Submandibular gland resection and bilateral parotid duct ligation as a management for chronic drooling in cerebral palsy

The control of chronic drooling in cerebral palsy has been difficult in the past. Previous methods to control drooling include the Wilkie procedure, which diverts the salivary flow from the parotid glands by means of surgically created tunnels to the tonsillar fossa, along with submandibular gland resection. An alternative is submandibular gland resection with bilateral parotid duct ligation. Previous published studies using this method have resulted in good to excellent results, but population sizes were felt to be too small to be conclusive. Since 1979, a total of 58 patients have been treated by parotid duct ligation with submandibular gland resection, and 86 percent have shown good to excellent results. These results compare favorably with those published by Wilkie. Also, parotid duct ligation is technically easier, associated with less postoperative morbidity, and has shown a decreased duration of hospitalization compared to parotid duct transposition.     

Effects of double ligation of Stensen's duct on the rabbit parotid gland

Salivary gland duct ligation is an alternative to gland excision for treating sialorrhea or reducing salivary gland size prior to tumor excision. Duct ligation also is used as an approach to study salivary gland aging, regeneration, radiotherapy, sialolithiasis and sialadenitis. Reports conflict about the contribution of each salivary cell population to gland size reduction after ductal ligation. Certain cell populations, especially acini, reportedly undergo atrophy, apoptosis and proliferation during reduction of gland size. Acini also have been reported to de-differentiate into ducts. These contradictory results have been attributed to different animal or salivary gland models, or to methods of ligation. We report here a bilateral double ligature technique for rabbit parotid glands with histologic observations at 1, 7, 14, 30, 60 days after ligation. A large battery of special stains and immunohistochemical procedures was employed to define the cell populations. Four stages with overlapping features were observed that led to progressive shutdown of gland activities: 1) marked atrophy of the acinar cells occurred by 14 days, 2) response to and removal of the secretory material trapped in the acinar and ductal lumens mainly between 30 and 60 days, 3) reduction in the number of parenchymal (mostly acinar) cells by apoptosis that occurred mainly between 14–30 days, and 4) maintenance of steady-state at 60 days with a low rate of fluid, protein, and glycoprotein secretion, which greatly decreased the number of leukocytes engaged in the removal of the luminal contents. The main post- ligation characteristics were dilation of ductal and acinar lumens, massive transient infiltration of mostly heterophils (rabbit polymorphonuclear leukocytes), acinar atrophy, and apoptosis of both acinar and ductal cells. Proliferation was uncommon except in the larger ducts. By 30 days, the distribution of myoepithelial cells had spread from exclusively investing the intercalated ducts pre-ligation to surrounding a majority of the residual duct-like structures, many of which clearly were atrophic acini. Thus, both atrophy and apoptosis made major contributions to the post-ligation reduction in gland size. Structures also occurred with both ductal and acinar markers that suggested acini differentiating into ducts. Overall, the reaction to duct ligation proceeded at a considerably slower pace in the rabbit parotid glands than has been reported for the salivary glands of the rat.     

Cysts, masses, and tumors of the accessory parotid gland.

An accessory parotid gland occurs in approximately 21 percent of human subjects. It is located anterior to the main parotid gland, usually just above Stensen's duct and connected by its own duct to the latter. Any lesions that can occur in the main parotid gland can also arise in an accessory parotid gland. For the excision of lesions of the accessory parotid gland, we prefer to turn the same cervicofacial flap used for a lateral or total parotidectomy. This permits one to fully visualize the superficial and deep main parotid segments, the trunk and the branches of the facial nerve, and the accessory parotid gland along with its duct system and Stensen's duct.     

The influence of the testis on the fertilizing life of spermatozoa in the ligated vas deferens of the golden hamster

Spermatozoa in the vas deferens of the hamster lose their fertilizing capacity 3 days after ligation of the initial part of the duct and after 2 days if the testes are removed at the time of ligation. Sham-ligation had no effect on the fertilizing life of vasal spermatozoa on the contralateral side even 3 days after bilateral castration. Unilateral castration for 3 days had no effect on the fertilizing capacity of spermatozoa from the ipsilateral unobstructed duct, whereas no eggs were fertilized by spermatozoa from the contralateral ligated duct associated with the remaining testis. Unlike testosterone, 5alpha-dihydrotestosterone injected daily or implanted subcutaneously in Silastic tubes maintained normal fertilizing capacity for 2 days in castrates and for 3 days in intact males. Within each group, ligation had no effect on the level of fructose in the seminal vesicle on that side compared with the level in the gland on the other side.     

