Normal Parotid Gland Research Articles

Buccal salivary cysts in association with a congenital parotid salivary fistula

Congenital parotid salivary fistulas are unusual entities that can arise from accessory parotid glands or, even more infrequently, from normal parotid glands via an aberrant Stensen's duct. A unique case of a congenital parotid salivary fistula presented in a four-week-old infant as polycystic swelling of the buccal region, with cyst contents draining to a cutaneous pit near the oral commissure. This patient offered an initial diagnostic challenge until it became evident that the drainage represented a salivary fistula. The case is used here to highlight the overlapping clinical and pathologic features shared between type I branchial cleft anomalies and congenital salivary cysts. This case is the second report of buccal salivary cysts in structural association with a congenital parotid salivary fistula and the first such case in which a normal Stensen's duct orifice has been preserved.

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.

Molecular Identification and Physiological Roles of Parotid Acinar Cell Maxi-K Channels

The physiological success of fluid-secreting tissues relies on a regulated interplay between Ca(2+)-activated Cl(-) and K(+) channels. Parotid acinar cells express two types of Ca(2+)-activated K(+) channels: intermediate conductance IK1 channels and maxi-K channels. The IK1 channel is encoded by the K(Ca)3.1 gene, and the K(Ca)1.1 gene is a likely candidate for the maxi-K channel. To confirm the genetic identity of the maxi-K channel and to probe its specific roles, we studied parotid glands in mice with the K(Ca)1.1 gene ablated. Parotid acinar cells from these animals lacked maxi-K channels, confirming their genetic identity. The stimulated parotid gland fluid secretion rate was normal, but the sodium and potassium content of the secreted fluid was altered. In addition, we found that the regulatory volume decrease in acinar cells was substantially impaired in K(Ca)1.1-null animals. We examined fluid secretion from animals with both K(+) channel genes deleted. The secretion rate was severely reduced, and the ion content of the secreted fluid was significantly changed. We measured the membrane potentials of acinar cells from wild-type mice and from animals with either or both K(+) channel genes ablated. They revealed that the observed functional effects on fluid secretion reflected alterations in cell membrane voltage. Our findings show that the maxi-K channels are critical for the regulatory volume decrease in these cells and that they play an important role in the sodium uptake and potassium secretion process in the ducts of these fluid-secreting salivary glands.

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.

Salivary Gland Tumors at in Vivo Proton MR Spectroscopy

To prospectively evaluate whether proton magnetic resonance (MR) spectroscopy can be used to characterize salivary gland tumors (SGTs). Ethics committee approval and informed consent were obtained. Hydrogen 1 ((1)H) MR spectroscopy was performed with echo times of 136 and 272 msec at 1.5 T in both SGTs and normal parotid glands. Spectra were analyzed in the time domain by using prior knowledge in the fitting procedure to obtain peak amplitudes of choline (Cho), creatine (Cr), and unsuppressed water. Mean Cho/Cr and Cho/water ratios for each subgroup of SGTs were obtained, and results were compared by using a nonparametric t test. Successful spectra were acquired in 56 patients (35 men, 21 women; mean age, 56 years) with a total of nine malignant tumors and 47 benign SGTs (24 Warthin tumors, 22 pleomorphic adenomas, one oncocytoma). At an echo time of 136 msec, Cho/Cr ratios were obtained in 26 (47%) of 55 spectra, with a mean value (+/- standard deviation) of 1.73 +/- 0.47, 5.49 +/- 1.86, 3.46 +/- 0.84, and 2.45 for malignant tumors, Warthin tumors, pleomorphic adenomas, and oncocytoma, respectively. Differences were significant between Warthin tumors and pleomorphic adenomas (P = .028) and between benign SGTs and malignant tumors (P < .001). At an echo time of 272 msec, Cho/Cr ratios were obtained in 16 (30%) of 53 spectra, with a mean value of 2.27 +/- 0.69, 6.92 +/- 1.47, and 3.67 +/- 1.23 for malignant tumors, Warthin tumors, and pleomorphic adenomas, respectively. Differences were also significant between Warthin tumors and pleomorphic adenomas (P = .041) and benign SGTs and malignant tumors (P = .004). There was a significant difference in mean Cho/water ratio for Warthin tumors versus pleomorphic adenomas at echo times of 136 msec (P = .003) and 272 msec (P = .002) but not for benign SGTs versus malignant tumors. (1)H MR spectroscopy may be used to characterize SGTs, but a larger study is required to validate these initial results.

