Minor Salivary Gland Tumors

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.

Salivary gland neoplasms are reported to represent between 1 and 5 per cent of all head and neck tumors. Based on National Cancer Institute data, Auclair, et al estimate between 2.2 and 2.5 cases of salivary gland tumors per 100,000 people occur each year in the United States. Various series from around the world report annual incidence for all salivary gland neoplasms to be between 0.4 to 13.5 cases per 100,000.

There are four large series describing 22,866 salivary gland neoplasms reported in the literature. These series are from the Armed Forces Institute of Pathology in 1991, Memorial Sloan Kettering in 1986, Pathology Institute University of Hamberg 1986, and the British Salivary Gland Panel in 1985. Of these 22,866 salivary gland neoplasms, 5,539 or 23% were localized to the minor salivary glands. Based on this data for every 100 parotid tumors, there are about 40 minor salivary gland tumors, 15 submandibular tumors and 1 sublingual tumor.

Most salivary gland neoplasms occur in the third to fifth decade and have a slight female predominance.

Of the 5539 minor salivary gland lesions, 44% were benign and 56% were malignant. This is in sharp contrast to the commonly quoted 80% malignancy rate which is derived from Spiro's 607 patients from Memorial Sloan Kettering Cancer Center. Spiro states in his articles that his data may be biased by his patient population.

While the paired parotid, submandibular, and sublingual glands comprise the major salivary glands, the minor salivary glands include approximately 500-1,000 simple tuboalveolar glands distributed throughout the submucosa of the upper aerodigestive tract. These glands are predominately mucous secreting. The minor salivary glands contribute to the mucous blanket of the respiratory tract which traps and clears particulate matter. In the oral cavity, the minor salivary glands produce most of the saliva not secreted at mealtime, which moistens and protects the mucous membranes; They facilitate taste deglutition and guard against cavities.

Approximately 450 to 750 minor salivary glands are present intraorally, located in the mucosa of the lips and cheeks, hard and soft palate, uvula, floor of mouth, posterior tongue, retromolar trigone, and peritonsillar area. The largest concentration of intraoral salivary glands is on the hard palate. Other mucous secreting glands of identical histology are present in the nose, nasopharynx, paranasal sinuses, larynx, tracheobronchial tree, and lacrimal glands. Heterotopic glands have been reported in lymph nodes, middle ear, body of the mandible, neck, hypopharynx, sternoclavicular joint, pituitary gland, and along the thyroglossal duct.

The salivary gland unit is composed of acini of serous or mucous cells which drain through the intercalated duct, striated duct, and excretory duct. Myoepithelial cells surround the acinar cells and the intercalated duct. The myoepithelial cells contract forcing saliva through the ductal system. Stem cells which give rise to the different elements of the salivary glands are present in the basal layer of the excretory duct and intercalated duct.

In 1953, Foote and Frazell published a paper categorizing salivary neoplasms which helped standardize pathologic diagnosis. Over the years updated classification schemes have been proposed. The most recent classification is depicted here and was published in 1991 by the World Health Organization. This classification encompasses all salivary gland neoplasms and places them into three groups: adenomas, carcinomas, and other tumors involving the salivary glands. The classification also includes salivary gland disorders which may be mistaken for neoplasms.

These entities can be differentiated based on clinical findings, characteristic histologic features, and immunohistochemical staining.

The multicellular theory asserts that salivary gland neoplasms arise from the adult differentiated counterpart of the salivary gland unit. Acinous tumors arise from the acinar cells, oncocytic tumors arise from the striated duct cells, mixed tumors develop from the intercalated duct and myoepithelial cells, and squamous cell and mucoepidermoid carcinomas develop from the excretory duct cells.
The bicellular theory states that the basal cells of the excretory and intercalated duct act as stem cells. The stem cells of the intercalated ducts give rise to acinous cell carcinoma, adenoid cystic carcinoma, mixed tumors, oncocytic tumors and Warthin's tumor while the stem cells of the excretory duct give rise to squamous cell and mucoepidermoid carcinoma.

Radiation exposure has been associated with the development of salivary gland neoplasms. Long-term observation of 82,000 people exposed to atomic bombs in Hiroshima and Nagasaki demonstrated a 3.5-fold relative risk for benign tumors and 11-fold relative risk for malignant tumors.

