Journal of oral pathology最新文献

Fibrous histiocytomas of the oral and maxillofacial regions are rare. The present study analyzes a sample of 63 cases from the literature together with 7 personally observed cases. Age, sex, site, size, clinical behaviour, treatment and survival were evaluated and related to a histological classification based on that of Rosai (1981). Lesions were assessed for histological criteria which would place them in one of 2 groups: fibrous histiocytoma (FH) or pleomorphic fibrous histiocytoma (PFH). Within these 2 histological groups the cases were subdivided into clinically benign, aggressive or malignant lesions. Thirty-nine cases (56.0%) were classified as FH and 31 cases (44.0%) as PFH. The mean age of male patients with PFH was significantly higher than female patients with FH (t = 3.05; d.f. 37; p less than 0.0025). Lesions in the PFH group involved bone more frequently than those in the FH group (Yate's Chi2 = 16.66; d.f. 1; p less than 0.00025). Lesions involving bone for both histological groups were more likely to be aggressive or malignant than soft-tissue lesions (Yate's Chi2 = 29.9; d.f. 1; p less than 0.00025). Soft-tissue lesions were usually less than 5 cm in greatest diameter. Radiographic features of malignancy for lesions with bone involvement is of prognostic importance regardless of the histological appearance of the lesion. The majority of the lesions under study were from the deep tissues of the oral and maxillofacial regions.

Stimulation of cell-mediated immunity (CMI) by 2,4 dinitrochlorobenzene (DNCB) was reported to be effective in clinical regression of some carcinomas and precancerous lesions. This study investigated development of CMI in rat submaxillary salivary glands with dermal application of DNCB to provide a model for the study of immunotherapy in salivary gland neoplasia. Twenty rats received 0.02 ml of 0.5% DNCB in 4:1 acetone corn-oil applied with a glass rod to 3 cm2 of clipped ventral skin of the neck covering the submaxillary salivary gland on 2 successive days. Ten days later, the submaxillary glands were challenged with an injection of 0.02 ml of DNCB. Thirty-two h later the animals were killed and the glands examined grossly and microscopically. Thirty control animals were sensitized and challenged, (a) 10 with 0.5% DNCB, then vehicle only, (b) 10 with vehicle only, then 0.5% DNCB, and (c) 10 with vehicle both times. Gross examination of experimental and control glands disclosed moderate edema and congestion. Microscopically, experimental glands showed inflammatory changes including infiltration, vascular congestion and perivascular cuffing of lymphocytes. Regional lymph nodes showed proliferation of cortical germinal centers only. Control glands showed acute vascular congestion in group (a), and absence of microscopic features of delayed hypersensitivity.

The distribution of immunoglobulins and fibrinogen in normal and inflamed oral mucosa was examined by direct immunofluorescence using enzyme-treated sections of formalin-fixed, paraffin-embedded tissue. Plasma proteins were found inter- and intracellularly in the surface epithelium in most of the normal and all of the inflamed mucosal specimens. This diffusion of plasma proteins into the surface epithelium was shown to contribute to the appearance of edematous epithelial cells and eosinophilic bodies ("keratin pools"). The results clearly demonstrate that oral epithelium is not to be regarded as a covering membrane isolated from the underlying connective tissue. Furthermore, the study confirms that immunohistochemical studies can be performed on enzyme-pretreated sections of routinely fixed and embedded tissue although it is emphasized that the method is not of universal applicability.

The article deals with the use of glucocorticosteroids in the treatment of the oral manifestations of Systemic Lupus Erythematosus (SLE), Discoid Lupus Erythematosus (DLE), Rheumatoid Arthritis (RA) in the temporomandibular joint, Pemphigus Vulgaris, Pemphigoid, Erythema Multiforme Exudativum (EME), Lichen Planus (LP), and Recurrent Aphthous Ulcerations (RAU). The benefit from steroids is discussed on the basis of current knowledge of etiology and pathogenesis of the various disorders. All of them are characterized by inflammation which appears secondary to a hypersensitivity reaction against autocomponents. Glucocorticoids do not interfere with the primary disease mechanisms. But it is concluded from the literature, that because of anti-inflammatory and immunosuppressive effects of the hormones, it seems reasonable to profit from steroids as palliatives in acute phases of the diseases and/or as long-term suppressors of the general host defense.

