Diagnosis and Management of Salivary Gland Disorders

As experts in the oral and maxillofacial region, the practicing dentist and dental specialist may be required to perform the necessary assessment, diagnosis, and management of a variety of salivary gland disorders ranging from minor, self-limiting disease processes to more significant disorders of the major and minor salivary glands; thus a thorough practical knowledge of the incidence, demographics, embryology, anatomy, and pathophysiology is necessary to manage these patients in the most appropriate manner. This chapter reviews the anatomy and physiology of salivary glands, as well as the etiologies, diagnostic methods, contemporary radiographic evaluation, and medical and surgical management of a variety of salivary gland disorders, including sialolithiasis and obstructive phenomena (e.g., mucocele and ranula), acute and chronic salivary gland infections, traumatic salivary gland disorders, Sjögren syndrome, necrotizing sialometaplasia, and benign and malignant salivary gland tumors.

Embryology, Anatomy, and Physiology

The salivary glands are divided into two groups: (1) the major glands and (2) the minor glands . All salivary glands develop from the embryonic oral cavity as buds of epithelium that extend into the underlying mesenchymal tissues. These epithelial ingrowths, or anlages, are apparent anatomically at 8 weeks’ gestation ( Fig. 21.1 ) and then branch to form a primitive ductal system that eventually becomes canalized to provide the basic salivary gland unit for the production and drainage of salivary secretions ( Fig. 21.2 ). This unit consists of an acinus (or secretory unit), which is a cluster of cells including myoepithelial cells and acinar (secretory) cells with secretory granules that coalesce into the collecting ducts that include the intercalated duct , followed by the striated duct , and finally the excretory duct ; each ductal unit consists of unique acinar cells with branching ducts. The minor salivary glands begin to develop around the fortieth day in utero, whereas the larger major glands begin to develop slightly earlier, at about the thirty-fifth day in utero. At around the seventh or eighth month in utero, secretory cells called acini begin to develop around the ductal system. The acinar cells of the salivary glands are classified either as serous cells , which produce a thin, watery serous secretion, or mucous cells , which produce a thicker, more viscous mucous secretion. The minor salivary glands are well developed and functional in the newborn infant. The acini of the minor salivary glands produce primarily mucous secretions, although some are composed of serous cells as well; this results in the classification of these minor glands as mixed . Between 800 and 1000 minor salivary glands are present throughout the portions of the oral cavity that are covered by mucous membranes, with a few exceptions, such as the anterior third of the hard palate, the attached gingiva, and the dorsal surface of the anterior third of the tongue. The well-established locations of the minor salivary glands are referred to as labial , buccal , palatine , tonsillar (Weber glands), retromolar (Carmalt glands), and lingual glands . The lingual glands are divided into three groups of glands: (1) inferior apical glands (of Blandin and Nuhn), (2) taste buds (Ebner glands), and (3) posterior lubricating glands ( Table 21.1 ).

Fig. 21.1, Embryologic development of the major salivary glands.

TABLE 21.1

Salivary Gland Embryology and Anatomy

	Minor Salivary Glands	Major Salivary Glands
In utero development	Day 40	Day 35
Number of glands	800–1000 minor glands	6 (3 paired glands)
Types of glands	Labial	Parotid
	Buccal	Submandibular
	Palatine	Sublingual
	Tonsillar (Weber glands)
	Retromolar (Carmalt glands)
	Lingual 1 Inferior apical glands (of Blandin and Nuhn) 2 Taste buds (Ebner glands) 3 Posterior lubricating glands

The major salivary glands are paired structures and include the parotid , submandibular , and sublingual glands . The parotid glands contain primarily serous acini with few mucous cells. Serous cells are cuboidal cells with eosinophilic secretory granules and produce thin, watery secretions with a low viscosity (1.5 Pa • s). Conversely, the sublingual glands are, for the most part, composed of mucous cells, which are clear low columnar cells with nuclei polarized away from the lumen of the acini, and produce a thick secretion with high viscosity (13.4 Pa • s). The submandibular glands are mixed glands, made up of approximately equal numbers of serous and mucous acini and thus produce a secretion with an intermediate viscosity of 3.4 Pa • s.

