Globular hyaline masses in the stroma of ameloblastoma: histopathologic and histochemical study.

A microscopical study of 15 intraosseous ameloblastomas revealed the presence of globular hyaline masses in only one of them (6.6%). These masses were confined to the stroma of plexiform areas and especially in regions undergoing cystic degeneration. They were periodic acid-Schiff positive and showed an affinity for acid dyes such as phloxine, acid fuchsin, orange G and picric acid. Regarding their pathogenesis, they are probably formed from extravasation of plasma glycoproteins, condensing and taking up a spheroidal shape in the liquid micro-environment of stromal degeneration under the influence of capillary phenomena.

Granular cell lesions of the jaws and oral cavity: a clinicopathologic, immunohistochemical, and ultrastructural study.

A clinicopathological, immunohistochemical, and ultrastructural study of 44 oral granular cell lesions was performed. A total of 35 mucosal granular cell tumors, 4 granular cell ameloblastomas, 1 lichen planus with granular cell change, and 3 congenital epulides of the newborn were studied. Pseudoepitheliomatous hyperplasia was found to occur in only a minority of these cases. Immunohistochemically, the majority of granular cell lesions were uniformly positive for S-100 protein and focally positive for vimentin in one half of the cases, suggestive of origin from a Schwann cell or a precursor mesenchymal cell. Congenital epulis of the newborn and central odontogenic granular cell tumor were negative for S-100 protein, epithelial membrane antigen (EMA), and prekeratin, suggesting a mesenchymal origin for these lesions.

Immunoreactivity of granular cell lesions of skin, mucosa, and jaw.

Granular cell lesions from many different sites share similar light and electron microscopic features. Immunologically, however, these lesions do not appear to be a homogenous group. This study determines the extent of immunologic heterogeneity of granular cell lesions from a wide variety of sites in skin, mucosa, and jaw. Thirty-one granular cell lesions (26 granular cell tumors [GCT] and five other granular cell lesions) from 18 different sites were evaluated immunohistochemically for keratins, vimentin, desmin, muscle actin, ACT, HLA-DR, and S-100 protein. Paraffin-embedded sections were utilized with an avidin-biotin complex immunoperoxidase technique. Except for ameloblastomas, all lesions were negative for keratin and positive for vimentin. All lesions were negative for desmin and actin. Positive ACT reactivity was found in one of seven GCT of tongue, a colonic lesion, a nose lesion, and a granular cell ameloblastic fibroma. All lesions were positive for HLA-DR except a few in which fixation appeared inadequate. S-100 immunoreactivity was found in all lesions except the congenital epulis, a GCT of the skin of the nose, a colonic lesion, and the odontogenic tumors. The antigenic profile of GCT of skin and mucosa is consistent with Schwann cell origin. However, some GCT and other granular cell lesions appear to be derived from macrophages, epithelial cells, or other cells. The expression of HLA-DR by granular cells is believed to be unrelated to cellular origin but rather to some common immunologic function.

Patterns of expression of intermediate filaments in ameloblastoma and human fetal tooth germ.

Monoclonal antibodies (Mab) were used to study the expression of cytokeratins and vimentin in various histological types of ameloblastoma and in human fetal tooth germ. The ameloblastoma and the tooth germ epithelia showed characteristics of both simple glandular and stratified squamous epithelial cells. Cytokeratin No. 18 was detected focally in most ameloblastomas studied but not in fetal odontogenic epithelia. Cytokeratins Nos. 8 and 19 were expressed in all epithelial elements of ameloblastomas and tooth germs. Only two tumors showed focally characteristics of keratinizing epithelia also seen in dental lamina but not in the enamel organ. All tumors except the granular cell ameloblastoma showed a variable coexpression of vimentin and cytokeratins in their neoplastic epithelia. A similar coexpression was detected in the stellate reticulum cells of the developing tooth. Ameloblastoma and human tooth germ epithelia share complex pattern of cytokeratin polypeptides together with coexpression of vimentin. The results strongly support the theory that ameloblastomas are of odontogenic origin and not direct derivatives of basal cells of oral epithelium or epidermis.

The treatment of adamantinoma of the tibia by wide resection and allograft bone transplantation.

Since 1975, nine patients who had adamantinoma of the tibia were treated by the orthopaedic oncology service of the Massachusetts General Hospital and the Children's Hospital, Boston, Massachusetts. All patients were followed for two years or more or until a relapse occurred (mean length of follow-up, 5.3 years). Five of the patients were female and four were male; their ages ranged from fourteen to fifty-six years (mean, 19.1 years). The treatment consisted of staging, wide surgical resection of the tumor, and insertion of a segment of intercalary bone allograft (eight patients) or an osteoarticular segment (one patient). All grafts were fixed with compression plates and screws. All but two of the allografts had united at both the proximal and the distal host-donor junction site by twelve months. None of the patients had a local recurrence but pulmonary metastases developed in one. Four of the patients had complications that affected the final result. The functional results were excellent in five patients, good in one, fair in one, and a failure in two. Seven of the nine patients were asymptomatic and fully functional at the time of writing; only one needed a brace to walk. On the basis of this experience we recommend wide resection and implantation of an intercalary allograft in the treatment of adamantinoma of the tibia.

The relationship between the keratocyst antigen (KCA) and keratin.