Role of the Accessory Parotid Gland in the Etiology of Parotitis: Statistical Analysis of Sialographic Features

This retrospective study aimed to identify if the existence of the accessory parotid gland correlated with the etiology of parotitis. This may aid the development of better treatment strategies in the future. Sialographic features of cases with parotitis and healthy subjects were reviewed. The chi-square test was used to compare the incidence of accessory parotid gland between the groups. The Student’s t test was used to compare the length of Stensen’s duct, the length from the orifice to the confluence of the accessory duct, and the angle between the accessory duct and Stensen’s duct between the groups. The incidence of accessory parotid gland in patients with parotitis was 71.8% (28/39), which was significantly higher than that in healthy subjects (P = 0.005). Patients with parotitis had a longer Stensen’s duct than healthy subjects (P = 0.003). There was no significant difference in the length from the orifice to the confluence of the accessory duct or the angle between the accessory duct and Stensen’s duct (P = 0.136 and 0.511, respectively) between the groups.The accessory parotid gland might play a role in the pathogenesis of parotitis. The existence of an accessory parotid gland is likely to interfere with salivary flow. Computational fluid dynamics analysis of salivary flow in the ductal system would be useful in future etiologic studies on parotitis.     

Hyperglycemic factor in submandibular glands and its etiological relations to diabetes mellitus in mice.

Bilateral ligation of both the submandibular and parotid ducts of adult normal and mutant hyperinsulinemic diabetic mice resulted in a significant hypoglycemic effect. Therefore, we postulated that duct ligation may result in the removal of hyperglycemic factor (Hoshino et al., 1976) rather than a change in insulin sensitivity. Indeed, no change in specific binding of 125I-insulin was observed in membrane fractions from several tissues obtained from mice of either sex or strains before and after duct ligation. After slices of the submandibular gland were incubated for 4 hr in Eagle's medium, an aliquot of the culture medium was injected i.p. into normal adult mice. A signigicant hyperglycemic effect was observed in 30 min in the injected animals. Eluates obtained by gel filtration of the crude extract of the submandibular gland were injected into normal adult mice, and hyperglycemia ensued. Thus, it is postulated that ligation of salivary ducts results in glandular atrophy and disappearance of the hyperglycemic factor which in turn leads to hypoglycemia and amelioration of diabetes mellitus, particularly of hyperinsulinemic type.     

LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice

Although it is clear that bile acid accumulation is the major initiator of fibrosis caused by cholestatic liver disease, endotoxemia is a common side effect. However, the depletion of hepatic macrophages with gadolinium chloride blunts hepatic fibrosis. Because endotoxin is a key activator of hepatic macrophages, this study was designed to test the hypothesis that LPS signaling through CD14 contributes to hepatic fibrosis caused by experimental cholestasis. Wild-type mice and CD14 knockout mice (CD14(-/-)) underwent sham operation or bile duct ligation and were killed 3 wk later. Measures of liver injury, such as focal necrosis, biliary cell proliferation, and inflammatory cell influx, were not significantly different among the strains 3 wk after bile duct ligation. Markers of liver fibrosis such as Sirius red staining, liver hydroxyproline, and alpha-smooth muscle actin expression were blunted in CD14(-/-) mice compared with wild-type mice after bile duct ligation. Despite no difference in lymphocyte infiltration, the macrophage/monocyte activation marker OX42 (CD11b) and the oxidative stress/lipid peroxidation marker 4-hydroxynonenal were significantly upregulated in wild-type mice after bile duct ligation but not in CD14(-/-) mice. Increased profibrogenic cytokine mRNA expression in the liver after bile duct ligation was significantly blunted in CD14(-/-) mice compared with the wild type. The hypothesis that LPS was involved in experimental cholestatic liver fibrosis was tested using mice deficient in LPS-binding protein (LBP(-/-)). LBP(-/-) mice had less liver injury and fibrosis (Siruis red staining and hydroxyproline content) compared with wild-type mice after bile duct ligation. In conclusion, these data demonstrate that endotoxin in a CD14-dependent manner exacerbates hepatic fibrogenesis and macrophage activation to produce oxidants and cytokines after bile duct ligation.     

