Various types of parotid gland tumors are discussed from nonneoplastic to both benign and malignant neoplasms. The anatomic relationship of the facial nerve is discussed as it exits the stylomastoid foramen and courses through the parotid gland. The effect of certain tumors on facial nerve function is also characterized. Details on which types of parotid tumors are more likely to affect facial nerve function and different prognostic predictors of return to function are evaluated. In addition, the prognostic value of tumor size and histologic type of parotid tumor is included.
Key points
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The different types of parotid gland tumors, nonneoplastic and both benign and malignant neoplasms, are discussed.
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In general, benign tumors do not affect facial nerve function. However, there are some rare cases of benign tumors invading the stylomastoid foramen, and through compression, presenting with facial nerve paresis/paralysis.
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Facial nerve paresis/paralysis is a poor prognostic indication and is associated with size and aggressiveness of parotid tumor.
Introduction
Approximately 25% of parotid masses are nonneoplastic; the remaining 75% are neoplastic. Salivary gland tumors are relatively rare and constitute only 3% to 4% of all head and neck neoplasms. Approximately 70% of salivary gland tumors arise in the parotid gland. Although most minor salivary gland tumors are malignant, three-fourths of parotid tumors are benign. The most common malignant types of tumor in the parotid gland are mucoepidermoid carcinoma (30%), adenoid cystic carcinoma, and malignant mixed tumors. Traditionally, facial nerve paralysis or paresis is an ominous sign that a parotid mass is most likely malignant and has invaded the facial nerve. However, this is not always the case because there have been case reports indicating that some benign tumors of the parotid gland can invade the stylomastoid foramen, and through compression, can cause paresis or paralysis.
At least 2 theories of tumorigenesis have been proposed for salivary gland neoplasms. In the first, the multicellular theory, each type of neoplasm is thought to originate from a distinctive cell type within the salivary gland unit. Therefore, Warthin and oncocytic tumors are thought to arise from striated ductal cells, acinic cell tumors from acinar cells, and mixed tumors from intercalated duct and myoepithelial cells. This theory is supported by the observation that all differentiated salivary cell types retain the ability to undergo mitosis and regenerate. The second theory, the bicellular reserve cell theory, assumes that the origin of the various types of salivary neoplasms can be traced to the basal cells of either the excretory or the intercalated duct. According to this theory, either of these 2 cells can act as a reserve cell with the potential for differentiation into a variety of epithelial cells. So despite the seeming heterogeneity of salivary tumors, all of them are thought to arise from 1 of 2 pluripotent stem cell populations. In this theory, adenomatoid tumors, including pleomorphic adenoma, and oncocytic tumors are derived from the reserve cell of the intercalated duct, whereas epidermoid tumors, such as squamous cell and mucoepidermoid carcinomas, are derived from the reserve cells of the excretory duct. Some reports provide molecular evidence to support the reserve cell theory of salivary gland tumorigenesis.
Introduction
Approximately 25% of parotid masses are nonneoplastic; the remaining 75% are neoplastic. Salivary gland tumors are relatively rare and constitute only 3% to 4% of all head and neck neoplasms. Approximately 70% of salivary gland tumors arise in the parotid gland. Although most minor salivary gland tumors are malignant, three-fourths of parotid tumors are benign. The most common malignant types of tumor in the parotid gland are mucoepidermoid carcinoma (30%), adenoid cystic carcinoma, and malignant mixed tumors. Traditionally, facial nerve paralysis or paresis is an ominous sign that a parotid mass is most likely malignant and has invaded the facial nerve. However, this is not always the case because there have been case reports indicating that some benign tumors of the parotid gland can invade the stylomastoid foramen, and through compression, can cause paresis or paralysis.
At least 2 theories of tumorigenesis have been proposed for salivary gland neoplasms. In the first, the multicellular theory, each type of neoplasm is thought to originate from a distinctive cell type within the salivary gland unit. Therefore, Warthin and oncocytic tumors are thought to arise from striated ductal cells, acinic cell tumors from acinar cells, and mixed tumors from intercalated duct and myoepithelial cells. This theory is supported by the observation that all differentiated salivary cell types retain the ability to undergo mitosis and regenerate. The second theory, the bicellular reserve cell theory, assumes that the origin of the various types of salivary neoplasms can be traced to the basal cells of either the excretory or the intercalated duct. According to this theory, either of these 2 cells can act as a reserve cell with the potential for differentiation into a variety of epithelial cells. So despite the seeming heterogeneity of salivary tumors, all of them are thought to arise from 1 of 2 pluripotent stem cell populations. In this theory, adenomatoid tumors, including pleomorphic adenoma, and oncocytic tumors are derived from the reserve cell of the intercalated duct, whereas epidermoid tumors, such as squamous cell and mucoepidermoid carcinomas, are derived from the reserve cells of the excretory duct. Some reports provide molecular evidence to support the reserve cell theory of salivary gland tumorigenesis.
