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PubMed1990

[Intramandibular inclusions of salivary gland tissue].

Salivary gland tissue inclusions in the mandible appear as well delimited radiolucency areas, asymptomatic, usually located in the mandibular angle and sometimes in the premolar canine and symphysis regions. The examination of 8,500 radiographs has demonstrated an incidence of one radiolucent area at the mandibular angle every 500 radiographs. Our result is slightly inferior to the mean reported in the literature. Seven cases were examined. Six of them have been treated surgically and histologically. At exploration a defect in the lingual cortical plate was found. The cavities were filled by salivary gland tissue. The contents of the cavities were attached via the lingual cortical defect to the near salivary gland. The cause of such radiolucency situated in the mandibular angle seems to be an altered resorption and apposition process of the bone triggered by a modification of the salivary glands elasticity; on the contrary, the salivary inclusions in the symphysis region is referred to as embryonic origin. In the literature different terms are used often in relation with a pathogenetical hypothesis; in this paper we suggest rather a description terminology such as intramandibular salivary tissue.

Adult↗
PubMed2004

Insect-malaria parasites interactions: the salivary gland.

Mosquito salivary glands are organs specialized in the production of a complex mix of molecules that digest carbohydrates from plant nectars, and facilitate blood feeding by the lubrication of mouthparts and the inhibition of homeostasis. Malaria sporozoites invade salivary glands and are injected with the saliva into vertebrate hosts during blood feeding. Sporozoites utilize molecules on their surface coat and outer pellicle membrane to adhere and invade specific regions of the salivary gland lobes. They transverse the secretory cells and are stored in the salivary duct, where transcription of new genes prepares them for vertebrate host invasion. Although it is probably that specific carbohydrate molecules on the surface of salivary glands function as parasites receptors, these have not been identified, neither other molecules nor mechanisms used by the parasite to invade, survive and mature within these organs. The recent advances in the sequence of the genomes of Anopheles gambiae and Plasmodium falciparum, and new developments in genomics and proteomics may help to elucidate the participating molecules, their regulation and interactions.

Aedes↗
PubMed2005

Fusion oncogenes and tumor type specificity--insights from salivary gland tumors.

Salivary gland tumors are frequently characterized by recurrent chromosome translocations, which have recently been shown to result in pathogenetically relevant fusion oncogenes. These genes encode novel fusion proteins as well as ectopically expressed normal or truncated proteins, and are found in both benign and malignant salivary gland tumors. The major targets of the translocations are DNA-binding transcription factors (PLAG1 and HMGA2) involved in growth factor signaling and cell cycle regulation, and coactivators of the Notch (MAML2) and cAMP (TORC1) signaling pathways. Identification of these fusion oncogenes has contributed to our knowledge of molecular pathways leading to epithelial tumors in general, and to salivary gland tumors in particular. Interestingly, the fusions in salivary gland tumors do not seem to be as tumor type specific as those in leukemias and sarcomas. Instead, they may function by activating basic transformation pathways that can function in multiple cell types. The downstream gene products of these fusions will be important targets for development of new intracellular therapeutic strategies.

Animals↗
PubMed1989

[Sialidase in rat salivary glands. Characteristics of soluble sialidase in salivary glands and other tissues].

