Definition/General
Introduction:
Sialadenitis represents inflammation of salivary glands with acute or chronic patterns
Most common non-neoplastic condition affecting salivary glands
FNAC shows characteristic inflammatory cellular infiltrate with reactive epithelial changes
Causes include infection, autoimmune disease, obstruction
Important to distinguish from neoplastic conditions.
Origin:
Results from ductal obstruction (stones, strictures)
Viral infections (mumps, EBV, CMV)
Bacterial infections (Staphylococcus, Streptococcus)
Autoimmune conditions (Sjogren syndrome)
Radiation-induced sialadenitis
Drug-induced dry mouth.
Classification:
Acute sialadenitis: bacterial or viral
Chronic sialadenitis: obstructive or autoimmune
Chronic sclerosing sialadenitis (Kuttner tumor)
Granulomatous sialadenitis
Milan System: Category II - Non-neoplastic
Grading based on inflammatory activity.
Epidemiology:
Common condition affecting all age groups
Acute forms more common in children
Chronic forms peak in middle age
Autoimmune sialadenitis shows female predominance
Parotid and submandibular glands equally affected
Indian population: high prevalence due to endemic infections.
Clinical Features
Presentation:
Acute: painful, rapid swelling
Fever and malaise
Purulent discharge from duct
Chronic: recurrent swelling
Meal-related pain
Reduced salivary flow
Firm, enlarged gland.
Symptoms:
Pain and swelling (main symptoms)
Dry mouth (xerostomia)
Difficulty swallowing
Bad taste (purulent discharge)
Fever (acute cases)
Trismus (severe cases)
Regional lymphadenopathy.
Risk Factors:
Dehydration
Poor oral hygiene
Salivary stones
Autoimmune diseases
Radiation therapy
Medications (anticholinergics, diuretics)
Systemic illnesses
Immunocompromised states.
Screening:
Clinical examination for gland enlargement
Ductal massage to assess discharge
Sialography for ductal anatomy
Ultrasound for stones/masses
CT/MRI for chronic cases
Autoimmune workup if indicated.
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Gross Description
Appearance:
FNAC aspirate often purulent or turbid
Acute: thick, cloudy appearance
Chronic: viscous, mucoid
Volume varies 0.5-3 ml
May contain debris and inflammatory exudate.
Characteristics:
Acute: purulent consistency
Contains neutrophils and bacteria
Chronic: mucoid quality
Contains lymphoid aggregates
Cellular debris prominent
Absence of mucin (unlike tumors).
Size Location:
Sample adequacy depends on inflammatory phase
Acute cases yield abundant inflammatory cells
Chronic cases may be paucicellular
Multiple sampling may be needed
Avoid heavily inflamed areas for interpretation.
Multifocality:
Bilateral involvement in autoimmune disease
Multiple gland involvement possible
Focal vs diffuse inflammation
Associated lymphadenopathy
Systemic autoimmune manifestations.
Microscopic Description
Histological Features:
Acute: predominant neutrophilic infiltrate
Bacterial colonies may be seen
Chronic: lymphoplasmacytic infiltrate
Lymphoid aggregates and germinal centers
Reactive epithelial changes
Fibrosis in chronic cases.
Cellular Characteristics:
Acute: neutrophils and macrophages
Reactive epithelial cells with enlarged nuclei
Chronic: lymphocytes and plasma cells
Tingible body macrophages
Immunoblasts scattered
Epithelial metaplasia (squamous, oncocytic).
Architectural Patterns:
Diffuse inflammatory infiltrate
Lymphoepithelial lesions (chronic)
Germinal center formation
Ductal dilatation and destruction
Stromal fibrosis
Acinar atrophy.
Grading Criteria:
Based on inflammatory activity
Acute inflammation: neutrophil predominance
Chronic active: mixed inflammation
Chronic inactive: lymphocyte predominance with fibrosis
Autoimmune: lymphoepithelial lesions
Focus score for Sjogren syndrome.