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.

Immunocytochemical localization of mK1, a true tissue kallikrein, in the mouse parotid gland: sexual dimorphism and effects of castration and hypophysectomy

In the normal parotid glands of mice at 12 weeks of age, mK1, a true tissue kallikrein, was detected at the apical rim of the striated ducts (SDs). Sexual dimorphism in the immunostaining intensity in parotid glands was seen, i.e., immunostaining was more intense in males than in females. Under electron microscopy, secretory granules, being small in size, and condensed at the subluminal cytoplasm, were labeled with immunogold particles showing the presence of mK1. These secretory granules were rather abundant and large in males. Castration in males reduced the immunoreactivity of mK1 in the SD cells because of a decrease in the number and size of secretory granules as revealed by electron microscopy. Hypophysectomy in male mice resulted in considerable loss of immunoreactivity for mK1, which was characterized under electron microscopy by complete disappearance or significant reduction of secretory granules in many SD cells. These results suggest that mK1 expression in the SD cells of murine parotid glands is regulated by pituitary-dependent hormones, and sexual dimorphism of mK1 expression is regulated by androgens.

Comparative study and application of MR sialography using different pulse sequences

目的 评价MR涎管造影的各种序列技术和临床应用.方法依次采用短时反转恢复序列(STIR)、重T2加权快速自旋回波序列(重T2WI FSE)、单次激发快速自旋回波序列(SS FSE),厚层扫描,快速采集,于服用维生素C(Vit C)前后分别扫描.检查了30例,其中13例为志愿者,17例为可疑涎管异常者.结果3种序列均能显示正常腮腺和颌下腺主导管.13例志愿者STIR序列均能清晰显示涎管1级和2级分支,2例能显示管径约为0.8 mm的末梢分支;重T2WI FSE序列可清晰显示13例志愿者1级分支、10例2级分支;SS FSE序列可显示10例涎管1级分支、6例2级分支.STIR序列能清晰显示患者主导管和涎管1、2级分支;重T2WI FSE序列清晰显示患者12例涎管1级、8例2级分支;SS FSE序列清晰显示患者10例1级分支、4例2级分支.17例可疑异常者,腺体炎症7例,急性炎症主导管稍增粗,末梢导管呈点、球状扩张;颌下腺癌1例,导管受压移位,呈截断状改变;良性肿瘤7例,涎管受压移位,无中断;干燥综合征及涎腺病各1例,涎管未见明显异常.16例患者含服Vit C 0.2 g后5 min重复扫描,涎管显示较前增粗.结论MR涎管造影能清晰显示腮腺和颌下腺导管系统,其中STIR序列能清晰显示导管2级分支,是1种显示涎管的非侵袭性方法,含服Vit C后可使唾液分泌增多,从而使涎管显示率增加,具有较高的临床实用价值。

Clinical and ultracytochemical investigation of sialadenosis.

The records of 65 patients with sialadenosis treated between 1989 and 2002 at Tokyo Women's Medical University Hospital were studied clinically and ultracytochemically, focusing on the secretory granules of the acinar cells. Biopsies of parotid glands were performed in 18 patients. The obtained parotid tissues were investigated electron microscopically and ultracytochemically. For the ultracytochemistry of carbohydrates, the periodic acid-methenamine silver method (PAM) and lectin-gold technology were used. An immunohistochemical study using anti-alpha-amylase antibody was also undertaken. Light microscopically, the acinar cells of the parotid glands of sialadenosis patients were pale and swollen. Ultrastructurally, most secretory granules of the acinar cells were homogeneous and could be classified into two types: electron-lucent and electron-dense. The former type was seen mainly in patients with anorexia nervosa and bulimia, while the latter type was predominantly found in patients with hypertension or diabetes mellitus. Both types of granule reacted uniformly with PAM. Acinar cells from normal parotid glands contained spherical dense cores which showed little reaction. The peripheral rims of the granules were strongly stained. Lectin-gold binding in the granules showed a similar pattern to PAM staining. Immunohistochemically, the acinar cells of the sialadenosis patients reacted with anti-alpha-amylase antibody. The dark granular type showed more intense reaction than the light granular type. These findings suggest that amylase and glycoconjugates are present in the secretory granules in sialadenosis although the granule structure is abnormal, being enlarged by disturbance of normal protein synthesis and release at the cellular level and by dense-core formation in the granules.

