Tumors of the salivary glands are uncommon and represent 2-4% of head and neck neoplasms. They may be divided into three broad categories, as follows:
The salivary glands are divided into two broad categories, major and minor. The major salivary glands include the following:
The minor glands are dispersed throughout the upper aerodigestive submucosa (ie, palate, lip, pharynx, nasopharynx, larynx, and parapharyngeal space). (See Benign Tumors of Minor Salivary Glands.)
About 70% of salivary gland tumors (SGTs) originate in the parotid gland. The remaining tumors arise in the submandibular gland (8%) and minor salivary glands (22%). Although 75% of parotid gland tumors are benign, slightly more than 50% of tumors of the submandibular gland and 80% of minor SGTs are found to be malignant. Pleomorphic adenomas (benign mixed tumors) are the most common benign SGTs, accounting for 85% of all salivary gland neoplasms. The ubiquitous deposition of the minor salivary glands complicates the diagnosis and management of SGTs. The approach for a suspected tumor of the minor salivary glands begins with a thorough history and a physical examination.
SGTs usually manifest as an enlargement or growth of the major salivary glands. Depending on the location of the gland, they can present with nerve compression symptoms when patients are seen later in the course with larger tumors. Investigate and exclude a history of weight loss, underlying infectious processes (eg, chest pain, cough, lymphadenopathy), and clinical indications of lymphoma type B symptoms (eg, night sweats, fever).
Radiographic imaging (computed tomography [CT] with or without magnetic resonance imaging [MRI]) and a histopathologic diagnosis (obtained based on fine-needle aspiration biopsy [FNAB]) often provide useful information prior to definitive surgical therapy. [1, 2, 3]
From 1650 to 1750, salivary gland surgery was limited to the treatment of ranulas and oral calculi. The concept of surgical excision of a parotid tumor has been attributed to Bertrandi in 1802. The initial applications of this surgery included an extensive approach, causing serious disfiguration and disability.
By approximately 1850, the focus shifted toward dissection and the intimate relation between the facial nerve and the parotid gland. Attempts were made to perform the surgery with nerve preservation. John C Warren, MD, was the first to use ether inhalation anesthesia during his resection of a parotid tumor in Boston in 1846. In 1892, Codreanu (a Romanian native) performed the first total parotidectomy with facial nerve preservation. Grafting of the facial nerve after resection was attempted in the early 1950s.
In 1958, Beahrs and Adson eloquently described the relevant anatomy and surgical technique of current parotid gland surgery.  They stressed surgical landmarks for avoiding injury to the main trunk and branches of the facial nerve and advocated complete removal of the superficial portion of the parotid gland for noninvasive lesions confined to that portion of the gland. 
The parotid gland is situated in the musculoskeletal recess formed by portions of the temporal bone, atlas, and mandible, along with their related muscles. The gland has a superficial lobe and a deep lobe, between which runs the extratemporal portion of the facial nerve. The deep lobe is in contact with the parapharyngeal space. The deep cervical fascia surrounds the parotid gland. This fascia has an anteroinferior portion that becomes the stylomandibular ligament, separating the parotid gland from the submandibular gland.
The facial nerve exits the stylomastoid foramen just posterior to the base of the styloid, gives off small branches to the postauricular and posterior belly of the digastric muscles, and then turns anterolaterally. The main trunk then becomes embedded in parotid tissue and divides into temporofacial and cervicofacial branches just superficial to the retromandibular vein and external carotid artery. Beyond this point, the nerve anatomy varies. In general, however, there are five peripheral nerve branches, as follows:
Surgical landmarks for the main trunk of the facial nerve include the tragal pointer and the tympanomastoid suture line. (See the images below.)
The submandibular gland encompasses most of the submandibular or digastric triangle. Like the parotid gland, the submandibular gland can be divided into a superficial and deep lobe on the basis of the relation to the mylohyoid. The marginal mandibular branch of the facial nerve courses between the deep surface of the platysma and the superficial aspect of the fascia that lies over the submandibular gland. The facial artery and vein are located just deep to this nerve, and ligation and superior traction of these vascular structures can prevent nerve injury.
Along the posterior border of the mylohyoid are located the lingual nerve and submandibular duct (Wharton duct). The hypoglossal nerve courses deep to the tendon of the digastric and then lies medial to the deep cervical fascia.
The sublingual gland occupies the same anatomic space as the submandibular gland, located between the mylohyoid and the hyoglossus. Because the gland is rather superficial, covered by only a thin layer of oral mucosa, it can often be palpated in the floor of the mouth.
The minor salivary glands are widely dispersed throughout the upper respiratory tract, including the palate, lip, pharynx, nasopharynx, larynx, and parapharyngeal space. The greatest densities of glands are located in the hard (250 glands) and soft (150 glands) palates.
The histogenesis of SGTs is based on the salivary gland unit (see the image below). According to the multicellular theory of SGTs, pleomorphic adenomas originate from the intercalated duct cells and myoepithelial cells; oncocytic tumors originate from the striated duct cells; acinic cell tumors originate from the acinar cells; and mucoepidermoid and squamous cell tumors originate from the excretory duct cells.
Although the etiology of SGTs is unknown, the involvement of environmental or genetic factors has been suggested.  Radiation exposure has been linked to the development of the benign Warthin tumor and to the malignant mucoepidermoid carcinoma. Epstein-Barr virus may be a factor in the development of lymphoepithelial tumors of the salivary glands. Genetic alterations (eg, allelic loss, monosomy and polysomy, and structural rearrangement) have been studied as factors in the development of SGTs.
SGTs represent 2-3% of head and neck neoplasms. Of the SGTs, 85% are pleomorphic adenomas. SGTs are more common in women than in men, with the peak incidence in the third and fourth decades of life. Pleomorphic adenomas make up 70% of parotid gland tumors and 50% of submandibular gland tumors.
Warthin tumors (adenolymphomas) account for 5-15% of SGTs. Warthin tumors are the second most common neoplasm of the parotid gland. They are more common in men than in women, with peak incidence in the fifth and sixth decades of life. (See the image below.)
Of minor SGTs, 50% are malignant. Mucoepidermoid cancer is the most common parotid malignancy. Overall, adenoid cystic carcinoma is the most common malignant tumor of all minor salivary glands and, specifically, the submandibular gland.
With the appropriate treatment of benign SGTs (ie, complete excision or superficial parotidectomy), the outcome is excellent, and the recurrence rate is very low.