AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Sialadenitis of the submandibular gland is a relatively commonly encountered yet infrequently discussed topic. Causes range from simple infection to autoimmune etiologies. Although not as frequent as sialadenitis of the parotid gland, it represents an important area of clinical relevance to the otolaryngologist and other specialists. The following discusses the basic science of the submandibular gland, as well as the more common causes of sialadenitis and sialadenosis of the submandibular gland.

Anatomy

The submandibular gland, along with the parotid and sublingual glands, comprise the major salivary glands. The minor salivary glands are scattered along the upper aerodigestive tract, including the lips, mucosa of the oral cavity, pharynx, and hard palate.

The submandibular gland is the second largest (approximate weight, 10 g) of the major salivary glands (the parotid gland is the largest). Anatomically, it is situated in the submandibular triangle of the neck.

The gland itself can be arbitrarily divided into superficial and deep lobes based on its relationship to the mylohyoid muscle, the former lying superficial to the muscle, and the latter wrapping around the posterior aspect of the muscle. The gland itself lies on the hyoglossus muscle, superficial to both the hypoglossal and the lingual nerves, the latter supplying parasympathetic innervation by way of the chorda tympani nerve (from cranial nerve VII) and the submandibular ganglion. The duct of the submandibular gland, also known as the Wharton duct, exits the gland from the deep lobe, passing through the floor of the mouth, and opening in close proximity to the lingual frenulum.

Pathophysiology

The salivary glands serve numerous functions, including lubrication; enzymatic degradation of food substances; production of hormones, antibodies, and other blood group–reactive substances; mediation of taste; and antimicrobial protection. The regulation of salivary flow is primarily through the autonomic system and, most importantly, the parasympathetic division. In the case of the submandibular gland, this is mediated through the submandibular ganglion. Presynaptic fibers are derived from the superior salivatory nucleus and carried by the chorda tympani nerve, which joins the lingual nerve traveling towards the ganglion. Postsynaptic fibers extend from the ganglion to the gland itself.

Saliva is produced in the glandular subunit. The fluid component of the saliva is derived from the perfusing blood vessels in proximity to the gland, while the macromolecular composition is derived from secretory granules within the acinar cells. The saliva is produced in the acinus. Myoepithelial cells, containing contractile elements, are located along the periphery of the acinus. Upon contraction of these myoepithelial cells, the saliva is secreted into the ductal system.

The exact mechanism of salivary secretion is not completely understood but is believed to be under the influence of a cyclic AMP (adenosine 3,'5'-cyclic monophosphate) and a calcium-activated phosphorylation mechanism. The salivary secretions are then modified by a variety of cell types along a series of ducts, including the striated, intercalated, and excretory ducts, before finally being excreted through the Wharton duct into the oral cavity.

The concentration of mucus is higher in the submandibular gland, accounting for the viscous nature of its secretions relative to the other salivary glands. This increased viscosity, and subsequent relatively slower flow, contributes to the propensity for salivary gland calculi and stasis in certain disease states.

Frequency

United States

The exact frequency of submandibular sialadenitis is unclear. The incidence of acute suppurative parotitis has been reported at 0.01-0.02% of all hospital admissions. The submandibular gland is suggested to account for approximately 10% of all cases of sialadenitis of the major salivary glands. Extrapolation would suggest an incidence of 0.001-0.002%, but this is unconfirmed.

Race

No race predilection per se exists.

Sex

No sex predilection per se exists.

Age

Although no obvious age predilection exists, per se, sialadenitis as a whole tends to occur in the older, debilitated, or dehydrated patient.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

Submandibular sialadenitis takes several forms. The diagnostic workup of any submandibular enlargement begins with a thorough history. This should include onset, duration of symptoms, recurrence, recent operative history, recent dental work, and thorough drug history, immunization history (specifically measles, mumps, rubella [MMR] vaccine), past medical (specifically autoimmune) history, past surgical history, and history of radiation therapy. Inquire as to associated fever or chills, weight loss, presence of a mass, bilaterality or unilaterality, skin changes, lymphadenopathy, keratitis, shortness of breath, oral discharge, dental pain, or skin discharge.

Physical

Physical examination should begin with the gland itself. The gland should be palpated for the presence of calculi. Examine the ductal opening for purulence. Palpation should extend into the floor of mouth as well as the soft tissue of the tongue, cheek, and neck. Lingual papillary atrophy should be looked for, as well as loss of enamel from the tooth surface (the latter may be associated with bulimia). All of the major salivary glands should be examined for masses, symmetry, and the presence of discharge. The presence of lymphadenopathy should be noted. The eyes should be examined for any presence of interstitial keratitis. A quick cranial nerve examination should be conducted with particular attention to cranial nerves VII and XII. The lungs should be examined and a chest radiograph ordered if suspected pulmonary involvement exists.