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.

Immunohistochemical distribution of CD9 in parotid gland tumors

Objective: CD9 is a member of the tetra-membrane-spanning glycoprotein family called tetraspanin. CD9 suppresses breeding and motion in some types of cancer cells. At present, the expression of CD9 in the salivary gland has not yet been elucidated. Methods: We examined the expression of CD9 not only in the normal salivary glands of human embryo and adults but also in the parotid gland tumors using immunohistochemical staining. Results: CD9 was not detected in embryos at 18 weeks of gestation, but was observed at 24 weeks in the salivary gland. CD9 was constantly detected in the adult normal parotid gland. In benign parotid gland tumors, CD9 was present in the 11 of 16 pleomorphic adenomas, every Warthin tumors (18/18) and basal cell adenoma (1/1). In contrast, positive staining for CD9 in malignant parotid tumors was observed in only the case of mucoepidermoid carcinomas. Neither acinic cell carcinomas or adenoid cystic carcinomas did show positive reaction in examined cases. The localization of CD9 was also observed in intercalated duct cells. Conclusion: There was a statistically significant reduced expression of CD9 in malignant parotid gland tumors as compared to benign parotid gland tumors ( P=0.003).

PyV-mT-induced parotid gland hyperplasia as detected by altered lectin reactivity is not modulated by inducible nitric oxide deficiency

The parotid gland was one of the first organs recognised to be sensitive to the transforming effects of polyomavirus. This study examines parotid gland pathology in mice expressing the polyomavirus middle T (PyV-mT) under the control of the mouse mammary tumour virus long terminal repeat (MMTV-LTR) to (1) demonstrate the utility of this model for studying premalignant disease; (2) identify early lesions by lectin staining and (3) determine effects of the inducible nitric oxide synthase (iNOS) in modulating tumorigenesis. The middle T oncogene is expressed in the parotid glands in addition to the mammary glands and results in the formation of parotid hyperplasias in 100% of transgenic female mice. These hyperplasias have the features of intraepithelial neoplasia including hypertrophic cells with prominent nucleoli and abnormal mitoses. Focal areas of parotid hyperplasia can be identified using peanut agglutinin (PNA), a lectin that recognises the tumour associated T antigen. In contrast to normal parotid gland, areas of hyperplasia do not bind PNA. Mice deficient in iNOS, an enzyme implicated in the promotion of tumorigenesis, were bred into the PyV-mT model. The loss of iNOS did not impact on the number or size of parotid gland hyperplasias, suggesting that NO produced by this enzyme is not a key regulator of PyV-mT-induced parotid gland hyperplasia. The consistent development of parotid hyperplasias in PyV-mT mice and clear identification of these lesions by loss of PNA lectin reactivity provides a useful model for studying early molecular changes in parotid tumorigenesis.

Unilateral agenesis of the parotid gland: an unusual entity

Agenesis of the parotid gland is extremely rare with only few cases reported in the medical literature. This entity can be important to diagnose as occasionally the normal parotid gland can be mistaken for a tumor due to the facial asymmetry. In this article, we present the case of an isolated unilateral parotid gland agenesis in a young child. The entity is discussed along with important associated conditions that should be ruled out. These include amongst others first and second branchial arch anomalies, as well as the Levy-Hollister or lacrimo-auriculo-dentodigital syndrome.

Ultrastructural localization of epidermal growth factor receptor in human parotid gland.

