[Intraoral radiographic studies of sialolithiasis of the submandibular gland. Illustration using a patient case report].
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To investigate membrane changes in development of the exocrine cells of the rat submandibular gland (SMG), biochemical and cytochemical studies of adenylate cyclase activity were performed on prenatal and postnatal glands. SMG rudiments and glands were studied from 15 days of gestation op to birth and 1, 2, 3, 4 and 24 weeks after birth. Glands were chemically assayed for adenylate cyclase activity using the procedures of Salomon and coworkers and cytochemically studied using a procedure which was verified biochemically. At 15-16 days of gestation basal adenylate cyclase activity was low and no staining could be observed. Adenylate cyclase activity rose six-fold from the 16th to the 18th day of gestation. Adenylate cyclase staining became evident along the surface of most of the cells of the rudiment at this time. Basal adenylate cyclase activity remained relatively constant from the 18th day of gestation up to 24 weeks of age. However, sequential changes were seen in the cytochemical localization, especially in relation to the apical plasma membrane of the developing secretory cells.
Immunohistochemical methods were used to study the effects of botulinum toxin A on the concentration of acetylcholinesterase in the submandibular gland of the rat. The toxin was injected into the glands of healthy adult female Wistar rats and immunohistochemistry performed on the excised organs. Morphometric measurements were also carried out to study changes of cell morphology after local applications of botulinum toxin A. Compared with untreated glands or glands injected with saline there was a decrease of acetylcholinesterase in the glands treated with botulinum toxin. As the cholinergic pathway of the autonomic nervous systems plays an important role in eliciting secretion from the salivary glands, inhibition of secretion by local application of botulinum toxin could be considered a therapeutic option for the treatment of various diseases affecting salivary gland function.
Sites of binding of eight different lectins (LTA, UEA I, WGA, SBA, DBA, CON A, PNA, RCA I) to cat submandibular gland were studied after exposure of tissue sections to sialidase, alpha-fucosidase, beta-galactosidase, alpha-mannosidase, beta-N-acetylglucosaminidase. All lectins were affected by enzymatic predigestion and the labeling of individual lectins was highly dependent upon the glycosidase used to pretreat the sections. Glycoconjugates of demilunar, acinar and ductal cells exhibited a different composition of terminal sequences. For example, fucose proved to form the disaccharide fucose-galactose in demilunar and acinar cells, whereas it was present with the sequence fucose-N-acetyl-D-glucosamine in striated duct cells. Sialic acid participated both to the terminal sequence sialic acid-galactose and sialic acid-N-acetyl-D-galactosamine either in demilunar or in ductal cells. Lectin labeling combined with glycosidase digestion was also helpful in verifying the influence of neighbouring oligosaccharides on the affinity of lectins for the respective sugars.
Basal cell adenoma is a well recognized histopathologic variant of monomorphic adenoma of salivary gland, but in recent years there have been occasional reports of malignant basal cell tumors of major salivary glands. We present a case report of one such basal cell adenocarcinoma arising in the submandibular gland and discuss the differential diagnosis and distinction from a basal cell adenoma. We also review the published literature on basal cell adenocarcinoma. This is the first case of basal cell adenocarcinoma to be studied in detail by both immunohistochemistry and electron microscopy. There has been debate in the past as to the cell of origin of salivary gland basal cell tumors and specifically as to whether myoepithelial differentiation occurs in these tumors. The immunohistochemical and ultrastructural features of this case provide evidence for a dual population of ductal and myoepithelial cells. A flow cytometric analysis of nuclear deoxyribonucleic acid content showed the presence of DNA aneuploidy within one tissue block.
