腮腺主导管结扎诱导萎缩后的组织转归

背景：人体大唾液腺常因受到头颈部肿瘤放射治疗、舍格伦综合征及涎腺炎等因素的影响发生腺体萎缩,目前对长期萎缩性腮腺内组织形态变化的观察仍较少。 目的：观察腮腺主导管结扎诱导腮腺萎缩后的组织转归。 方法：通过结扎SD大鼠右侧腮腺主导管诱导腺体萎缩,采用苏木精-伊红染色观察正常腮腺及导管结扎后0(对照),1,3,7,14,30,60 d萎缩性腮腺组织内腺泡、导管细胞的面积;免疫组织化学染色定量分析肌上皮细胞在腮腺萎缩不同时间点的数量分布变化。 结果与结论：结扎腮腺主导管后腺泡细胞出现快速凋亡,至14 d时已基本消失。随着腺体萎缩,间质逐渐纤维化并伴随炎性细胞浸润,组织内形成大量导管样结构,导管面积逐渐增加,到14 d时达到顶峰,随后逐渐减少,导管样结构呈典型的双套层结构,结扎各时间点腺泡、导管面积与对照组比较差异均有显著性意义(P < 0.05)。结扎后7 d内肌上皮细胞数量快速增加,随后肌上皮细胞数量增长缓慢,维持在一定的范围。表明腮腺主导管结扎诱导腺体萎缩早期腺泡细胞快速消失,出现大量导管样结构,肌上皮反应性增殖,随着腺体的萎缩由导管样结构及肌上皮细胞组成“双套层”结构可能抑制腺体的进一步萎缩。     

Intercalated duct cells in the rat parotid gland may behave as tissue stem cells

This study was conducted to determine whether intercalated duct cells in the rat parotid gland have the properties of tissue stem cells. After induction of cellular proliferation by repeated administration of isoproterenol (IPR), a β-adrenergic agonist, proliferation activity in acinar, intralobular, and intercalated ductal cells was quantified using Ki-67 immunohistochemistry. The total number of each type of component cell in a gland was also estimated in the course of IPR treatment. IPR was found to induce proliferation of acinar and intercalated duct cells, but not intralobular duct cells. The total number of acinar cells in a gland on day 5 of IPR treatment was 1.6 times of that at day 0 (baseline). In contrast, the total numbers of intercalated and intralobular duct cells did not change from baseline, indicating a high possibility that the proliferated intercalated duct cells differentiated into acinar cells. On days 2 to 3 of IPR treatment, intercalated duct cells with amylase-positive secretory granules were recognized in a region very close to the acini, and were suspected of being transitional cells from intercalated duct to acinar cells. This quantitative study indicates that intercalated duct cells may have the properties of tissue stem cells upon IPR stimulation.     

Salivary duct carcinoma in situ of the parotid gland

Aims: To describe three cases of purely in situ salivary duct carcinoma, so as better to define the entity. Methods and results: Three primary tumours of the parotid gland are presented, in each case composed of cysts and ducts and lined by high nuclear grade epithelial cells. All parts of each tumour were surrounded by a myoepithelial cell rim and there was no evidence of invasion. The tumour cells expressed immunohistochemical markers seen in invasive salivary duct carcinoma of usual (high‐grade) type. In two cases the androgen receptor (AR) reaction was strong, but there was no immunohistochemical expression of HER2 protein or gene amplification by in situ hybridization. In the remaining case, fewer nuclei stained for AR, but both HER2 protein and gene amplification were demonstrated. Conclusions: Salivary duct carcinoma in situ is morphologically similar to breast ductal carcinoma in situ and, although our cases are few, salivary duct carcinoma in situ can possibly be subdivided into luminal and non‐luminal cell types, as can analogous mammary neoplasms. The present study cannot determine whether low‐grade cribriform cystadenocarcinoma, architecturally similar but immunohistochemically different, is part of the spectrum of salivary duct carcinoma in situ, or whether it represents a separate entity.     