The parotid glands , the largest salivary glands, lie superficial to the posterior aspect of the masseter muscles and the ascending rami of the mandible, in an “inverted triangular” shape below the zygomatic arch. Peripheral portions of the parotid glands may extend to the mastoid process, along the anterior aspect of the sternocleidomastoid muscle, and around the posterior border of the mandible into the pterygomandibular space ( Fig. 21.3 ). The major branches of the seventh cranial (facial, VII) nerve roughly divide the parotid gland into a superficial lobe and a deep lobe and course anteriorly from the exit of the nerve from the stylomastoid foramen to innervate the muscles of facial expression. Since the parotid gland contains the terminal branches of the facial nerve, this may explain why a mandibular block local anesthetic injection may result in transient facial paralysis if the anesthetic solution is deposited into the parotid gland as it extends around the posterior border of the mandible into the pterygomandibular space. Small ducts from various regions of the parotid gland coalesce at the anterosuperior aspect of the parotid gland to form the Stensen duct , which is the major duct of the parotid gland. The Stensen duct is about 1 to 3 mm in diameter and 6 cm in length. Occasionally a normal anatomic variation occurs in which an accessory parotid duct may aid the Stensen duct in the drainage of salivary secretions. In addition, an accessory portion of the parotid gland may be present anywhere along the course of the Stensen duct. The duct traverses anteriorly from the parotid gland hilum and courses in a position superficial to the masseter muscle. At the location of the anterior edge of the masseter muscle, the Stensen duct turns sharply in a medial direction and pierces through the fibers of the buccinator muscle. The Stensen duct opens into the oral cavity through the buccal mucosa as a punctum in the maxillary posterior buccal vestibule, usually adjacent to the maxillary first or second molar. The parotid gland receives neural innervation from the ninth cranial (glossopharyngeal) nerve via the auriculotemporal nerve from the otic ganglion (see Fig. 21.7 ).

Fig. 21.3, Parotid gland anatomy. The facial nerve branches divide the gland into superficial and deep lobes. The Stensen duct courses superficial to the masseter muscle then curves sharply to pierce the buccinator muscle and enter the oral cavity.

The submandibular glands are located in the “submandibular triangle” of the neck, which is a triangle formed by (1) the anterior belly of the digastric muscle, (2) the posterior belly of the digastric muscle, and (3) the inferior border of the mandible ( Fig. 21.4 ). The posterosuperior portion of the gland curves upward around and above the posterior border of the mylohyoid muscle and gives rise at the hilum to the major duct of the submandibular gland known as the Wharton duct . This duct passes forward along the superior surface of the mylohyoid muscle in the sublingual space, adjacent to the lingual nerve. The anatomic relationship in this area is such that the lingual nerve loops under the Wharton duct, from lateral to medial, in the posterior floor of the mouth; the lingual nerve then branches to provide sensory input to the anterior two-thirds of the tongue on each side of the tongue. Of course the glossopharyngeal nerve provides sensation to the posterior one-third of each side of the tongue, and the chorda tympani branch of the facial nerve provides taste sensation to the anterior two-thirds of the tongue. The Wharton duct continues forward in a straight line, and the lingual nerve traverses under the duct from a lateral position (beginning in the pterygomandibular space after separating from the inferior alveolar nerve) to a medial position. In a medial position, the Wharton duct is vulnerable to injury in the third molar region during third molar extraction surgery because it lies in a position close to the medial surface of the internal oblique ridge of the posterior mandible. Subsequently, as mentioned, the nerve turns in a medial direction to branch extensively into the tongue musculature bilaterally. The Wharton duct is about 5 cm in length, and the duct lumen is 2 to 4 mm in diameter. The Wharton duct opens into the floor of the mouth via a muscular punctum located close to the mandibular incisors at the most anterior aspect of the junction of the lingual frenum and the floor of the mouth. The punctum is a constricted portion of the duct, and it functions to limit retrograde flow of bacteria-laden oral fluids into the ductal system. This is particularly important since this punctum limits retrograde entry of those bacteria that tend to colonize around the ductal orifices, such as Staphylococcus aureus and Streptococcus species.