Numerous studies of patients who received radiotherapy for benign conditions detected an increased risk for salivary gland neoplasms. Most of these tumors occur in the parotid gland, and like radiation-induced thyroid cancer, there is a long latency period between radiation exposure and neoplasm development.

Certain occupational exposures have also been associated with salivary gland neoplasms. The association between adenocarcinoma of the paranasal sinuses and wood workers has also been described in the literature. Other risky occupations include asbestos mining, rubber manufacturing, and plumbing.

It is interesting to note, that unlike other cancers of the head and neck, smoking tobacco and consuming alcohol are not associated with increased risk.

While no formal clinical staging exists for reporting neoplasms of the minor salivary glands, Spiro, et al., in 1991 reported that staging criteria used for squamous cell carcinoma were useful for predicting treatment results. Adenoid cystic carcinoma was a notable exception, since staging was of no value in predicting survival rates in these patients.

Computed tomography is useful to evaluate bone erosion and lesions of the paranasal sinuses.In a series of 9 minor salivary gland tumors evaluated by contrast enhanced computed tomography and magnetic resonance imaging, 4 lesions were missed by CT, while all lesions were identified on MRI, leading the Kaneda, et al, in 1994 to conclude that MRI is superior to CT for evaluation minor salivary gland lesions.

In general, on MRI benign lesions appear as well-defined, inhomogeneous masses, without peripheral enhancement on T1-weighted images and they appear hyperintense on T2-weighted images. While malignant lesions also appear inhomogenous, and hyperintense on T2-weighted images, they appear ill-defined, and have peripheral enhancement on T1-weighted images. It is hypothesized that this peripheral enhancement represents hemorrhage. Kaneda et al, warn that these findings are only suggestive of malignancy and specific diagnosis must be made by histopathologic examination.

Fine-needle aspiration of salivary gland lesions may provide preoperative tissue diagnosis. Sismanis, et al in 1981 reported a 74% overall accuracy rate based on a series of 51 fine needle aspirations. The advantages of fine needle aspiration include its safety, cost, and speed. This may be useful in patients who are poor operative risks. One disadvantage of fine needle aspiration is that architectural features and tissue invasion can not be evaluated.

In Conley's editorial response to Sismanis' paper he warns "All surgeons would be prudent to recognize the limitations of this specific technique of needle aspiration and take it for precisely what it represents." He goes on to say "The pleomorphic nature of this variety of neoplasm makes it dangerous to make any management decisions on the basis solely of a smear proffered to the pathologist."

Frozen section evaluation of tissue is an important adjunct in diagnosis and treatment of salivary gland neoplasms. A series of 100 major and minor salivary neoplasm specimens examined by Ringual, et al in 1986 revealed a 92% accuracy rate for a specific diagnosis. No unnecessary radical surgery was performed. Auclair's review of the literature in 1991 revealed an overall accuracy of 96.2% based on 21 series. Accuracy was only 77% for malignant lesions. False negative readings are most common with mucoepidermoid carcinoma and are usually caused by sampling errors. The whole specimen should be sent to the pathologist who should decide which areas to evaluate.

In addition to determining the specific pathology, frozen sections are useful to evaluate perineural invasion and margins. Auclair warns that "it is important to remember that a therapeutic decision should never be made on the basis of a frozen section diagnosis alone; is should always be made in conjunction with the clinical findings."

Minor salivary gland tumors occur in the oral cavity or oropharynx in almost 90% of cases. Four percent of minor salivary gland tumors occur in the nasal cavity, nasopharynx, and paranasal sinuses. This is probably an underestimate of the true prevalence of these lesions. Batsakis states that there is no histologic difference between mucous glands of the nose and paranasal sinuses, and other minor salivary glands, yet some pathologists, including the pathogists at the Armed Forces Institute of Pathology, do not classify tumors of this anatomic site as salivary gland tumors. In Spiro's series from Memorial Sloan Kettering, neoplasms from the nasal cavity, nasopharynx, and paranasal sinuses represent nearly 25% of his patients, which maybe a more accurate estimate of the their incidence. Other minor salivary gland tumors have been described in the larynx, trachea, neck, ear, lacrimal glands, and heterotopic salivary tissue.