Sarcomatoid salivary duct carcinoma of the parotid gland

Salivary duct carcinoma (SDC) is a high-grade neoplasm known to histologically resemble high-grade ductal carcinoma in situ of the breast. We describe 3 cases of sarcomatoid salivary duct carcinoma, a heretofore unreported variant of SDC. Each case was a composite of SDC and sarcomatoid carcinoma and histologically similar to reported cases arising in the breast. The clinicopathologic features, including immunohistochemistry, of 3 cases were investigated. In the 3 men, ages 56, 68, and 70 years, the resected parotid tumors measured 1.5, 3.5, and 1.5 cm, respectively. Only the 3.5-cm tumor extended beyond the parotid gland into soft tissue. This patient died at 3 years with pulmonary metastases. The other patients were free of disease at 6 and 12 months. Histologically, each case was a composite of usual-type SDC and sarcomatoid carcinoma. SDC showed typical cribriform architecture, whereas anaplastic, spindled cells constituted the sarcomatoid areas. Immunohistochemically, epithelial elements stained as follows: cytokeratin (AE1/AE3 & CAM 5.2) positive in 3 of 3 cases, EMA positive in 3 of 3 cases, vimentin negative in 3 of 3 cases, desmin negative in 3 of 3 cases, c-erbB-2 positive in 1 of 2 cases. Sarcomatoid elements stained as follows: AE1/AE3 negative in 3 of 3 cases, CAM 5.2 rare positive cell in 1 of 3 cases, EMA focally positive in 3 of 3 cases, vimentin positive in 3 of 3 cases, desmin negative in 3 of 3 cases, c-erbB-2 negative in 2 of 2 cases. Electron microscopy, performed in one case, showed scattered junctional complexes congruent with epithelial differentiation. Immunohistochemical results, EMA and CAM 5.2 positivity, and ultrastructural findings supported our belief that these unique biphasic tumors represented SDC with sarcomatoid carcinoma. We conclude an element of sarcomatoid carcinoma rarely may arise in association with SDC, and it is erroneous to diagnose such tumors as "carcinosarcoma."     

胸导管结扎对大鼠脂质代谢和胰组织结构的影响

目的:探讨胸导管结扎对脂质代谢的影响,揭示淋巴回流障碍诱发胰组织的显微和超微结构变化.方法:SD大鼠随机分为假手术对照组和结扎胸导管模型组.术后6个月取静脉血标本进行血脂检测;部分胰组织标本,H-E和刚果红染色光镜观察;部分胰组织进行透射电镜观察.结果:(1)模型组大鼠游离脂肪酸和甘油三酯浓度明显下降,胆固醇浓度无显著变化.(2)光镜观察显示模型组大鼠的胰腺小叶间隙增宽,脂肪堆积和淋巴管扩张.(3)透射电镜观察显示模型组大鼠的胰岛细胞间隙增宽,细胞间隙及细胞内可见大量脂滴样物质、红细胞和胶原原纤维样结构.结论:胸导管结扎可引起胰腺结构变化和影响胰腺的内、外分泌功能.     

Crystalloids in salivary duct cysts of the human parotid gland

Summary Crystalloids found in salivary duct cysts of the human parotid gland were examined by scanning electron microscopical observations with electron probe X-ray microanalysis. The cystic spaces were filled with numerous crystalloids which had a variety of forms with slight eosinophilic and glassy appearance. Scanning electron microscopically, crystalloids were hexagonal and rhombohedral in shape, and cutting the surface showed a polycyclic structure or regular parallel lamination. By electron probe X-ray microanalysis, sulphur was the only detected element. The present study suggests that crystalloids resulted from deposition from supersaturated saliva containing sulphur containing compounds into the cystic lumen or into epithelial cytoplasm.     

X-ray microanalysis of the rat parotid gland after chronic sympathectomimetic stimulation

The effects of chronic treatment with isoproterenol, reserpine, prenalterol, and terbutaline on rat parotid gland were investigated by electron microscopy and X-ray microanalysis. Chronic isoproterenol treatment induced lower potassium and calcium concentrations in the acinar cells. The cells were enlarged and contained more and larger zymogen granules than acinar cells in the controls. The zymogen granules contained markedly less sulfur, potassium, and calcium than in control animals. Prenalterol had effects similar to those of isoproterenol, but less pronounced, whereas terbutaline had no significant effects. Chronic treatment with reserpine caused a decrease in calcium levels but did not affect potassium levels. The changes in elemental composition in parotid acinar cells after chronic treatment with isoproterenol and reserpine differed from those induced by the same treatment in the submandibular gland of the rat.     

