Salivary Gland Disorders

Obstructive/stasis mechanisms

• Sialolithiasis: calcium phosphate–rich stones form where flow is slow, alkaline, and mucin-dense — hence the submandibular predominance (Wharton duct drains uphill against gravity); stones cause postprandial colic and set up ascending infection
• Ductal stricture or mucus plugging: prior instrumentation, chronic inflammation, or radioiodine exposure narrows the duct; the American Thyroid Association notes sialadenitis and xerostomia as recognized adverse effects of I-131 therapy, since the sodium-iodide symporter concentrates iodine in salivary epithelium

Infectious

• Bacterial (suppurative) sialadenitis: retrograde spread of oral flora — S. aureus plus anaerobes — when flow falls (dehydration, postoperative state, intubation, tube feeding)
• Viral: mumps paramyxovirus remains the classic cause in undervaccinated children; CDC/ACIP two-dose MMR schedule is the modifiable protection. HIV produces benign lymphoepithelial cysts with bilateral parotid enlargement

• Obstruction-mediated pathology: Sialoliths (salivary stones composed of calcium phosphate and mucin) or mucus plugs block salivary ducts, causing retrograde pressure, ductal dilation, acinar atrophy, and secondary bacterial infection (typically Staphylococcus aureus); obstruction most commonly affects the submandibular gland due to its mucoid secretions and narrow Wharton's duct
• Inflammatory/autoimmune mechanisms: In Sjögren syndrome, CD4+ T cells infiltrate and destroy acinar tissue through autoimmune attack on muscarinic-3 receptors and mitochondrial antigens (anti-SS-A/Ro and anti-SS-B/La antibodies), leading to progressive xerostomia; similarly, sarcoidosis causes noncaseating granulomatous infiltration of gland parenchyma
• Infectious pathogenesis: Viral infection (mumps paramyxovirus, CMV, EBV, HIV) causes direct cytolytic destruction of acinar cells and ductal epithelium; bacterial sialadenitis occurs when salivary flow decreases (dehydration, medications) allowing ascending infection through ducts, with subsequent abscess and ductal stricture formation
• Radiation-induced glandular atrophy: High-dose radiation (>20 Gy) to head/neck causes direct acinar cell apoptosis, fibroblast proliferation, collagen deposition, and ductular obliteration, resulting in permanent xerostomia
• Neoplastic transformation: Salivary gland tumors arise from epithelial, myoepithelial, or mesenchymal components; parotid tumors are more commonly benign (80%), while submandibular and minor gland tumors carry higher malignancy risk (50%); specific translocations drive tumor types (e.g., t(9;22) in acinic cell carcinoma)

• Acute bacterial sialadenitis: Sudden onset of pain, swelling, and erythema over affected gland (typically parotid); purulent discharge from duct opening; fever and systemic toxicity; risk factors include dehydration, anticholinergics, post-surgical states, and poor oral hygiene
• Chronic sialadenitis: Recurrent episodes of gland swelling and pain; history of sialolith passage; episodes triggered by eating; xerostomia and recurrent infections develop as gland atrophies
• Sjögren syndrome presentation: Dry mouth (xerostomia) and dry eyes (keratoconjunctivitis sicca) as cardinal features; bilateral parotid gland swelling and tenderness; associated systemic features including arthralgias, fatigue, Raynaud phenomenon, and increased risk of lymphoma
• Sialoliths/obstructive disease: Colicky pain and swelling of affected gland, worsening with eating or sour stimuli (lemon drops); palpable stone in floor of mouth (submandibular) or in duct opening; swelling subsides between meals if obstruction is intermittent
• Mumps (parotitis): Bilateral parotid enlargement and tenderness; fever, malaise, and trismus; typically in unvaccinated children; complications include meningitis, deafness, orchitis, and pancreatitis
• Salivary gland tumors: Painless, progressive swelling; long-standing mass often indicates indolent process; red flags include rapid growth, facial nerve paralysis, skin fixation, ulceration, and trismus (suggesting malignancy or deep lobe involvement)
• Xerostomia (dry mouth): Difficulty chewing/swallowing, burning sensation, increased cavities and oral candidiasis; associated medications include anticholinergics, antihistamines, SSRIs, and diuretics