Trypsin-like and chymotrypsin-like esteroprotease isozymes of the mouse submandibular gland were separated by isoelectric focusing. In normal female mice the following pI-isozyme activities were found; pI-4.6, -5.6 (shoulder), -5.8, -7.1, and -9.9, hydrolytic activities for benzoylarginine ethylester (BAEE) (trypsin-like enzymes), and pI-4.7 and -10.3 hydrolytic activities for acetyltyrosine ethylester (ATEE) (chymotrypsin-like enzymes). In mice with testicular feminization (Tfm mice), only pI4.6 hydrolytic activity for BAEE was found; no ATEE hydrolytic activity was detected. In normal female mice, both 5 alpha-dihydrotestosterone (5 alpha-DHT) and tri-iodo-L-thyronine (T3) significantly increased all these isozymes except the pI-4.6 hydrolytic activity for BAEE. In Tfm mice, T3 also increased all these isozymes except the pI-4.6 hydrolytic activity for BAEE, but 5 alpha-DHT had no effect on any enzymes. These results suggest that the pI-4.6 hydrolytic activity for BAEE is non-inducible by the two hormones. Androgen does not seem to be involved in the inductions of these esteroproteases by T3.
The vasoregulatory role of nitric oxide (NO) and angiotensin II type 1 (AT(1)) receptors in the circulation of the submandibular gland (SMG) of rats was studied. The glandular blood flow was determined by means of laser Doppler flowmetry and rubidium isotope technique. The data obtained by these two methods correlated well (r = 0.77; P < 0.01). The AT(1) receptor antagonist candesartan (0.5 mg kg(-1), i.v.) reduced the vascular resistance in the SMG by 37 % (P < 0.05). By contrast, the NO synthase blocker L-NAME (15 mg kg(-1), i.v.) significantly increased vascular resistance in the SMG both in candesartan-treated (P < 0.001) and non-treated (P < 0.001) animals. The increase in resistance was greater (P < 0.05) after previous blockade of AT(1) receptors. These findings suggest that the AT(1) receptors have an important role in the vasoregulation of the SMG in the rat. As a result of AT(1) blockade, NO-dependent tone of glandular vessels may be enhanced significantly.
The paper presents the merits and drawbacks of vascular pedicled flaps of thyroid and submandibular glands in the reconstructive surgery following partial laryngectomy (combined with the resection of tongue base if necessary), as well as the results of clinical, radiological, radionucleoloid++ and histological investigation carried out in 81 cases with various extend of neoplasm (T1-T4). The average observation period was 8.2 (min. 1, max. 14) years. The discussed flaps were satisfactorily elastic and rigid, allowed formation in monobloc even complex structures (for instance vocal cord, arytenoid eminence, lateral wall of the larynx) with the high healing rate (1 total and 2 partial losses only), with an insignificant degree of atrophy in the larynx and a considerably greater one in the tongue base (despite a very difficient cover with mucosa), as well as a small local recidive range (3/81 cases all coming from the tissue out of the flap). With the above data, the discussed flaps seem to be superior in many respects to the materials conventionally used in the reconstruction of the larynx. A subclinical form of hypothyreosis (reduced level of T3, T4 and TSH) was stated in 1 case only, whereas xerostomy was not observed in any. The detailed oncological and functional results obtained in the whole group of patients will be published in another paper.
We studied the distributions of laminin-5 and hemidesmosome components, HD1/plectin and BP230, in the submandibular glands of adult and developing mice. In adult mice, laminin-5 was expressed in the basement membranes of both the myoepithelial cells and excretory ducts. The former expression was predictable because laminin-5 is a ligand for hemidesmosomes, which appear in myoepithelial cells and stratified epithelium. However, the latter expression pattern suggested that the non-stratified epithelium of the excretory duct might also be associated with hemidesmosomes. During fetal development, laminin-5 was found in the basement membrane of developing ducts but not epithelial end buds in which future lobules are formed by epithelial branching. The expression of HD1/plectin but not BP230 was noted in the developing duct at early embryonic stages, indicating the presence of type II hemidesmosomes. Expression of BP230 appeared in the excretory duct epithelium at around the day of birth. At this stage, the typical hemidesmosome was observed in the duct epithelium. Our results suggest that laminin-5 is involved in duct development rather than epithelial branching. The results also suggest that the developing duct epithelium interacts with laminin-5 through the type II hemidesmosome, which later matures into a typical hemidesmosome upon the onset of expression of BP230.