Mitogen-activated protein kinase up-regulation and activation during rat parotid gland atrophy and regeneration: role of epidermal growth factor and beta2-adrenergic receptors

Abstract The rat secretory ductal obstruction model has been widely used to assess salivary gland injury, growth, and differentiation. In this study, a novel ductal obstruction and release procedure was used to explore the signaling pathways leading to salivary gland regeneration. Rats underwent bilateral parotid ductal obstruction in which the duct was occluded against a plastic disk subcutaneously and released by external ligature removal. This ductal obstruction/release procedure was validated to produce glandular atrophy and regeneration with histological analysis and periodic acid-Schiff staining. Immunoblot analysis indicated that during ductal obstruction and the early post-release period (day 7), expression of immunoreactive proliferating cell nuclear antigen and vimentin was increased in the parotid glands compared with sham-operated animals. Immunohistochemical staining and immunoblots revealed up-regulation of the mitogen-activated protein kinases (MAPKs), extracellular signal-regulated receptor kinase (ERK)1/2, and p38 during the atrophic and regeneration phases of ductal obstruction/release. Similarly, increases in activated, i.e., phosphorylated, ERK1/2 (pERK1/2) and p38 (phospho-p38) were demonstrable in both ductal and recovering acinar cells, with pERKs expressed predominantly in the nuclei and phospho-p38 distributed throughout the cells. Furthermore, levels of epidermal growth factor (EGF) receptor and β2-adrenergic receptor (β2-AR) were elevated in the ligated glands and at day 7 post-release; β1-AR levels did not change over the same time period. These results support the view that cell proliferation is involved in duct ligation-induced atrophy of the rat parotid gland and gland recovery upon ligature removal. Up-regulation of ERKs and p38, and the activation of these MAPKs by up-regulated EGF and β2-ARs, may be important signaling components underlying glandular atrophy and subsequent regeneration.     

Sebaceous lymphadenoma identified by fine needle aspiration biopsy: a case report

BACKGROUND: Sebaceous lymphadenoma of the parotid gland is a rare benign neoplasm. This is the first reported case of fine needle aspiration biopsy (FNAB) findings for sebaceous lymphadenoma of the parotid gland. CASE: A 60-year-old male presented with painless, bilateral parotid swelling noted for 5 months. The swelling was more pronounced on the right. Examination revealed bilaterally prominent parotid glands with diffuse firmness but no discrete masses. There was no evidence of facial nerve dysfunction. Laboratory evaluation was negative for infectious and autoimmune etiologies. Magnetic resonance imaging revealed bilateral cystic parotid masses. FNAB of the right parotid was obtained to assist with preoperative counseling. It revealed lymphoid and salivary gland parenchymal cells. The patient underwent a right superficial parotidectomy. The surgical specimen of the parotid mass confirmed the diagnosis of sebaceous lymphadenoma on the tissue section. The contralateral parotid mass had not been excised at this writing. CONCLUSION: This report is the first to describe the FNAB findings of the unusual benign parotid neoplasm sebaceous lymphadenoma. Though the definitive diagnosis of any parotid mass requires tissue, generally obtained via parotidectomy, an FNAB diagnosis can be useful in counseling a patient prior to definitive biopsy.     

Surgical treatment of drooling by bilateral parotid duct ligation and submandibular gland resection.

We have followed 14 patients for up to 6 years after they had submaxillary gland resections and parotid duct ligations for drooling. Good to excellent results were found in more than 85 percent of them in the control saliva, and there have been no recurrences or fistulae. This procedure is technically simple to do, and it is associated with less morbidity than surgical relocation of the parotid ducts.     