80-90% of tumors in the nose and paranasal sinuses are squamous cell carcinomas. Minor salivary gland tumors represent only 4-8% of paranasal sinus neoplasms.These lesions which have been likened to "a fire which smolders unnoticed within the walls of a house," typically present after a long course of symptoms including nasal obstruction, rhinorrhea, "polyps", and epistaxis, and may be beyond control when the diagnosis is finally made.

Clinicians need to maintain a high index of suspicion when patients with these common symptoms do not respond to conventional therapy. Adenocarcinoma and adenoid cystic carcinoma are the most common histologies present in this region. Malignant lesions most commonly arise from the maxillary sinuses, ethmoid sinuses, high nasal cavity and nasopharynx. Pleomorphic adenomas most commonly arises in the nasal cavity.

Minor salivary gland neoplasms account for less than 1% of all malignancies of the larynx. The location of these tumors corresponds to the location of mucous glands in the larynx. There are no minor salivary glands present on the free margin of the true vocal fold, the posterior surface of the epiglottis, and a portion of the aryepiglottic fold. In 1983, Dr. Donovan reported three cases of adenoid cystic carcinoma of the subglottic region. Subglottic tumors typically present with shortness of breath, dyspnea on exertion, and may be accompanied by hoarseness. Supraglottic tumors typically cause hoarseness and dysphagia. On endoscopy, patients typically have a submucosal mass with normal overlying respiratory epithelium. Patients may present with a neck mass. In the majority of patients symptoms have been present for greater than 6 months. The most common histologies in the larynx are adenoid cystic carcinoma and adenocarcinoma. Benign minor salivary gland tumors of the larynx are rare. Pleomorphic adenomas of the subglottis are the most frequently encountered benign minor salivary gland neoplasm of larynx.

Within the oral cavity 50% of tumors occur in the palate (mostly the hard palate), 22% occur in the lips, 12% occur in the buccal mucosa, 7% in the tongue, 5% in the floor of mouth and retromolar trigone, and 4% in the tonsillar region. In one series of 103 labial minor salivary gland tumors reported by Neville, et al. in 1988, it is interesting to note that 85% of the tumors were from the upper lip; and 15% were from the lower lip. Of the upper lip lesions 90% were benign, while 98.3% of the lower lip lesions were malignant.

Symptoms are based on location. Most frequently, patients complain of a painless mass, although pain, parasthesias, dysphagia, speech impairment, and referred otalgia may occur. On physical examination, these lesions typically present as smooth, non-ulcerated masses; unless previously biopsied. Benign lesions are typically mobile unless located on the palate or alveolar ridge. Neoplasms are usually located lateral to the midline in the palate, unlike palatine tori which are midline and bony hard.

The most common histology in the palate is pleomorphic adenoma accounting for 50% of all neoplastic lesions, 21% are mucoepidermoid carcinoma, adenocarcinoma and adenoid cystic carcinoma account for 8% of the lesions each. Lesions of the tongue, retromolar trigone, and floor of mouth are more likely than palatal lesions to be malignant.

Despite the lengthy list of neoplasms which may develop in minor salivary glands, 75% of benign lesions are pleomorphic adenomas or benign mixed tumors, and 20% of lesions are monomorphic adenomas.

Pleomorphic adenomas, also known as benign mixed tumors, represent 75% of all benign minor salivary gland tumors and are the most common neoplasm of the minor salivary glands. The palate is the most frequent location followed by the lips. Patients typically present with a painless slow-growing mass for periods up to years. Other symptoms are related to the anatomic site of lesion. Grossly, they are freely mobile, well-demarcated masses. Unlike parotid lesions, pleomorphic adenomas of the minor salivary glands tend to be unencapsulated. Recurrent lesions are typically multinodular.

Histologically they have a fibrous capsule and contain an admixture of epithelial, myoepithelial and stromal components. All components must be identified to diagnose pleomorphic adenomas, but one component may predominate. Necrosis and mitosis are rare. Epithelial cells are cytokeratin positive, and myoepithelial cells stain for cytokeratin, S-100 protein, glial fibrillary acidic protein, actin and vimentin.

Monomorphic adenomas represent 20% of the benign minor salivary glands. Monomorphic adenomas include basal cell adenoma, canulicular adenoma, oncocytoma, myoepithelioma, and Warthin's tumor. Unlike pleomorphic adenomas, monomorphic adenomas lack a stromal component. It is questionable if Warthin's tumor can arise in salivary glands other than the parotid since it originates in part from lymphoid tissue.