In this study, we elucidated some characteristics of soluble sialidases in the rat salivary glands, brain, liver and kidney. 1) Soluble sialidases in the submandibular and parotid glands were inactivated by about 75 and 60%, respectively, and the enzymes in the brain, liver and kidney were also inactivated by 16-48%, when preincubated at 40 degrees C for 1h. When preincubated at 60 degrees C, the enzymes in all tissues were completely inactivated within 10 min. 2) Ca2+ ion in low concentrations tended to activate soluble sialidases in both the submandibular and parotid glands, but had no apparent effect on the enzymes in the brain, liver and kidney. The enzyme in the submandibular gland tended to be activated also by low concentrations of Mg2+. Both Cu2+ and Hg2+ ions caused a marked inhibition on the soluble sialidases in all tissues. 3) The molecular weight of soluble sialidases in the submandibular and parotid glands was determined to be about 68,000 and 46,000, respectively, by means of Sephadex G-200 gel filtration. The molecular weight of the enzymes in the brain and liver was almost similar to that of the enzyme in the parotid gland. In the kidney, soluble sialidase was separated into two enzymes, one having high (more than 500,000) and the other having low (about 46,000) molecular weight. 4) By isoelectric focusing analysis, three isozymes were detected in the submandibular gland and brain sialidases and two isozymes detected in the enzymes of other tissues. The isoelectric point of the major isozymes in the submandibular and parotid glands was 6.4 and 6.9 respectively. In the brain, liver and kidney sialidases, the isozymes with isoelectric point in the range of 4.4 to 6.7 were detected.

Animals↗
PubMed1979

Relationship between phosphatidylinositol synthesis and recovery of 5-hydroxytryptamine-responsive Ca2+ flux in blowfly salivary glands.

Each salivary gland contains about 135 pmol of phosphatidylinositol. In glands prelabelled by incubation for 1 h with [32P]Pi or [3H]inositol there was a subsequent breakdown of 80% of the labelled phosphatidylinositol over a 2 h incubation period with 10 micrometer-5-hydroxytryptamine. However, there was no detectable decrease either in total phosphatidylinositol based on phosphorus analysis by chemical estimation or in the radioactivity of [32P]phosphatidylinositol in salivary glands of flies raised from the larval stage on diets containing[32P]Pi and whose phospholipids were uniformly labelled. These results suggest that the pool of phosphatidylinositol involved with Ca2+ gating is a small fraction of the total phosphatidylinositol content. Furthermore it is this small compartment that is preferentially radioactively labelled during short-term incubations with radioactively labelled precursors. In salivary glands incubated for 2 h with 10 micrometer-5-hydroxytryptamine there was a marked decrease in the flux of 45Ca2+ across the gland. After removal of the hormone, incubation of salivary glands for 1 h in the presence of 2mM-inositol, but not choline or ethanolamine, resulted in a recovery of hormone-responsive 45Ca2+ flux. Quantitative studies revealed that less than 9 pmol of phosphatidylinositol must be formed to fully restoret he 5-hydroxytryptamine-responsive 45Ca2+ flux.

Biological Transport↗
PubMed1994

Analysis of Epstein-Barr virus-encoded small RNA 1 expression in benign lymphoepithelial salivary gland lesions.

Salivary gland enlargement resulting from benign lymphoepithelial lesions may be seen in patients with Sjögren's syndrome (SS) and in the early stages of human immunodeficiency virus (HIV) infection. Although the pathogenesis of these lesions is thought to differ in SS and HIV infection, Epstein-Barr virus (EBV) has been suggested as a pathogenetic agent in both cases. We have assessed the presence of latent EBV infection in a series of 15 lymphoepithelial salivary gland lesions using RNA-RNA in situ hybridization with digoxigenin-labeled riboprobes complementary to the abundantly-expressed EBV-encoded small RNA 1 (EBER1). Two of four benign lymphoepithelial lesions (BLEL) from patients seropositive for HIV expressed EBER1 in lymphocyte nuclei in a fashion similar to that described previously in HIV-associated persistent generalized lymphadenopathy (PGL). By contrast, EBER1 was not expressed in any of four BLEL from patients with SS, or seven lymphoepithelial cysts (LEC) and BLEL from patients with neither HIV infection nor SS. These data suggest that latent EBV infection does not play a major pathogenetic role in the lymphoepithelial salivary gland lesions associated with SS or those seen in patients without systemic disease. In the case of HIV-associated salivary gland lesions, the data are consistent with earlier proposals that these BLEL result from the involvement of intraparotid lymph nodes by PGL.

Adult↗
PubMed1984

A cytochemical study on the salivary gland pleomorphic adenoma (mixed tumor) and the fetal and adult salivary gland.