Fig. 21.4, Submandibular gland anatomy. The submandibular triangle is formed by the anterior and posterior bellies of the digastric muscles and inferior border of the mandible. A portion of the gland may extend above the mylohyoid muscle. The Wharton duct courses superiorly and anteriorly to exit in the anterior floor of the mouth.

The sublingual glands are located on the superior surface of the mylohyoid muscle, in the sublingual space, and are separated from the oral cavity by a thin layer of oral mucosa in the anterior floor of the mouth ( Fig. 21.5 ). The main acinar ducts throughout the sublingual glands are called Bartholin ducts and in most instances coalesce to form 8 to 20 ducts of Rivinus. These Rivinus ducts are short and small in diameter, and they open individually, directly into the anterior floor of the mouth on a crest of mucosa known as the plica sublingualis ; or, alternatively, they may open indirectly through connections to the submandibular duct and then into the oral cavity via the Wharton duct . The sublingual and submandibular glands are innervated by the facial (VII) nerve through the submandibular ganglion via the chorda tympani nerve (see Fig. 21.8 ).

Fig. 21.5, Sublingual gland anatomy. Note the relationship of the Wharton duct and the lingual nerve.

The functions of saliva are to provide lubrication for speech and mastication, produce enzymes for digestion, and produce compounds with antibacterial properties ( Table 21.2 ). The salivary glands produce approximately 1000 to 1500 mL of saliva per day, with the highest flow rates occurring during meal times. The relative contributions of each salivary gland to the total daily production vary, with the submandibular gland providing 70%, the parotid gland 25%, the sublingual gland 3% to 4%, and the minor salivary glands contributing only trace amounts of saliva ( Table 21.3 ). The electrolyte composition of saliva also varies between the major salivary glands, with the parotid gland concentrations generally higher than the submandibular gland, except for submandibular gland calcium concentration, which is approximately twice the concentration of parotid calcium levels. The relative viscosities of saliva vary according to the specific gland involved and correspond to the relative percentages of mucous and serous cells in the gland; thus the highest viscosity saliva is found in the sublingual gland secretions composed of mostly mucous cells, followed by the submandibular gland secretions (mixed mucous and serous cells), and lastly, the parotid gland secretions with the lowest viscosity, which are composed mainly of serous cells ( Fig. 21.6 ). Of note, the daily production of saliva begins to decrease gradually after the age of 20 years because of increased intraparenchymal fibrosis as well as decreased neural secretory stimulation.

TABLE 21.2

Composition of Normal Adult Saliva

	Parotid Gland	Submandibular Gland
Amino acids	1.5 mg/dL	<1 mg/dL
Ammonia	0.3 mg/dL	0.2 mg/dL
Bicarbonate	20 mEq/L	18 mEq/L
Calcium	2 mEq/L	3.6 mEq/L
Chloride	23 mEq/L	20 mEq/L
Cholesterol	<1 mg/dL	<1 mg/dL
Fatty acids	1 mg/dL	<1 mg/dL
Glucose	<1 mg/dL	<1 mg/dL
Magnesium	0.2 mEq/L	0.3 mEq/L
Phosphate	6 mEq/L	4.5 mEq/L
Potassium	20 mEq/L	17 mEq/L
Proteins	250 mg/dL	<150 mg/dL
Sodium	23 mEq/L	21 mEq/L
Urea	15 mg/dL	7 mg/dL
Uric acid	3 mg/dL	2 mg/dL

TABLE 21.3

Daily Saliva Production by Salivary Gland

Gland	Production
Submandibular gland	70%
Parotid gland	25%
Sublingual gland	3%–4%
Minor glands	Trace

Fig. 21.6, (A) Parotid gland histology (serous cells). (B) Sublingual gland (mucous cells). (C) Submandibular gland (mixed mucous and serous cells). Note that some of the mucous cells (lighter color) have associated surrounding serous demilunes (darker color).