The relationship of the keratocyst antigen (KCA), the soluble component present in most keratocyst fluids, and keratin, was studied with immunofluorescence microscopy comparing their distribution in developing mouse embryonic teeth and in human ameloblastomas. In these tissues both molecules showed a strong codistribution in epithelial cells. In the embryonic teeth both molecules were present in the stratum intermedium cells between the stellate reticulum cells and ameloblasts, but the secretory ends of the ameloblasts showed fluorescent staining only for keratin. The relationship was further investigated by comparing the physicochemical characteristics of KCA and keratin. Results on immunoblotting and two-dimensional gel electrophoresis showed that KCA existed in keratocyst fluid as a 60-68,000 dalton polypeptide with an isoelectric point of pI 6.8. Immunoblotting analysis of various isolated keratins revealed a typical polypeptide pattern of each keratin when anti-KCA antiserum was used for staining. These findings suggest that KCA and keratin are related molecules and that KCA may be a soluble component of keratin.

Adamantinoma of the tibia. An ultrastructural and immunohistochemical study.

The light microscopic, ultrastructural, and immunohistochemical characteristics of two tibial adamantinomas are presented. The immunohistochemical studies utilized specific antibodies against Factor VIII-related antigen and keratin protein, considered as markers for endothelial and epithelial cells, respectively. These revealed positive staining for keratin in the tumor cells of both cases, whereas Factor VIII was not found in either. Ultrastructurally, both tumors had tonofilaments, desmosomes, gap junctions, microvillous-like projections, and basement membranes. Patient 1 had disease that was histologically of the classic spindle cell type; the disease of Patient 2 was atypical and closely resembled an epithelioid angiosarcoma. Immunohistochemical and ultrastructural findings in each case indicate an epithelial component in tibial adamantinoma.

Glycosaminoglycans in fluid aspirates from odontogenic cysts.

Glycosaminoglycans and proteoglycans were analysed in keratinizing and nonkeratinizing odontogenic cyst fluids. Hyaluronic acid showed the highest incidence and abundance amongst the glycosaminoglycans detected. Appreciable amounts of chondroitin-4-sulphate were also observed, particularly in the dental cysts, with lesser amounts of the other glycosaminoglycans. Heparan sulphate showed a higher incidence and abundance in the keratocyst than the other cysts, whilst chondroitin-6-sulphate could not be detected in any of the cysts. A considerable proportion of the glycosaminoglycans of the fluids appeared to be complexed with protein and was released only after proteolytic digestion. The origin of these macromolecules is uncertain although it is likely that they are derived from both the connective tissue and the epithelium of the cyst wall.

Oral granular cell lesions. An immunohistochemical study with emphasis on intermediate-sized filaments proteins.

Six cases of oral granular cell lesions were studied with respect to intermediate-sized filaments (IF), peanut lectin binding (PNL) and muramidase activity by means of the peroxidase antiperoxidase technique. The tumours included three granular cell myoblastomas of the tongue (GCM) two cases of congenital gingival granular cell tumour (CGGT) and one granular cell ameloblastoma (GCA). Every tumour studied showed intracytoplasmic PNL binding whereas muramidase was negative in all cases. Vimentin expression was demonstrated in the CGGT and to a lesser extent in the GCM, but was absent in the GCA which was positive for keratin. Desmin and glial fibrillary acidic protein (GFAP) were not present in any of the lesions. These data demonstrate that PNL binding might be considered to be a common feature of granular cells regardless of their histogenesis. Lysosomes are supposed to represent the intracellular binding sites for this marker. Moreover it is shown that histomorphological identity between the granular cells of CGGT and GCA does not signify identity in histogenesis since the former are of mesenchymal derivation while the latter, from their intermediate filament protein types appear to originate from epithelium.

Adamantinoma of bone. An electron microscopic and immunohistochemical study.

Adamantinoma of bone is a rare tumor, and fine structural analysis has been done in only a few cases. We report four cases studied by electron microscopy and immunohistochemical methods. Ultrastructural evaluation revealed a characteristic constellation of features, including intracellular bundles of type I microfilaments, moderate numbers of evenly dispersed mitochondria, scattered profiles of rough endoplasmic reticulum, occasional Golgi bodies and lysosomes, and scattered glycogen particles. Microvillous processes and desmosomes were identified in all tumors. Well-formed basement membranes enveloped cell clusters but did not surround individual cells. Intercellular basement membrane-like material also was found focally in pools. Ultrastructural features of endothelial differentiation, including Weibel-Palade bodies, micropinocytotic vesicles, and tight junctions, were not identified. Immunoperoxidase stains for coagulation factor VIII (von Willebrand factor) and blood group antigens were negative, whereas similar stains for keratin were positive. Our findings strongly suggest that adamantinoma is a neoplasm expressing definite epithelial, rather than endothelial, characteristics.

Fibrinolytic activity in cystic lesions of jaw bones.

The fibrinolytic activity in the tissues of cystic lesions of jaw bones was investigated by the semiquantitative method of Astrup. The specimens examined were ameloblastoma (9 cases), follicular cyst (8 cases) and radicular cyst (14 cases). High fibrinolytic activity was observed in ameloblastoma, while in radicular cyst the activity was variable. It is suggested that in radicular cyst inflammatory episodes play an important role in activating local fibrinolysis, while in ameloblastoma the tissue itself has a great capacity to induce locally activated plasmin.