We studied the pleomorphic adenoma of the salivary gland ultrastructurally and cytochemically [Mg2+-activated adenosine triphosphatase (Mg2+-ATPase)], compared it with normal human fetal and adult salivary glands, and evaluated the histogenesis of this tumor. In the adult salivary gland, reaction products shows Mg2+-ATPase activity were localized in the plasma membranes of myoepithelial cells adjacent to the acinar cells or intercalated duct cells. However, in the salivary gland of the 16-week fetus, they were seen along all adjoining plasma membranes of the cells of terminal buds and duct-like structures. The present case of pleomorphic adenoma comprised two histological components: solid and myxomatous areas. Reaction products were seen along adjoining plasma membranes of both light and dark cells in solid areas.

Adenoma, Pleomorphic↗
PubMed1994

Myoepithelium of salivary glands.

In salivary glands and other exocrine organs, there are starfish-shaped cells that lie between the basal lamina and the acinar and ductal cells. These have structural features of both epithelium and smooth muscle cells, and so are called myoepithelial cells. Their functions include contraction when the gland is stimulated to secrete, compressing or reinforcing the underlying parenchymal cells, thus aiding in the expulsion of saliva and preventing damage to the other cells. They also may aid in the propagation of secretory and other stimuli. Their common developmental origin with the basal cells of the larger ducts is displayed in the mature glands by shared structural and immunohistochemical features, but most such basal cells do not have the distinguishing features of myoepithelial cells, such as myofibrils. Although myoepithelial cells can be identified by light microscopy through enzyme histochemistry and special stains and immunohistochemistry for their myofibrils, these techniques can be misleading in salivary gland neoplasms. Thus, the most reliable means of identifying neoplastic myoepithelial cells is with a combination of histochemistry and electron microscopy. The extent to which these cells are derived from undifferentiated stem cells in both normal and neoplastic growth is controversial. The presentation here of transmission electron microscopy (TEM) of well-differentiated myoepithelial cells in mitotic division indicates that stem cells are not necessarily the only source of myoepithelial cells in the later stages of salivary gland development or in neoplasia.

Animals↗
PubMed1996

A 2 week pair-fed study of early X-irradiation effects on rat major salivary gland function.

Salivary gland function is affected shortly after irradiation of the head and neck. An intense oral mucositis develops after exposure and may interfere with ingestion. The effects of restricted food and water intake on the secretory output of rat major salivary glands were examined. Parotid and submandibular salivary output and body weight were measured in rats at 4, 8, 11 and 14 days after 15 Gy X-irradiation of the head and neck. Comparisons were made with two groups: a non-irradiated group with food and water intake restricted to that of the irradiated group (pair-fed), and a non-irradiated, ad libitum-fed control group. Parotid saliva output was significantly decreased in the irradiated group at 4, 8, and 11 days compared with the control group. The pair-fed rats also had significantly decreased parotid output at these time points and their parotid function did not differ from that of the irradiated animals. At 14 days, all three groups demonstrated similar parotid function. Submandibular salivary output was not affected to the same extent. Only at a single time point (11 days) was flow significantly decreased in the irradiated group. Total body weight was less than that of control rats for both the irradiated and pair-fed animals at all time points. These results suggest that the early effects of radiation on salivary glands are due, in part, to limited intake of food and water during the immediate post-irradiation period.

Analysis of Variance↗
PubMed1993

Salivary gland tumors.

Salivary gland cancers continue to pose both diagnostic and treatment dilemmas. Over the past year, a great deal has been written concerning salivary gland tumors in children, fine needle aspiration for salivary gland neoplasms, prognostic factors, and pathologic evaluation and treatment. Some of the more important findings include imaging studies and approaches to the human immunodeficiency virus-positive patient with parotid enlargement, the molecular biology of salivary cancer, and the pitfalls of fine needle aspiration cytology. The necessity of facial nerve sacrifice in parotid surgery for malignancy is debated, and the classification of tumors is clarified.

Child↗
PubMed1997

Lupus erythematosus profundus around the salivary glands: a case resembling submandibular salivary gland disease.