Salivary duct carcinoma of the parotid gland: report of a rare case with a comparative study of aspiration cytology and histomorphology

BACKGROUND: Salivary duct carcinomas affecting primarily the parotid gland are extremely rare (0.2-2% of all salivary gland tumors). These carcinomas are considered to be of high grade malignancy, with mortality in up to 70% of cases. They usually affect elderly males and less often young adults. Despite the fact that the histomorphologic characteristics of this tumor are always necessary for its classification, several authors have reported that the cytopathologic approach, using fine needle aspiration (FNA) cytology, can establish the final diagnosis. The aim of this paper is to present a rare case of salivary duct carcinoma of the parotid gland with no typical microscopic findings that was diagnosed by FNA cytology through a combination of techniques on biopsy material. CASE: A 56-year-old male presented with a right parotid mass measuring 6 cm in diameter. The mass appeared to expand subcutaneously and infiltrate the skin of the neck region. Biopsy material from both the mass and skin was obtained using FNA and processed with conventional, cell block and liquid-based cytology techniques. A core biopsy was also performed on the mass for histologic evaluation. CONCLUSION: The findings were consistent with a salivary duct carcinoma of the parotid gland and were confirmed by the histologic report. FNA cytology combined with such techniques as liquid-based cytology provides the potential for the final diagnosis. Liquid-based cytology can improve the cellular morphology of the material and allows immunocytochemistry and other diagnostic techniques. The application of such techniques is significantly restricted by conventional processing; thus, combining liquid-based cytology with other techniques expands the boundaries of cytology as a diagnostic test.     

Immunolocalization of electroneutral Na(+)-HCO cotransporters in human and rat salivary glands

Patterns of salivary HCO secretion vary widely among species and among individual glands. In particular, virtually nothing is known about the molecular identity of the HCO transporters involved in human salivary secretion. We have therefore examined the distribution of several known members of the Na(+)-HCO cotransporter (NBC) family in the parotid and submandibular glands. By use of a combination of RT-PCR and immunoblotting analyses, the electroneutral cotransporters NBC3 and NBCn1 mRNA and protein expression were detected in both human and rat tissues. Immunohistochemistry demonstrated that NBC3 was present at the apical membranes of acinar and duct cells in both human and rat parotid and submandibular glands. NBCn1 was strongly expressed at the basolateral membrane of striated duct cells but not in the acinar cells in the human salivary glands, whereas little or no NBCn1 labeling was observed in the rat salivary glands. The presence of NBCn1 at the basolateral membrane of human striated duct cells suggests that it may contribute to ductal HCO secretion. In contrast, the expression of NBC3 at the apical membranes of acinar and duct cells in both human and rat salivary glands indicates a possible role of this isoform in HCO salvage under resting conditions.     

TNF-alpha and leptin in experimental liver fibrosis models induced by carbon tetrachloride and by common bile duct ligation

In this study we investigated TNF-alpha and leptin levels in two different liver fibrosis models induced by carbon tetrachloride (CCl(4)) and common bile duct ligation (CBDL). A total of 36 male rats of Albino-Wistar strain were allocated to three groups. One of the groups was the control. The second group received 0.15 ml 100 g(-1) CCl(4) subcutaneously for 6 weeks, 3 days per week. The third group underwent common bile duct ligation (CBDL) and was monitored for 4 weeks. Histopathological investigation included fibrosis, steatosis and inflammation. Serum IL-6 and TNF-alpha levels were analysed by ELISA methods and leptin was analysed by RIA. Fibrosis and steatosis increased significantly in the CCl(4) group in comparison with the CBDL group (p < 0.01; p < 0.001). Leptin and TNF-alpha levels in CCl(4) group were higher than those in the CBDL and control groups (p < 0.05). TNF-alpha and leptin levels were not related to each another in either the CCl(4) group or the CBDL group (r=0.22, p > 0.05; r=0.19, p > 0.05). The IL-6 level was higher in the CCl(4) group in relation to severity of inflammation (p < 0.05). TNF-alpha and leptin levels were higher in animals with liver fibrosis induced by CCl(4), than they were in those whose liver fibrosis was induced by common bile duct ligation. Leptin and TNF-alpha may be less effective on the development of liver fibrosis in the group which underwent common bile duct ligation.     