Ductal papillomas including sialadenoma papilliferum, intraductal papilloma and inverted ductal papilloma represent the remaining 5% of neoplasms.

Of malignant minor salivary gland neoplasms, 38% are mucoepidermoid carcinoma, followed by adenoid cystic carcinoma 22%, adenocarcinoma 22%, 5% are mixed malignant, and 5% are acinic cell carcinoma.

Mucoepidermoid carcinoma is the most common malignant minor salivary gland tumor representing 38% of malignant neoplasms. Mucoepidermoid carcinomas occur most commonly in the palate and can be divided into 3 grades: low, intermediate, and high. Lower grade lesions typically have a higher number of mucous secreting cells and may form cystic structures. Individual cell keratinization may occur while keratin pearls and intracellular bridges are rare. On immunohistochemical staining, mucoepidermoid carcinomas are cytokeratin positive; S-100 protein, glial fibrillary acidic protein, and actin negative.

The clinical presentation and course of mucoepidermoid carcinoma correlates with the grade of the lesion. Low grade and intermediate grade lesions can be treated with wide-local excision and neck-dissection in clinically positive necks. High-grade lesions require wide-block surgical excision. Neck dissection and post-operative irradiation are also recommended.

Adenoid cystic carcinoma accounts for 22% of minor salivary gland malignancies. These neoplasms occur most commonly in the palate. and frequently spread by perineural invasion; this can present clinically as a cranial nerve palsy or loss of sensation. Three histologic types are described: cribiform, tubular and solid. The tubular pattern is thought to have the best prognosis and the solid pattern the worst prognosis. All three types are characterized by fairly uniform-sized cells with small hyperchromatic nuclei, scant cytoplasm, and indistinct cell borders.

Immunohistochemistry reveals two cell populations: ductal cells which are positive for cytokeratin, S-100 protein, epithelial membrane antigen, and carcinoembyonic antigen; and myoepithelial cells which are positive for cytokeratin, S-100 protein, actin, and glial fibrillary acidic protein.

In the past. the aggressiveness of adenoid cystic carcinoma has been underestimated because of its relatively benign histologic appearance and favorable short-term treatment results.

Treatment usually consists of wide surgical excision and radiotherapy for residual microscopic disease, perineural invasion, inoperable or recurrent disease. Small lesions without perineural invasion or bone erosion can be treated by surgery alone. Long-term follow-up is mandatory.

Adenocarcinoma represents 22% of minor salivary gland neoplasms. Several forms have been described including papillary, sessile, alveolar-mucoid, and a group of tumors which occurs almost exclusively in the oral minor salivary glands known as polymorphous low-grade adenocarcinoma. Polymorphous low-grade adenocarcinoma only represents 3% of malignant minor salivary gland neoplasms. Papillary adenocarcinoma located in the ethmoids is the histology most often associated with woodworkers.

Adenocarcinomas display heterogeneous histology, but common to all lesions is the presence of glands and absence of epidermoid differentiation. In higher grade lesions, glandular elements may be more difficult to identify. In polymorphous low-grade adenocarcinoma a variety of growth patterns are present usually within the same lesion. A tendency toward perivascular and perineural invasion is present. Mitotic figures are rare and necrosis is not seen. In all adenocarcinomas, immunohistochemical staining is positive for cytokeratin, epithelial membrane antigen, and S-100 protein. Carcinoembryonic antigen, actin, and glial fibrillary acidic protein are variably immunoreactive.

Treatment for adenocarcinomas include conservative but complete surgical excision, neck dissection with clinical evidence of cervical lymph node metastasis. Postoperative radiotherapy may be beneficial in high grade lesions. With the exception of polymorphous low-grade adenocarcinoma, adenocarcinomas tend to recur locally.

Acinic cell carcinoma represents 5% of malignant minor salivary gland neoplasms. This tumor is usually circumscribed and may have a variety of growth patterns: solid, microcystic, papillary-cystic, and follicular. These lesions may be multifocal. Cell types present in these lesions include acinic cells, intercalated duct cells, vacuolated cells, clear cells, and nonspecific glandular cells. These lesions are cytokeratin positive and have variable immunoreactivity to S-100 protein and vimentin. Complete surgical excision is the treatment of choice.