In a 29 year old Japanese woman with SLE, a bilateral submandibular mass was detected. Computed tomographic (CT) scan suggested inflammatory changes around the submandibular glands. Histological findings of the deep skin biopsy showed typical changes of lupus erythematosus profundus (LEP). LEP should be considered in the differential diagnosis of an unexplained submandibular mass in a subject with SLE.

Adult↗
PubMed1984

Characterization of tick antigens inducing host immune resistance. I. Immunization of guinea pigs with Amblyomma americanum-derived salivary gland extracts and identification of an important salivary gland protein antigen with guinea pig anti-tick antibodies.

Guinea pigs immunized by subcutaneous injection of an emulsion of incomplete Freund's adjuvant (IFA) containing tick salivary gland extract antigens (SGA) from partially fed female ticks expressed a significant level of tick rejection when challenged 17 days later. This level of tick rejection was similar to animals actively sensitized by tick feeding and challenged at the same time. SGA emulsified with complete Freund's adjuvant (CFA) or administered with saline was ineffective. However, ticks that fed on animals immunized with SGA+IFA or SGA+CFA expressed significant reductions in engorgement weight. SGA was active when prepared with or without protease inhibitors. The minimum effective immunizing dose of SGA was between 100 and 280 micrograms per animal. Extracts made from salivary gland-derived cement material (CA) from partially fed female ticks administered at 50 micrograms in IFA induced levels of tick rejection comparable to animals immunized with 280 micrograms of SGA+IFA. Sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS/PAGE) of 35S- and 125I-radiolabeled SGA and CA extracts immunoprecipitated by guinea pig anti-tick serum that transferred immune resistance demonstrated a unique protein of 20,000 m.w. Serum from animals immunized with SGA+IFA (successful immunization) recognized this same protein, whereas serum from animals immunized with SGA+CFA (unsuccessful immunization) did not. The results of this study suggest that a 20,000 m.w. protein derived from the tick salivary gland may be responsible for the induction and perhaps elicitation of host immune resistance responses to Amblyomma americanum ticks.

Animals↗
PubMed1983

[The accessory salivary glands in Sjögren's syndrome. Histological and ultrastructural study. Correlations with sialographic changes in the principal glands].

139 salivary gland biopsies have been studied in patients with Sjögren's syndrome. Histologically, we classified labial salivary gland injuries (127 cases) in 3 groups based on striated duct distension: first, some tubular ectasia with few interstitial lymphoid cells; second, much ectasia associated with many lymphoid cells and early pericanalar sclerosis; third, intensive ectasia, scarce lymphocytes, severe peri and intralobular sclerosis and extensive destruction of acini. This grading is positively correlated with that of parotid biopsies and also with abnormalies on 60 parotid sialographic radiogramms performed simultaneously. Histoenzymological and ultrastructural studies demonstrate, at an early stage of the disease, epithelial and myoepithelial alterations in striated ducts, with tubular ectasia. Simultaneously, an intensive regeneration from intercalated ducts takes place. Nevertheless that regeneration fails to repair myoepithelial cells. Furthermore, young myoid cells, leaving tubular walls, migrate in interstitial tissue and are responsible for accumulation of membranoid material and later of collagen sclerosis.

Adult↗
PubMed1991

Modulation of T and B cell proliferative responses by factors present in rat salivary glands.

Rat salivary gland culture supernatants (SGSN) were shown to inhibit the proliferation of rat spleen cells induced by the mitogens concanavalin A (ConA), phytohaemagglutinin (PHA), pokeweed mitogen (PWM), lipopolysaccharide (LPS) and S. typhimurium mitogen (STM). The responses of B cells were more markedly inhibited than the responses of T cells. Factors contained in SGSN which had a molecular weight smaller than 3500 inhibited all responses, whereas factors greater than 3500 only inhibited responses induced by PWM, LPS or STM. Factors present in SGSN also inhibited the proliferation of two B cell hybridoma cell lines, as well as the IL-2-responsive cell line CTLL-2 and the IL-4-responsive cell line CT.4S. However, SGSN factors having a molecular weight greater than 3500 did not inhibit CTLL-2 proliferation. These data indicate that rat salivary glands contain factors which differentially regulate T and B cell proliferative responses in vitro and which may modulate localized immune responses in the salivary gland in vivo.

