| Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Benign Parotid Masses The salivary glands can be divided into two groups: the minor group and the major group. There are about 600 – 1000 minor glands. They are unpaired, and line the entire oral cavity. The major salivary glands are paired, and include the parotid glands, the submandibular glands and the sublingual glands. Parotid gland development begins in about the 5 th to 6 th week of development. The primordium develops from the oral ectoderm and progresses into the surrounding mesenchyme. The parotid gland develops posteriorly while the facial nerve migrates anteriorly. The parotid gland eventually envelops the nerve. The parotid gland is contained in the parotid space, which is bounded superiorly by the zygoma, posteriorly by the external auditory canal, inferiorly by the styloid process, styloid muscle and great vessels. The tail of the parotid extends posteriorly over the mastoid tip and lies over the sternocleidomastoid muscle. Stensen’s duct, which is approximately 4-7-cm long, arises from the anterior border of gland. The duct exits from the lateral surface of the masseter muscle, penetrates the buccal fat pad and buccinator muscle to enter into the oral cavity, usually opposite just the second maxillary molar. Anatomically, the gland is a contiguous unit; however, surgically it is separated into a superficial and deep lobe by the facial nerve. A branch of the auricular temporal nerve, which carries postganglionic parasympathetic fibers from the otoganglion, innervates the gland. These fibers stimulate secretion. Injury to these fibers could lead to aberrant re-intervation with the skin sweat glands resulting in what is known as Fry’s Syndrome. The parotid fascia is a continuation of the superficial layer of the deep cervical fascia within which there are multiple nodes, which serve as the drainage basin for the face. The superficial nodes drain the parotid gland, the external auditory canal, the pinna, the scalp, eyelids and lacrimal glands. The deep nodes within the parotid gland drain the external auditory canal, the parotid gland itself, the middle ear, nasopharynx and soft palate. The salivary gland unit consists of an acinus and a duct. The acinus may contain serous or mucus cells or both. The acinus drains into a series of ducts, which are all differentiated. The intercalated duct is relatively unspecialized. The striated ducts are thought to play an important role in electrolyte and water transport. Here is the histologic examination of a normal parotid gland. The serous acini predominate, but you can see some mucinous acini here. The glands are each an acinus and duct unit, which are surrounded by contractile epithelial cells, which facilitate in salivary flow. Two theories exist regarding the development of histogenesis of salivary gland neoplasms. According to the multi cellular theory, neoplasms arise from different mature cells that are different counterparts within the salivary gland unit. Ancocytic tumors are believed to arise from striated duct cells, acinus cell tumors from acinar cells, and mixed tumors from intercalated duct cells and myoepithelial cells. The other theory, the bicellular theory, states that basal cells of the excretory and intercalated duct serve as stem cells or reserve cells for the differentiation of the salivary gland units, and that neoplasms arise from either one of these reserve cells. Therefore, Warthins tumors, oncocytic tumors, adenoid cystic, carcinoma and acinus tumors are thought to arise from intercalated duct reserve cells and squamous cell, mucoepidermoid carcinoma and other more malignant neoplasms are thought to arise from the expiatory duct reserve cells. Salivary gland tumors comprise 3% - 4% of all head and neck neoplasms. Ninety-five percent of all salivary gland neoplasms occur in adults. Seventy to eight percent of these are thought to arise in parotid gland and 70% - 80% of these are usually benign. Most benign parotid neoplasms present as a painless, slow-growing mass. Patients may have symptoms for more than three to ten years. Any sudden increase in size may cause suspicion related to infection, superimposed infections, cystic degeneration, and hemorrhage of malignant degeneration of the mass. Often times these neoplasms are freely mobile, well circumscribed lesions. Usually there is no overlying skin change and no evidence of facial nerve injury or involvement. Salivary neoplasms have been described and classified by several authors, including the 1972 World Health Organization classification Pleomorphic adenoma is the most common salivary gland neoplasm, accounting for 50% - 70% of all parotid neoplasms. Originally described in 1866 as a benign mixed tumor, it was originally thought to be derived from both epithelial and mesenchymal elements. In 1948 the name was changed to pleomorphic adenoma, better fitting its suspected unicellular origins. It is now thought to be derived from intercalated duct cells. Seventy to eighty percent of pleomorphic adenomas occur at the tail of the parotid and exist superficial to the nerve. However, 10% originate in the deep lobe and as many as 10% - 15% involve both lobes. There is a slight female predominance and it is most commonly seen in the third to sixth decades of life. There are no known specific etiologic factors. Clinically, as with most parotid neoplasms, pleomorphic adenoma usually presents as a firm, freely mobile mass located at the tail of the parotid. Usually it is a unifocal or unilocular type mass. The gross appearance on surgical section is usually well