The epidermal growth factor receptor (EGFR) is widely distributed in several organs in which, following interaction with its ligand, it can affect development and differentiation. The aim of this study was to define the distribution of EGFR in human parotid gland by means of a post-embedding immunogold staining method. Normal human parotid glands obtained at surgery were routinely prepared for electron microscopy. Semithin and ultrathin sections were treated for immunocytochemistry using a mouse monoclonal antibody specific for EGFR and a goat anti-mouse gold conjugated secondary antiserum. At the light microscope level, EGFR reactivity was revealed by a specific dark staining in both acinar and ductal cells. At the electron microscope level, EGFR was strongly stained in the cytoplasmic compartments and occasionally labeled on cell surfaces. In acinar cells, it appeared to be associated with small vesicles of uncertain nature that were scattered among the secretory granules. EGFR-positive vesicles were also observed in the ductal cells, with the most intense labeling being localized in striated ducts. Since cytoplasmic vesicles were previously found to be EGF-positive, these results may be due to the presence of the EGF-EGFR complex that is internalized after binding of EGF to the surface EGFR.

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.

Quantitative analysis of normal major salivary glands using computed tomography

Objectives: We sought to calculate the size and the computed tomography (CT) number of normal parotid and submandibular glands and to evaluate their relationship with respect to sex, age, and obesity in the Korean population. Study Design: The authors investigated the axial CT images of 42 healthy volunteers. The maximum cross-sectional area (MCSA) was used as an indicator of the size of the gland. Three regions of interest on axial scans were selected to calculate the mean CT number. Results: There was a significant decrease in the mean MCSA of the submandibular gland and the CT number of both glands with age. The MCSA of the submandibular gland in males was larger than that in females. There was a close correlation between the parotid and the submandibular glands with respect to the CT number, as well as between the left and right glands with respect to the MCSA and the CT number. The body mass index was positively correlated with the MCSA of the parotid gland, whereas the body mass indexes and the CT numbers of both glands were negatively correlated. Conclusions: Both age and obesity are closely correlated with the size and the CT number of the major salivary glands. Moreover, the correlation between the CT numbers of the parotid and the submandibular glands may be used for diagnostic purposes. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:240-4)

Distribution of MUC1 in the normal human oral cavity is localized to the ducts of minor salivary glands

The change in expression of MUC1 from health to disease forms the basis of its use as a potential disease marker. Previous attempts at isolating MUC1 from normal, healthy human oral mucosa have, however, drawn conflicting conclusions as to its presence. Furthermore, when MUC1 was detected in the oral glycocalyx, it was not clear which cells were synthesising it. We examined human oral glycocalyx using pooled buccal smears from 50 normal individuals. Following isopycnic density centrifugation and membrane extraction with octyl glucoside and saponin, MUC1 was detected with the polyclonal antibody CT1. Immunohistochemistry using antibodies CT1 and BC2 was performed on sections from eight labial, seven palatal, four buccal, three retromolar pad, three dorsum of tongue and two ventral surface of tongue biopsies. In-situ hybridisation using MUC1 and cytoplasmic tail oligoprobes on sections from four palatal, seven labial and two retromolar pad biopsies was also carried out. MUC1 mRNA could only be detected in the minor salivary mucous glands. MUC1 has already been identified in the ducts of normal parotid and submandibular gland, and our findings demonstrate a similar distribution in minor salivary glands. We conclude that when present in the normal oral glycocalyx, the only oral source of MUC1 is from cell membranes of the minor salivary glands.

Warthin's tumor of parotid gland on Tc-99m pertechnetate scintigraphy with lemon juice stimulation: Tc-99m uptake, size, and pathologic correlation.