The neurosecretory control of salivary production is derived from sympathetic and parasympathetic stimulation. The sympathetic innervation originates from the superior cervical ganglion nerve supply to the salivary glands via the vast arterial vascular plexus of the face. Parasympathetic control is different for each of the major salivary glands. The parasympathetic innervation to the parotid gland originates from the tympanic branch of the glossopharyngeal nerve (IX), which then travels via the lesser petrosal nerve to the otic ganglion. Postganglionic parasympathetic nerves then travel via the auriculotemporal nerve to the parotid gland ( Fig. 21.7 ). The parasympathetic control of the submandibular and sublingual glands originates in the superior salivatory nucleus, which travels via the facial nerve (chorda tympani branch) to the submandibular ganglion. Postganglionic parasympathetic nerves then travel directly to the submandibular gland or with the lingual nerve to the sublingual gland ( Fig. 21.8 ).

Fig. 21.7, Parotid gland innervation. CN, Cranial nerve.

Fig. 21.8, Submandibular and sublingual gland innervation. CN, Cranial nerve.

Diagnostic Modalities

History and Clinical Examination

The most important components of diagnosis in salivary gland disorders, as with other disease processes, are the patient history and clinical examination. In most cases, the patient will guide the doctor to the diagnosis merely by relating the events that have occurred in association with the presenting chief complaint. Specific questions should focus on the specific nature of the complaint(s), and whether the symptoms are exacerbated during mealtimes, which may indicate an obstructive phenomenon, or whether inadequate hydration has resulted in decreased salivary flow, if comorbidities may have contributed to the salivary gland complaints (e.g., autoimmune disease), or whether trauma has occurred (e.g., lip biting resulting in a mucocele). The astute clinician must perform a thorough clinical evaluation, and in many instances, the diagnosis can be determined without the need for further diagnostic testing. The clinical examination should include inspection and a bimanual palpation of the specific salivary gland with a determination of adequacy and normalcy of salivary flow, which may be accomplished through “milking” of the main duct of the gland to encourage drainage to assess the quantity and quality of the saliva produced. On occasion a lacrimal probe may be required to obturate the punctum of the gland duct (generally for the Stensen and Wharton ducts) to clear a mucous plug, salivary “sludge,” or a small calculus so that a patent ductal system and normal salivary flow can be restored. At the very least, the clinician may be able to develop a differential diagnosis and categorize the problem as reactive, obstructive, inflammatory, infectious, metabolic, neoplastic, developmental, or traumatic, and this designation will guide further appropriate diagnostic testing. Occasionally the clinician may find it necessary to use any of several diagnostic modalities, including serum or salivary fluid electrolytes, salivary gland imaging studies, functional salivary studies, endoscopic salivary procedures, and salivary biopsy procedures to assist in establishing a diagnosis in salivary gland disease.

Salivary Gland Radiology

Plain-Film Radiographs

The primary purpose of plain films , or two-dimensional radiographs, in the assessment of salivary gland disease is to identify salivary stones (calculi), although only 80% to 85% of all stones are radiopaque and therefore visible radiographically. The incidence of radiopaque stones varies, depending on the specific gland involved, compared with the parotid glands having less radiopaque stones than the submandibular gland ( Table 21.4 ). A mandibular occlusal radiograph is most useful for detecting sublingual and submandibular gland calculi in the anterior floor of the mouth ( Fig. 21.9 ), although a high false-negative rate for detecting radiolucent stones or mucous plugs as the cause of obstruction does exist. In addition, a mandibular occlusal film may miss a posteriorly located stone. Periapical radiographs can show calculi in each salivary gland or duct, including minor salivary glands, depending on film placement. In most instances, when the stone is visible radiographically, the radiographic image corresponds in size and shape to the actual stone morphology. Panoramic radiographs can reveal stones in the parotid gland and may identify posteriorly located submandibular stones ( Fig. 21.10 ).

TABLE 21.4

Incidence of Radiopaque (vs. Radiolucent) Stones

Location	Incidence
Submandibular gland	80% radiopaque
Parotid gland	40% radiopaque
Sublingual gland	20% radiopaque
Minor glands	Rare

Fig. 21.9, (A) Mandibular occlusal radiograph showing a radiopaque sialolith (arrow) . (B) Submandibular sialolith (1 cm) after intraoral removal.

