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Submandibular gland mucocele should be remembered in the differential diagnosis of swelling at the submandibular triangle. In the cystic lesion of the submandibular area, the biochemical analysis of aspirated material for amylase should be performed. The cases with submandibular gland mucocele should be treated by removing the lesion with both the submandibular and the sublingual glands.
Sympathectomy (Sx) of the submandibular gland was induced at various postnatal ages by ip administration of a single dose of reserpine or by unilateral excision of a superior cervical ganglion. If animals were 12 days old or less at the time of drug administration, [Ca] of the submandibular gland was not measurably increased 24 hr later; if rats were 14 days of age or older, [Ca] of the gland 24 hr after reserpine injection was nearly double that of untreated controls. Two days after surgical Sx, [Ca] of the denervated submandibular gland was unchanged from that of the innervated member of a pair if animals were less than 14 days of age at the time of denervation; [Ca] was twice that of glands of control rats if animals were older than 14 days of age when the denervation was performed. The anti-tumor agent, cyclocytidine (CC), given daily for 3 days in an ip dose of 500 mg/kg, also caused a two- to threefold increase in [Ca] of the submandibular gland when rats were more than 12 days of age at the time of the initial injection of the drug, but in rats younger than this age, CC caused no change in the [Ca] of the submandibular gland. Present data show that there are age-related differences in the ability of the submandibular gland to accumulate calcium following sympathetic denervation or treatment with a norepinephrine-releasing drug. These differences may be attributed either to incomplete development of calcium transport mechanisms, or incomplete development of the sympathetic innervation before 14 days of age.
Regeneration of submandibular gland (SMG) secretory parenchyma is remarkably impaired in salivary gland diseases and under experimental conditions such as in tissue culture and after isografting. In our study acinar regeneration was found to depend on the site where the SMG tissue was implanted. Implantation of several 2-3 mm3 fragments of SMG subcutaneously in the back of the same donor adult male rat resulted in initial necrosis and mononuclear cell infiltration of the autograft. Then there was epithelial proliferation with the appearance within 28 days of lobules which contained numerous duct-like structures and only a few or no acini. In contrast, implanting SMG fragments in the anatomical bed of the donor gland resulted in the appearance of a more differentiated autograft. Although the initial tissue changes were similar to those seen in the autografts in the subcutaneous tissues of the back, the SMG autograft in the neck also contained numerous acini by 42 and 56 days after implantation. These data support the view that the implantation site influences the course of cytodifferentiation in SMG autografts.
Rat submandibular gland (RSMG) cells have been immortalized with a retrovirus vector which encodes the adenovirus 12S E1A gene product. The immortalized cells were epithelial-like in nature and displayed a beta-adrenergic coupled rise in intracellular cAMP upon exposure to norepinephrine. Western- and lectin-blotting experiments of cell lysates demonstrated the presence of blood group A-reactive oligosaccharides. Such oligosaccharides are characteristic of RSMG mucin-glycoproteins. These cells appear to be suitable for use in analysis of cell-specific factors which regulate RSMG glycosylation.
Is the differential kinetics of secretion of saliva between the parotid and submandibular glands responsible for the relative difference in radiosensitivity? Radiation-induced dysfunction is more often noted in the parotid glands than the submandibular glands. This difference in susceptibility is often attributed to the difference in the cellular composition of these glands. During our studies using 99Tcm-pertechnetate to quantitate salivary gland function in patients treated with radioiodine, we noted frequent unstimulated discharge of saliva from the submandibular glands compared with parotid secretion. We hypothesize that the relative resistance of the submandibular glands could be due to the differential kinetics of the parotid and submandibular glands, as evidenced by using 99Tcm-pertechnetate to study their function.