Causes

• Acute sialadenitis: Acute sialadenitis is an acute inflammation of a salivary gland.
• • Patients typically present with erythema over the area, pain, tenderness upon palpation, and swelling. Frank cellulitis and induration of adjacent soft tissues may be present. Purulent material may be observed being expressed from the Wharton duct, particularly upon milking the gland. Rarely, a cutaneous fistula may occur, with spontaneous drainage of purulent material. The inflammation is secondary to an infectious process.
  • The most common organism is Staphylococcus aureus. Other bacterial organisms include Streptococcus viridans, Haemophilus influenzae, Streptococcus pyogenes, and Escherichia coli. The infection is often the result of dehydration with overgrowth of the oral flora. The most common causes are postoperative dehydration, radiation therapy, and immunosuppression (eg, diabetes mellitus, organ transplant, chemotherapy, human immunodeficiency virus).
  • Of note, infection of the submandibular gland is rare in the neonate and prepubescent child. When it does occur, similar pathogens have been identified, including Pseudomonas aeruginosa and group B streptococci. Physical examination, in addition to the symptoms described above, includes failure to thrive and irritability. Progression may occur, involving the contralateral gland. The etiology of this entity is unclear.
  • Although less common than bacteria, several viruses have been implicated in submandibular sialadenitis. These include the mumps virus, which typically affects the parotid gland but can affect the submandibular gland as well. Other viruses include HIV, coxsackievirus, parainfluenza types I and II, influenza A, and herpes.
  • Infection of the submandibular gland can result in the formation of a submandibular abscess. In this state, the patient may appear toxic, with features similar to acute submandibular sialadenitis. Spiking fevers are not uncommon. This is a serious condition requiring strict attention because of the possibility that the abscess may spread to involve other deep neck spaces of the neck. Trismus may be indicative of parapharyngeal involvement. Progression to Ludwig angina, a life-threatening infection of the submental and sublingual spaces, although rare, can occur.
• Chronic sialadenitis: Chronic sialadenitis, in contrast, is typically less painful and is associated with recurrent enlargement of the gland (often following meals) typically without erythema. The chronic form of the disease is associated with conditions linked to decreased salivary flow, rather than dehydration. These conditions include calculi, salivary stasis, and a change in the fluid and electrolyte composition of the gland.
• Sialolithiasis: Salivary calculi (sialolithiasis) relate to the formation and deposition of concretions within the ductal system of the gland.
• • Eighty percent of all salivary calculi occur in the submandibular gland, with approximately 70% of these demonstrable as radio-opacities on routine plain radiography consisting of intraoral occlusal radiographs.
  • The calculi vary in size and may be single or multiple. The formation of calculi is associated with chronic sialadenitis, and in particular, the recurrent nature of the problem.
  • The exact mechanism of stone formation is unclear, but it appears to be related to the following conditions:
    • Salivary stagnation
    • Epithelial injury along the duct resulting in sialolith formation, which acts as a nidus for further stone formation
    • Precipitation of calcium salts
  • The stones themselves are typically composed of calcium phosphate or calcium carbonate in association with other salts and organic material such as glycoproteins, desquamated cellular residue, and mucopolysaccharides.
  • Patients most often present with a colicky postprandial swelling of the gland. The course of the disease is typically relapsing and remitting until a final definitive treatment, usually in the form of surgery, is undertaken.
• Autoimmune sialadenitis: Autoimmune diseases, in particular Sjögren syndrome, can be associated with sialadenitis. Although preferentially affecting the parotid gland, the submandibular and minor salivary glands are also affected. The disease, which is associated with keratoconjunctivitis sicca, xerostomia, salivary gland enlargement, and lingual papillary atrophy, is confirmed through biopsy of the minor salivary glands of the lip. Numerous laboratory tests are also used to confirm the diagnosis, such as autoantibodies Sjögren syndrome A (SS-A) and Sjögren syndrome B (SS-B), rheumatoid factor, and antinuclear antibodies.
• Sialadenosis: Sialadenosis refers to nonneoplastic noninflammatory swelling in association with acinar hypertrophy and ductal atrophy.
• • Etiologies fall into 5 major categories.
    • Nutritional (eg, vitamin deficiency, bulimia)
    • Endocrine (eg, diabetes mellitus, hypothyroidism)
    • Metabolic (eg, obesity, cirrhosis, malabsorption)
    • Inflammatory/autoimmune (eg Sjögren disease, Heerfordt syndrome)
    • Drug induced (eg, thiourea)
  • Physical examination shows a nontender swelling that is often bilateral and symmetric but can be unilateral and asymmetric.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