The malignant mixed tumor refers to two distinct neoplasms carcinoma ex-pleomorphic adenoma and carcinosarcoma.

Carcinoma ex-pleomorphic adenoma most commonly is a focus of adenocarcinoma arising in a pleomorphic adenoma, but can be almost any histology arising in a pleomorphic adenoma. These lesions usually present as longstanding painless masses that rapidly enlarge over a 3 to 6 month period. They often become painful and fixed. Treatment is surgical, and recurrence is common.

Carcinosarcoma consists of a mixture of malignant epithelial and mesenchymal elements. These rare lesions are typically poorly circumscribed, infiltrative lesions and commonly are composed of an epithelial component like moderate to poorly differentiated ductal carcinoma and sarcomatous component like chrondrosarcoma. Treatment is surgical excision, followed by neck dissection and radiotherapy for palpable disease and chemotherapy for distant metastasis.

Other malignant epithelial neoplasms reported in the minor salivary glands include adenosquamous, epithelial-myoepithelial cell carcinoma, cell carcinoma, oncocytic carcinoma, squamous cell carcinoma, and undifferentiated carcinoma.

Surgery is the treatment of choice for minor salivary gland neoplasms. According to Gates "The first excision should be the most definitive and comprehensive; treatment of recurrent disease is generally futile. In general, the largest excision that can be performed without physiologic mutilation should be carried out."

Benign neoplasms can be treated solely with surgical excision. Pleomorphic adenomas must be completely excised with an adequate margin. Incomplete excision increases the risk for recurrence and the difficulty of future resections. Recurrent pleomorphic adenomas of the palate may be associated with skull base invasion through the palatine foramen. It is uncommon for other benign neoplasms to recur after complete surgical extirpation.

Surgical removal of paranasal sinus neoplasms may require combined intracranial and extracranial approaches to resection. Although in a paper from 1983, Dr. Goepfert warns "an ultraradical approach seems to be unwarranted if it fails to remove all gross disease." Maxillary sinus lesions can usually be managed with maxillectomy and orbital exenteration if the orbit is involved.

Laryngeal neoplasms require wide surgical excision with either partial laryngectomy, laryngectomy, or larygopharyngectomy.

Treatment of oral cavity neoplasms includes complete surgical excision which may require a palatectomy for palate lesions, removal of the buccinator muscle for cheek lesions, and removal of the maxilla of mandible if they are involved.

The affinity of adenoid cystic carcinoma for perineural invasion requires special attention. In adenoid cystic carcinoma of the palate, the greater palatine nerve should be identified and submitted for frozen section. Although it is probably controversial today, Weisberger and his group at MD Anderson, in 1979 recommend tracing the greater palatine nerve to the foramen rotundum in an attempt to obtain clear surgical margins. In 1989, Weber et al. from MD Anderson advocated tracing the mental nerve in a retrograde fashion for adenoid cystic carcinomas of the lip with perineural invasion. If these maneuvers fail to produce clear margins than postoperative radiation is indicated.

Neck dissections are recommended for clinically positive necks, and in patients with high-grade mucoepidermoid carcinoma.

The effect of radiation therapy on minor salivary gland neoplasms was retrospectively studied in a group of 160 patients at MD Anderson Cancer Center in 1994. Garden, et al recommend the use of radiation in patients with perineural invasion, positive margins, high-grade histology, recurrence, and in patients with neck disease. Microinvasion of small unnamed nerves is not an indication for radiotherapy. They recommend a dose of 6000 cGray over 6 weeks. Treatment should commence as soon as possible after surgery. In the mid-1960's when high-grade lesions were treated only by surgery recurrence rates were reported to be as high as 50%. In this series only 12% had a local recurrence, while 36% of patients relapsed with distant metastasis. Radiation also increases local control in unresectable and inoperable lesions.

Based on a series of 52 patients, Ellis et al, in 1988 claim that radiation therapy alone is effective in patients with early-stage minor salivary gland tumors, and surgery can be reserved for salvage.

Complications of radiotherapy are rare but include serous otitis media with decreased hearing, visual impairment or blindness, and bone necrosis.