In a rat submandibular rudiment on day 16, both laminin (LM) and type IV collagen (Col-IV) were found in all cases to colocalize not only in the basement membrane, but also in the rough endoplasmic reticulum of the epithelial cells, indicating that the synthesis of the components of basement membrane is greatly enhanced at this particular stage of extensive branch formation. Using the submandibular gland from a 16-day embryo, the model system was developed to determine the structural organization of the basement membrane. The pre-existing basement membrane was digested with collagenase and dispase, causing its complete disappearance. The subsequent gradual reconstruction of an authentic basement membrane was confirmed by electron microscopy and immunohistochemistry of LM and Col-IV. In the model system, this recovery started at 4 h of culture, and formation was complete by 8 h. During the recovery, thick bundles of actin filaments appeared transitionally in the basal cytoplasm. Electron microscopic analysis indicated two precursor structures, aggregated fuzzy fibers (type 1 extracellular matrix (ECM)) and 10-nm-thick strand piles (type 2 ECM), and an authentic basement membrane structure appeared during the course of membrane reconstruction. LM and Col-IV were always located together in these three structures. These observations clearly indicate that the precursors, containing LM, Col-IV and most likely heparan sulfate proteoglycan, appeared to form immediately following their secretion into the extracellular space, and assembled into the rigid structure of basement membrane within 8 h. The ultrastructural and immunohistochemical process of basement membrane reconstruction appeared to coincide closely with that of the glomerular basement membrane in developing kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
The submandibular glands of 4-week-old rats were dissociated by a procedure involving digestions with collagenase and hyaluronidase, chelation of divalent cations and mechanical force. A suspension of single cells was obtained in low yield by centrifugation in a Ficoll-containing medium. Immediately after dissociation and after a culture period of 16-18 hr the dissociated cells were tested for agglutinability by concanavalin A (Con A). Using ferritin (tfer)-conjugated Con A the lectin binding by the isolated acinar cells was also studied. The dissociated cells were agglutinated by low concentrations of Con A and bound Fer-Con A molecules on their entire surface without any indication of polarization of the cell membrane. There was a considerable cell to cell variation in the amount of Fer-Con A binding which was, in general, sparse and patchy. The contact surfaces between agglutinated cells revealed a dense binding of Fer-Con A molecules irrespective of the types of cells participating in the agglutination reaction. Cells cultured for 16-18 hr were no longer agglutinated by Con A. As compared to the freshly dissociated cells the cultured acinar cells revealed a more uniform and denser binding of Fer-Con A molecules. Furthermore, there were more lectin molecules bound to the cell surface corresponding to the basal part of the cell, where the nucleus and most of the rough surface endoplasmic reticulum were located, than to the apical cell surface. It is suggested that the higher density of lectin-binding sites on the cell surface in the vicinity of the cisternae of the rough endoplasmic reticulum indicates insertion sites of newly synthesized membrane glycoproteins.
Extracts of the submandibular gland (SMG) of rats contain fractions that stimulate the in vitro proliferation of Con A-treated lymphocytes. One of the stimulatory fractions was also shown to induce in vivo immunosuppression in rats and mice in several experimental models. Since many other biologically active factors of the SMG had been found to be hormone dependent, we investigated the effects on the immunosuppressive factor of hypophysectomy (Hx) and of hormonal reconstitution in male Fischer rats. Hx induced a marked atrophy of the SMG together with an almost complete disappearance of both the in vitro lymphocyte-stimulating activity and the in vivo immunosuppressive activity, the latter assayed with the contact sensitivity reaction in mice. The treatment of the Hx rats with pituitary hormones demonstrated that prolactin (PRL), thyroid stimulating hormone (TSH), and luteinizing hormone (LH) induced a significant reconstitution of these biological activities, growth hormone led to the recovery of the lymphocyte-stimulating activity but not of the immunosuppressive activity, while follicle-stimulating hormone, and adrenocorticotropic hormone did not induce any recovery of these biological activities. In view of the positive results obtained with TSH and LH further experiments were done to compare the effects of thyroid and sex hormones with those of PRL. The results demonstrated that testosterone and thyroid hormones induced significant recovery of the lymphocyte-stimulating and the immunosuppressive activity. The combination of these two hormones with PRL produced the most effective results. On the other hand, estrogens and progesterone had no significant effects. These results confirm the effectiveness of androgens and thyroid hormones in stimulating the production of biologically active factors by the SMG. Moreover, they demonstrate that PRL, a hormone not previously considered to increase the activity of the SMG, stimulates the production of immunoregulatory factors in Hx animals.