Dissociation of rat parotid gland.

Rat parotid gland was dissociated by sequential collagenase and hyaluronidase digestions, chelation with ethylenediaminetetraacetic acid, and mild shearing force to yield predominantly single cells. The isolated acinar cells retained their morphologic characteristics and their amylase activity. The functional integrity of the isolated cells was assessed by measuring their secretory response to isoproterenol, epinephrine, and carbamylcholine and by their ability to incorporate radioactively labeled leucine and thymidine. The discharge of amylase from the dissociated cells was not effected by isoproterenol or norepinephrine and the response to carbamylcholine was minimal. The data indicate a destruction or perturbation of hormone receptors during the dissociation procedure. The maintenance of the cells in culture for up to 18 hours failed to restore the responsiveness of the isolated parotid gland acinar cells to isoproterenol. The isolated cells incorporated 14C-leucine into proteins at a linear rate between 30 and 180 minutes. Chromatographic and electrophoretic profiles of newly synthesized proteins indicated that all major proteins synthesized in vivo were also synthesized by the isolated cells. The isolated cells incorporated tritiated thymidine into DNA. Furthermore, stimulation of DNA synthesis by isoproterenol in vivo was reflected by a higher rate of thymidine incorporation by the isolated cells as compared with controls. The dissociated parotid gland cells offer a convenient system for studying various cellular processes, particularly the synthesis of macromolecules with high specific activity. However, some functions, notably the response to beta- adrenergic agonists, are lost during the dissociation procedure.     

Intraoral duct ligation without inclusion of the parasympathetic nerve supply induces rat submandibular gland atrophy

The atrophic effect of ligating the main duct of the right submandibular gland was examined in rat using a novel intraoral approach that did not include the chorda lingual (CL) nerve. Comparison was made with the effect of duct ligation including the attached CL nerve as carried out in previous studies. In all animals, the contralateral, unligated left submandibular gland was used as a control. At different times (1, 2, 7, 14 and 21 days) after ligation, glands were removed and weighed. Tissue was fixed for morphological analysis and homogenized for biochemical assay of secretory proteins. After 21 days, ligated glands showed a significant decrease in wet weight compared with unligated glands. Weight loss was the greatest (P < 0.05) in glands ligated with the CL nerve included. Light microscopy revealed that following ligation, an initial inflammatory reaction was followed by severe atrophy of acini and granular ducts. The atrophy was less severe when the CL nerve was not ligated. Secretory proteins were decreased from day 1 onwards following duct ligation in both groups. It can be concluded that most of the atrophy induced by duct ligation is independent of damage caused to the parasympathetic nerve supply, although the latter causes a greater atrophy presumably due to denervation.     

Postnatal development of the duct system in the mouse parotid gland

The morphology of the parotid gland in adult mice is mouse strain-specific. C57BL/6 and C3H/He strains of mouse are representatives of two types of the morphology identified previously. The postnatal development of such morphologic differences was investigated by sialography of excised glands of these strains of mouse. It was observed that the mouse strain-dependent morphological characteristics were already present at birth, except for the branching pattern of the peripheral duct system, which became differentiated at 3 weeks of age. These results indicate that the C3H/He mouse-specific branching pattern of the peripheral ducts reflects the profile of matured secretory units and ducts, and that the C57BL/6 mouse-specific pattern resembles that of an immature C3H/He mouse.     

Regeneration of the parotid gland in the rat

Summary Parotid gland regeneration was studied in rats in which all of the left gland and part (50–60%) of the right had been removed. In young rats weighing 60–100 g, regeneration occurred in 19% of cases, as judged by the restoration of the weight of the organ. The weight of the glands did not always reach the initial level, however, and averaged 80% of the weight in control animals.The number of cases with gland regeneration increased in adult rats when the capsule was left open after the operation. Histological investigation showed that regeneration does not occur by growth starting at the injured surface, but rather by the proliferation of the secretory epithelium (regenerative hypertrophy) of the acini over the whole organ.(Presented by Active Member AMN SSSR V. V. Parin) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 50, No. 10, pp. 113–118, October, 1960     

