Normal Parotid Gland Tissue Research Articles

Expression of CD44v6 and COX-2 in pleomorphic adenomas and carcinomas of parotid gland

To investigate the correlation between CD44v6 and cyclooxygenase-2(COX-2) expression and recurrence and deterioration of pleomorphic adenoma of parotid gland. Immunohistochemistry was used to detect the expression of CD44v6 and COX-2 in 19 normal parotid tissues, 25 primary pleomorphic adenomas, 15 first recurrent pleomorphic adenoma, 15 second recurrent pleomorphic adenoma and 13 cancer in pleomorphic adenomas. The correlation between CD44v6 and COX-2 and the recurrence and deterioration of pleomorphic adenomas was evaluated using SPSS 15.0 software package. The positive expression rate of CD44v6 in normal parotid gland, primary pleomorphic adenoma, first recurrent pleomorphic adenoma, second recurrent pleomorphic adenoma and cancer was 5.26%, 44.00%, 60.00%, 93.37% and 100.00%, respectively;and the positive expression rate of COX-2 was 10.53%, 40.00%, 63.33%, 93.37% and 100.00%, respectively. There was significant difference in the positive expression intensity of CD44v6 and COX-2 among the groups (P<0.05). The positive expression rate and intensity of CD44v6 and COX-2 in normal parotid gland tissue were significantly lower than those in other groups (P<0.05). There was no significant difference in the positive expression rate and intensity of CD44v6 between primary pleomorphic adenoma and first recurrent pleomorphic adenoma (P>0.05). There was no significant difference in the expression intensity of COX-2 between the two groups (P>0.05), but the positive expression rate of COX-2 between the two groups was not significant(P>0.05). The positive expression rate and intensity of CD44v6 and COX-2 in the second recurrent pleomorphic adenoma were significantly higher than those in the first recurrent pleomorphic adenoma(P<0.05), but there was no significant difference between the two groups(P>0.05). CD44v6 in the second recurrent pleomorphic adenoma and cancer was significantly higher than that in the first recurrent pleomorphic adenoma(P<0.05). There was no significant difference in the expression rate and intensity of COX-2 (P>0.05). CD44v6 and COX-2 may play an important role in promoting occurrence, invasion, recurrence and deterioration of pleomorphic adenoma through synergistic action.

Conservative Surgical Treatment of Benign Parotid Tumors: Extracapsular Dissection

Parotid tumor resection, parotidectomy, is a surgical procedure that requires considerable experience from surgeons in most of the cases because of the risk of facial nerve damage. In addition, it is often times difficult to identify and preserve the facial nerve during the procedure, because it requires removal of a considerable amount of normal parotid tissue even when it is not related to the location of the tumor itself. Post-operative cosmetic problems and complications associated with inevitable removal of the normal parotid gland tissue cannot be ignored. For these reasons, parotidectomy has been evolved over the years to ensure the oncological safety, avoid complications, and improve functional and cosmetic results. Recently, the use and importance of extracapsular dissection (ECD) has become more recognized because it is a more conservative surgical method than partial superficial parotidectomy with preservation of facial nerve function, minimization of functional and cosmetic complications, and limited removal of unnecessary normal parotid gland tissue. Herein, we review the literatures related to ECD for benign parotid tumors and explain the efficacy of this emerging procedure based on the previous study results reported by the authors.

A reliable multiclass classification model for identifying the subtypes of parotid neoplasms constructed with variable combination population analysis and partial least squares regression based on Raman spectra

Pleomorphic adenoma (PA), Warthin's tumor (WT) and mucoepidermoid carcinoma (MEC) are three common subtypes of salivary gland tumors, for which the occurrence site is located in the parotid gland. Accurately diagnosing the subtypes of parotid tumors plays a vital role in the surgical treatment. Unfortunately, the current studies mainly focus on the binary classification of parotid tumors. The preoperative multi-classification of them has still been underexplored. For the purpose of broadening the application area of the predictive models and facilitating the clinical preoperative diagnosis, we suggested a multi-classification model, which was constructed by combining the variable combination population analysis (VCPA) algorithm with the partial least squares regression (PLSR), to simultaneously discriminate the three subtypes of parotid tumors as well as the normal parotid gland tissue based on the Raman spectra of the tissue samples. In addition, we investigated the impact of generating Raman spectra from different sampling locations on the reliability of the predictive models. For the validation set, the overall accuracy in predicting the subtypes of parotid tumors and the normal parotid gland tissue was 0.867. Similarly, the accuracies achieved by the models constructed with the Raman spectra from two different sampling locations were 0.877 and 0.883, respectively, indicating the minor influence of the sampling locations on the predictive models. Our findings can be helpful for establishing the method of rapidly diagnosing the salivary gland tumors preoperatively in clinics. Moreover, the characteristic wavenumbers used in model construction were highly associated with the variations of the structures and contents of nucleic acids, collagen, proteins, lipids and DNA/RNA in gland tissue, which revealed the mainly difference among three types of parotid tumors and can be conductive to better understanding the molecular mechanisms of them.