The differential diagnosis of submandibular sialadenitis and sialadenosis includes the following:

Infectious (acute) cause - Bacterial or viral disease

Inflammatory cause - Sialolithiasis, radiation-induced disease

Autoimmune cause - Sjögren disease, lupus

Granulomatous cause - Tuberculosis, tularemia, sarcoidosis, catscratch disease, actinomycosis

Drug-related cause - Thiourea

Neoplastic (benign) cause - Pleomorphic/monomorphic adenoma, oncocytoma, ductal papilloma, hemangioma, foreign body, ranula, lymphoepithelial cyst

Neoplastic (malignant) cause - Adenoid cystic carcinoma, mucoepidermoid carcinoma, adenocarcinoma, undifferentiated carcinoma, malignant oncocytoma, squamous cell carcinoma

Endocrine cause - Hypothyroidism, diabetes mellitus

Metabolic cause - Vitamin deficiency, cirrhosis, obesity, bulimia, malabsorption

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• In evaluating the patient with sialadenitis, steps should be taken in the following order: history, physical examination, culture, laboratory investigation, radiography, and if indicated, fine-needle aspiration biopsy (see History and Physical).
• Laboratory investigations should begin with culture of the offending gland (if possible, prior to the administration of antibiotics).
• Blood cultures should be obtained in the patient exhibiting bacteremia or sepsis.
• As a rule, needle aspiration of a suspected abscess is not indicated.
• Routine electrolytes and complete blood cell count with differential should be obtained to assess for any evidence of dehydration or systemic infection.
• If a diagnosis of autoimmunity is entertained, serum analysis for antinuclear antibody, SS-A, SS-B, and erythrocyte sedimentation rate should be conducted.

Imaging Studies

• Numerous radiologic techniques are available in submandibular imaging. Deciding which study to obtain first is often difficult. Examination selection should be based in part on the suspected cause of the problem. The authors' institution tends to begin with plain radiography, followed by the use of computed tomography scanning with combined sialography.
• Of all the radiologic examinations available, one of the simplest is conventional plain radiography.¹ Anteroposterior, lateral, and oblique intraoral occlusal views are used. This technique is particularly valuable in evaluating the presence of calculi, which are radio-opaque in approximately 70% of cases. These radiographs are limited in that they do not provide any information about the ductal system or soft tissues.
• Sialography can be used to evaluate sialolithiasis or other obstructive entities, as well as inflammatory and neoplastic disease.
• • In this technique, a water-soluble medium such as meglumine diatrizoate is injected into the Wharton duct and lateral, oblique, and anteroposterior plain radiographs are obtained in order to assess the ductal arborization.
  • Contraindications for this test are iodine allergy and acute sialadenitis.
  • Any filling defects (eg, calculi), retained secretions (eg, chronic sialadenitis), stricture formation (eg, inflammation), extravasation (eg, Sjögren disease), or irregularly contoured borders (eg, neoplasm) are noted.
• Ultrasonography can be used to differentiate between solid versus cystic lesions of the gland. It can also be used to differentiate intrinsic from extrinsic disease and can be helpful in identification of abscess formation.
• Computed tomography scanning is an excellent modality in differentiating intrinsic versus extrinsic glandular disease. It is also extremely valuable in defining abscess formation versus phlegmon. It is limited in evaluating the ductal system unless combined with simultaneous sialography.
• Magnetic resonance imaging is of little utility in sialadenitis or sialadenosis. It does not allow evaluation of the ductal system, and it is not helpful in defining calcifications. It is an excellent tool for soft tissue definition and is invaluable in instances of suspected neoplasia.

Procedures

• Fine-needle aspiration and biopsy
• • Open biopsy of the lip should be considered when the diagnosis of Sjögren disease is contemplated.
  • If suspicion of a solid neoplasm masquerading as sialadenitis is significant, a fine-needle aspiration with biopsy should be undertaken. The management and differential diagnosis of submandibular neoplasms is beyond the scope of the current discussion.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Medical Care

Management of submandibular sialadenitis and sialadenosis involves a wide range of approaches, from conservative medical management to more aggressive surgical intervention.