According to Kaplan et al in 1986 the indications for chemotherapy in salivary gland neoplasms are recurrent, inoperable or metastatic disease. In a review of 116 cases, they report a 10% complete response rate and 40% overall response rate. The responses were short-lived lasting only 6 to 8 months. Cisplatinum, adriamycin, and 5-fluorouracil were identified as active agents against adenoid cystic carcinoma, acinous cell carcinoma, adenocarcinoma, and mixed malignant tumors; and Carboplatinum, methotrexate and 5- fluorouracil were active against mucoepidermoid carcinoma. Chemotherapy was palliative, relieving pain in many cases.

In 1982, Dr. Sessions and a group from Baylor reported the use of intra-arterial cisplatinum for adenoid cystic carcinoma and emphasized that this technique may be particularly useful in tumors of the minor salivary glands. According to Dr. Sessions, intra-arterial administration of cisplatin may shrink the size of the primary tumor and enhance the success of later surgery, or may offer substantial palliation.

According to the National Cancer Institute Cancer Information Service, there is currently an ongoing phase II clinical trial evaluating the response rate of metastatic and recurrent salivary gland malignancies to taxol (paclitaxel).

In Spiro's 1991 review of 436 previously untreated minor salivary gland neoplasms, he found the 5 year survival for malignant neoplasms was 73%, 10 year survival was 56%, 15 year survival was 46% and the 20 year survival was 35% for patients treated with surgery. This data was compared to a similar cohort of patients with major salivary gland neoplasms and no difference in survival was found. Patients with sinus primaries had a significantly lower overall survival rate compared to patients with oral lesions at 10 years.

Spiro also divided minor salivary gland malignancies into two groups: low-grade neoplasms including low-grade mucoepidermoid carcinoma, low grade adenocarcinoma, and acinic cell carcinoma; and high-grade malignancies including malignant mixed tumor, high grade mucoepidermoid tumors, high grade adenocarcinoma and adenoid cystic carcinoma. Patients with low-grade histologies had a significantly better survival rate over twenty years.

Low grade lesions had a 93% survival at 10 years compared to 42-58% at 10 years.

Although minor salivary gland neoplasms are infamous for late recurrence, 70% of recurrences appear within 2 years. Paranasal sinus lesions are particularly prone to recurrence, as are adenoid cystic carcinomas, adenocarcinomas, and pleomorphic adenomas excised without an adequate margin.There are reports of local recurrence developing over 20 years after initial treatment.

With regards to metastasis, in Spiro's series of 378 patients who had carcinomas of the minor salivary glands, at least 19% developed distant spread with the likelihood significantly increased if the neck was clinically positive at presentation. The incidence of distant metastasis for adenoid cystic carcinoma is reported to be between 25%-50%. The most frequent sites being the lung and bone. With adenoid cystic carcinoma, surgical excision of isolated pulmonary metastasis is indicated due to its indolent nature.

Non-neoplastic minor salivary gland pathologies, categorized as tumor-like lesions in the World Health Organization classification, also occur and may be mistaken for neoplastic processes. Of the listed conditions, three commonly occur in the minor salivary glands -- Necrotizing sialometaplasia, benign lymphoepithelial lesions and salivary gland cysts.

Sialadenosis, oncocytosis, and chronic lymphoid hyperplasia typically occur in the parotid glands, and chronic sclerosisng sialadenitis occurs in the submandibular gland.

Necrotizing sialometaplasia, or salivary gland infarction, is most commonly localized to the palate and occurs in patients in the sixth to seventh decade. This lesion is usually caused by trauma, or previous surgery. Because of its ulcerative appearance, it may be confused with a malignancy. These lesions heal spontaneously.

Benign lymphoepithealial lesions are a local manifestation of Sjogrens syndrome and are characterized by recurrent painful swelling of the parotid glands. Similar lesions also occur in the minor salivary glands, particularly the lips. These lesions are associated with an increased risk of developing lymphoma.

Also of note, 75% of salivary glands cysts, or mucoceles, occur in the minor salivary glands predominantly in the lower lip and floor of mouth.

23% of salivary gland neoplasms occur in the minor salivary glands.
of these lesions 44% of the neoplasms are benign; 56% malignant
The most common location is in oral cavity and in the oral cavity the most common location is the palate. The most common neoplasm overall is pleomorphic adenoma.
The most common malignant neoplasms are mucoepidermoid, adenoid cystic, and adenocarcinoma
MRI is superior to CT scan for imaging minor salivary tumors
Optimal management considers: local control; neck treatment, radiation, and chemotherapy;
treatment modifications are dictated by site and histology
Long term follow-up is mandatory.