Novel differential diagnostic method for superficial/deep tumor of the parotid gland using ultrasonography

The purpose of this study was to prepare the ultrasonographic diagnostic criteria on parotid tumors for preoperative differentiation of superficial and deep tumors. We evaluated 154 patients with a benign parotid tumor who underwent surgery. The minimum thickness of normal parotid gland tissue between the parotideomasseteric fascia and tumor (minimum fascia-tumor distance [MFTD]) was measured on preoperative ultrasonography and compared among tumors at different locations, and the optimum cutoff value to differentiate a deep tumor was identified. The MFTD showed significant differences between superficial and deep tumors and between inferior pole and deep tumors. The sensitivity, specificity, and accuracy of an MFTD ≥3 mm for the differentiation of deep tumors were 85%, 91%, and 89%. A tumor with an MFTD ≥3 mm on preoperative ultrasonography is very likely to be a deep tumor based on a new differentiation method for deep parotid tumors considering those present at other locations.

Giant cell reparative granuloma of parotid region – A case report

Giant cell reparative granuloma is a benign neoplastic lesion primarily affecting mandible and maxilla. Giant cell reparative granuloma of parotid region has never been reported in the literature. We report a case of giant cell reparative granuloma of parotid region infiltrating the whole of whole parotid gland, probably arising from the zygomatic bone. Total conservative parotidectomy was done to completely excise the lesion. Histological examination revealed multinucleate giant cells with areas of fibrosis and hemosiderin deposits surrounded by normal parotid gland tissue.

A Rare Case of Chronic Sialadenitis of Accessory Parotid Gland

The accessory parotid gland is salivary tissue adjacent to stenson's duct that is separated from the main parotid gland and lying on masseter muscle. It has secondary duct empting into the stenson's duct. The differential diagnosis of mid-cheek masses include pathology arising from normal anatomic structures or from variations of normal accessory parotid gland tissue. Surgical resection is the treatment of choice for the accessory parotid gland tumor. We report a case of accessory parotid gland with chronic sialadenitis in a 26years old male with the diagnosis and treatment. Accessory parotid gland pathologies should be included in the differential diagnosis of a patient presently with a mid-cheek mass.

O.542 Management of malignant parotid gland tumors

We report a case of pleomorphic adenoma which was assessed pre-operatively as arising from the accessory parotid gland. Computed tomography (CT)-sialography provided information about the relationship between the tumor and the remaining normal accessory parotid tissue, and fine-needle aspiration of the tumor provided additional information as to the histologic features of the tumor, i.e. it was identified as of salivary origin. Zygomatic and buccal branches of the facial nerve extended over the accessory parotid gland tumor and the parotid duct was located just beneath the tumor. Therefore, pre-operative assessment of the tumor's nature was important for prevention of facial nerve damage and salivary fistula. The normal accessory parotid gland tissue associated with the accessory parotid tumor was histologically different from that of normal parotid gland tissue dissected in other patients with pleomorphic adenoma of the parotid gland. It is suggested that the difference in cell composition between these glands affects the development of the associated tumors.

Do Magnetic Resonance Imaging and Ultrasound Add Anything to the Preoperative Workup of Parotid Gland Tumors?

To assess the additional value of magnetic resonance imaging (MRI) and ultrasound (US) to physical examination (PE) and fine needle aspiration cytology (FNAC) in the preoperative determination of the location and histology of parotid gland tumors. Prospectively, 99 patients with 77 benign and 22 malignant lesions were included; 82 underwent parotidectomy. FNAC was performed in 88 patients. On PE, the location of the tumor was predicted. Eighty-nine patients had MRI and 47 US. Various characteristics and the presumed diagnosis were assessed. Furthermore, the location of the tumor in relation to the facial nerve was predicted. The results were compared with the definite histology and the location during surgery. Of the MRI characteristics, incomplete demarcation from normal parotid gland tissue showed the highest positive predictive value (PPV) for malignancy of 0.48. Of the US characteristics, enlarged lymph nodes yielded the highest PPV for malignancy of 0.5. Cytology correctly predicted the benign or malignant nature of the tumor in all cases. Superficial location was well predicted on PE with a PPV of 0.8, slightly better on MRI (PPV of 0.87), and worse on US (PPV of 0.7). FNAC is the only accurate investigation for classifying a parotid gland tumor as benign or malignant. Palpation and MRI are superior to US in predicting tumor location. Because the results for palpation and MRI are almost equal, MRI should only be reserved for specific cases, and not routinely requested.