• Clinical examination: Palpate glands for size, consistency, tenderness, fluctuance; visualize duct opening for purulent discharge; bidigital palpation of floor of mouth for submandibular sialoliths; assess facial nerve function (CN VII) to evaluate for mass effect or malignancy
• Imaging modality selection: Ultrasound is first-line imaging for acute inflammation and stones (high sensitivity for sialoliths >2 mm); CT preferred for deep lobe involvement and surgical planning; MRI with sialography provides best soft tissue detail and can visualize ductal system; avoid radiation in young patients
• Sialography/sialendoscopy: Direct visualization of ductal system to identify strictures, stones, or mucus plugs; sialendoscopy is both diagnostic and therapeutic, allowing stone removal and ductal dilation
• Sjögren syndrome diagnosis (requires 4 of 6 items): Positive anti-SSA/Ro or anti-SSB/La antibodies, positive rheumatoid factor, ocular staining score ≥5, abnormal Schirmer test (<5 mm wetting in 5 minutes), abnormal Saxon test (unstimulated whole saliva <2 g in 2 minutes), or positive minor salivary gland biopsy showing lymphocytic infiltration (focus score ≥1)
• Fine needle aspiration (FNA): Gold standard for evaluating salivary gland masses; low morbidity; can distinguish benign from malignant lesions and guide further management; core biopsy reserved for indeterminate FNA results
• Viral serology: Mumps IgM/IgG; CMV, EBV, and HIV testing in immunocompromised; provides confirmatory diagnosis in viral sialadenitis
• Salivary flow rate measurement: Stimulated (chewing paraffin) and unstimulated tests quantify hyposalivation; flow <0.5 mL/min unstimulated or <1 mL/min stimulated confirms xerostomia

• Acute bacterial sialadenitis — first-line: IV antibiotics covering gram-positive cocci and anaerobes (e.g., cefoxitin 2 g IV q6h or ampicillin-sulbactam 3 g IV q6h); supportive care with hydration, warm compresses, NSAIDs (ibuprofen 600 mg PO q6h); sialagogues (lemon drops, sugarless candy) to promote salivary flow; if no improvement within 48-72 hours, consider imaging to exclude abscess
• Salivary obstruction/sialoliths: Conservative management with hydration and oral hygiene; sialagogues and warm massage to promote stone passage; ultrasound-guided sialolith removal or sialendoscopy for symptomatic stones; submandibular gland sialectomy reserved for chronic obstruction with recurrent infection and glandular atrophy (higher morbidity due to marginal mandibular nerve risk)
• Chronic sialadenitis management: Aggressive oral hygiene and frequent water intake; sialagogues (sugar-free lemon drops, pilocarpine 5 mg PO q6h as systemic agent); low-dose prophylactic antibiotics during high-risk periods; gland-sparing therapy preferred; gland excision only if recurrent infections significantly impact quality of life
• Sjögren syndrome treatment: First-line symptomatic management with artificial saliva, sugar-free lozenges, and pilocarpine (5 mg PO TID-QID) or cevimeline (30 mg PO TID) to stimulate residual secretory function; immunosuppression for systemic manifestations with hydroxychloroquine (200-400 mg PO daily) for arthralgias and rituximab (anti-CD20 monoclonal antibody) for severe disease; aggressive dental care and fluoride prophylaxis to prevent caries