encapsulated or pseudo encapsulated and tannish-white, with a very smooth, homogenous appearance. Recurrent disease however, can be multi nodular. The recurrence rates approach 5% following an adequate primary excision. Previously higher recurrence rates were reported, usually secondary to simple enucleation procedures. Histologically pleomorphic adenoma is comprised of an admixture of epithelial and myoepithelial components, as well as stromal components. The epithelial component can have squamous differentiation with keratinized pearls. The stromal component can be a varying admixture of mucoid, myxomatous and fibrous cells that exist in chondroid areas. Pleomorphic adenoma can be further classified into four types: predominantly myxoid, equally myxoid and cellular, predominantly cellular, and extremely cellular. The capsule may be variable and incomplete with different pseudopod extensions beyond the capsule. There have been incidental case reports of benign disease with metastatic spread, and rare reports of malignant transformation. This has usually been in patients with long-standing disease, usually greater than ten years. Complete surgical excision is the treatment of choice, usually requiring a superficial parotidectomy or a total parotidectomy. It is important to insure an adequate margin of normal tissue, not just enucleation, as this leads to higher recurrence rates. Pleomorphic adenoma is not particularly radiosensitive and therefore, radiation therapy is usually reserved for unresectable or nonsurgical candidates. Warthin’s tumor, also known as papillary cyst adenoma lymphomatosum, was first described in 1929 by Warthin. It comprises 5% - 6% of all salivary gland tumors, and up to 12% of benign parotid gland tumors. There is a male predominance and it has been linked with tobacco use. The peak incidence for Warhin’s tumor is in the fifth to sixth decade of life. It is important to recognize that bilateral disease may be present in up 14% of cases, often may not be concurrent disease, and that up to 18% of patients present with pain. The gross section of a Warthin’s tumor is usually a well encapsulated, brownish lesion of soft tissue with multiple cystic space and papillary projections. There may be solid white nodular areas within the mass and this is representative of mature lymphoid follicles. The tumor is thought to originate from salivary gland duct epithelium. Papillary and cystic lesions consist of epithelial and lymphoid elements. The epithelial component that lines the papillary projections is comprised of a double layer of oncococytes. The lymphoid component consists of mature lymphoid follicles, often with mature germinal centers. Treatment consists of complete surgical excision with an adequate cuff with normal tissue. Recurrent disease is usually secondary to either inadequate primary excision or multi focal disease. Malignant transformation, while reported, is extremely rare. Among the rarer benign tumors is myoepithelioma, which accounts for less than 1% of all salivary neoplasms. There is no gender predilection reported and it is usually seen in adults in the third to sixth decade. The gross appearance of myoepithelioma is usually well circumscribed, with a smooth bosselated appearance and relatively homogeneous. Histologically, it is also well incapsulated. It is composed of monomorphic spindle-shaped cells or the more plasmacytoid type cells in a fasicular or swirling pattern. The cells are usually uniform and there is minimal surrounding stroma. Again, complete excision is curative. Basal cell adenoma accounts for 2% of all salivary type tumors. It is considered one of the monomorphic adenomas. Again, there is no gender predilection and the underlying etiology for the development of these tumors is unclear. Basal cell adenoma is thought to be derived from both ductal and myoepithelial cells. Histologically it is characterized by basaloid appearing cells that can be subdivided into different morphologic patterns: the trabecular pattern, the tubular pattern, membranous pattern and solid pattern. Usually these patients present with a solitary mass; however, the membranous type can present as a multi focal lesion. Again, complete surgical excision is curative. Oncocytoma accounts for less than 1% of all salivary gland neoplasms. There is no gender predilection. Oncocytic metaplasia is the transformation of ductal and acinar epithelium into oncocyte. Usually this does not occur until after 50 years of age. The proliferation of oncocytes then progresses with age and explains why oncocytoma usually do not present until the sixth to eighth decade of life. Oncocytoma can be differentiated from oncocytic hyperplasia in that oncocytomas are usually more well circumscribed and organized. Usually, oncobytoma presents as a painless mass and is usually seen in the parotid gland. Histologically it is an encapsulated tumor with a trabecular or cord like or organoid pattern that is separated by thin fibro-connective stroma. Predominantly, you see these large polyhedral cells with abundant granular eosinophilic cytoplasms. The granular eosinophilic cytoplasm is usually secondary to mitochondrial hyperplasia; however, a clear cell variant may also be seen. Again, the treatment for oncocytoma is complete surgical excision. Radiotherapy is not indicated because oncocytes are thought to be radioresistant. Recurrence is rare. Sebaceous glands are found in normal parotid gland tissue up to 10% of the time; however, the presence of a sebaceous adenoma is extremely rare, less than 1% of all adenomas of the major salivary