Evidence of lymphangiogenesis in Warthin’s tumor of the parotid gland

The details of the pathogenesis of cystadenolymphoma (Warthin's tumor) of the parotid gland are still unclear. Neovascularization is considered to be a pivotal factor for solid tumor progression and biological behavior of the tumor. Using double-labeling immunohistochemistry for LYVE-1 and CD34 (specific markers for lymphatic and vascular endothelial cells, respectively) this study analyzes lymphatic vessel density (LVD) and blood vessel density (BVD) in 10 Warthin's tumors and 10 pleomorphic adenomas of the parotid gland as well as in 5 normal parotid glands and 5 normal parotid lymph nodes. There was no significant difference in the intratumoral LVD and BVD among pleomorphic adenoma and normal parotid gland tissue. In contrast, the intratumoral LVD and BVD were significantly higher in Warthin's tumor than pleomorphic adenoma, normal parotid gland and parotid lymph node (P<0.0001 versus P<0.004). The increase in lymphatic vessels in Warthin's tumor suggests that epithelial tumor cells might promote lymphangiogenesis in this kind of lesions.

Genes associated with early development, apoptosis and cell cycle regulation define a gene expression profile of adenoid cystic carcinoma

Adenoid cystic carcinoma (ACC) is an uncommon salivary gland malignancy characterized by indolent yet relentless growth that exhibits inherent resistance to systemic chemotherapy, surgical salvage and conventional radiotherapy. We used microarray analysis to characterize gene expression changes associated with ACC. Eight ACC patient specimens were compared with normal parotid gland tissue and the ACC3 cell line. Differentially expressed genes were identified (512 total) using supervised analysis methods and functional categories assigned using OntoExpress. Genes associated with morphogenesis, neurogenesis, proliferation and apoptosis characterized ACC tumors. Genes associated with saliva production and immune response characterized normal parotid tissues while the ACC3 cell line expressed genes primarily associated with proliferation, chromosome maintenance and the cell cycle. These results demonstrate that ACC tumors express genes associated with early developmental processes including morphogenesis and neurogenesis implicating oncogenic events that result in dedifferentiation of normal salivary glands.

Tumors of the accessory lobe of the parotid gland: a 10-year experience.

The differential diagnosis of midcheek masses include pathology arising from normal anatomic structures or from variations of normal accessory parotid gland tissue. Accessory parotid gland tissue has been described as salivary tissue adjacent to Stenson's duct that is separate from the main body of the parotid gland. We report our 10-year experience with the diagnosis and treatment of eight accessory parotid gland neoplasms that have been followed by the senior authors. This is a retrospective review of our experience with eight accessory parotid gland neoplasms. A literature review and retrospective chart review of our experience with accessory parotid gland tumors over the past 10 years. The presentation, evaluation, management, treatment, and outcome were recorded. Eight cases of accessory lobe parotid tumors were identified, which have been followed since the date of initial treatment. All of the patients presented with a slowly growing cheek mass. There was one case of carcinoma expleomorphic adenoma, one case of undifferentiated carcinoma (small cell carcinoma), one case of basal cell adenocarcinoma, one case of benign salivary cyst, two cases of pleomorphic adenoma, and two cases of monomorphic adenoma. A standard facelift approach or modified Blair incision was used to excise these tumors. Neoplasms of the accessory parotid gland are rare. Management of these tumors include a high index of suspicion, good understanding of the anatomy, and meticulous surgical approach.