Effects of saliva from chronically reserpinized rat on Na and K transport in perfused main excretory duct of submandibular gland of normal rat

Reserpine (RES) (0.5 mg/kg body wt, ip) was administered to rats for 7 days. On Day 8 saliva was evoked from these animals by intraperitoneal injection of pilocarpine nitrate (10 mg/kg body wt) and saliva from submandibular and parotid glands was collected separately. These collected salivas were used to perfuse through the main ducts of the submandibular glands of normal rats. After a control period of perfusion of the main duct with bicarbonate saline solution, parotid saliva from RES rats was perfused through the duct followed by regular perfusion. There was inhibition of Na absorption (22%) and K secretion (23%). Moreover, when submandibular saliva from treated rat was perfused through the main duct prior to regular perfusion, there was a decrease in Na absorption (31%) and K secretion (28%). In contrast, perfusion of the main duct with either parotid or submandibular saliva from normal rats caused no significant changes in Na and K transport. The present experiments confirm previous studies that there is some Na-inhibitory factor(s) present in saliva of the chronically RES-treated rat.     

The involvement of altered vesicle transport in redistribution of Ca2+, Mg2+-ATPase in cholestatic rat liver

Vectorial sorting of plasma membrane protein-containing vesicles is essential for the establishment and maintenance of cell polarity. In the present study, the involvement of altered vesicle transport in the redistribution of membrane-bound Ca2+, Mg2+-ATPase resulting from cholestasis was investigated in hepatocytes. Cholestasis was induced in rat liver by common bile duct ligation. Ca2+, Mg2+-ATPase activity was demonstrated histochemically at the light and electron microscopical levels. Microtubules, an important factor for transcellular transport of vesicles, were studied in situ by immunofluorescence microscopy and electron microscopy in detergent-extracted preparations. The results showed that microtubules underwent significant changes after common bile duct ligation. The most pronounced alteration was focal accumulation of -tubulin in the cytoplasm of hepato cytes after 7 days of common bile duct ligation. At the electron microscopical level, the number of microtubules was increased considerably. In control livers, the activity of Ca2+, Mg2+-ATPase was localized only at the apical plasma membrane of hepatocytes, but it was also present at the basolateral plasma membrane after common bile duct ligation. The number of intracellular vesicles containing Ca2+, Mg2+-ATPase activity was increased strikingly, and some of them were associated with lateral membrane domains in which Ca2+, Mg2+-ATPase activity was found. It is concluded that common bile duct ligation induces the rearrangement of microtubules, which may disturb vectorial transport of Ca2+, Mg2+-ATPase-containing vesicles in hepatocytes, leading to the redistribution of Ca2+, Mg2+-ATPase. © 1998 Chapman & Hall     

Histoarchitecture of the human parotid duct. Light-microscopic study

A light-microscopical study of the histoarchitecture of the human parotid duct was carried out. The parotid duct, much like other excretory passages, possessed three histological coats: mucosa, muscular layer and adventitia. The mucous epithelium was composed of the innermost tall columnar cells and the basal cubical cells. Numerous, circular elastic fibers were in close vicinity to the epithelium. The muscular layer consisted of smooth muscular fibers running in longitudinal direction. The adventitia consisted of lipofibrous connective tissue and contained many vessels. The result of the present study suggests that the parotid duct contributes to control of salivary secretion, since its architecture is basically similar to that of other excretory passages which have peristaltic activity.     

新生小鼠缺氧缺血性脑损伤模型的制作研究

目的：通过对动物模型的制作模拟新生儿围产期缺氧缺血性脑损伤,研究其脑组织病理变化,为新生儿缺氧缺血性脑损伤的病理生理的研究以及进一步有效的治疗提供实验基础。方法：将40只7d新生昆明小鼠分四组,分别为正常组（A组）、单侧颈总动脉结扎组（B组）、单侧颈总动脉结扎＋缺氧组（C组）和双侧颈总动脉结扎组（D组）。单侧颈总动脉结扎组（B组）行右侧颈总动脉结扎;单侧颈总动脉结扎＋缺氧组（C组）行右侧颈总动脉结扎后将其置于20℃的恒温50mL密闭容器中,分不同的时间将其取出;双侧颈总动脉结扎组（D组）行双侧颈总动脉结扎,各组术后均送回母鼠身边继续母乳喂养,三天后再作病理检测。结果：行单侧颈总动脉结扎加缺氧60min时,小鼠结扎侧皮质及海马区出现病理改变,随着缺氧时间延长（90rain、100min、120min）病变范围逐渐扩大,病理改变越明显。结论：本实验显示单侧颈总动脉结扎同时缺氧一定时间可以导致小鼠脑组织损伤,脑细胞发生病理改变,且皮层及海马区域的神经细胞对缺氧缺血最为敏感,从而为进一步研究新生儿缺氧缺血性脑损伤提供了较为可靠的模型。     

Morphological, micromorphological and histochemical studies on the parotid salivary glands of the one-humped camel (Camelus dromedarius).

