Submandibular Sialadenitis/Sialadenosis Clinical Presentation

Updated: Apr 18, 2022
  • Author: Adi Yoskovitch, MD, MSc; Chief Editor: Arlen D Meyers, MD, MBA  more...
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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 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.



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.

A study by Naylor et al indicated that risk factors for acute sialadenitis after skull base surgery, though poorly understood, “may include extreme flexion and/or rotation of the head and neck.” [4]

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.


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 formatio

  • 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 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.