The physicochemical property and immunohistochemical localization of progestin (P) and estrogen (E) receptors (PR and ER) were examined in the submandibular gland (SMG) of 5-8-week-old castrated rats. The localization of epidermal growth factor (EGF) was simultaneously examined in the same tissue. The tissue cytosols from male and female rats specifically bound 3H-promegestone (3H-R5020) and 3H-estradiol-17 beta with high affinity and low capacity; the values were within the range of those reported for other tissues. However, E-treatment suppressed the specific P-binding in the female, whereas it did not in the male. On the contrary, E-treatment did not at all suppress specific E-binding in both sexes. Monoclonal antibodies against PR and ER were mainly located in the epithelium of the excretory duct and granular convoluted tubule, but not in the acinus. The monoclonal antibodies were also located in the large polygonal cell with irregular cell border, probably macrophage in the tissue. The EGF-immunoreactivity was observed in the epithelium of the same tissue region as that in which the monoclonal antibodies were located. The present results clearly suggest that the rat SMG tissue contains specific PR and ER that are mainly located in the epithelium of the duct system where EGF-producing cells are also located. The possibility that P and E may influence EGF-production through their receptors in this tissue was discussed.
The effects of local intraarterial infusions of VIP, acetylcholine (ACh), substance P, isoprenaline and bradykinin on submandibular gland blood flow and salivary secretion were studied in cats. It was found that VIP (10(-14) to 10(-10) mol/min) caused an atropine resistant vasodilation but no salivary secretion. Several hundred fold higher doses of exogenous VIP had to be infused than the amounts of VIP seen in the venous outflow during maximal nerve stimulation at a similar vasodilatory response. ACh infusions (5 X 10(-12) to 5 X 10(-8) mol/min) caused both a muscarinic vasodilation and salivary secretion. ACh was about 100 times less potent than VIP as a vasodilating agent. Both ACh and VIP induced in high doses a vasodilatory response similar to that seen during parasympathetic nerve stimulation at 15 Hz. ACh by itself did in the present doses, however, only induce about 50-60% of the maximal secretory response. Combined infusions of ACh and VIP, had mostly an additive effect on vasodilation. The salivatory volume response to ACh was potentiated by VIP and to a smaller extent also by isoprenaline. This potentiating effect may be due to a direct effect on secretory elements as well as partly to the additional increase in blood flow. Bradykinin was about 1 000 times less potent than VIP as a vasodilating agent. Substance P (10(-9) mol/min) only caused a weak vasodilation. Since there is evidence that ACh and VIP coexist within the same neurons and are both released upon parasympathetic nervous activation, the present findings suggest that the secretory and vasodilatory responses may be caused by an interaction between these two agents.
This investigation was undertaken to clarify the oxygen uptake caused by adrenaline, noradrenaline and pilocarpine in rat submandibular gland. 1. Adrenaline (55 microM), noradrenaline (55 microM) and pilocarpine (10 microM) significantly stimulated the oxygen uptake. 2. When Na+ in Ringer solution was substituted by Li+ or choline, the stimulation by adrenaline, noradrenaline and pilocarpine was blocked. However, when Na+ (50%) was contained in the Li+ -Ringer solution, the response by these agents were observed. 3. When K+ in the Ringer solution was removed, the stimulation by adrenaline and noradrenaline was observed, but that by pilocarpine was not. 4. Adrenaline-, noradrenaline- and pilocarpine-induced oxygen uptake was not observed when Ca2+-deficient tissue was incubated in Ca2+-free Ringer solution. When the normal tissue was incubated in Ca2+-free Ringer solution, the stimulation by adrenaline and noradrenaline was observed, but that by pilocarpine was diminished. 5. The oxygen uptake of Ca2+-deficient tissue due to adrenaline and noradrenaline was recovered by the addition of 3 or 5 mM Ca2+ to the Ca2+-free Ringer solution, while the response of pilocarpine was recovered by the addition of 5 mM Ca2+. 6. The stimulation by adrenaline, noradrenaline and pilocarpine was considerably blocked by the addition of 2.5 or 5 mM La3+ to the Ringer solution. 7. The stimulation by adrenaline and noradrenaline was significantly blocked by the addition of 5 mM procaine. On the other hand, the stimulation by pilocarpine was blocked by 0.5 or 5 mM procaine. These results suggest that the increase in the oxygen uptake seen with adrenaline, noradrenaline and pilocarpine is dependent on the presence of Na+ and Ca2+.