Animals↗
PubMed2001

[Myoepithelial differentiation markers in salivary gland neoplasia].

Salivary gland tumors frequently present myoepithelial cell differentiation that is not always easily identified on routinely stained sections. Recently novel markers of myoepithelium have been studied, such as calponin (CALP), caldesmon (CALD), and smooth muscle myosin heavy chain. These markers, together with smooth muscle actin may be useful tools for identifying myoepithelial cells. We immunohistochemically studied a series of 23 benign and malignant salivary gland tumors using antibodies to these four markers. The tumors were classified as follows: pleomorphic adenoma (n = 8), basal cell adenoma (n = 3), myoepithelioma with plasmacytoid cells (n = 2), epithelial-myoepithelial cell carcinoma (n = 6) and adenoid cystic carcinoma (n = 4). All tumors were positive for at least one of the four markers. CALP and smooth muscle actin were the markers more frequently expressed. Positivity was mostly located in the myoepithelial cells that constitute the external layer of the glandular or tubular neoplastic structures. In poorly differentiated epithelial myoepithelial carcinomas, composed of solid sheets of neoplastic cells and sometimes of clear cells, immunohistochemical staining for myoepithelial markers evidenced rudimentary glandular structures. CALP and smooth muscle actin were positive in the two cases of myoepithelioma with plasmacytoid cells. In conclusion, the combined staining with four markers helps to disclose myoepithelial cell differentiation and can be a useful tool for the correct histopathological diagnosis of salivary gland tumors. Among the four markers studied, CALP and smooth muscle actin were the most useful to identify myoepithelial cell differentiation.

Actins↗
PubMed1987

Systemic therapy of salivary gland hypofunction.

Salivary gland hypofunction occurs most often as a consequence of numerous drug therapies, anti-neoplastic treatments, or systemic disease. There are no universally accepted means of treating gland dysfunction and the resultant subjective xerostomia. A few studies have suggested that treatment of underlying inflammatory connective tissue disease will improve salivary performance in Sjögren's syndrome. Most of these reports, however, have either been limited to a small number of patients or have failed to include objective measures of salivary gland output. A larger body of literature deals with attempts using many different sialogogues to stimulate salivary function in a variety of conditions. Again, many studies have failed to document salivary improvement objectively. Recently, interest has focused on three drugs: bromhexine, anethole-trithione, and pilocarpine hydrochloride. Studies with these agents are reviewed, and current clinical investigations with pilocarpine are presented in detail.

Anethole Trithione↗
PubMed1996

Wegener's granulomatosis presenting as major salivary gland enlargement.

Salivary gland involvement is rare in Wegener's granulomatosis. We report the first case of widespread major salivary gland enlargement as part of the presentation of this disease. A review of the few reported cases in the literature suggests that salivary gland involvement may be associated with a limited form of the disease and an improved prognosis. The anti-neutrophil cytoplasmic antibody (c-ANCA) assay remains the gold standard of diagnosis but care should be exercised in the interpretation of results. This patient responded well to current immunosuppressive therapy.

Female↗
PubMed1996

Oncocytic adenocarcinoma of minor salivary gland. An unusual glossal presentation of a minor salivary gland tumor.

A case of an unusual oncocytic variant of minor salivary gland adenocarcinoma presenting in the base of the tongue in a 79 year old male with a remote history of regional radiotherapy is presented. The tumor had a striking morphologic similarity to the more common granular cell tumor, with which it could have been easily confused, leading to significant misdiagnosis. The light microscopic, cytologic, immunohistochemical and electron microscopic features are presented, with a discussion of the differentiating features of this lesion compared to other more common benign and malignant glossal tumors.

Adenocarcinoma↗