glands. Microscopically, you see mostly squamous cells with focal sebaceous differentiation. Again, complete surgical excision is the treatment of choice. In the pediatric population, sialoblastoma is a rare congenital or perinatal aggressive lesion that usually presents within the first few months of life and has known aggressive potential, with very low-grade malignant potential as well. It usually involves, or is present in, only the major salivary glands. Seventy-five percent of sialoblastomas present in the parotid glands. These patients may present as firm nodular lesions and it may be fixed. There have been reports of patients presenting with underlying facial nerve paralysis as well. Histologically, sialoblastoma consists of islands of primitive basaloid cells. Hemangioma is another parotid mass that presents in the pediatric population, occurring primarily in children less than one year old, and accounting for 50% of parotid masses in children. These may be the capillary or cavernous type. It may also be associated with cutaneous hemangiomas overlying this. The usual treatment of these is watchful waiting, as 95% of these spontaneously involute within five years. There may be a period of rapid growth within the fourth to six month of life. Other mesenchymal tumors that may present in the parotid, other than the epithelial type tumors, include lipoma, which also comprises less than 1% of parotid gland neoplasms. There is a slight male predominance. These are characterized by all fairly slow, painless growth. Again, excision is curative. Lymphangioma may occasionally involve the salivary gland, but is usually more commonly seen as an extension of cystic hygroma. These are more commonly seen in submandibular gland area; however, the parotid gland has been reported. Other neoplasms include intraparotid schwannoma of cranial nerve VII and neurofibroma. However, these are extremely rare. It is important to recognize that there are also a host of other tumor like conditions that may mimic a benign parotid neoplasm, including benign lymphoepithelial lesions, also termed Mikuliez’s disease or myoepithelial sialoadenitis. It is often seen in association with patients with Sjogren’s syndrome and usually these patients present with a recurrent, firm swelling or diffused swelling of the gland. Histologically, it is characterized by lymphocytic infiltration of the gland, which eventually leads to parenchymal atrophy. It is also important to be aware that these patients are at an increased risk of developing non-Hodgkin’s lymphoma. Chronic sclerosing sialoadenitis may also be seen. This is a chronic inflammatory disease resulting in a firm mass and may often be associated with recurrent pain. It is more commonly seen in the submandibular gland; however it has also been seen in the parotid gland and it is usually related to duct obstruction and sialolithiasis. Histologically, there is chronic focal inflammation, duct ectasia distal to the obstruction, acinar atrophy and extensive fibrosis. Salivary duct cysts can result from chronic obstruction as well. These develop from marked cystic dilations at the salivary ducts that are distal to the obstruction. They may be present in 2% - 3% of all parotid gland lesion. Again, excision is curative. Lymphoepithelial cysts are similar histologically to salivary duct cysts and can also have a similar clinical presentation. The differentiating feature is that lymphoepithelial cysts have dense lymphoid tissue within the cystic wall. In the absence of HIV status these usually present as just a unilateral cystic mass. They usually present in the fourth to fifth decade of life and there is a slight male predominance. These can be differentiated from Warthin’s tumors, which also can present as multiple cystic masses, by presenting more as a unilocular lesion and by not having the papillary configuration of the Warthin’s tumors. In the presence of HIV, you may see multiple lymphoepithelial cysts. These are lymphoid hyperplasia of the salivary glands, most commonly presenting in the parotid gland. The proliferation of duct epithelium gives rise to these cysts in the epithelial island and you may also get the parotid adenopathy. It eventually leads to effacement of the gland as well. It can often be an early manifestation or presenting sign of HIV. Lastly, is sialoadenosis. This is a non-neoplastic, non-inflammatory enlargement of the gland, often secondary to different metabolic factors or secretory dysfunction. It is usually secondary to systemic disease, such as diabetes, thyroid insufficiency, malnutrition, and alcoholism or liver cirrhosis. The salivary gland dysfunction is thought to be due to peripheral autonomic neuropathy. It is characterized by an initial acinar hypertrophy followed by progressive parenchymal atrophy and replacement and effacement with fat. There are a few imaging modalities that assist in the diagnosis; however, general routine use of imaging of small, well-defined masses usually in the superficial lobe located at the tail are not warranted, because these imaging modalities are not likely to alter management. However, imaging may be helpful in assisting with management or diagnosis when there is clinical suspicion of malignancy, questions of deep lobe involvement or questions in diagnosis. CT scan with contrast provides good resolution and is usually the modality of choice. It helps differentiated between intraglandular and extraglandular masses. It may help in the differentiation between benign and malignant disease and assist in assessing for bony involvement of destruction. However, it