Fig. 21.10, (A) Panoramic radiograph demonstrates a right submandibular sialolith (arrows) . (B) Panoramic radiograph showing right parotid stone in Stensen duct (arrowhead) .

Sialography

The gold standard in diagnostic salivary gland radiology is sialography , although this diagnostic study is performed less commonly today with fewer radiologists having the necessary expertise to perform sialography. Sialography is indicated as an aid in the detection of radiopaque and radiolucent (15% to 20%) stones, as well as mucous plugs, because it can identify obstruction within the ductal system. In addition, sialography is also useful in the assessment of the extent of destruction of the salivary duct or gland parenchyma or both as a result of obstructive, inflammatory, traumatic, and neoplastic diseases. Also, sialography may be used as a therapeutic maneuver because the ductal system is dilated during the study, and small mucous plugs or necrotic debris (or “sludge”) may be cleared during the injection of contrast medium into the ductal system.

The sialography technique can be easily performed under local anesthesia and includes the following steps: (1) cannulation of the salivary duct (Stensen or Wharton duct) with a plastic or metal catheter ( Fig. 21.11 ), (2) injection of a radiographic contrast medium into the ductal system and the substance of the gland, and (3) acquisition of a series of radiographic images at various time points during this process. Approximately 0.5 to 1 mL of contrast material may be injected into the duct and gland before the patient begins to experience pain from ductal distension and retrograde filling of the gland parenchyma. The two types of contrast media available for sialographic studies are water-soluble solutions and oil-based solutions. Both types of contrast material contain relatively high concentrations (25% to 40%) of iodine. Most clinicians prefer to use water-soluble media, which are more miscible with salivary secretions, more easily injected, disseminated into the finer portions of the ductal system, and, after the study is completed, more readily eliminated from the gland by drainage through the duct or systemic absorption from the gland and excretion through the kidneys. Oil-based media are more viscous and require a higher injection pressure to visualize the smaller ductules compared with water-soluble media. As a result, oil-based media usually produce more discomfort to the patient during the injection process. Oil-based media are poorly eliminated from the ductal system and may cause persistent iatrogenic ductal obstruction following the sialogram. Also, any residual oil-based contrast medium not absorbed by the gland may produce severe foreign-body reactions and glandular necrosis following the sialogram. In addition, if the patient has ductal disruption resulting from chronic inflammatory changes, the extravasation of oil-based media into soft tissue around the gland may cause significantly more soft tissue damage compared with the water-soluble material.

Fig. 21.11, Cannulation of the Stensen duct with a plastic catheter and traction on the cheek to straighten the ductal curvature in this area.

Sialography provides the preliminary step in outlining the ductal morphology and localizing an obstruction, if present, thus providing a route map for therapeutic intervention. Important information that may be obtained during the sialogram study includes the size, number, position, and mobility of a stone(s), as well as the diameter of the distal duct and presence of stenosis within the ductal system. A complete sialogram consists of three distinct phases, depending on the time at which the radiograph is obtained after injection of the contrast material:

1
Ductal phase ( Fig. 21.12 ), which occurs almost immediately after injection of contrast material and allows visualization of the major ducts
2
Acinar phase ( Fig. 21.13 ), which begins within minutes after the ductal system has become fully opacified with contrast medium and the gland parenchyma becomes subsequently filled with contrast material
3
Evacuation phase ( Fig. 21.14 ), which assesses normal secretory clearance and elimination function of the gland to determine whether any evidence remains of retention of contrast medium in the gland or ductal system during a period greater than 5 minutes after the contrast has been injected into the ductal system

Digital subtraction sialography has been shown to provide superior images of the ductal system, particularly images of the area where the path of the duct overlies, or is obstructed by, bony structures or the dentition. A normal ductal phase of a sialogram shows a large primary duct branching gradually and smoothly into secondary and terminal ductules, like the branches of a tree. In the acinar phase of the sialogram, the even distribution of contrast medium throughout the gland results in opacification of the entire acinoparenchyma that outlines the gland and its lobules. When a stone or mucous plug obstructs a salivary duct, continued functional secretion by the gland produces distention of the ductal system proximal to the obstruction (seen during the ductal phase of the sialogram) and finally leads to pressure atrophy of the parenchyma of the gland (seen during the acinar phase of the sialogram; Fig. 21.15 ). For the evacuation phase of the study, the retention of any contrast medium in the gland or ductal system beyond 5 minutes is considered abnormal, and the contrast should be eliminated completely out of the gland and ducts as seen on the final postevacuation radiograph.

