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.

Immunohistochemical localization of intermediate filament proteins in calcifying epithelial odontogenic tumors.

Three calcifying epithelial odontogenic tumors (CEOT) were examined immunohistochemically. The localization of intermediate filaments was characterized through the use of polyclonal anti-keratin antiserum (TK which detects 41-65 kd keratins), 2 monoclonal keratin antibodies (PKK1 specific for the 44, 46, 52 & 53 kd keratins and KL1, specific for the 55-57 kd keratins) and monoclonal antibodies for vimentin and desmin. The tumor epithelial cells were slightly positive or negative for PKK1 detectable keratins, but slightly to strongly positive for KL1 and TK antibodies. Tumor epithelium was slightly positive for vimentin but negative for desmin. The tumor foci were composed of both dark-staining and pale-staining cells; the former had a more intense reaction with KL1 and TK antibodies than the latter. Homogeneous acellular material was either PAS-positive or negative, with or without calcification, and keratin-negative.

Ameloblastic fibroma: growth potentiality of odontogenic epithelium and coexpression of intermediate filament proteins in fibromatous cells.

Four cases of ameloblastic fibroma are described immunohistochemically in terms of intermediate-sized proteins in both epithelial and mesodermal components. Keratin proteins were demonstrated by polyclonal anti-keratin antiserum (TK: detecting 41-65 kDa keratins) and 2 monoclonal antibodies to keratin (KL1: 55-57 kDa, PKK1: 44, 46, 52 and 54 kDa), and monoclonal antibodies to vimentin and desmin. Two types of odontogenic epithelial tumour cells were discriminated: undifferentiated odontogenic cells and common ameloblastoma cells. Keratin expression was found to be stronger in undifferentiated cells than in the ameloblastoma cells. Undifferentiated cells were PAS-positive, while ameloblastoma cells were negative. Fibroma cells were strongly positive for vimentin, and negative for desmin. Keratin proteins were also expressed slightly. Thus, coexpression of keratin and vimentin was seen in fibroma cells. Histogenesis is discussed from the standpoint of the distribution patterns of keratin and vimentin, as well as with respect to the histopathology.

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.

Soluble proteins in fluid from non-keratinizing jaw cysts in man.

Fluids from non-keratinizing cysts of the jaws contain the main proteins found in plasma. The low relative concentration of macromolecular non-immunoglobulin proteins shows that there is no free passage of plasma proteins into the cyst fluid. Sufficient evidence was found to conclude that the immunoglobulins in cyst fluid are partly produced locally and partly derived from plasma. Cyst fluid immunoglobulins have antibody activity to rabbit erythrocytes. Accumulation of cyst fluid is primarily due to inadequate lymphatic drainage of the cyst cavity. Differential diagnosis between various types of non-keratinizing cysts cannot be based on the plasma protein patterns of their fluids.

The calcifying epithelial odontogenic tumor. A review and analysis of 113 cases.

A review of the world literature has revealed 113 cases of the calcifying epithelial odontogenic tumor. The clinical, radiographic, and histopathologic features are analyzed. Various treatments that have been carried out are related to the frequency of recurrence. The theories of histogenesis are discussed and an attempt is made to explain the nature and origin of the amyloid-like substance.

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.

Amyloid-like material in odontogenic tumors.

Various types of odontogenic tumors (epithelial, mesodermal, and mixed tumors) were studied for the presence of amyloid material. Highman's Congo red and Wolman's standard toluidine blue methods were used for diagnosing amyloid. Of all types of odontogenic tumors studied, only the calcifying epithelial odontogenic tumors contained material that might be interpreted as amyloid-like.

Glycoproteins in fluid from non-keratinizing jaw cysts.

Fluid from 47 non-keratinizing jaw cysts and autologous serum were separated by electrophoresis on cellulose acetate membranes and stained for glycoproteins. All cyst fluids contained glycoproteins, but the separation patterns differed from those of serum. The major carbohydrate-bearing fractions of cyst fluid migrated with alpha2- and gamma-globulins, while in serum alpha2 and beta-glycoproteins contained most bound carbohydrates. The appearance of the gamma-globulin patterns indicated local synthesis and accumulation of cyst fluid gamma-globulins. The other glycoproteins most likely had escaped from plasma. Electrophoretograms of cyst fluid stained for glycosaminoglycans revealed that cystic glycoproteins often were complexed with glycosaminoglycans, causing more or less distorted separation patterns.