A 35-year-old gentleman presented with a three week history of a painless submucosal mass at the junction of the hard and soft palate on the right. The patient had no lymphadenopathy or neurologic deficits. A biopsy revealed adenoid cystic carcinoma. An MRI revealed a well-demarcated 2.0 cm mass confined to the soft palate. The mass was intermediate density with peripheral enhancement on T1-weighted images and hyperintense on T2-weighted images. The patient underwent a right partial palatectomy, and skin graft placement. Pathologic examination demonstrated a 3.0 x 2.0 x 1.7 cm adenoid cystic carcinoma originating in the soft palate. Perineural invasion was identified in areas adjacent to the main tumor mass. The margins were free of tumor. Postoperatively, the patient received 6000 cGy over 6 weeks to opposing lateral fields from the level of the palate to the base of skull. The patient is currently doing well 4 months after his initial procedure.

Auclair PL, et al. Salivary gland neoplasms: general considerations. In: Ellis GL, Auclair PL, Gnepp DR, editors. Surgical Pathology of the Salivary Glands, 1st ed. Philadelphia: W.B. Saunders Company, 1991:135-164.

Auclair PL, Goode RK, Ellis GL. Mucoepidermoid carcinoma of intraoral salivary glands. Cancer 1992;69:2021-2030.

Bardwil JM, Reynolds CT, Ibanez ML, Luna MA. Report of one hundred tumors of the minor salivary glands. Am J Surg 1966;112:493-497.

Batsakis JG, Chinn E, Regezi JA, Repola DA. The pathology of head and neck tumors: salivary glands, part 2. Head Neck Surg 1978;1:167-180.

Batsakis JG, Holtz F, Sueper RH. Adenocarcinoma of the nasal and paranasal cavities. Arch Otolaryngol 1962;77:625-633.

Batsakis JG, Regezi JA. The pathology of head and neck tumors: salivary glands, part 1. Head Neck Surg 1978;1:59-68.

Brown RL, Bishop EL, Girardeau HS. Tumors of the minor salivary glands. Cancer 1959;12:40-46.

Chaudhry AP, Vickers RA, Gorlin RJ. Intraoral minor salivary gland tumors: an analysis of 1,414 cases.Oral Surg Oral Med Oral Pathol 1961;14:1194-1226.

Da-quan M, Guang-Yan Y. Tumours of the minor salivary glands: A clinicopathologic study of 243 cases. Acta Otolaryngol 1987;103:325-331.

Donovan DT, Conley J. Adnenoid cystic carcinoma of the subglottic region. Ann Otol Rhinol Laryngol 1983;92:491-495.

Ellis ER, Million RR, Mendenhall WM, Parsons JT, Cassisi NJ. The use of radiation therapy in the management of minor salivary gland tumors. Int J Radiation Oncology Biol Phys 1988;15:613-617.

Eveson JW, Cawson RA. Salivary gland tumors: a review of 2,410 cases with particular reference to histological types, site, age, and sex distribution. J Pathol 1985;146:51-58.

Garden AS, Weber RS, Ang KK, Morrison WH, Matre J, Peters LJ. Postoperative radiation therapy for malignant tumors of the minor salivary glands. Cancer 1994;73:2563-2569.

Gates GA. Malignant neoplasms of the minor salivary glands. NEJM 1982;306:718-722.

Giannoni C, El-Naggar AK, Ordonez NG, Tu ZN, Austin J, Luna MA, Batsakis JG. c-erbB-2/neu oncogene and Ki-67 analysis in the assessment of palatal salivary gland neoplasms. Otolaryngol Head Neck Surg 1995;112:391-398.

Goepfert H, Giraldo AA, Byers RM, Luna MA. Salivary gland tumors of the base of the tongue. Arch Otolaryngol 1976;102:391-395.

Goepfert H, Luna MA, Lindberg RD, White AK. Malignant salivary gland tumors of the paranasal sinuses and nasal cavity. Arch Otolaryngol 1983;109:662-668.

Jenkins DW, Spaulding CA, Constable WC, Cantrell RW. Minor salivary gland tumors: the role of radiotherapy. Am J Otolaryngol 1989;10:250-256.