Crude extracts from submandibular glands of the rat, rabbit, guinea pig and macaque monkey contained high activities of branched-chain amino acid aminotransferase comparable to those from the heart and kidney. In each species, the isoelectric point and relative elution volume on Sephacryl of the aminotransferase from the submandibular gland had the same values as the heart enzyme. The enzyme of rat submandibular gland was partially purified; the properties of the purified enzyme suggest that it is the same type as that from the heart.
OBJECTIVE: It was aimed to analyze the biometric changes in ipsilateral submandibular glands of patients with unilateral chorda tympani (ChT) section during otological operations, compared with change in size of the contralateral glands and with those of healthy subjects. METHODS: 29 patients with unilateral complete ChT section and 29 healthy subjects with identical ages, genders, and weights to the patient group were examined ultrasonographically. The patients having a mean duration to follow-up examination of 32 months (2-84 months) were subdivided into two groups by their time to follow-up as short-term patient group (2-12 months, 14 patients) and long-term patient group (13-84 months, 15 patients). The ultrasonographic dimensions and volumes of submandibular glands were compared statistically between the groups. RESULTS: In the patient group, the glands on the contralateral, non-operated side were found to be greater than the ipsilateral, denervated glands in terms of both paramandibular depth dimension (P<0.05) and volume (P<0.01). The differences could be determined only in long-term patient group. When comparing the submandibular glands of the patient group with those of the control group, it was found that paramandibular depth dimension and volume of the submandibular glands on the contralateral, non-operated side were statistically greater (P<0.01). There was no difference between submandibular glands on the operated side of the patient group and those of the control group (P>0.05). CONCLUSION: The late (13-84 months) biometric results of ChT damage on submandibular gland were significant for increase in the size of the contralateral, non-denervated submandibular gland. An atrophying effect was not ascertained in the submandibular glands denervated parasympathetically due to the section of the ChT.
Histopathological studies were made on the submandibular glands, obtained from 207 autopsy cases of patients, ranging in age from 40-98 years who had not had collagen diseases. Focal lymphocytic infiltration of the submandibular glands was more frequently seen in the cases of patients over 70 years (80.3%) than in those of under 70 years (53.8%). Generally, the incidence of focal lymphocytic infiltration showed a trend to gradual increase with age. Immunohistochemically, a predominance of T cells (60-80%) was found in submandibular lesions with the majority (60-70%) belonging to the Leu 3a+ subset (Helper/Inducer) and with less than 20% belonging to the Leu 2a+ subset (Cytotoxic/Suppressor). The percentage of Leu 2a+ subset was found to increase in the lesion of the periacinar area, and the acinar parenchyma appeared gradually to be damaged by the infiltrating lymphocytes. The findings in the present study suggest that focal lymphocytic infiltration in submandibular glands is a focal sign of immunological disorder, based on the autoimmunity associated with aging.
Effects of experimental diabetes on rat submandibular glands have been documented, but earlier reports suggested that diabetes caused an extensive cellular degeneration and a replacement of the parenchymal cells by fibrous connective tissue. Such observations, however, are difficult to reconcile with the relatively normal physiological responsiveness of the gland (Anderson and Suleiman, 1989). This study, therefore, reexamined the histological, histochemical and ultrastructural effects of streptozotocin-induced diabetes on rat submandibular glands. The tissues were examined at 3 weeks, and 3 and 6 months after the induction of diabetes, and compared with glands from age-matched controls by both light and electron microscopy. Light microscopically, the proportional volumes of the acini and granular ducts remained constant in control rats at about 48% and 38% respectively. In diabetic animals the volume density of the acini increased progressively to 62%, whereas that of the granular ducts decreased to 20%. The diameter and number of granular ducts were reduced in diabetic animals, but acinar cell profile area was only affected 6 months after the induction of diabetes. Ultrastructurally, there was an accumulation of lipid in the acinar cells and, with increasing duration of diabetes, the number of autophagic structures in both the acini and the granular ducts increased. Although there was evidence of some cellular degeneration it was never excessive. Morphometry showed that the volume density of secretory granules within the acinar cells was unaffected, but there was a significant reduction in the volume density of secretory granules within the granular ducts. Thus, in the rat submandibular gland the greatest effect of streptozotocin-induced diabetes was to cause hypotrophic changes in the cells of the granular ducts. The relative contributions of a direct effect of insulin insufficiency and the hypogonadal effects of diabetes, however, are not known.