Immunohistochemistry
Positive Markers:
Epithelial cells: CK7 positive
CK8/18 positive
EMA positive
Inflammatory cells: CD20 positive (B cells)
CD3 positive (T cells)
CD68 positive (macrophages)
IgG4 positive (subset).
Negative Markers:
Epithelial cells: p63 negative (unless squamous metaplasia)
S-100 negative
Chromogranin negative
Calponin negative
Inflammatory cells maintain appropriate lineage markers.
Diagnostic Utility:
IHC rarely needed for typical sialadenitis
May help identify epithelial components
Useful to exclude lymphoma (polyclonal vs monoclonal)
IgG4 staining for IgG4-related disease
Viral markers if suspected.
Molecular Subtypes:
IgG4-related sialadenitis: IgG4+ plasma cells >30%
Autoimmune sialadenitis: polyclonal inflammatory infiltrate
Infectious sialadenitis: pathogen-specific patterns
Drug-induced: specific medication history.
Molecular/Genetic
Genetic Mutations:
No specific genetic mutations in inflammatory sialadenitis
Autoimmune forms may show HLA associations
Sjogren syndrome: HLA-DR3, HLA-DR2
Reactive changes in epithelium
Polyclonal B cell proliferation.
Molecular Markers:
Inflammatory cytokines elevated
Autoantibodies in autoimmune disease
Polyclonal immunoglobulin patterns
Normal tumor suppressor expression
Reactive proliferation markers
Tissue repair factors.
Prognostic Significance:
Excellent prognosis with appropriate treatment
Acute forms resolve completely
Chronic forms may cause permanent damage
Autoimmune sialadenitis: risk of lymphoma development (1-5%)
Functional assessment important for outcome.
Therapeutic Targets:
Antibiotics for bacterial infection
Antivirals for specific viral infections
Anti-inflammatory agents
Immunosuppressants for autoimmune disease
Ductal interventions for obstruction
Symptomatic treatment for dry mouth.
Differential Diagnosis
Similar Entities:
Lymphoma (MALT lymphoma)
Warthin tumor (lymphoid component)
Chronic sialadenitis vs tumor
IgG4-related disease
Granulomatous disease (sarcoid, TB)
Kimura disease (eosinophilic infiltrate).
Distinguishing Features:
Sialadenitis: Polyclonal inflammatory infiltrate
Reactive epithelial changes
Mixed inflammation
Lymphoma: Monoclonal B cells
Light chain restriction
Warthin tumor: Oncocytic epithelium
Organized lymphoid tissue
IgG4 disease: IgG4+ plasma cells
Storiform fibrosis
Granulomatous: Epithelioid granulomas.
Diagnostic Challenges:
Distinguishing reactive from neoplastic
Lymphoepithelial lesions may mimic carcinoma
Atypical reactive changes
Sampling adequacy in fibrotic areas
Clinical correlation essential
Flow cytometry for lymphoid lesions.
Rare Variants:
Necrotizing sialadenitis
Eosinophilic sialadenitis
Granulomatous sialadenitis
Xanthogranulomatous sialadenitis
IgG4-related sialadenitis
Radiation-induced sialadenitis
Actinomycosis.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Fine needle aspiration from [location] salivary gland
Specimen Adequacy
Adequate for evaluation - contains inflammatory cells and reactive epithelium
Inflammatory Pattern
[Acute/chronic] inflammatory infiltrate with predominant [neutrophils/lymphocytes]
Epithelial Changes
Reactive epithelial cells with enlarged nuclei and prominent nucleoli
Microorganisms
[Present/absent] - [specify if identified]
Background
Inflammatory background with cellular debris and proteinaceous material
Milan System Category
Category II - Non-neoplastic (inflammatory)
Cytological Diagnosis
[Acute/chronic] sialadenitis
Recommendation
Clinical correlation recommended. Culture for bacterial pathogens if acute. Consider autoimmune workup if chronic