Standard, and most effective, therapy to date is glandular sialadenectomy, which is associated with fairly low operative morbidity; however, in recent times, the administration of steroid (which can shrink the inflammatory lesion and is known to reduce serum IgG4 values) has been considered favorably, and may be useful in younger patients or those who refuse surgery.

The cause and pathogenesis of this chronic condition are not very well understood. Several factors have been postulated:

- Formation of a hard salivary calculus or sialolith by accumulation of calcium salts in the duct of the salivary gland (a process known as Sialolithiasis). This has been proposed as the most common cause for Küttner's tumor of the submandibular gland, with sialoliths observed in an appreciable proportion of cases. However, sialolith involvement may not be found in many cases.

- Abnormalities of the salivary gland ducts leading to excessive accumulation or retention of ductal secretions, which can excite chronic inflammations.

- Immune, especially autoimmune, cause - which has gained steam, given the observation that the tissue of the glands is overrun with lymphoid immune cells and fibrous connective tissue, as well as corroboration from markedly similar lesions (with histologic and immunohistochemical findings) seen elsewhere in the body. The presence of abundant Immunoglobulin G4 (IgG4) associated with Plasma cells infiltrating into the salivary glands, as well as increased serum IgG4 concentration, has been noted with patients with Küttner's tumor.

This chronic condition is primarily observed in adult (40–70 years) patients. However, Küttner's tumor, with prominent immunopathological features, has been described in an 11-year-old boy in Brazil in 2012.

As recognition of IgG4-RD is relatively recent, there are limited studies on its epidemiology. It is therefore difficult to make an accurate estimation of prevalence. Furthermore, age of onset is almost impossible to estimate; age at diagnosis is frequently misused as the age of onset.

A 2011 study estimated the incidence of IgG4-RD in Japan at 2.8–10.8/million population, with a median age of onset of 58 years.

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

Most patients will fully recover from dacryoadenitis. For conditions with more serious causes, such as sarcoidosis, the prognosis is that of the underlying condition.

Infections involving the salivary glands can be viral or bacterial (or rarely fungal).

- Mumps is the most common viral sialadenitis. It usually occurs in children, and there is preauricular pain (pain felt in front of the ear), swelling of the parotid, fever, chills, and headaches.

- Bacterial sialadentitis is usually caused by ascending organisms from the oral cavity. Risk factors include reduced salivary flow rate.

- Human immunodeficiency virus-associated salivary gland disease (HIV-SGD).

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

Acute dacryoadenitis is most commonly due to viral or bacterial infection. Common causes include mumps, Epstein-Barr virus, staphylococcus, and gonococcus.

Chronic dacryoadenitis is usually due to noninfectious inflammatory disorders. Examples include sarcoidosis, thyroid eye disease, and orbital pseudotumor.

A salivary diverticulum (plural "diverticuli") is a small pouch or out-pocketing of the duct system of a major salivary gland. Such diverticuli typically cause pooling of saliva and recurrent sialadenitis, especially parotitis. A diverticulum may also cause a sialolith to form.

The condition can be diagnosed by sialography. Affected individuals may "milk" the salivary gland to encourage flow of saliva through the duct.

Published studies on the survival of SS patients are limited in varied respects, perhaps owing to the relatively small sample sizes, and secondary SS is associated with other autoimmune diseases. However, results from a number of studies indicated, compared to other autoimmune diseases, SS is associated with a notably high incidence of malignant non-Hodgkin lymphoma (NHL). NHL is the cancer derived from white blood cells. About 5% of patients with SS will develop some form of lymphoid malignancy. Patients with severe cases are much more likely to develop lymphomas than patients with mild or moderate cases. The most common lymphomas are salivary extranodal marginal zone B cell lymphomas (MALT lymphomas in the salivary glands) and diffuse large B-cell lymphoma.

Lymphomagenesis in primary SS patients is considered as a multistep process, with the first step being chronic stimulation of autoimmune B cells, especially B cells that produce rheumatoid factor at sites targeted by the disease. This increases the frequency of oncogenic mutation, leading to any dysfunction at checkpoints of autoimmune B-cell activation to transform into malignancy. A study's finding has concluded the continuous stimulation of autoimmune B cells, leading to subtle germinal abnormalities in genes having specific consequences in B cells, which underlies the susceptibility to lymphoma.

Apart from this notably higher incidence of malignant NHL, SS patients show only modest or clinically insignificant deterioration in specific organ-related function, which explains the only slight increases in mortality rates of SS patients in comparison with the remainder of the population.

