be involved in oncogenesis, malignant potential, and tumor cell differentiation.     

Immunohistochemical detection of uPA, uPAR, PAI-1, and maspin in ameloblastic tumors

BACKGROUND: To evaluate the roles of extracellular matrix (ECM)-degrading serine proteinase in progression of odontogenic tumors, expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1), and maspin was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 45 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against uPA, uPAR, PAI-1, and maspin. RESULTS: Immunohistochemical reactivity for uPA, uPAR, PAI-1, and maspin was detected in normal and neoplastic odontogenic tissues: uPA was recognized predominantly in mesenchymal cells, uPAR was evident in epithelial cells, PAI-1 was found in both epithelial and mesenchymal cells, and maspin was expressed only in epithelial cells. The levels of uPA and uPAR immunoreactivity in ameloblastic tumors were slightly higher than the levels in tooth germs, while PAI-1 reactivity in ameloblastomas tended to be lower than that in tooth germs. The level of maspin immunoreactivity in ameloblastomas was significantly higher than that in tooth germs, and ameloblastic carcinoma showed decreased maspin reactivity. CONCLUSION: Expression of uPA, uPAR, PAI-1, and maspin in tooth germs and ameloblastic tumors suggests that interactions among these molecules contribute to ECM degradation and cell migration during tooth development and tumor progression. Altered expression of the serine proteinase and its associated molecules in ameloblastic tumors may be involved in oncogenesis of odontogenic epithelium.