A case of simultaneous pleomorphic adenomas of the right parotid and ipsilateral submandibular glands was reported. The patient was a 68-year-old woman who had a ten-year history of an otherwise asymptomatic non-enlarging mass in the parotid gland and a slowly enlarging mass in the submandibular gland. Microscopically, the parotid tumor consisted of predominant spindle-shaped cell proliferations with myxoid stroma in places. The submandibular gland tumor showed tubular and trabecular formations with stroma consisting of hyalinized fibrous connective tissues. Simultaneous pleomorphic adenomas in the salivary glands are so rare that only 23 cases can be found in the literature. Additionally, only five tumors occurring simultaneously in the parotid and submandibular glands are reported in the literature. Our case seems to be the sixth of simultaneous pleomorphic adenomas of the parotid and submandibular glands.
Elafin, a bifunctional protein, has the NH(2)-terminal domain functions as a transglutaminase substrate for crosslinking to lysine-containing proteins and the COOH-terminal whey acidic protein domain as a potent anti-elastase. Human fetal submandibular glands (n=100) and adult submandibular glands (n=10) were used to elucidate the expression pattern of elafin in the developmental processes of human submandibular gland by immunohistochemistry, in situ hybridization, and western blot analysis. Elafin mRNA was expressed both in the gland epithelium and intralobular mesenchymal tissue of fetal submandibular gland in an early developmental stage (10-18 weeks) and an early intermediate developmental stage (EIDS; 19-24 weeks). The elafin antigen was also found in the intralobular mesenchyme of submandibular gland in the same stages. Thereafter, elafin was transitionally expressed in the ducts and acini of submandibular glands. In the late intermediate developmental stage (LIDS; 25-32 weeks) and the late developmental stage (LDS; 33-40 weeks), elafin became markedly positive in the excretory and striated ducts but weakly positive in the intralobular mesenchymal tissue. The elafin was heavily present in the excretory and striated ducts of adult submandibular gland, while it was sparse in the intralobular mesenchymal tissues. Western blot analysis showed the protein extracts from submandibular glands of EIDS, LIDS, and LDS, adult submandibular gland, fetal tissues (8 weeks), and adult parotid saliva migrated into multiple bands, about 25, 50, 65, and 140 kDa, which were higher than the putative size of elafin protein, 12 kDa. These data suggest that elafin, anti-elastase, is an essential component highly utilized during the morphogenetic processes of fetal salivary gland development and continuously plays a role for the protection of the tubuloalveolar structures of adult salivary gland.