IgG4-related ophthalmic disease (IgG4-ROD) is the recommended term to describe orbital (eye socket) manifestations of the systemic condition IgG4-related disease, which is characterised by infiltration of lymphocytes and plasma cells and subsequent fibrosis in involved structures. It can involve one or more of the orbital structures.

Frequently involved structures include the lacrimal glands, extraocular muscles, infraorbital nerve, supraorbital nerve and eyelids. It has also been speculated that ligneous conjunctivitis may be a manifestation of IgG4-related disease (IgG4-RD).

As is the case with other manifestations of IgG4-related disease, a prompt response to steroid therapy is a characteristic feature of IgG4-ROD in most cases, unless significant fibrosis has already occurred.

Among the complications discussed above, women with anti-Ro/SS-A and anti-La/SS-B antibodies who become pregnant, have an increased rate of neonatal lupus erythematosus with congenital heart block requiring a pacemaker. Type I cryoglobulinemia is a known complication of SS.

IgG4-related disease (IgG4-RD), formerly known as IgG4-related systemic disease, is a chronic inflammatory condition characterized by tissue infiltration with lymphocytes and IgG4-secreting plasma cells, various degrees of fibrosis (scarring) and a usually prompt response to oral steroids. In approximately 51–70% of people with this disease, "serum" IgG4 concentrations are elevated during an acute phase.

It is a relapsing–remitting disease associated with a tendency to mass forming, tissue-destructive lesions in multiple sites, with a characteristic histopathological appearance in whichever site is involved. Inflammation and the deposition of connective tissue in affected anatomical sites can lead to organ dysfunction, or even organ failure, if not treated.

Early detection is important to avoid organ damage and potentially serious complications. Treatment is recommended in all symptomatic cases of IgG4-RD and also in asymptomatic IgG4-RD involving certain anatomical sites.

This is a rare condition, probably caused by an allergic reaction, in which there is sudden swelling of the salivary glands. It is associated with other allergic conditions such as asthma, urticaria, allergic rhinitis and food allergy.

Salivary gland aplasia (also termed salivary gland agenesis) is the congenital absence of salivary glands. Usually the term relates to the absence of some or all of the major salivary glands.

It is a rare condition, and most known cases have been in association with syndromes of the ectodermal tissues, particularly the lacrimal apparatus. Example syndromes which have been reported with salivary gland aplasia include hereditary ectodermal dysplasia, mandibulofacial dysostosis and hemifacial microsomia.

The main significance of the condition is a lack of saliva, causing xerostomia (dry mouth), with accompanying susceptibility to dental caries (tooth decay), infections of the mouth, and upper respiratory tract infections (e.g., candidiasis, ascending sialadenitis, laryngitis and pharyngitis). Patients with salivary gland aplasia typically require regular application of topical fluoride to prevent tooth decay.

These are also collectively known as chronic punctate parotitis or chronic autoimmune parotitis.

"Sjögren's syndrome:"

Chronic inflammation of the salivary glands may also be an autoimmune disease known as Sjögren's syndrome. The disease most commonly appears in people aged 40–60 years, but it may affect small children. In Sjögren syndrome, the prevalence of parotitis in women versus men is approximately 9:1. The involved parotid gland is enlarged and tender at times. The cause is unknown. The syndrome is often characterized by excessive dryness in the eyes, mouth, nose, vagina, and skin.

"Lymphoepithelial lesion of Godwin:"

Most frequently associated with a circumscribed tumor with the histologic features of Sjögren syndrome. This designation has also fallen out of favour.

Sialodochitis (also termed ductal sialadenitis), is inflammation of the duct system of a salivary gland. This is compared to sialadenitis, which is inflammation of the gland parenchyma.

Sialodochitis may be associated with salivary duct strictures and salivary stones.

It is common in both the parotid glands and submandibular glands.

The treatment is as for sialadenitis.

"Acute bacterial parotitis:"

is most often caused by a bacterial infection of Staphylococcus aureus but may be caused by any commensal bacteria.

"Parotitis as Extrapulmonary Tuberculosis:"

The mycobacterium that cause tuberculosis can also cause parotid infection. Those infected tend to have enlarged, nontender, but moderately painful glands. The diagnosis is made by typical chest radiograph findings, cultures, or histologic diagnosis after the gland has been removed. When diagnosed and treated with antitubercular medications, the gland may return to normal in 1–3 months.

"Acute viral parotitis (mumps):"

The most common viral cause of parotitis is mumps. Routine vaccinations have dropped the incidence of mumps to a very low level. Mumps resolves on its own in about ten days.

"HIV parotitis:" Generalized lymphadenopathy has long been associated with HIV, but the localized enlargement of the parotid gland is less well known.

Symptoms, if any, can be mild even in the presence of significant swelling or masses.