The aim of this study was to evaluate the usefulness of technetium-99m (Tc-99m) pertechnetate scintigraphy with lemon juice stimulation in the diagnosis of Warthin's tumor and its correlation with Tc-99m uptake, tumor size, and histologic subtype. Tc-99m pertechnetate scintigraphy before and after lemon juice stimulation and pathologic specimens of 34 Warthin's tumors and 47 non-Warthin's lesions were retrospectively evaluated. Tc-99m uptake of Warthin's tumors before and after stimulation was visually graded as follows: absent; indeterminate; low grade; definite; and strong. Tumor size was defined as maximum diameter of the tumor measured from the surgical specimen. Warthin's tumors were classified into three histologic subtypes according to the ratio of epithelial and lymphoid stromal components: predominant epithelial; intermediate; and low-grade epithelial types. Eighteen of 34 (53%) Warthin's tumors and one benign lymphoepithelial cyst showed higher uptake than that of the normal parotid gland on Tc-99m scintigraphy before lemon juice stimulation. Thirty-two of the 34 (94%) Warthin's tumors, one benign lymphoepithelial cyst, one pleomorphic adenoma, and one oncocytoma revealed higher uptake than that of the normal parotid gland on Tc-99m scintigraphy after lemon juice stimulation. The mean size was 37 mm in strong uptake Warthin's tumors, 24 mm in definite uptake tumors, 19 mm in low-grade uptake tumors, and 12 mm in low-grade uptake tumors excluding those tumors with large cystic component. There was a significant correlation between tumor size and degree of Tc-99m uptake after lemon juice stimulation. However, there was no correlation between histologic subtype and Tc-99m uptake, and histologic subtype and tumor size in Warthin's tumors. Our study concludes that Tc-99m pertechnetate scintigraphy with lemon juice stimulation is useful for the detection and diagnosis of Warthin's tumor. The degree of uptake in Warthin's tumor on Tc-99m scintigraphy with lemon juice stimulation depends mainly on tumor size and the presence of large cystic component in it.

Immunolocalisation of cartilage-derived retinoic acid-sensitive protein in pleomorphic adenoma of the parotid salivary gland.

Pleomorphic adenoma of the parotid salivary glands often contains chondroid elements and may exhibit cartilaginous and osseous differentiation, although the latter is extremely rare. Twenty-nine pleomorphic adenomas (PAs) of the parotid gland were examined immunohistochemically for the distribution of cartilage-derived retinoic acid-sensitive protein (CD-RAP), a recently described marker of chondrocytes, which may be important in the morphogenesis and development of the salivary gland. In the normal parotid gland, the ductal cells expressed CD-RAP, but not the myoepithelial cells. In the pleomorphic salivary adenomas, the duct-like cells, but not the myoepithelial cells, expressed CD-RAP. Since many authorities consider myoepithelial cells to be the source of the chondroid matrix, it is surprising that these cells do not express the chondrocytic marker, CD-RAP. Putative neoplastic myoepithelium in the pleomorphic adenoma and some cells in the myxochondroid areas expressed S-100 and calponin.

Parotid gland tissues investigated by picosecond time-gated and optical spectroscopic imaging techniques

Near-infrared (NIR) time-resolved and spectroscopic transillumination imaging techniques are used to investigate normal tissues and Warthin's tumor of human parotid glands. The time-sliced imaging arrangement uses 120-fs, 1-kHz repetition-rate, 800-nm pulses from a Ti: sapphire laser and amplifier system for sample illumination and an ultrafast gated intensified camera system (UGICS) for recording two-dimensional (2-D) images using transmitted light. Images recorded with earlier temporal slices (approximately first 100 ps) of transmitted light highlight the tumor, while those recorded with later temporal slices (later than 200 ps) accentuate normal tissues. The spectroscopic imaging arrangement uses 1210-1300 nm tunable output of a Cr: forsterite laser for sample illumination, a Fourier space gate to discriminate against multiple-scattered light, and a NIR area camera to record 2-D images. The tumor region in the specimen appears brighter than the normal region in spectroscopic images recorded with light of different wavelengths. A wavelength-dependent variation in the ratio of light transmission through the tumor to that through the normal parotid gland is observed. Differences in scattering and wavelength-dependent absorption characteristics of normal parotid gland and Warthin's tumor provide a consistent explanation of these observed features. Histopathological analysis of the specimen sheds light on the probable origin of the differences in scattering and absorption characteristics.