is important to recognize that CT scan usually does not provide any helpful information on the histologic diagnosis. Only in the diagnosis of lipoma can the CT assist, when the calculi within the gland can be seen. MRI is another imaging modality technique and it may be a useful adjunct to CT. It is superior to CT in demonstrating internal architecture of the salivary gland and is more helpful in delineating the interface between normal tissue and the tumor. MRI may also be helpful in assessing for perineural involvement. Other imaging modalities are no longer very popular, but ultrasonography is also available and may be helpful in differentiating between cystic and solid lesions; however, its use is usually limited just to very superficial disease. Sialography, while inadequate in the evaluation of mass lesions, may be helpful in the assessment of intraductal disease. There is also CT sialography, which is helpful in delineating the ductal system; however, the use of CT sialography will impede the visualization of mass lesion and the demarkation of the mass. Fine needle aspiration is an option in the diagnosis of parotid gland lesions, but the use of FNA is controversial. Opponents of FNA argue that it is unlikely to change the management, particularly in a straightforward, small, superficial mass at the tail of the parotid. The opponents of FNA also state that the results are inconsistent and FNA incurs unnecessary cost. However, advocates of FNA say that this is a relatively low cost, safe and easy to perform procedure and may assist in the management of the patient. In one study, Howler et al looked at 100 different patients who underwent fine needle aspiration for parotid mass. Overall, he found that FNA results led to a change in management in 35% of patients, usually in a change of diagnosis between neoplastic and inflammatory disease. There are multiple studies researching the accuracy and reliability of FNA with variable results, but overall the sensitivity approximates 85% - 99% over the specificity of 96% - 100%. Therefore, proponents of FNA say that it is relatively low cost and may be helpful. Obviously, the accuracy of this modality depends on adequate sampling and the skill of your cyto pathologists. It should be kept in mind that highly cellular samples should be examined with caution, and different cystic lesions should be aspirated more than once. In the past, parotid neoplasms were treated with simple extracapsular enucleation and this often resulted in very high recurrence rates, as high as 45-50%. In 1984, Dr. Donovan emphasized the importance of removing the tumor with an adequate cuff of normal tissue. He emphasized the need to avoid invasion of the capsule, minimizing tumor spillage, as this can lead to feeding and recurrence and understanding and emphasizing the nature of the pathology and that microscopic extensions can often exist to extend beyond what may appear to the growth capsule. Case Report: G.T. is a 67-year-old man who presented to the Otolaryngology clinic complaining of a slowly growing painless mass over the left parotid region for the last three years. He was concerned that it was increasing in size over the last several months. He denied any other symptoms. His past medical history was remarkable only for hypertension. His social history was negative for alcohol or tobacco use. On physical examination, he had a 3cm firm mass located at the left tail of parotid region. His facial nerve function was symmetric bilaterally and fully intact. The remainder of the head and neck exam was unremarkable. He subsequently underwent a superficial parotidectomy. Frozen section pathology was consistent with pleomorphic adenoma. Based on this finding, no further intervention was pursued. Post-operatively, his facial nerve function remained intact. Final pathology confirmed the diagnosis of pleomorphic adenoma. 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Tumors of the Salivary Glands. Washington, DC: Armed Forces Institute of Pathology; 1996. Hanna EY, Suen JY. Neoplasms of the Salivary Glands. Cummings CW, ed. Otolaryngology Head & Neck Surgery, 3 rd ed. St. Louis: Mosby; 1998. pp 1255-1302. Helmus C. Conservative vs superficial parotidectomy for benign lesions of the parotid tail. Arch Otolaryngol Head Neck Surg 1999;125:1164-1165. Helmus C. Subtotal parotidectomy: A 10-year review (1985 to 1994). Laryngoscope 1997;107:1024-1027. Pinkston JA, Cole P. Incidence rates of salivary gland tumors: Results from a population-based study. Otolaryngol Head Neck Surg 1999;120:834-840. Orvidas LJ, Kasperbauer JL, Lewis JE, Olsen KD, Lesnick TG. Pediatric parotid masses. Arch Otolaryngol Head Neck Surg 2000;126:177-184. Rodriguez-Bigas MA, Sako K, Razack MS, Shedd DP, Bakamjian VY. Benign parotid tumors: A 24-year experience. J Surg Oncol 1991;46:156-161. Spiro RH. Diagnosis and pitfalls in the treatment of parotid tumors. Semin Surg Oncol 1991;7:20-24. Spiro RH. Salivary neoplasms: Overview of a 35-year experience with 2807 patients. Head Neck Surg 1986;8:177-184. Van der Wal JE, Leverstein H, Snow GB, Kraaijenhagen HA, van der Waal I. Parotid gland tumors: Histologic reevaluation and reclassification of 478 cases. Head Neck 1998;20:204-207. Wenig BM. Atlas of Head and Neck Pathology. Philadelphia: Saunders; 1993. pp 283-295. Yoo GH, Eisele DW, Askin FB, Driben JS, Johns ME. Warthin’s tumor:A 40 year-experience at the Johns Hopkins Hospital. Laryngoscope 1994;104:799-803. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2005 Baylor College of Medicine
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