• One management scheme is as follows:
• • Acute sialadenitis
    • Medical management - Hydration, antibiotics (oral versus parenteral), warm compresses and massage, sialogogues
    • Surgical management - Consideration of incision and drainage versus excision of the gland in cases refractory to antibiotics, incision and drainage with abscess formation, gland excision in cases of recurrent acute sialadenitis
  • Salivary calculi
    • Medical management - Hydration, compression and massage, antibiotics for the infected gland
    • Surgical management - Duct cannulation with stone removal, gland excision in recurrent cases
  • Sjögren disease
    • Medical management - Hydration, dental hygiene, rheumatology and dental referral
    • Surgical management - Gland excision not usually needed unless recurrent acute sialadenitis
  • Sialadenosis
    • Medical management - Treatment of underlying cause
    • Surgical management - Not indicated
• Medical management centers on eliminating the causative factor.
• • Acute sialadenitis
    • In cases of acute sialadenitis, adequate hydration should be ensured and electrolyte imbalances corrected.
    • Patients are most often treated on an outpatient basis, with the administration of a single dose of parenteral antibiotics in an emergency department, followed by oral antibiotics for a period of 7-10 days. Clindamycin (900 mg IV q8h or 300 mg PO q8h) is an excellent choice and provides good coverage against typical organisms.
    • Patients who exhibit significant morbidity, are significantly dehydrated, or are septic should be admitted to hospital. In this latter group of patients, CT scanning of the area should be performed. If a large abscess is noted, incision and drainage should be considered. Small abscesses typically respond to conservative methods.
    • In cases refractory to antibiotics, viral and atypical bacterial causes should be considered.
  • Sialolithiasis
    • Patients with sialolithiasis should be initially treated with hydration, warm compresses, and gland massage.
    • Antibiotics are indicated in patients exhibiting infection.
  • Sjögren disease
    • In those patients with Sjögren disease, hydration and prevention of complications should be undertaken.
    • Dental hygiene should be strictly maintained in order to prevent carries, and dental and rheumatology consults should be sought. Gland excision is rarely indicated.
  • Sialadenosis: Sialadenosis should be managed expectantly. Treatment should be directed towards managing the underlying problem and achieving homeostasis. Gland excision is not indicated.

Surgical Care

• Acute sialadenitis
• • Patients who exhibit significant morbidity, are significantly dehydrated, or are septic should be admitted to hospital. In this latter group of patients, CT scanning of the area should be performed. If a large abscess is noted, incision and drainage should be considered. Small abscesses typically respond to conservative methods.
  • In patients with recurrent acute attacks, gland excision during a period of quiescence should be considered. Serial CT scanning is often useful.
• Sialolithiasis
• • In patients with calculi in proximity of the opening of the Wharton duct, the duct can be cannulated, dilated, and the stone removed via a transoral approach.
  • Patients with deep intraparenchymal stones or multiple stones should have their glands excised on an elective basis. Ultrasonic lithotripsy is rarely effective and is not offered at the authors' institution.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics

Therapy must cover all likely pathogens in the context of this clinical setting.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Further Inpatient Care

• Patients requiring inpatient management should be monitored on a daily basis and preferably twice daily.
• In order to ascertain the progression or improvement of acute sialadenitis, serial CT scanning may be warranted.
• Patients with sialolithiasis should be treated conservatively during the acute exacerbation stage and should be monitored after discharge for definitive surgical intervention.

Further Outpatient Care

• For patients with acute sialadenitis not requiring admission, follow-up visit should be 3 days from the first visit and then 1 week later (with improvement).
• Patients with chronic sialadenitis/sialolithiasis and autoimmune sialadenitis or sialadenosis should be seen on a regular basis and if acute exacerbation of the problem occurs.

In/Out Patient Meds

• In addition to the antibiotics, patients may be treated with any form of nonsteroidal anti-inflammatory medications. Narcotics may be needed in severe cases, and increasing pain refractory to medications is often an indication for admission for further evaluation.
• In addition, medications predisposing to xerostomia should be avoided where possible. These include antiparkinsonian, antiemetics, antinauseants, over-the-counter and prescription cold medications, antidepressants, antihypertensive agents, diuretics, anticholinergics, antianxiety agents, and decongestants.

Complications

• The most serious complication of acute sialadenitis is the formation of an abscess. Management is described above.
• Complications of chronic sialadenitis and autoimmune sialadenitis are most often dental in nature because of the decreased function of the gland and the protective effect provided against caries.
• Chronic inflammation of the gland with or without calculi often renders the gland difficult to excise because of the loss of normal tissue planes.