The morphology, blood and nerve supply of the parotid salivary glands of the one-humped camel were studied in detail. The intraglandular portion of the duct system was also examined. The histological and histochemical studies showed that the parotid salivary glands of the camel are of the tubuloacinar type and are serumocoid in nature. The secretory acini and tubules show themselves in 3 different forms according to the different phases of their secretory cycle. The duct system of the gland contains goblet cells between its lining epithelium. The intercalated ducts show ampullation followed by narrowing that help in mixing the secretion. Intraepithelial glands are found in the terminal part of the parotid duct.     

Polyphenols from Camellia sinenesis attenuate experimental cholestasis-induced liver fibrosis in rats

Accumulation of hydrophobic bile acids during cholestasis leads to generation of oxygen free radicals in the liver. Accordingly, this study investigated whether polyphenols from green tea Camellia sinenesis, which are potent free radical scavengers, decrease hepatic injury caused by experimental cholestasis. Rats were fed a standard chow or a diet containing 0.1% polyphenolic extracts from C. sinenesis starting 3 days before bile duct ligation. After bile duct ligation, serum alanine transaminase increased to 760 U/l after 1 day in rats fed a control diet. Focal necrosis and bile duct proliferation were also observed after 1-2 days, and fibrosis developed 2-3 wk after bile duct ligation. Additionally, procollagen-alpha1(I) mRNA increased 30-fold 3 wk after bile duct ligation, accompanied by increased expression of alpha-smooth muscle actin and transforming growth factor-beta and the accumulation of 4-hydroxynenonal, an end product of lipid peroxidation. Polyphenol feeding blocked or blunted all of these bile duct ligation-dependent changes by 45-73%. Together, the results indicate that cholestasis due to bile duct ligation causes liver injury by mechanisms involving oxidative stress. Polyphenols from C. sinenesis scavenge oxygen radicals and prevent activation of stellate cells, thereby minimizing liver fibrosis.     

Forskolin-Induced Clearance of the Fluorescent Dye Sulforhodamine from Rat Parotid Intralobular Duct Lumen: Visualization of the Secretory Function under a Confocal Laser Scanning Microscope

Cyclic AMP evokes fluid secretion with bicarbonate in exocrine ducts. Clearance of fluorescent dyes from rat parotid intralobular ducts by forskolin was visualized as a fluorescence change in the duct luminal space by optical sectioning under a confocal laser scanning microscope to clarify the secretory function in the ducts. When the isolated rat parotid intralobular duct segments were superfused with membrane-impermeable fluorescent dyes during the experimental period, fluorescent dyes were passively moved into the duct space. Forskolin and isobutylmethylxanthine decreased the fluorescence of anionic dye, sulforhodamine B, and neutral dye, dextran tetramethyl-rhodamine, in the duct space, suggesting that the forskolin-induced clearance of fluorescent dyes might be the result of fluid secretion in the ducts. Methazolamide inhibited a forskolin-induced sustained decrease in duct fluorescence and intracellular acidification. Low concentrations of external Cl?, DIDS, bumetanide and amiloride did not markedly inhibit a forskolin-induced decrease in duct fluorescence. These findings suggest that a major portion of the steady decrease in duct fluorescence by forskolin was related to intracellular HCO3? production, not the uptake mechanism of external Cl?. Glibenclamide, NPPB, DPC and DMA inhibited the forskolin-induced decrease. Forskolin evokes the clearance of fluorescent dyes from duct space possibly due to fluid secretion in rat parotid ducts, associated with secretion through CFTR and DPC-sensitive anion channels of carbonic anhydrase-dependent bicarbonate linked with the Na+/H+ exchange mechanism.