Facial nerve
The main trunk of the facial nerve exits the skull base via the stylomastoid foramen, immediately producing 3 small branches: the posterior auricular, posterior digastric, and stylohyoid nerves. The facial nerve then courses laterally around the styloid process and is immediately superficial to the posterior belly of the digastric muscle. As the nerve continues caudally, it pierces the posterior capsule of the parotid gland. The main trunk typically bifurcates in to the zygomaticotemporal branch and the cervicofacial branch at the pes anserinus, also known as the goose’s foot, and thereafter into the temporal, zygomatic, buccal, marginal, and cervical branches. The pes anserinus is about 1.3 cm from the stylomastoid foramen. The nerve continues within the gland, going lateral to the posterior facial vein or retromandibular vein and the more medially situated external carotid artery. The nerve then divides via variable anatomic patterns into the temporal, zygomatic, buccal, mandibular, and cervical branches ( Fig. 1 ). There is an important nerve that connects the facial nerve and the mandibular nerve (V3): the auriculotemporal nerve. Tumor from a parotid malignancy can extend along this nerve and then spread in a retrograde manner along the trigeminal nerve. Thus, transection of this nerve in appropriate cases is an important surgical consideration when dealing with parotid malignancies.
Regardless of whether they are benign or malignant, tumors of the parotid gland usually present as a painless swelling. There are some nonneoplastic parotid tumors that should be also be considered, such as lymphoepithelial lesions caused by lymphomas or human immunodeficiency virus, and granulomatous masses caused by sarcoidosis and Sjorgren syndrome. These masses tend to present as diffuse swelling or multiple swellings and less so as a discrete parotid tumor. They do not typically cause any deficit in the function of the facial nerve. Neoplastic benign tumors are usually present for a long duration and have a slow growth rate. However, patients may indicate that they incidentally noticed the appearance of a lump. Rapid increase in the size of a long-standing mass should raise the suspicion of malignant transformation of a pre-existing benign tumor but may be due to inflammation or cystic degeneration, most commonly associated with Warthin tumor. Patients who come to medical attention with a mass in the parotid gland should be asked about a history of cancer of the scalp or facial skin. Metastasis to the parotid gland from skin cancer, including melanoma, may be diagnosed by a careful examination of these areas for evidence of a skin cancer or a scar from a previous excision.
On examination, benign tumors of the parotid gland are usually well defined, nontender, and freely mobile. They are commonly located in the “tail” of the parotid gland but may be present anywhere in the superficial or deep lobe. Tumors may originate entirely from the deep lobe or they may extend from the superficial to the deep lobe through the relatively narrow stylomandibular tunnel, which gives the appearance of a dumbbell tumor. In either case, the tumor may extend to the parapharyngeal space and may displace the oropharyngeal wall medially. The presence of pain, facial nerve paresis or paralysis, fixation of the mass to the overlying skin or underlying structures, and associated cervical adenopathy usually indicates the presence of malignancy. It should be noted, however, that these findings usually indicate local or regional extension of the tumor, and the diagnosis of parotid malignancy should not await the development of these signs and symptoms. The possibility of malignancy should be ruled out in patients with any mass in the parotid gland. A mass in the parotid gland will usually require cytologic or histologic evaluation with fine-needle aspiration (FNA) biopsy or parotidectomy.
Facial nerve paralysis is most commonly associated with parotid undifferentiated carcinoma (24%), squamous cell carcinoma (19%), adenoid cystic carcinoma (17%), adenocarcinoma (11%), mucoepidermoid carcinoma (9%), carcinoma ex pleomorphic adenoma (7%), and acinic cell carcinoma (1%). Overall, if the facial nerve is paralyzed at clinical presentation, the 5-year survival rate is only between 9% and 14%. Pain on presentation of a parotid mass most likely indicates perineural invasion, which greatly increases the likelihood of malignancy in a patient with a parotid mass. Of patients with malignant parotid tumors, 7% to 20% present with facial nerve weakness or paralysis, which rarely accompanies benign lesions and indicates a poor prognosis. Facial nerve tumor invasion and therefore functional paresis or paralysis often correlate directly with an increased rate of nodal metastasis of up to 66% to 77%. These patients have an average survival of 2.7 years and a 10-year survival of 14% to 26%.
The House-Brackmann Facial Nerve Grading System is widely used to characterize the degree of facial paralysis. Having common nomenclature in order to communicate the severity of the facial nerve paresis is important to standardize. In this scale, grade I is assigned to normal function, and grade VI represents complete paralysis. Intermediate grades vary according to function at rest and with effort ( Tables 1 and 2 ).
| Grade | Description | Gross Function | Resting Appearance | Dynamic Appearance |
|---|---|---|---|---|
| 1 | Normal | Normal | Normal | Normal |
| 2 | Mild dysfunction | Slight weakness with effort, may have mild synkinesis | Normal | Mild oral and forehead asymmetry; complete eye closure with minimal effort |
| 3 | Moderate dysfunction | Obvious asymmetry with movement, noticeable synkinesis, or contracture | Normal | Mild oral asymmetry, complete eye closure with effort, slight forehead movement |
| 4 | Moderately severe dysfunction | Obvious asymmetry, disfiguring asymmetry | Normal | Asymmetrical mouth, incomplete eye closure, no forehead movement |
| 5 | Severe dysfunction | Barely perceptible movement | Asymmetric | Slight oral/nasal movement with effort, incomplete eye closure |
| 6 | Total paralysis | None | Asymmetric | No movement |