Fig. 21.15, Sialogram of right submandibular gland. Obstruction of duct by a radiolucent sialolith (arrows) has caused inflammatory dilation of the proximal duct (sialodochitis) and loss of normal parenchyma of the gland (sialadenitis).

Sialodochitis is a dilation of the salivary duct resulting from epithelial atrophy as a result of repeated inflammatory or infectious processes, with irregular narrowing caused by reparative fibrosis (i.e., “sausage link” pattern; Fig. 21.16 ). Sialadenitis represents inflammation mainly involving the acinoparenchyma of the gland. Patients with sialadenitis experience saccular dilation of the acini of the gland resulting from acinar atrophy and infection, which results in “pruning” of the normal arborization of the small ductal system of the gland ( Fig. 21.17 ). Centrally located lesions or tumors that occupy a part of the gland or impinge on its surface will displace the normal ductal anatomy. On sialographic images, the ducts adjacent to the lesion are draped and stretched in a curvilinear fashion around the mass, producing a characteristic “ball-in-hand” appearance ( Fig. 21.18 ).

Fig. 21.16, (A) Sialogram of left parotid gland. The characteristic “sausage link” appearance of the duct indicates ductal damage from obstructive disease with irregular narrowing of duct caused by reparative fibrosis (sialodochitis). (B) Diagram inset of obstruction with proximal dilation of the ductal system.

Fig. 21.17, Parotid sialadenitis with acinar destruction from chronic disease. Inset shows “pruning of the tree” caused by acinar destruction.

Fig. 21.18, Sialogram of left parotid gland illustrates the “ball-in-hand” phenomenon (arrows) . The filling defect indicates a tumor of the gland with displacement of normal surrounding ductal anatomy. Inset shows “ball-in-hand” phenomenon caused by tumor displacement of the gland.

Sialograms are specialized radiologic studies performed by oral-maxillofacial surgeons and some interventional radiologists trained in the technique, although this is performed less commonly today than in the past. Those inexperienced in the performance of, or proper interpretation of, the sialogram should not attempt this examination. The three contraindications to sialography are (1) acute salivary gland infections , because a disrupted ductal epithelium may allow extravasation of contrast medium into the soft tissues and cause severe pain and possibly a foreign-body reaction; (2) patients with a history of iodine sensitivity , especially a severe allergic reaction after a previous radiologic examination using contrast medium; and (3) preceding a thyroid gland study , because retained iodine in the salivary gland or ductal system may interfere with interpretation of the thyroid gland scan.

Computed Tomography, Magnetic Resonance Imaging, Ultrasonography, and Positron Emission Tomography

The use of computed tomography (CT) has been generally reserved for the assessment of mass lesions of the salivary glands. Although CT scanning results in radiation exposure to patients, it is less invasive than sialography and does not require the use of contrast material or operator expertise in the sialography procedure. In addition, CT scanning can demonstrate salivary gland calculi, especially submandibular stones that are located posteriorly in the duct, at the hilum of the gland, or in the substance of the gland itself ( Fig. 21.19 ). Three-dimensional CT imaging can allow much better resolution and delineation of the stone and of the ductal system in a noninvasive fashion ( Fig. 21.20 ). The office-based cone-beam computed tomography (CBCT) technology has been evaluated with regard to the diagnosis of sialolithiasis in the major salivary glands, and, compared with ultrasonography, it was found to have high sensitivity and specificity. While dental artifacts and patient movement that result in poor image quality may limit its diagnostic value, the availability, low cost, and lower radiation doses of CBCT, compared with medical-grade CT imaging, makes it a valuable alternative for a noninvasive diagnosis of sialolithiasis.

