This is a case report of a recurrent lesion diagnosed histologically as a unicystic ameloblastoma. The concomitant presence of a traumatic neuroma was observed within the wall of the recurrent lesion. The mode of development of the traumatic neuroma, and the reason for the recurrence were presented.
Ameloblastomas formed 1.1 percent of all oral pathology cases reported. The race, sex and age group distribution of 133 cases are shown. The peak age incidence (70.6 percent) was between 11-40 years. The mandible was involved 9 times more commonly than the maxilla. The anatomical sites of distribution, clinical and radiological features, histological variants and their correlation are discussed. Twenty two patients (15 percent) had ameloblastomas associated with a dentigerous cyst and/or unerupted teeth. Ameloblastomas with the above clinical features represented a much less aggressive form of neoplasm. The authors could not correlate histological variants of ameloblastoma with recurrence rates. The various treatment methods and the respective recurrence rates are outlined. Radiotherapy and marsupialization as treatment of ameloblastoma are not recommended. The indications for enucleation curettage, resection en bloc, segmental resection and hemimandibulectomy
are emphasized. Ameloblastomas involving the maxilla should be treated by complete removal en bloc with a margin of normal tissue. Since ameloblastoma has the capacity to recur after several years of apparent cure patients who have been treated for ameloblastoma must be followed up periodically during their life time. So far no case of ameloblastoma in this study has shown evidence
ofmetastasis.
This article consists of two selected case reports of a recently named odontogenic tumour, unicystic ameloblastoma. The clinical and radiographic findings of the two cases mimic that of odontogenic cysts but not dentigerous cysts as in most reported, cases. Histologically, either a normal or ameloblastomatous cyst lining is evident. Other features of ameloblastoma are present within the cyst wall or as luminal nodules within the cystic space. A review of the literature indicates that this is a non-aggressive tumour with a low recurrence rate.
A case is described of ameloblastoma of the mandible presenting with multiple recurrences and subsequent extension to the maxilla with resultant transformation into an aggressive (malignant?) epithelial odontogenic ghost cell tumour. The latter is a rare, biologically virulent entity that affects mainly males, exhibits a preference for the maxilla and is histologically characterized by atypical malignant odontogenic epithelium associated with areas of ghost cell formation and varying amounts of dentinoid.
A case is described of ameloblastoma of maxilla presenting with numerous calcified keratin pearls. The significance of cellular variation in relation to the behavioural potential of the ameloblastoma in general is briefly discussed.
Clinical, radiological and histological characteristics of the peripheral ameloblastoma are briefly outlined. A case found occurring in the palate and presenting with atypical histological features is reported. The differential diagnosis of this lesion, its treatment and histogenesis are discussed.
Two cases of either peripheral odontogenic fibroma (POF) (WHO type) or peripheral ameloblastoma are reported. Their immunohistochemical characteristics were investigated in an attempt to clarify their histogenesis. The results showed that the epithelial component of this neoplasm tended to retain its distinct odontogenic character and expressed a keratin profile different from that of the overlying oral epithelium from which both cases most probably originated. The connective tissue element of these tumors was vimentin-positive and S-100 protein negative, confirming their mesodermal nature but precluding the possibility of ectomesenchymal derivation. No reactivity for desmin was noted.
Granular cell ameloblastoma (GCA) is a well recognized variant of follicular ameloblastoma with extensive granular cell change. In contrast, plexiform granular cell odontogenic tumor (PGCOT) is a rare and recently described lesion characterized histologically by a monophasic plexiform pattern of granular cells. In this paper, two cases of an unusual granular cell odontogenic tumor exhibiting combined features of these two entities are described along with their immunohistochemical characteristics. The granular cells of both the GCA and PGCOT areas showed similar patterns of expression for keratin and S-100, which differed from those of typical ameloblastoma. No reactivity for desmin or vimentin was noted. The histomorphologic and immunohistochemical features of these hybrid tumors suggest that the granular cells present have a common origin, most probably the odontogenic epithelium.
Seventeen cases of desmoplastic ameloblastoma were examined immunohistochemically. Immunoperoxidase techniques were applied for detection of keratin, desmin, vimentin and S-100 protein expression in these tumors. The tumor epithelium of desmoplastic ameloblastoma exhibited weak, focal, inconstant keratin staining, weak, variable expression of S-100 protein, desmin immunoreactivity of mild to moderate intensity and vimentin non-reactivity. The pertinent literature on the immunohistochemistry of ameloblastomas is briefly reviewed.
Seventeen cases are reported of desmoplastic variant of ameloblastoma of the jaws observed during the years 1967-1991. There were 12 females and 5 males, and these consisted of 7 Chinese, 6 Malays, 2 Indians, 1 Sikh and 1 Kadazan. Their ages at diagnosis ranged from 21-60 years with a mean of 36.6 years. There were 10 mandibular and 7 maxillary tumours. Of these, 14 cases involved the anterior segment with extension to the premolar region in 5 cases. 60% of cases were radiologically suggestive of fibro-osseous lesions. The main mode of treatment was resection and 1 case presented with recurrence. The findings of this study were compared with those of previous reports.
