Circumscribed salivary duct carcinoma of the palate: a non-threatening variant.
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Previously we have shown that nicotinamide prevents spontaneously occurring diabetes associated with insulitis in non-obese diabetic (NOD) mice. In this study we injected nicotinamide (0.5 mg/g) or saline (0.01 ml/g) into female NOD mice daily during a period between 4 and 16 weeks of age. At the end of the treatment, periductal and perivascular lymphocytic infiltration in submandibular glands was observed in 91% of saline-injected control mice and 36% of nicotinamide-injected mice (P less than 0.01). No significant difference was observed in the prevalence of anti-salivary duct antibodies or antinuclear antibodies between the nicotinamide group and the saline group. Nicotinamide may alter cell-mediated, but not humoral, immunity to salivary gland cells, resulting in the prevention of submandibulitis.
We present a 65-year-old man with an enlarged mass in the right parotid gland. A fine-needle aspiration cytology suspected Warthin's tumor. The ill-defined margin of the tumor in diagnostic imaging and unexpected clinical course of the occurrence of facial nerve paralysis suggested malignant neoplasm. The patient was treated with surgical resection of the primary site and neck following radiation therapy. Pathologic diagnosis was a salivary duct carcinoma. Difficulty in early diagnosis of this tumor may result in local extension, early metastasis to regional lymph nodes and distant sites, and death.
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Salivary flow rate and the concentrations of electrolytes in parotid saliva and arterial plasma from anaesthetized sodium-replete sheep were measured before, during and after ipsilateral intracaroitd infusion of acetylcholine at 10 nmol min-1 to ascertain whether anaesthesia altered the relation between salivary flow and sodium concentration. The potential difference (PD) between the lumen of the parotid duct and the vascular system was also measured. Concentrations of salivary sodium and phosphate were decreased and potassium concentration and total CO2 content were increased when rate of salivary flow was increased by acetylcholine infusion. Salivary chloride concentration was reduced in five experiments and increased in three experiments when flow rate was elevated. Thus the flow-composition relations of parotid saliva from anaesthetized sheep were essentially the same as those for saliva from conscious animals. The PD between the lumen of the parotid duct and blood at resting flow rates was 9.4 +/- 1.07 mV, lumen negative. At high flow rates, stimulated by acetylcholine infusion, the PD increased to 21.9 +/- 2.20 mV, lumen negative. This increase in PD of the duct epithelium appeared to depend on changes in the composition of saliva arriving at the site of potential measurement.
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An investigation was undertaken to study the distribution of enzymes associated with submandibular gland salivary calculi. Ten calculi were freeze-sectioned and incubated for acid and alkaline phosphatases and for lactate, succinate and maleate dehydrogenases. All calculi were partly covered by a 50-210 micrometers wide zone of organic material consisting of connective tissue and metaplastic squamous epithelium facing the mineralized calculus, or of a structureless substance attached to the mineralized calculus. The epithelium showed an intense staining reaction for acid phosphatase and lactate dehydrogenase and a moderate reaction for succinate dehydrogenase throughout all levels of the epithelium. The structureless peripheral zone exhibited a moderate activity of acid phosphatase and succinate dehydrogenase located to an area close to the mineralized matrix. Also alkaline phosphatase and lactate dehydrogenase were found in a special pattern in the structureless zone. Sodium fluoride and sodium vanadate added to the incubation medium inhibited acid phosphatase activity whereas cupric chloride only lowered the staining reaction. Enzyme activity was found only within the peripheral zone of organic material with one exception. The results suggest that the calcification process of salivary calculi is not a passive calcification of necrotic material or mucin but rather an active process promoted by enzymes in the surrounding organic substances.
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The duct cells of the mandibular glands of mice (and many other mammalian salivary glands) absorb NaCl from an isotonic, Na+-rich primary saliva, formed by the gland's secretory endpieces, utilising an amiloride-sensitive Na+ channel in the apical (luminal) domain of the plasma membranes. The present study focuses on the mechanisms whereby the apical membrane Na+ conductance is controlled so that the rate of Na+ influx from lumen to cytosol via the Na+ channels is matched to the rate of Na+ extrusion from cytosol to interstitium via the basolateral Na+-K+-ATPase (so called homocellular regulation or epithelial cross-talk). Our results show that the apical membrane Na+ conductance is not controlled by a sensor of extracellular (luminal) Na+, as has been previously believed, but by sensors of cytosolic Na+ and Cl- which down-regulate the Na+ channels when the cytosolic concentration of either ion increases. These effects of cytosolic Na+ and Cl- are mediated, respectively, by G proteins of the Gi and Go subclasses.
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