Continuing Education Activity
Submandibular sialadenitis and sialadenosis are 2 common causes of submandibular gland swelling. Submandibular sialadenitis is characterized by inflammation due to salivary stasis, leading to bacterial infection from the oral cavity. In contrast, sialadenosis is a non-inflammatory, benign swelling often associated with underlying metabolic disorders. Both conditions can lead to significant discomfort and complications if not properly managed. Early recognition and intervention are key to preventing progression, with chronic sialadenitis requiring attention to underlying factors to reduce recurrence and improve quality of life.
In this course, participants learn to identify the etiology, clinical features, and management strategies for both submandibular sialadenitis and sialadenosis. The course emphasizes the importance of early diagnosis and conservative management to improve patient outcomes. Collaboration with an interprofessional team, including otolaryngologists, dentists, and radiologists, is highlighted, which enhances care by ensuring comprehensive evaluation, accurate diagnosis, and coordinated treatment, ultimately reducing complications and improving long-term patient quality of life.
Objectives:
Identify the clinical signs and symptoms of submandibular sialadenitis and sialadenosis.
Differentiate between inflammatory submandibular sialadenitis and non-inflammatory sialadenosis based on clinical presentation and patient history.
Implement conservative management strategies to treat early-stage submandibular sialadenitis and prevent progression.
Communicate clear and accurate information across the interprofessional healthcare team to coordinate patient care, including shared findings from imaging, pathology, and clinical evaluations.
Access free multiple choice questions on this topic.
Introduction
The submandibular glands are paired major salivary glands located within the submandibular triangle, covered by the investing layer of deep cervical fascia. The mylohyoid muscle separates the superficial and deep lobes of these glands. Saliva drains from the submandibular glands into the mouth via Wharton duct, which courses between the sublingual gland and hyoglossus muscle, opening near the frenulum on the floor of the mouth.[1] Parasympathetic stimulation increases saliva secretion, while sympathetic stimulation reduces it. Saliva is rich in potassium and low in sodium, containing substances that begin food breakdown and maintain the oral cavity’s health, including immunoglobulin A (IgA).
Sialadenitis refers to the inflammation of a salivary gland. Submandibular sialadenitis is less common than parotid involvement. Acute sialadenitis typically results from bacterial or viral infections, presenting with rapid-onset pain and swelling. Chronic sialadenitis involves recurrent or persistent inflammation, often due to obstruction, such as salivary stones or strictures, and usually presents with swelling but without erythema. Sialadenosis is a non-neoplastic, non-inflammatory enlargement of the salivary glands, characterized by acinar hypertrophy and ductal atrophy; this presents as painless, often bilateral, symmetric swelling and is frequently associated with underlying metabolic conditions.
Etiology
Causes of Submandibular Sialadenitis
Infectious causes
Bacterial: Often polymicrobial
Staphylococcal aureus: the most common organism
Hemophilus influenza
Gram-negative aerobes (eg, Enterobacteriaceae)
Anaerobes: Prevotella, Fusobacterium, Peptostreptococcus
Obstructive causes
Sialolithiasis
Ductal stricture
Ductal foreign body eg, fish bone, hair, grass blade
External compression of duct, eg, denture flanges
Drug-induced sialadenitis
Clozapine
I-asparaginase
Phenylbutazone
Granulomatous sialadenitis
Causes of Sialadenosis
Endocrinal disorders
Diabetic mellitus
Hypothyroidism
Metabolic disorders
Obesity
Cirrhosis
Malabsorption
Epidemiology
The exact prevalence of submandibular sialadenitis is not clear. Submandibular gland sialadenitis accounts for about 10% of all cases of sialadenitis and accounts for about 0.001% to 0.002% of all hospital admissions. There is no age or sex predilection for this condition; however, it commonly affects patients who are older or dehydrated. Sialadenosis is the most common cause of salivary gland swelling in the United States.
Pathophysiology
Major risk factors for sialadenitis include reduced salivary secretion and duct obstruction. Hyposecretion of saliva can occur in those who are dehydrated, immunocompromised, or undernourished, and patients after surgery. Medications that decrease salivary flow, like antihistaminics, diuretics, and 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 (eg, 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 older age, poor oral hygiene, postoperative state, intubation, and 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 bacteria include Streptococcus viridans, Haemophilus influenza, Enterobacteriaceae spp, and anaerobes like Prevotella, Fusobacterium spp, Peptostreptococcus. Viral sialadenitis can result from mumps, parainfluenza, Epstein-Barr virus, and human immunodeficiency virus.
Histopathology
In acute suppurative submandibular sialadenitis, interstitial neutrophilic infiltration and necrosis with acinar destruction are present. Vacuolar changes in the acini cells and lymphocytic infiltration are more common in viral sialadenitis. Dilated duct with calculi, chronic inflammation, and fibrosis are 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
The history and physical examination play a crucial role in the evaluation of submandibular swelling; the history should address many factors, including:
Duration of symptoms (acute vs chronic)
The number of glands involved
Discomfort associated with swelling
Foul taste in the mouth
Frequency of symptoms
Aggravating factors (association with meals or salivary stimulants)
Constitutional symptoms (fever, viral prodrome, weight loss)
Systemic symptoms (eg, joint pain, dry eyes, and mouth )
Medical comorbidities (eg, alcohol use, diabetes, bulimia, liver disease, autoimmune disease)
History of radiation treatment
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, and tenderness—massage of the gland to express salivary discharge from duct orifice and note the type of discharge. A focused cranial nerve exam is necessary to evaluate the facial nerve and trigeminal nerve, especially the mandibular branch and an examination of cervical lymph nodes is also required. Fever may also 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. Massaging 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 (eg, 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.