Four cases of either combined occurrence of ameloblastoma and odontogenic keratocyst or a rare keratinising variant of ameloblastoma are presented. The cardinal histomorphologic characteristics are simultaneous occurrence of ameloblastomatous epithelial islands with central keratinisation and multiple keratinising cysts. Immunohistochemically the tumour elements were keratin positive and occasionally S-100 protein and desmin positive. Major differential diagnosis of these neoplasms are discussed.
A case of unicystic ameloblastoma which recurred after 15 years showing unusual histological features is reported. The prominent pseudo-glandular features present are described. This case highlights the importance of extensive histological examination for more characteristic features of ameloblastoma to reach a correct diagnosis.
Granular cell ameloblastomas are uncommon lesions accounting for about 3-5% of all histologic subtypes of ameloblastoma. The plexiform granular cell odontogenic tumour, on the other hand, is a newly described lesion characterised by a monophasic plexiform pattern of granular cells. This article reports a tumour found occurring in the left mandible of a 67-year-old Indian male which histologically showed features of both the aforementioned lesions.
Ameloblastoma is an aggressive odontogenic tumor, which arises from odontogenic epithelium. Ameloblastomas can present in several clinical and histomorphological patterns. The granular cell variant accounts for only 3.5% to 5% of ameloblastomas. We have presented two cases of granular cell ameloblastoma (GCA) occurring in a 44-year-old and 50-year-old man, respectively. Case No. 1 on incisional biopsy was diagnosed as unicystic ameloblastoma (UA), which later after excisional biopsy was finally diagnosed as GCA owing to the features observed in excisional biopsied tissue. Case No. 2 on incisional biopsy showed darker and lighter stained cells arranged in small follicular pattern, and anastomosing cords. Meticulous immunohistochemistry, histochemical examination and careful literature search helped us to diagnose it as GCA. We have made an attempt to elucidate the diagnosis of GCA especially in cases of GCA with unusual granular component.
The ameloblastoma is the most common and clinically significant odontogenic epithelial neoplasm known for its locally-invasive behaviour and high recurrence risk. Epithelial-to-mesenchymal transition (EMT) is a fundamental process whereby epithelial cells lose their epithelial characteristics and gain mesenchymal properties. EMT induction via transcription repression has been investigated in ameloblastoma. However, morphologically evident mesenchymal phenotypic transition remains ill-defined. To determine this, 24 unicystic (UA), 34 solid/multicystic (SA) and 18 recurrent ameloblastoma (RA) were immunohistochemically examined for three EMT-related mesenchymal markers, alpha smooth muscle actin (α-SMA), osteonectin and neuronal cadherin (N-cadherin). All three factors were heterogeneously detected in ameloblastoma samples (α-SMA, n=71/76, 93.4%; osteonectin, n=72/76, 94.7%; N-cadherin, n=24/76, 31.6%). In the tumoural parenchyma, immunoreactive cells were not morphologically distinct from their non-reactive cellular counterparts. Rather, α-SMA and osteonectin predominantly labelled the cytoplasm of central polyhedral > peripheral columnar/cuboidal tumour cells. N-cadherin demonstrated weak-to-moderate circumferential membranous staining in both neoplastic cell types and cytoplasmic expression in spindle-celled epithelium of desmoplastic amelobastoma. For all tumour subsets, α-SMA and osteonectin scored significantly higher in the stroma > parenchyma whilst α-SMA was overexpressed along the tumour invasive front > centre (p<0.05). Stromal N-cadherin scored higher in SA > UA and RA > UA (p<0.05). Other clinicopathological parameters showed no significant associations. Taken together, acquisition of mesenchymal traits without morphologically evident mesenchymal alteration suggests partial EMT in ameloblastoma. Stromal upregulation of these proteins in SA and RA implicates a role in local invasiveness.
Notch signaling has been implicated in cell fate decisions during odontogenesis and tumorigenesis of some odontogenic neoplasms; however, its role in solid/multicystic (SA), unicystic (UA), and recurrent (RA) ameloblastoma remains unclear. The aim of this study was to determine Notch receptor and ligand expressions in these subtypes and to speculate on their significance.
To determine the distribution patterns of bone resorption regulators, receptor activator of nuclear factor κ-B (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) in recurrent ameloblastoma (RAs) and to clarify their impact on the biologic behavior of these neoplasms.
This report details a case of mandibular peripheral ameloblastoma having a clear cell component. The latter consisted of ovoid cells with vacuolated or clear cytoplasm and vesicular or pyknotic nuclei that may be disposed as discrete clusters or show direct transition from typical acanthomatous areas. Comparison of this lesion with other odontogenic and nonodontogenic tumors that contain clear cells is discussed in the context of the differential diagnosis.
The term Unicystic Ameloblastoma (UA) refers to those cystic lesions that show clinical and radiological characteristics of an odontogenic cyst but on histological examination show a typical ameloblastomatous epithelium lining part of the cyst cavity, with or without luminal and/or mural tumor growth. Till date, lot of controversies exist among oral surgeons and oral pathologists regarding this entity. An attempt is being made here to discuss all the diagnostic dilemmas associated with UA.