The interaction of neurotransmitters and hormones with specific receptors on the plasma membranes of cells results in enzyme secretion from exocrine glands. However, the effects of agonists on the release of kallikrein and tonin from the rat submandibular gland have not yet been evaluated systematically. The purpose of the present study was to investigate the effects of norepinephrine, isoproterenol, methacholine, and cholecystokinin on the simultaneous release of kallikrein and tonin from the rat submandibular gland. Submandibular gland slices were incubated in vitro at 37 degrees C in a modified Krebs-Ringer medium containing 0.2% each of glucose and bovine serum albumin and bubbled with a gas mixture of 95% O2 and 5% CO2. Glandular kallikrein and tonin secreted into the incubation medium were determined by specific radioimmunoassays. Norepinephrine at 10(-5) M concentration increased kallikrein secretion from a control value of 7.7 +/- 1.5 to 114.7 +/- 26.9 ng/min/mg tissues (p less than .01), and at 10(-4) M concentration kallikrein secretion increased to 265.9 +/- 58.3 ng/min/mg tissue (p less than .01). Similarly, norepinephrine at 10(-5) M enhanced the release of tonin from a basal rate of 4.4 +/- 0.6 to 57 +/- 14.4 ng/min/mg tissue (p less than .05), and at 10(-4) M the rate increased to 91.3 +/- 20.0 ng/min/mg tissue (p less than .01). In contrast, isoproterenol, methacholine, and cholecystokinin did not increase the secretion of kallikrein or tonin. We conclude that the secretion of kallikrein and tonin from rat submandibular glands upon sympathetic stimulation is mediated through stimulation of alpha-adrenoceptors only.
PURPOSE: To evaluate the MR appearance of normal and pathologic states of the submandibular gland. METHODS: MR images of 22 healthy subjects and 21 patients with histopathologically confirmed disorders of the submandibular gland (five pleomorphic adenomas, two hemangiomas, two malignant lymphomas, one adenoid cystic carcinoma, one squamous cell carcinoma, and 10 cases of sialadenitis) were reviewed. RESULTS: All normal submandibular glands showed higher signal intensity than surrounding muscle but lower intensity than fat on T1-weighted and T2-weighted images. Postcontrast images showed moderate enhancement of the gland. All the tumors had lower signal intensity than the normal submandibular gland on T1-weighted images and had intermediate to high (n = 8) or high (n = 3) signal intensity relative to the normal submandibular gland on T2-weighted images. Six of seven benign tumors were well defined, and three of four malignant tumors were poorly defined. In all cases of sialadenitis, the submandibular gland showed diffusely different signal intensities from the normal gland on both T1-weighted and T2-weighted images. Eight cases of chronic sialadenitis showed lower T2-weighted signal intensities than the normal gland, and this can be explained histopathologically by marked fibrosis and cellular infiltration. CONCLUSIONS: MR imaging can show the presence, extent, margins, and signal intensity changes of pathologic conditions of the submandibular gland.
The submandibular gland of the white Wistar rats was examined. The animals were given Metizol for 21 days and 42 days at the dose of 1 mg/kg b.m./24 h. The submandibular gland samples were taken for histological and histochemical examination. Then they were stained with hematoxylin and eosine as well as by Masson's, PAS's and Feulgen's method. The mean area of section of cell nuclei was measured. The results of examination were counted statistically. The following changes were noticed: After 21 days of administration of Metizol in the submandibular gland the mean area of the tubules was increased. The quantity of tubules increased as well. In the tubules cells some more secretion was noticed. The follicles shrank. After 42 days of administration of Metizol the appearance, number and stainability of the tubules and follicles were similar to control group.
OBJECTIVE: To study the toxicity of lead poisoning to submandibular gland and its effects on nerve growth factor (NGF) gene expression in mice. METHODS: An experimental model with lead poisoning was established and its histopathological changes in the submandibular gland of mice were observed under light and electronic microscopes. Effects of lead poisoning on expression of NGF mRNA in submandibular gland were analyzed quantitatively by human NGF DNA probe labelled with digoxin with in situ hybridization. RESULTS: Body weight of the mice with experimental lead poisoning reduced, and their lead levels in blood and submandibular gland increased. Lobular atrophy, fibrous hypertrophy, angiectasis of the stroma and enlargement of lobule interstitial in mouse submandibular gland with lead poisoning could be found under light and electron microscopes. Their rough surfaced endoplasmic reticulum was extended and mitochondrion swollen. Graphic analysis showed that diameters of the secretory striate ducts and granular tubules decreased in the mice with lead poisoning. Results of in situ hybridization indicated that hybridized signals in the granular and secretory striate ducts and granular tubules reduced significantly, and NGF mRNA expression decreased. CONCLUSION: Lead is toxic to the submandibular gland of mice and can affect their NGF gene expression.