Fig. 21.19, (A) Axial computed tomography (CT) scan of the mandible and floor of mouth shows a posterior submandibular sialolith (arrow) . (B) Coronal CT scan showing a two stones in the submandibular duct near the gland hilum.

Fig. 21.20, (A) Three-dimensional computed tomography (3D-CT) scan showing a large submandibular stone (S) . (B) 3D-CT scan showing irregular narrowing and destruction of the submandibular duct from chronic inflammation (arrows) .

Magnetic resonance imaging (MRI) is superior to CT in delineating soft tissue details of salivary gland lesions, specifically tumors or other mass lesions, with no radiation exposure to the patient or the necessity of contrast enhancement. Three-dimensional MRI reconstruction and MRI virtual endoscopy of the ductal system have shown promising results in the visualization of abnormalities in conditions such as Sjögren syndrome, sialolithiasis, cysts, tumors, and inflammatory conditions. These advances in MRI may prove beneficial in evaluating and understanding the relationship of the ductal system to surrounding tissues as well as the endoluminal conditions of the ducts.

Current advances in ultrasonography technology have made this imaging modality extremely valuable in diagnosis of salivary gland pathology. Ultrasonography can provide high-resolution images, is noninvasive, has a low cost, and is an easily performed procedure that allows for accurate evaluation of the parotid and submandibular glands. In salivary gland tumor evaluation, important information regarding vascularization can be obtained with color Doppler ultrasonographic examination, which may aid in the differentiation of benign and malignant disease processes. Ultrasonography represents the most common examination method for nodular lesions and is useful to guide biopsies for diagnostic purposes (e.g., fine-needle aspiration [FNA] biopsy ), especially when the clinical examination is limited because of a small size or difficult access location of the nodule. Finally, ultrasonography, with intraductal injection of contrast material, has been proposed as a complementary method for evaluation of obstructive salivary gland disease. In addition to the examination of the ductal system of the gland, parenchymal evaluation is possible with this ultrasound technique.

The role of fluorodeoxyglucose positron emission tomography (FDG-PET) scanning has been examined in the assessment and workup of salivary gland malignancies for diagnostic and treatment planning purposes. Initial reports have found FDG-PET to be of low value in distinguishing between benign and malignant lesions, as well as in the management of salivary gland malignancies. More recent studies though have demonstrated that the diagnostic accuracy of FDG-PET for the prediction of pathologic tumor extent and nodal involvement was superior to conventional CT for high-grade malignancies. Furthermore, FDG-PET was found to be clinically useful in both the initial tumor staging, as well as in the accurate evaluation of nodal involvement by cervical lymph node level and posttreatment evaluation and monitoring for recurrences ( Fig. 21.21 ).

Fig. 21.21, (A) Computed tomography scan of malignant neoplasm of right submandibular gland. (B) Corresponding fluorodeoxyglucose positron emission tomography scan showing the same malignant neoplasm of right submandibular gland.

Salivary Scintigraphy (Radioactive Isotope Scanning)

The use of nuclear imaging in the form of radioactive isotope scanning, or salivary scintigraphy (sialoscintigraphy) , allows a thorough evaluation of the salivary gland parenchyma with regard to the presence of mass lesions, as well as the function of the gland itself. This study uses a radioactive isotope, usually technetium-99m injected intravenously, which becomes distributed throughout the body and is taken up preferentially by a variety of tissues with an active rate of biological turnover, including the salivary glands. The major limitation of this study, other than radiation exposure, is the poor resolution of the images obtained. Salivary gland scintigraphy may demonstrate increased uptake of radioactive isotope in an acutely inflamed gland or decreased uptake in a chronically inflamed gland, as well as the presence of a mass lesion, either benign or malignant in nature. Perhaps the most valuable application of sialoscintigraphy is in the diagnosis, therapeutic decision-making, and follow-up of patients with Sjögren syndrome. The American-European Consensus Group in 2002 established the scintigraphy scoring system (0 to 12 scale) and, based upon this scoring system, an abnormal scintigraphy study is an established criterion used in the diagnosis of Sjögren syndrome.

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