Emergencies — recognize immediately

• Deep neck space extension / parapharyngeal or submandibular abscess: infection tracks along fascial planes from an obstructed, infected gland; trismus, floor-of-mouth elevation, muffled hot potato voice, drooling, or stridor signal impending airway loss. Ludwig angina from submandibular involvement is an airway emergency — secure the airway first, then contrast CT and surgical drainage with IDSA-consistent broad-spectrum coverage of oral streptococci, S. aureus, and anaerobes
• Descending mediastinitis: retropharyngeal spread; widened mediastinum or air on CT, sepsis physiology — surgical emergency
• Suppurative parotitis with abscess: failure to defervesce after 48–72 hours of appropriate antibiotics plus fluctuance; ultrasound or CT confirms, drainage required

Disease complications

• Gland atrophy and recurrent sialadenitis: chronic obstruction causes acinar loss and fibrosis; swelling stops fluctuating and the gland becomes small and firm
• MALT lymphoma in Sjögren disease: chronic lymphoid stimulation; the signal is a persistently hard, unilateral, enlarging parotid mass, new cryoglobulins, or falling complement — biopsy, do not observe
• Rampant cervical/root caries and oral candidiasis from loss of salivary buffering and IgA
• Anti-Ro/SSA transplacental passage causing neonatal lupus and congenital complete heart block, which ACOG and ACR address with fetal cardiac surveillance in antibody-positive pregnancy
• Mumps sequelae: orchitis, aseptic meningitis, pancreatitis, and unilateral sensorineural hearing loss
• Carcinoma ex pleomorphic adenoma: sudden growth or new facial weakness in a mass present for years

Treatment complications

• Facial nerve injury after parotidectomy — the nerve traverses the gland; intraoperative monitoring is standard
• Frey syndrome: aberrant parasympathetic auriculotemporal fibers reinnervate skin sweat glands; gustatory sweating and flushing, confirmed by the starch–iodine test, treated with botulinum toxin
• Marginal mandibular, lingual, or hypoglossal nerve injury after submandibular gland excision; great auricular nerve loss gives earlobe numbness
• Sialocele or salivary fistula; tumor spillage and recurrence after enucleation or incisional biopsy of pleomorphic adenoma

• Stones go submandibular, tumors go parotid: Wharton duct drains uphill and carries viscous mucinous saliva, so ~80–90% of sialoliths are submandibular; the parotid's serous, watery secretion resists stone formation but the gland hosts most neoplasms. Postprandial colicky swelling = stone until proven otherwise
• Duct anatomy is testable: Stensen duct opens opposite the second upper molar; Wharton duct opens at the floor-of-mouth papilla beside the frenulum. Purulent expression from Stensen duct with a tender, erythematous parotid in a dehydrated postoperative elderly patient is suppurative parotitis
• Facial nerve weakness plus a parotid mass = malignancy until disproven, because CN VII runs through the gland and benign tumors displace rather than invade. Best next step is FNA and cross-sectional imaging, then oncologic resection per NCCN Head and Neck Cancers guidance — never open incisional biopsy, which seeds tumor and creates fistula
• Tumor one-liners: pleomorphic adenoma — most common benign, chondromyxoid stroma, recurs if enucleated, can undergo malignant transformation; Warthin tumor — smokers, bilateral/multifocal, lymphoid stroma with germinal centers; mucoepidermoid carcinoma — most common malignancy, mucous plus squamoid cells, MAML2 fusion; adenoid cystic carcinoma — cribriform Swiss cheese pattern, perineural invasion causing pain and palsy, late pulmonary metastases
• The one association examiners love: Sjögren disease and parotid MALT lymphoma. A firm, unilateral, persistent parotid mass in a woman with sicca symptoms and anti-SSA/Ro is lymphoma, not a flare
• Common distractor — sialadenosis versus sialadenitis: bilateral, soft, painless, non-tender parotid enlargement in bulimia, alcoholism, or diabetes is acinar hypertrophy; antibiotics and imaging are the wrong answer, treat the underlying disorder
• Mumps is a vaccine-preventable stem: bilateral parotitis with orchitis or aseptic meningitis in an unimmunized child; prevention is the two-dose CDC/ACIP MMR schedule
• Xerostomia workup starts with the medication list — anticholinergics, antihistamines, tricyclics, and diuretics — before invoking autoimmune disease