Induced auto-allergic lesions in the submandibular glands of rats were studied by immunofluorescence. Direct staining with a goat anti-rat IgG conjugate was negative. Indirect immunofluorescence revealed a high incidence of anti-salivary-duct antibodies in sera from both control and experimental groups. In individual rats, no relationship was found between the presence or absence of serum anti-salivary antibodies and the presence or absence of salivary auto-allergic lesions. We conclude that the antibodies demonstrated do not play a role in the pathogenesis of the disease.

Parotid traumatization resulted in significant hyperamylasemia at 2 and 18 h, but resolved by 72 h after surgery. Traumatization of the exorbital lacrimal gland did not result in hyperamylasemia. Parotid duct ligation led to significantly increased amylase levels at 24 and 48 h, but resolved by 72 h.

The nature of the tumor cells in 5 cases of ameloblastomas was studied by immunohistochemistry, and the findings were compared with developing mouse and human teeth as well as with 5 cases of carcinomas in the oral region. The antigens investigated were keratin, an intracellular cytoskeletal protein typical of epithelial cells, and laminin, an extracellular matrix protein found in basement membranes. Our results show that keratin is expressed by all types of epithelial cells in ameloblastomas as well as in the epidermoid carcinomas, and developing teeth. The epithelial, keratin-positive tumor islands in the ameloblastomas were surrounded by a continuous line of laminin, in a pattern similar to that seen in developing tooth. Laminin was seen also around the epidermoid carcinomas but large areas devoid of laminin were constantly seen between the stroma and the neoplastic epithelium. This indicates a lack of proper basement membrane formation by the malignant epidermoid carcinomas. This may be due either to a diminished production or an increased degradation of basement membrane proteins by the carcinoma cells. Our results are in line with suggestions that ameloblastomas are derived from odontogenic epithelial cells. Immunostaining for keratin does not distinguish between carcinomas and the ameloblastomas. However, visualization of basement membrane proteins such as laminin can apparently be used in the differential diagnosis between ameloblastomas and carcinomas.

Apparent viscosities at different shear rates were measured for 3 types of saliva substitutes: (a) mucin-containing saliva; (b) substitutes based upon carboxymethylcellulose (CMC), and (c) solution of polyethylenoxide (PEO). The apparent viscosities were compared with those of human whole saliva. Human whole saliva and mucin-containing saliva substitutes appeared to be similar in their rheological properties. Both types of solution are viscoelastic solutions and adjust their apparent viscosities to their biological functions. Preparations containing CMC or PEO are non-Newtonian liquids. From this study it is concluded that mucin-containing saliva substitutes appear to be the best substitutes for natural saliva, as far as rheological properties are concerned.

The nature and location of intermediate filament proteins (IFP) may provide new insights into the origin and differentiation of neoplastic cells. An immunofluorescent study of these IFP in a case of a granular cell ameloblastoma revealed that all tumor cells contained the IFP keratin. Some granular cells, however, also contained the IFP vimentin, which is considered specific for mesenchymal tissues only. The implications of these observations are discussed. Study with monoclonal antibodies indicated the origin of the ameloblastoma from non-keratinized squamous epithelium. A comparison of the anti-keratin immunofluorescence pattern of the ameloblast-like cells in the present tumor with ameloblasts in the tooth germ revealed no similarities, indicating that despite some resemblance of the peripheral columnar cells to ameloblasts, these cells differ in other aspects.

Vitamin A deficiency (A-) is known to cause morphologic changes in tooth structures. However, its effects on glycosaminoglycan (GAG) distribution in dental pulp, and the role of retinoic acid (RA) in altering these effects are not clearly defined. Tissue changes induced by vitamin A deficiency and RA administration were evaluated histologically in incisors of rats fed on one of 3 different diets: a) vitamin A sufficient (A+); b) vitamin A deficient (A-); and c) vitamin A deficient supplemented with retinoic acid (A-/RA). Four weeks after the onset of vitamin A deficiency, all rats were killed and their 4 continuously erupting incisors evaluated histologically. A- rats had altered dentine and pulp with disrupted histodifferentiation of pulpal mesenchymal cells to normal odontoblasts. The frequency of these abnormalities in dentine and pulp was lower in A-/RA rats. The enamel organ was unremarkable in the 4-week deficient period. Using special stains, we noted that pulpal GAG accumulation in A- and A-/RA rats was limited to the lingual area, while in A+ rats, GAG were distributed throughout. These data suggest that vitamin A deficiency affects histodifferentiation of pulpal mesenchymal cells to odontoblasts, as well as GAG distribution in pulp. RA administration reduces the A- changes and therefore, appears to have some activity in dentinogenesis.