Lacrimal gland involvement may cause swelling of the upper eyelid, or proptosis if there is severe swelling. Other orbital masses or inflammation can result in visual disturbance (blurred vision, double vision, visual field impairment), restricted eye movements, pain or discomfort, numbness in the distribution of the supraorbital and/or infraorbital nerves, or proptosis.

IgG4-related ophthalmic disease has been estimated to account for approximately 25% of all cases of proptosis, eyelid swelling and other features of orbital swelling.

In chronic recurrent sialadenitis or chronic sclerosing sialadenitis, acute attacks are managed with conservative therapies such as hydration, analgesics (mainly NSAIDs), sialogogues to stimulate salivary secretion, and regular, gentle gland massage. If infection is present, appropriate cultures should be obtained, followed by empirical antibiotic therapy initially, for example amoxicillin/clavulanate or clindamycin which cover oral flora.

If there are attacks more than approximately 3 times per year or severe attacks, surgical excision of the affected gland should be considered.

Sialadenitis (sialoadenitis) is inflammation of a salivary gland. It may be subdivided temporally into acute, chronic and recurrent forms.

The prevalence of salivary stones in the general population is about 1.2% according to post mortem studies, but the prevalence of salivary stones which cause symptoms is about 0.45% in the general population. Sialolithiasis accounts for about 50% of all disease occurring in major salivary glands, and for about 66% of all obstructive salivary gland diseases. Salivary gland stones are twice as common in males as in females. The most common age range in which they occur is between 30 and 60, and they are uncommon in children.

In one report, about 20% of individuals with mealtime syndrome had strictures upon sialography. For unknown reasons, strictures seem to be more common in females.

While risk factors vary with age and gender, most of the common chronic diseases in the US are caused by dietary, lifestyle and metabolic risk factors that are also responsible for the resulting mortality. Therefore, these conditions might be prevented by behavioral changes, such as quitting smoking, adopting a healthy diet, and increasing physical activity. Social determinants are important risk factors for chronic diseases. Social factors, e.g., socioeconomic status, education level, and race/ethnicity, are a major cause for the disparities observed in the care of chronic disease. Lack of access and delay in receiving care result in worse outcomes for patients from minorities and underserved populations. Those barriers to medical care complicate patients monitoring and continuity in treatment.

In the US, Minorities and low-income populations are less likely to access and receive preventive services necessary to detect conditions at an early stage.

The majority of US health care and economic costs associated with medical conditions are for the costs of chronic diseases and conditions and associated health risk behaviors. Eighty-four percent of all health care spending in 2006 was for the 50% of the population who have one or more chronic medical conditions (CDC, 2014).

There are thought to be a series of stages that lead to the formation of a calculus ("lithogenesis"). Initially, factors such as abnormalities in calcium metabolism, dehydration, reduced salivary flow rate, altered acidity (pH) of saliva caused by oropharyngeal infections, and altered solubility of crystalloids, leading to precipitation of mineral salts, are involved. Other sources state that no systemic abnormality of calcium or phosphate metabolism is responsible.

The next stage involves the formation of a which is successively layered with organic and inorganic material, eventually forming a calcified mass. In about 15-20% of cases the sialolith will not be sufficiently calcified to appear radiopaque on a radiograph, and therefore be difficult to detect.

Other sources suggest a retrograde theory of lithogenesis, where food debris, bacteria or foreign bodies from the mouth enter the ducts of a salivary gland and are trapped by abnormalities in the sphincter mechanism of the duct opening (the papilla), which are reported in 90% of cases. Fragments of bacteria from salivary calculi were reported to be Streptococci species which are part of the normal oral microbiota and are present in dental plaque.

Stone formation occurs most commonly in the submandibular gland for several reasons. The concentration of calcium in saliva produced by the submandibular gland is twice that of the saliva produced by the parotid gland. The submandibular gland saliva is also relatively alkaline and mucous. The submandibular duct (Wharton's duct) is long, meaning that saliva secretions must travel further before being discharged into the mouth. The duct possesses two bends, the first at the posterior border of the mylohyoid muscle and the second near the duct orifice. The flow of saliva from the submandibular gland is often against gravity due to variations in the location of the duct orifice. The orifice itself is smaller than that of the parotid. These factors all promote slowing and stasis of saliva in the submandibular duct, making the formation of an obstruction with subsequent calcification more likely.

Salivary calculi sometimes are associated with other salivary diseases, e.g. sialoliths occur in two thirds of cases of chronic sialadenitis, although obstructive sialadenitis is often a consequence of sialolithiasis. Gout may also cause salivary stones, although in this case they are composed of uric acid crystals rather than the normal composition of salivary stones.