[1] Causes of sialadenitis are varied, including bacterial (most commonly Staphylococcus aureus), viral and autoimmune conditions.

Hypofunction of the salivary gland will reduce saliva production causing decreased protection against acid erosion and increased risk of dental decay.

The pattern of facial weakness is likely to include one or more branches of the nerve and is likely to be panfacial due to the widespread fibrosis within the gland.

[6] It was thought that morphological characteristics of the salivary ducts could also be a contributing factor, as stagnation of saliva due to these could perhaps cause an increased incidence of sialadenitis.

[6] One well known form of sarcoidosis is known as Heerfordt's syndrome which is characterized by facial nerve palsy, enlargement of the parotid and anterior uveitis.

[6] One study came to the conclusion that the presence of salivary calculi is the main indicator for the removal of the submandibular gland in patients where neoplasia is absent.

[8] This was because 82% of glands removed in an ENT department in Stockholm were found to have salivary calculi within them and all of these cases but one had chronic sialadenitis.

[9] The initial stage of acute bacterial sialadenitis involves[10] the accumulation of bacteria, neutrophils and inspissated fluid in lumen of ductal structures.

Damage to ductal epithelium results in sialodochitis (periductal inflammation), accumulation of neutrophils in glandular stroma, followed by acini necrosis with microabscesses formation.

Recurrent episodes result in the chronic stage, which involves the establishment of periductal lymph follicles and further destruction of salivary acini.

[10] Generally, in acute bacterial and viral sialadenitis cases, the lobular architecture of the gland is maintained or may be slightly expanded.

Chronic sialadenitis (also known as lymphoepithelial sialadenitis [LESA]) presents with 50% of[clarification needed] which are monoclonal by PCR while mucosa-associated lymphoid tissue (MALT) lymphoma has ducts surrounded by broad coronas of monocytoid cells, infiltration of interfollicular region by monocytoid cells or atypical plasma cells containing Dutcher bodies, monoclonality by immunohistochemistry or flow cytometry, and monocytoid infiltrates in regional lymph nodes.

In sialoithiasis, concomitant squamous metaplasia may be observed in the salivary ducts with dark calcific stone fragments.

[10] Chronic sclerosing sialadenitis is characterised by presence of three major criteria of[11] dense lymphoplasmacytic infiltrate, storiform pattern of fibrosis and obliterative phlebitis.

There are two features relatively inconsistent with diagnosis of IgG4-related disease which are the presence of epithelioid cell granulomas and a prominent neutrophilic infiltrate.

It composes of acini and ductal elements embedded in dense sclerotic stroma, and has a characteristic finding of large acinar cells present with abundant eosinophilic cytoplasmic granules.

[11] In autoimmune sialadenitis, activation of T and B cells that infiltrate the interstitium occurs due to a response to an unidentified antigen present in the salivary gland parenchyma.

In secondary Sjögren’s syndrome, periglandular fibrosis with the absence of inflammation may also be observed in addition to that of myoepithelial sialadenitis from the progressive systemic sclerosis.

Other factors to also consider include the type of gland affected as well as underlying conditions such as an autoimmune disease or ductal stones.

[10] May present with a history of recent surgical intervention or use of medications such as antihistamines, antidepressants, or anticholinergic agents.

A unilateral or bilateral painful swelling of the parotid or submandibular regions may be present upon a physical examination.

Chronic sclerosing sialadenitis typically presents unilaterally in submandibular gland that cannot be differentiated clinically from a neoplasm, with pain an inconsistent finding.

Characterised by persistent, asymptomatic bilateral swelling of parotid glands, and may represent as a manifestation of more widespread systemic disease.

Mandibular trismus – restricted mouth opening to its full extent (of approximately 40mm) may be present with large swellings typically due to acute bacterial infection of affected gland.

[12] If infection is present, appropriate cultures should be obtained, followed by empirical antibiotic therapy initially,[12] for example amoxicillin/clavulanate or clindamycin which cover oral flora.

If attacks occur more than approximately three times per year or are severe, surgical excision of the affected gland should be considered.

[4] In each group studied, most patients suffered from sialadenitis in their twenties but there was also found to be a significant number of females whose symptoms started in their thirties and forties.

[4] More women reported symptoms that were confirmed to be sialadenitis than men in this study, which may suggest that females are more likely to be affected but more research would need to be done to be sure of this.

[1] This study found that there was no predilection to any race, sex or age, although it was noted that sialadenitis in general tended to occur in people who are debilitated, dehydrated or older.

[13] Ascending acute bacterial parotitis used to be a common perimortal event but today this is no longer the case due to antibiotics and basic modern care, which means that patients will be much less likely to become dehydrated.