Aggressive invasive micropapillary salivary duct carcinoma of the parotid gland

The presence of invasive micropapillary component has been reported to be associated with salivary duct carcinoma and poor outcomes. Herein is described a rare case of invasive micropapillary salivary duct carcinoma of the parotid gland in a 60-year-old man. The micropapillary component was approximately 70% of the area of the tumor. Squamous differentiation was focally seen adjacent to the micropapillary component. On immunohistochemistry the ordinary salivary duct carcinoma component was positive for gross cystic disease fluid protein-15 (GCDFP-15), androgen receptor (AR), and HER2/neu, whereas both micropapillary and squamous components were negative for GCDFP-15 and AR. Immunohistochemical staining for D2-40 highlighted the lymph vessel invasion of tumor cells. This patient developed metastases in the lymph nodes of the neck, and also in the liver, lung, and brain. The lymph nodes and liver metastases had both ordinary salivary duct carcinoma and micropapillary components. The patient died of tumor 11 months after the initial surgical operation. The results support that the presence of micropapillary component is associated with more aggressive behavior of salivary duct carcinoma. It is also important for pathologists to recognize that GCDFP-15 and AR expression can be reduced in micropapillary carcinoma in the differential diagnosis of metastatic tumor.     

Cell death and cell proliferation during atrophy of the rat parotid gland induced by duct obstruction

Rat parotid gland atrophy after unilateral duct ligation was studied by light and electron microscopy. Death of secretory acinar cells, which took the form of apoptosis, resulted in their complete disappearance within 5 days. The remnants of the dying cells were mostly phagocytosed and degraded by macrophages within the glandular epithelium; a few were taken up by adjoining epithelial cells. The acinar cell deletion was accompanied by increased mitosis of striated and intercalated duct epithelial cells. However, over many weeks, there was enhanced apoptosis of duct cells, which eventually led to marked shortening of intercalated ducts. Apoptosis of capillary endothelial cells was observed and may account for the reduction in the capillary bed known to accompany gland atrophy. The end-stage lesion comprised small numbers of ducts in a condensed stroma. Compensatory hyperplasia, involving proliferation of duct and acinar cells, was demonstrated in the contralateral glands.     

Melatonin release by exocytosis in the rat parotid gland

Several beneficial effects on oral health are ascribed to melatonin. Due to its lipophilic nature, non‐protein‐bound circulating melatonin is usually thought to enter the saliva by passive diffusion through salivary acinar gland cells. Recently, however, using transmission electron microscopy (TEM), melatonin was found in acinar secretory granules of human salivary glands. To test the hypothesis that granular located melatonin is actively discharged into the saliva by exocytosis, i.e. contrary to the general belief, the β‐adrenergic receptor agonist isoprenaline, which causes the degranulation of acinar parotid serous cells, was administered to anaesthetised rats. Sixty minutes after an intravenous bolus injection of isoprenaline (5 mg kg^?1), the right parotid gland was removed; pre‐administration, the left control gland had been removed. Samples were processed to demonstrate melatonin reactivity using the immunogold staining method. Morphometric assessment was made using TEM. Gold particles labelling melatonin appeared to be preferentially associated with secretory granules, occurring in their matrix and at membrane level but, notably, it was also associated with vesicles, mitochondria and nuclei. Twenty‐six per cent of the total granular population (per 100 μm² per cell area) displayed melatonin labelling in the matrix; three‐quarters of this fraction disappeared (P < 0.01) in response to isoprenaline, and melatonin reactivity appeared in dilated lumina. Thus, evidence is provided of an alternative route for melatonin to reach the gland lumen and the oral cavity by active release through exocytosis, a process which is under the influence of parasympathetic and sympathetic nervous activity and is the final event along the so‐called regulated secretory pathway. During its stay in granules, anti‐oxidant melatonin may protect their protein/peptide constituents from damage.     

Salivary duct carcinoma of the parotid gland: the cytohistological features

A 62-year-old man presented with rapidly growing tumour in the right parotid region with associated pain and facial nerve palsy. Based on the fine needle aspiration cytology report of high-grade mucoepidermoid carcinoma, parotidectomy was performed which showed features of salivary duct carcinoma. The smears were reviewed to identify the potential pitfalls in the cytological diagnosis of salivary duct carcinoma.