Evaluation
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, including the following:
Culture and sensitivity of exudate from duct
Complete blood count to rule out infections
Imaging studies
[8]
X-ray: This can be useful to detect sialolith in chronic sialadenitis; around 70% to 80% of submandibular stones are radioopaque.
Ultrasonography: This can demonstrate sialolith (>1 mm) and abscess cavity, if present.
Computed tomography scan: This is indicated if conventional plain films are negative or when the clinical presentation is severe, and can demonstrate sialolith. In chronic sclerosing sialadenitis, the salivary gland may be enlarged or atrophic.
Distal subtraction angiography sialography: Acute inflammation is a relative contraindication; this study can detect sialolith, ductal stricture, and loss of parenchymal integrity if present in chronic sialadenitis.
Magnetic resonance imaging is warranted if neoplasia is suspected.
Anti–Sjögren-syndrome-related antigen A autoantibodies, SSB/anti-La, antinuclear antibody, rheumatoid factor tests: If sialadenitis secondary to connective tissue disorders is suspected.
Fine needle aspiration cytology of affected gland: Chronic sclerosing sialadenitis can present similarly to a tumor; fine needle aspiration is useful to exclude the presence of a neoplasm.
[9]
Treatment / Management
The treatment options for acute sialadenitis, chronic sialadenitis, and sialadenosis includes:
Acute sialadenitis: Most cases receive treatment with conservative medical management; this includes hydration, warm compresses, massage, pain relief with analgesics (eg, nonsteroidal anti-inflammatory drugs), and sialogogues. Empiric antibiotic therapy starts with amoxicillin/clavulanate or clindamycin. Antibiotic selection should be according to culture and sensitivity reports. Intravenous antibiotics may be necessary for severe cases. If soft tissue swelling is significant and there is no contraindication, corticosteroid therapy is an option. Rarely, acute suppurative sialadenitis can lead to abscess formation; surgical incision and drainage are indicated in these cases.
Chronic sialadenitis: Medical management includes hydration, oral hygiene, pain relief, and sialogogues. In cases of infection, broad-spectrum antibiotics are added. In the case of sialolithiasis, salivary gland stone removal should occur using interventional sialendoscopy or direct surgical removal.
[10][11] Extracorporeal shock wave lithotripsy, under ultrasonic guidance, is used for intraglandular duct stone removal.Recurrent sialadenitis (>3 episodes/year) or in chronic sclerosing sialadenitis: excision of the salivary gland is the recommendation.
Sialadenosis: This condition requires expectant management. Treatment of the underlying cause is the approach taken.
Differential Diagnosis
The differential diagnoses for submandibular sialadenitis and sialadenosis include the following:
Infectious causes: Bacterial (eg, Staphylococcus aureus) or viral (eg, mumps )
Granulomatous causes: Tuberculosis, sarcoidosis, cat scratch disease, actinomycosis
Autoimmune cause: Sjogren disease, systemic lupus erythematosus
Tumors: Pleomorphic adenoma, oncocytoma, ductal papilloma, adenoid cystic carcinoma, squamous cell carcinoma, mucoepidermoid carcinoma
Endocrine and metabolic causes: Hypothyroidism, diabetes mellitus, bulimia, cirrhosis, vitamin deficiency, malabsorption
Drug-related: Thiourea
Prognosis
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; the 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), and with the treatment of the underlying cause, sialadenosis has an excellent prognosis.
Complications
The complications that can manifest with submandibular sialadenitis and sialadenosis are as follows:
Recurrence
Abscess formation: Infection may spread along the fascial planes of the neck, causing a potentially serious complication. Incision and drainage are required.
Dental decay: Hypofunction of the salivary gland with reduced saliva production causes decreased protection from acid erosion, promoting dental decay.
Deterrence and Patient Education
Patients with sialadenitis should receive education about oral hygiene regimens (eg, 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 causes (eg, Sjogren syndrome) is essential. Patients with submandibular sialadenosis should focus on control of underlying factors (eg, hypothyroidism, diabetes, cirrhosis).
Enhancing Healthcare Team Outcomes
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. Chronic sialadenitis evaluation can involve interventional radiologists, otolaryngologists, rheumatologists, and internists. Communication between the healthcare team is essential for proper treatment and management, especially in chronic sialadenitis and sialolithiasis, a multidisciplinary approach helps to discern the cause of this condition and 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 clinician, 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 occur. For patients with acute sialadenitis who do not require admission, follow-up 3 days from the first visit and then 1 week later (with improvement) is recommended. Patients with chronic sialadenitis/sialolithiasis and autoimmune sialadenitis or sialadenosis should be followed up regularly and in acute exacerbations.
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Disclosure: Rabin Adhikari declares no relevant financial relationships with ineligible companies.
Disclosure: Abhinandan Soni declares no relevant financial relationships with ineligible companies.