A Study of MECT1-MAML2 in Mucoepidermoid Carcinoma and Warthin's Tumor of Salivary Glands

The t(11;19)(q21;p13) chromosomal translocation has been described in two distinct types of salivary gland neoplasms: mucoepidermoid carcinoma (MEC) and Warthin's tumor (WT). Since this translocation has been recently shown to generate a MECT1-MAML2 fusion gene, we evaluated 10 primary MEC and seven primary WT to further define the molecular association of these two entities using cytogenetic, as well as in situ hybridization (ISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses directed against the fusion gene. A karyotype was established in all neoplasms except for two MEC cases. Of the eight karyotyped MECs, five showed the t(11;19)(q21;p13), two had a normal karyotype, and one case presented a -Y and +X. Three of the WT revealed a normal karyotype and four had several abnormalities which did not involve chromosomes 11 and 19. ISH analysis performed in cytogenetic suspension and/or in tumor paraffin sections demonstrated MAML2 rearrangement in 7 of 10 cases of MEC: all five cases with t(11;19), one case with normal karyotype, and one unkaryotyped case. RT-PCR analysis confirmed the expression of the MECT1-MAML2 gene in all MEC cases that were positive by ISH analysis. Neither the t(11;19) nor MECT1-MAML2 was detected in any case of WT, nor in control samples from polymorphous low-grade adenocarcinoma, acinic cell carcinoma, or normal parotid gland tissue. We have demonstrated that ISH and RT-PCR are sensitive methods for detecting MECT1-MAML2 in MEC. In contrast, we did not detect the t(11;19) nor MECT1-MAML2 expression in seven cases of WT.

Histopathology of pleomorphic adenoma in the parotid gland: a prospective unselected series of 100 cases.

Histopathological characteristics of pleomorphic adenomas, especially of capsular alterations such as thin capsule areas, capsule-free regions, capsule penetration, satellite nodules, and pseudopodia in the different subtypes, are described. Prospective unselected series of 100 consecutive cases from 1997 to 2000. Light microscopic examination and semiquantitative analysis of the pleomorphic adenomas. Fifty-one (51%) pleomorphic adenomas were classified as myxoid (stroma-rich) type, 35 (35%) specimens as cellular type, and 14 (14%) as classic subtype. Ninety-seven percent of all tumors showed areas with thin (<20 microm) capsule independent of the tumor subtype. Tumors of myxoid subtype showed the absolute greatest regions of a thin capsule. Especially, tumors of myxoid type (71%) often had a distinct focal absence of encapsulation with tumor merging into normal parotid gland tissue; 11% of the cellular subtype and 43% of the classic subtype presented capsule-free areas. Thirty-three percent of the myxoid pleomorphic adenomas, 23% of the cellular subtype, and 21% of the classic subtype had satellite nodules or pseudopodia. Almost all pleomorphic adenomas have focally thin capsules. One-fourth of all pleomorphic adenomas contain abnormalities such as satellite nodules or pseudopodia. More than two-thirds of pleomorphic adenomas of the myxoid (stroma-rich) subtype and at least half of all tumors show a focal absence of the capsule. Therefore, enucleation or local dissection of the pleomorphic adenoma is not a sufficient surgical treatment of this special tumor entity. We recommend, depending on the location of the tumor, a lateral or total parotidectomy as the treatment of choice.

Accessory parotid gland tumor: a case report

We report a case of pleomorphic adenoma which was assessed pre-operatively as arising from the accessory parotid gland. Computed tomography (CT)-sialography provided information about the relationship between the tumor and the remaining normal accessory parotid tissue, and fine-needle aspiration of the tumor provided additional information as to the histologic features of the tumor, i.e. it was identified as of salivary origin. Zygomatic and buccal branches of the facial nerve extended over the accessory parotid gland tumor and the parotid duct was located just beneath the tumor. Therefore, pre-operative assessment of the tumor's nature was important for prevention of facial nerve damage and salivary fistula. The normal accessory parotid gland tissue associated with the accessory parotid tumor was histologically different from that of normal parotid gland tissue dissected in other patients with pleomorphic adenoma of the parotid gland. It is suggested that the difference in cell composition between these glands affects the development of the associated tumors.

ErbB-2/Her-2 gene amplification and overexpression in parotid gland tumors.

Proto-oncogenes represent a family of normal cellular genes that were identified on the basis of their similarity to genetic sequences with known tumorigenic or transforming potential. Accumulating evidence links alterations in either the structure, copy number, or expression of one or another of these genes to neoplasia. One such gene, called erbB-2/Her-2 was found amplified in an adenocarcinoma of the human salivary gland and has also been found associated with primary human breast cancer. Patients with multiple copies of the gene have had a shorter overall survival. In the present study, 21 tumors of the parotid gland were examined by Southern and Northern blot hybridization for amplification and possible overexpression of the erbB-2/Her-2 oncogene. Normal parotid gland tissue was used as negative control. The parotid gland lesions comprised 7 pleomorphic adenomas, 5 squamous cell carcinomas, 4 cases of chronic fibrotic sialadenosis, 3 mucoepidermoid carcinomas as well as 1 lymphoma and 1 cystadenolymphoma. Gene amplification was found in 1 of the pleomorphic adenomas, with 2 tumors showing a significant overexpression of the erbB-2/Her-2 oncogene. Because 3-5% of all pleomorphic adenomas undergo malignant transformation, close follow-up of patients is currently underway.