Prognosis

• The prognosis of acute sialadenitis is very good. Most cases are easily treated with conservative medical management, and admission is the exception, not the rule. Acute symptoms resolve within 1 week; however, edema in the area may last several weeks.
• Postsurgery, patients are often already admitted with appropriate intravenous antibiotics. These patients have a similar prognosis.
• Patients with chronic sialadenitis often have a relapsing and remitting course. Prognosis is dependent on the etiology.
• Patients with sialolithiasis require definitive surgical treatment in most cases, which results in an excellent prognosis.
• Patients with Sjögren or other autoimmune diseases are likely to have a protracted course related to systemic involvement.
• Patients with sialadenosis have a good prognosis, if their underlying problem is adequately controlled. Even if control is attained, bilateral swelling may be persistent.

Patient Education

• Patients with any form of sialadenitis should be educated as to the value of hydration and excellent oral hygiene. This lessens the severity of the attacks and prevents dental complications. Patients with sialadenosis should be educated regarding the mechanism of their underlying pathology and methods of maintaining control over them.
• For excellent patient education resources, visit eMedicine's Teeth and Mouth Center.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Submandibular calculus.
	View Full Size Image
Media type:  Image

Media file 2:  Sialogram with stenosis secondary to chronic sialadenosis.
	View Full Size Image
Media type:  X-RAY

Media file 3:  Submandibular abscess and associated Ludwig angina.
	View Full Size Image
Media type:  Image

Media file 4:  Submandibular neoplasm.
	View Full Size Image
Media type:  Image

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

1. Isacsson G, Isberg A, Haverling M, Lundquist PG. Salivary calculi and chronic sialoadenitis of the submandibular gland: a radiographic and histologic study. Oral Surg Oral Med Oral Pathol. Nov 1984;58(5):622-7. [Medline].
2. Batsakis JG. Physiology. In: Cummings CW, et al, eds. Otolaryngology Head and Neck Surgery. 3rd ed. St. Louis, Mo:. Mosby;1998:1210-1222.
3. Bradley PJ. Benign salivary gland disease. Hosp Med. Jul 2001;62(7):392-5. [Medline].
4. Chapman AH. The salivary glands, pharynx and esophagus. In: Sutton D, ed. Textbook of Radiology and Imaging. Vol 2. New York, NY:. Churchill Livingstone;1998:729-828.
5. Ching AS, Ahuja AT, King AD, et al. Comparison of the sonographic features of acalculous and calculous submandibular sialadenitis. J Clin Ultrasound. Jul-Aug 2001;29(6):332-8. [Medline].
6. Gayner SM, Kane WJ, McCaffrey. Infections of the salivary glands. In: Cummings CW, et al, eds. Otolaryngology Head and Neck Surgery. 3rd ed. St. Louis, Mo:. Mosby;1998:1234-1246.
7. Guerrissi JO, Taborda G. Endoscopic excision of the submandibular gland by an intraoral approach. J Craniofac Surg. May 2001;12(3):299-303. [Medline].
8. Haynes RC. Adrenocorticotropic hormone: adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. In: Goodman LS, Gilman AG, eds. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 8th ed. New York, NY:. Pergamon Press;1990:1431-1462.
9. Kaneda T, Minami M, Ozawa K, et al. MR of the submandibular gland: normal and pathologic states. AJNR Am J Neuroradiol. Sep 1996;17(8):1575-81. [Medline].
10. Matthews TW, Dardick I. Morphological alterations of salivary gland parenchyma in chronic sialadenitis. J Otolaryngol. Dec 1988;17(7):385-94. [Medline].
11. Rice DH. Diagnostic imaging. In: Cummings CW, et al, eds. Otolaryngology Head and Neck Surgery. 3rd ed. St. Louis, Mo:. Mosby;1998:1223-1233.
12. Rosai J. Major and minor salivary glands. In: Rosai J, ed. Ackerman's Surgical Pathology. Vol 1. St. Louis, Mo:. Mosby;1996:815-856.
13. Sande MA, Mandell GL. Antimicrobial agents. Tetracyclines, chloramphenicol, erythromycin, and miscellaneous antibacterial agents. In: Goodman LS, Gilman AG, et al, eds. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 8th ed. New York, NY:. Pergamon Press;1990:1117-1145.
14. Saunders JR Jr, Hirata RM, Jaques DA. Salivary glands. Surg Clin North Am. Feb 1986;66(1):59-81. [Medline].
15. Silvers AR, Som PM. Salivary glands. Radiol Clin North Am. Sep 1998;36(5):941-66, vi. [Medline].
16. Sumi M, Izumi M, Yonetsu K, Nakamura T. The MR imaging assessment of submandibular gland sialoadenitis secondary to sialolithiasis: correlation with CT and histopathologic findings. AJNR Am J Neuroradiol. Oct 1999;20(9):1737-43. [Medline].

Article Last Updated: Jul 23, 2008