Submandibular glands are major paired salivary glands. It is located in the submandibular triangle covered by the investing layer of deep cervical fascia. Mylohyoid muscle separates the superficial and deep lobe of the glands. Submandibular glands drain into the mouth via Wharton’s duct, which courses between the sublingual gland and hyoglossus muscle; it opens through a small opening lateral to the frenulum on the floor of the mouth.[1]
Parasympathetic stimulation increases saliva secretion, and sympathetic stimulation slows it down. Saliva is high in potassium, low in sodium; it contains substances that begin the breakdown of food, to maintain and protect the oral cavity environment, and immunoglobulin A (IgA).
Sialadenitis is inflammation of the salivary gland. Sialadenitis of the submandibular gland is less common than that of the parotid gland. Acute sialadenitis is usually due to bacterial or viral infections and usually presents with rapid onset pain and swelling.
Chronic sialadenitis is characterized by recurrent or persistent of the salivary gland. Chronic sialadenitis is usually due to obstruction, e.g., calculi, stricture, and usually presents with swelling without erythema.
Sialdenosis is nonneoplastic,non-inflammatory swelling of the salivary gland in association with acinar hypertrophy and ductal atrophy. Sialdenosis presents as non-tender swelling that is often bilateral and symmetric. Sialadenosis is often associated with systemic metabolic conditions.
Causes of Submandibular Sialadenitis
Causes of Sialadenosis
The exact prevalence of submandibular sialadenitis is not clear. Submandibular gland sialadenitis accounts for about 10% of all cases of sialadenitis. It accounts for about 0.001 to 0.002% of all hospital admissions. There is no age or sex predilection. It commonly affects older, dehydrated patients. Sialadenosis is the most common cause of salivary gland swelling in the US.
Major risk factors for sialadenitis include reduced salivary secretion and duct obstruction. Hyposecretion of saliva can occur in dehydrated people, postoperative patients, immunocompromised, and undernourished. Medications that decrease salivary flow like antihistaminics, diuretics,beta-blockers can predispose to sialadenitis. Decreased salivary production can occur in patients with a history of radiation to the head and neck region, long-standing xerostomia (e.g., Sjogren syndrome), and those with chronic illness. Salivary duct obstruction is usually due to sialolithiasis, ductal stricture, ductal foreign body, and external compression of the duct.
Other risk factors include old age, poor oral hygiene, postoperative state, intubation, use of anticholinergic agents.[7] Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection. Retrograde contamination of salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity is common. Usually, submandibular sialadenitis is polymicrobial. Staphylococcus aureus is the most frequently isolated organism. Other bacterias include Streptococcus viridans, Haemophilus influenza, Enterobacteriaceae spp, and anaerobes like Prevotella, Fusobacterium spp, Peptostreptococcus. Viral sialadenitis can result from mumps, parainfluenza, Epstein-Barr virus, HIV.
In acute suppurative submandibular sialadenitis, interstitial neutrophilic infiltration, necrosis with acinar destruction is present. Vacuolar changes in the acini cells and lymphocytic infiltration is more common in viral sialadenitis. Dilated duct with calculi, chronic inflammation, and fibrosis is evident in chronic sialadenitis due to sialolith. In sialadenosis, there is atrophy of parenchymal tissue and a compensatory increase in the amount of adipose tissue. Inflammatory infiltrates are absent.
History and physical examination have a crucial role in the evaluation of submandibular swelling. History should address many factors:
A physical exam includes a visual inspection of glands to observe the number of glands involved, erythema of overlying glands, palpation of the gland to note gland size, texture, tenderness—massage of the gland to express salivary discharge from duct orifice and note the type of discharge. A focussed cranial nerve exam is necessary to evaluate facial nerve and trigeminal nerve, especially the mandibular branch. An examination of cervical lymph nodes is also required.
Fever may be present.
On examination, the gland is swollen, indurated, and tender. Cervical lymphadenitis may be present in cases of infections. Chronic or recurrent sialadenitis causes repeated episodes of pain and swelling, often with meals and recurrent infections. Massage of the gland may reveal purulent saliva at the ductal orifice. Acute unifocal salivary gland swelling due to obstructive sialadenitis is usually the result of salivary gland stones and/or strictures and is characterized by intermittent gland swelling occurring with the stimulation of meals. Mechanical obstruction of salivary flow within the duct causes swelling of the gland.
Viral sialadenitis (e.g., mumps) presents with acute multifocal salivary gland swelling accompanied by constitutional symptoms, including fever, headache, malaise, and myalgia. Submandibular sialdenosis presents with painless bilateral submandibular enlargement and may be associated with mild discomfort.Approximately 50 % of cases are associated with recognized risk factors, including diabetes, metabolic syndrome, alcoholism, bulimia, malnutrition, and liver disease.
In addition to history and physical examination, evaluation of sialadenitis requires lab investigations, radiography, biopsy, if indicated, and other tests to rule out autoimmune etiology.
Acute sialadenitis has an excellent prognosis. Complete resolution is usually the expectation following conservative outpatient management. Most of the acute symptoms resolve in a week; however, edema takes a longer time to disappear. Chronic sialadenitis can have multiple relapses and remissions.
Prognosis is dependent on the etiology. If sialoliths require surgery, the prognosis is good. Symptoms of autoimmune sialadenitis often improve following medical management of the underlying condition (such as Sjogren's syndrome). With the treatment of the underlying cause, sialadenosis has an excellent prognosis.
Patients with sialadenitis should receive education about oral hygiene regimens (e.g., brushing teeth) and hydration. When the acute symptoms and tenderness have subsided, repeated massage of the submandibular gland can be an ongoing therapy. Avoid anticholinergic medications and diuretics. Treatment of underlying cause (e.g., Sjogren syndrome) is essential. Patients with submandibular sialadenosis should focus on control of underlying factors(e.g., hypothyroidism, diabetes, cirrhosis).
Submandibular sialadenitis and sialadenosis are common causes of submandibular swelling. Patients with acute sialadenitis usually present in outpatient primary care or dental care and sometimes in an emergency care setting. The patient is generally evaluated by a primary care physician, nurses, nurse practitioners, physician assistants, dentists, emergency medicine physicians. Chronic sialadenitis evaluation can involve interventional radiologists, otolaryngologists, rheumatologists, and internists.
Communication between the health care team is essential for proper treatment and management, especially in chronic sialadenitis and sialolithiasis. A multidisciplinary approach helps to find out the cause manage sialadenosis.
Open communication between different teams is essential. For example, during the management of chronic sialadenitis due to sialolith that fails, conservative management requires proper communication between the primary care physician, radiologist, and otolaryngologist are necessary. Patients should receive counsel regarding symptoms, oral hygiene, hydration, and warning signs suggesting the failure of conservative measures so that timely consultation and management can take place.
Patients with acute sialadenitis who do not require admission, follow-up three days from the first visit, and then one week later (with improvement)is recommended.
Patients with chronic sialadenitis/sialolithiasis and autoimmune sialadenitis or sialadenosis should be followed up regularly and in cases of acute exacerbations.
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