Kaneda T, Minami M, Ozawa K, et al. Imaging of the minor salivary glands. Oral Surg Oral Med Oral Pathol 1994;77:385-90.

Kaplan MJ, Johns ME, Cantrell RW. Chemotherapy for salivary gland cancer. Otolaryngol Head Neck Surg 1986;95:165-170.

Kim KH, Sung MW, Chung PS, Rhee CS, Park CI, Kim WH. Adenoid cystic carcinoma of the head and neck. Arch Otolaryngol 1994;120:721-726.

Kuhel W, Goepfert H, Luna M, Wendt C, Wolf P. Adenoid cystic carcinoma of the palate. Arch Otolaryngol 1992;118:243-247.

Neville BW, Damm DD, Weir JC, Fantasia JE. Labial salivary gland tumors. Cancer 1988;61:2113-2116.

Posner MR, Ervin TJ, Weichselbaum RR, Fabian RL, Miller D. Chemotherapy of advanced salivary gland neoplasms. Cancer 1982;50:2261-2264.

Regezi JA, Lloyd RV, Zarbo RJ, McClathchey KD. Minor salivary gland tumors: a histologic and immunohistochemical study. Cancer 1985;55:108-115.

Rigual NR, Milley P, Lore JM, Kaufman S. Accuracy of frozen-section diagnosis in salivary gland neoplasms. Head Neck Surg 1986;8:442-446.

Rounthwaite FJ, Frei JV, Wallace AC, Watson TA. The effect of radiotherapy in the treatment of adenoid cystic carcinoma of the head and neck arising in minor salivary glands. J Otolaryngol 1977;6:297-308.

Sadeghi A, Tran LM, Mark R, Sidrys J, Parker RG. Minor salivary gland tumors of the head and neck: Treatment Strategies and Prognosis. Am J Clin Oncol 1993;16:3-8.

Seifert G. Tumour-like lesions of the salivary glands: the new WHO classification. Path Res Pract 1992;188:836-846.

Sessions RB, Lehane DE, Smith RJH, Brian N, Suen JY. Intra-arterial cisplatin treatment of adenoid cystic carcinoma. Arch Otolaryngol 1982;108:221-224.

Sismannis A, Merriam JM, Kline TS, Davis RK, Shapshay SM, Strong MS. Diagnosis of salivary gland tumors by fine needle aspiration biopsy. Head Neck Surg 1981;3:482-489.

Smith SA. Radiation-induced salivary gland tumors. Arch Otolaryngol 1976;102:561-562.

Spiro RH, Koss LG, Hadju SI, Strong EW. Tumors of minor salivary origin: a clinicopathologic study of 492 cases. Cancer 1971;31:117-129.

Spiro RH, Thaler HT, Hicks WF, Kher UA, Huvos AH, Strong EW. The importance of clinical staging in minor salivary gland carcinoma. Am J Surg 1991;162:330-336.

Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2,807 patients. Head Neck Surg 1986;8:177-184.

Stillwagon GB, Smith RRL, Highstein C, Lee DJ. Adenoid cystic carcinoma of the supraglottic larynx. Am J Otolaryngol 1985;6:309-314.

Suen JY, Johns ME. Chemotherapy for salivary gland cancer. Laryngoscope 1982;92:235-239.

Waldron CA, El-Mofty SK, Gnepp DK. Tumors of the intraoral minor salivary glands: a demographic and histologic study of 426 cases. Oral Surg Oral Med Oral Pathol 1988;66:323-333.

Wang CC, Goodman M. Photon irradiation of unresectable carcinomas of salivary glands. Int J Radiation Oncology Biol Phys 1991;21:569-576.

Weber RS, Palmer JM, El-Naggar AE, McNeese MD, Guillamondegui OM, Byers RM. Minor salivary gland tumors of the lip and buccal mucosa. Laryngoscope 1989;99:6-9.

Weisberger E, Luna MA, Guillamondegui OM. Salivary gland cancers of the palate. Am J Surg 1979;138:584-587.

©2001-2006 Baylor College of Medicine
Bobby R. Alford Department of Otolaryngology-Head and Neck Surgery
Mail: One Baylor Plaza, NA102, Houston, TX 77030
Phone: 713-798-5906
E-mail: oto@bcm.edu

Last modified: Feb. 8, 2006