Increased Expression of the Enzyme 1-4-Galactosyltransferase is Associated with Human Parotid Neoplasms

Human biopsy samples of parotid gland neoplasms were examined for the level of enzyme activity of the glycosyltransferase, beta 1-4-galactosyltransferase. An analysis of an adenoid cystic carcinoma, Warthin's tumor, mucoepidermoid carcinoma, and five pleomorphic adenomas all revealed elevated levels of enzyme activity. Evidence for plasma membrane beta 1-4-galactosyltransferase activity was provided by membrane fractionation as well as intact cell enzyme assays. On the other hand, the major protein of human saliva, salivary alpha-amylase, was substantially reduced in the same tissue compared with adjacent normal parotid gland tissue. The trichloroacetic acid-soluble proteins isolated from gland homogenates were also reduced in two of the carcinoma samples but increased in the pleomorphic adenomas. Additionally, the proliferation of these cells, in vitro, could be retarded by culturing in media containing the galactosyltransferase specific modifier protein, alpha-lactalbumin, or the nucleotide sugar, UDP-galactose.

Immunohistochemical analyses of autoimmune sialadenitis in man

The immunoreactivity pattern for different monoclonal antibodies to cytokeratins and to vimentin in epimyoepithelial islands typical for glands of patients with Sjögren's syndrome has been compared with that of normal parotid gland tissue. Two types of epithelial island cells were observed: one had an intermediate filament protein pattern similar to that of ordinary duct epithelial cells of normal parotid gland. The other had an intermediate filament protein pattern typical of myoepithelial and/or basal duct cells in normal glands. Thus, we conclude that the islands are composed of a mixed population of gland cells on the basis of their content of cytokeratins or of cytokeratins and vimentin. These cells might originate from pluripotential reserve cells or from ordinary duct, myoepithelial and/or basal duct cells which may have undergone metaplasia.

Immunohistochemical investigation of lysozyme, lactoferrin, alpha 1-antitrypsin, alpha 1-antichymotrypsin and ferritin in parotid gland tumors.

Presence of lysozyme, lactoferrin, alpha 1-antitrypsin, alpha 1-antichymotrypsin and ferritin was examined by the immunoperoxidase method in 15 consecutive parotid gland tumors as well as in normal parotid gland tissue. Lysozyme and lactoferrin were detected in intercalated duct cells of normal tissue and in the epithelial component of pleomorphic adenomas. alpha 1-antitrypsin, alpha 1-antichymotrypsin and ferritin were found in both epithelial and mesenchymal components of pleomorphic adenomas but not in normal parotid tissue. In the epithelial component of adenolymphoma only alpha 1-antichymotrypsin and lactoferrin were observed. The results would support a tentative histogenetic link between the intercalated duct cell and the epithelial component of the pleomorphic adenoma.

Parotid benign tumors: comments on surgical treatment of 263 cases

263 patients with benign parotid gland tumors have been operated upon, from 1970 through 1980. Of this total number of tumors, according to their histopathologic examination, 185 corresponded to pleomorphic adenoma, 24 to Warthin's tumor, 10 to recurrent pleomorphic adenomas (at first operated on elsewhere) and 44 to miscellaneous tumors or tumor-like lesions (simple cyst, lymphoepithelial lesion, branchial cleft cysts, lymph node hyperplasia etc.). 25 cases of pleomorphic adenoma, operated on during the past 24 months, were not evaluated as far as recurrence is concerned, because their follow-up was insufficiently long. The operative procedures used by us for pleomorphic adenoma surgery were: (a) pericapsuiar (extracapsular) excision, with a margin of normal parotid gland tissue without preparation of the fascial nerve, for 98 small size and superficially sited pleomorphic adenomas (52.6%); (b) subtotal parotidectomy (superficial lobectomy) with preparation of the facial nerve for 78 tumors (42.5%); (c) total parotidectomy with preservation of the nerve for 9 tumors located on the deep lobe of the gland (4.9%). We did not see any permanent facial palsy, and not one case of recurrence.