Category Archives: Oral Pathology

Pleomorphic adenoma

  • The commonest salivary gland tumor
  • 60 – 85% of parotid tumours
  • 45 – 50% of minor gland tumors

Most common intra-oral site: Palate (other – parotid)

Incidence: 5th – 6th decades, F = 60% cases

Clinical: A slow growing, painless, rubbery swelling with intact overlying skin

NB: CA in PSA, 3% of tumors


  • A mixture of epithelial & mesenchymal components (myxoid, chondroid & mucoid areas, with architectural diversity)
  • Pseudoencapsulated with both intra- and extracapsular nodules representing growth of pseudopodia into the surrounding tissues → high recurrence rate


  • FNA
  • Core needle biopsy
  • Radio, US, CT, MRI


  • Surgical resection
  • Parotid – Superficial or total parotidectomy


Salivary gland tumors

Salivary gland tumors exhibit paradoxical behavior:

  • Malignancies – indolent
  • Benign tumors – aggressive


  • Parotid – 65%
  • Submandibular glands – 10%
  • Sublingual glands < 1%
  • Minor salivary glands – 25%

For the intra-oral tumors:

  • Palate – 55%
  • Upper lip – 20%


Two theories:

1. Bicellular theory: Neoplasms arise from stem cells in excretory and intercalated ducts

  • Intercalated ducts:
    • Pleomorphic adenoma
    • Warthin’s tumor
    • Oncocytoma
    • Acinic cell
    • Adenoid cystic
  • Excretory ducts:
    • Mucoepidermoid
    • Squamous cell

2. Multicellular theory: Neoplasm develops from various differentiated cells within the salivary gland unit

  • Acinar cells: Acinic cell carcinoma
  • Intercalated duct: Pleomorphic tumor
  • Striated duct: Oncocytic tumor
  • Excretory duct:
    • Mucoepidermoid
    • Squamous cell
Salivary duct

WHO classification of salivary gland tumors:

1) Adenomas: Benign

2) Carcinomas: Malignant

  • Mucoepidermoid carcinomas
  • Acinic cell carcinomas
  • Adenoid cystic carcinomas
  • Carcinoma arising from PSA
  • Pleomorphic low grade adenocarcinoma
  • Others

Other causes of inflammation – Salivary gland disease

Granulomatous disease

1. Sarcoidosis

Uncommon chronic multisystem disease, unknown cause

Epidemiology: Adult females of African origin


  • Granuloma formation in:
    • Lungs lymph nodes (particularly hilar nodes)
    • Salivary glands
    • Oral sites
  • Systematic features:
    • Erythema nodosum
    • Lymphadenopathy
    • Lung involvement
  • Oral features:
    • Enlarged salivary glands
    • Xerostomia
    • Gingival hyperplasia
    • Labial swelling

NB: Heerfordt’s syndrome (salivary and lacrimal swelling, facial palsy and uveitis) is rare


2. TB

  • Primary TB of the salivary glands:
    • Uncommon, usually unilateral, parotid most common affected
    • Believed to arise from spread of a focus of infection in tonsils
  • Secondary TB – may involve the salivary glands but tends to involve the SMG

3. Cat Scratch Disease

  • Does not involve the salivary glands directly, but involves the periparotid and
    submandibular triangle lymph nodes
  • May involve SG by contiguous spread
  • Bacteria is Bartonella Henselae(G-R)



True cysts of the parotid account for 2-5% of all parotid lesions

  1. Congenital:
  • Type 1 – Branchial arch cysts
  • Type 2 – Cysts are a duplication anomaly of the membranous and cartilaginous EAC
  1. Acquired:
  • Mucus extravasation vs. retention
  • Traumatic
  • Benign epithelial lesions
  • Association with tumors:
    • Pleomorphic adenoma
    • Adenoid Cystic Carcinoma
    • Mucoepidermoid Carcinoma
    • Warthin’s Tumor


  • Aka: pneumosialadenitis, wind parotitis, pneumatocele glandulae parotis
  • In the absence of gas-producing bacterial parotitis, gas in the parotid duct or gland is assumed to be due to the reflux of pressurized air from the mouth into Stenson’s duct.
  • May occur with episodes of increased intrabuccal pressure – glass blowers, trumpet players
  • Crepitations on palpation of gland
  • Swelling may resolve in minutes to hours, in some cases, days.
  • US and CT show air in the duct and gland
  • Antibiotics to prevent superimposed infection


  • Non inflammatory, non neoplastic swelling of salivary glands
  • Usually bilateral and painless, affecting the parotids

Etiology: Dysregulation of the autonomic innervation of the salivary glands.

  1. Drugs: Alcohol, Sympathomimetics (isoprenaline)
  2. Endocrine: Acromegaly, Diabetes mellitus, Pregnancy
  3. Metabolic: Liver cirrhosis, Anorexia nervosa/bulimia, Cystic fibrosis, Malnutrition
  4. HIV


Salivary duct obstruction

Sialolithiasis/salivary gland calculus


  • Xerostomic meds
  • Water hardness
  • Hypercalcemia
  • Tobacco smoking – cytotoxic effect on saliva, ↓ PMN phagocytic, ↓ salivary proteins
  • Gout – only systemic disease known to cause salivary calculi and these are composed of uric acid

Submandibular duct:

  • Inorganic deposits in the submandibular duct
  • Initiated by a nidus (which is frequently of bacterial origin) – acts as a focus for dystrophic calcification
  • The submandibular duct (wharton’s) is commonly affected due to:
  1. Its tortuous course and longer duct – which encourages stasis within the duct
  2. Higher mucous content in saliva
  3. Saliva more alkaline
  4. Higher concentration of calcium and phosphate in the saliva
  5. Tendency of the saliva to flow against gravity – leaching of inorganic residues
  • Ductal defects aggravate this condition – strictures and stenoses


  • Unilateral, painful salivary gland swelling + intermittent symptoms that appear on salivation
  • Acute ductal obstruction – may occur at meal time when saliva producing is at its maximum, the resultant swelling is sudden and can be painful (gustatory pain)
  • Gradually reduction of the swelling can result but it recurs repeatedly when flow is stimulated.
  • This process may continue until complete obstruction and/or infection occurs

Clinical history:

  • History of swellings / change over time
  • Trismus
  • Pain
  • Variation with meals
  • Bilateral
  • Dry mouth, dry eyes
  • Recent exposure to sick contacts (mumps)
  • Radiation history
  • Current medications


1. Inspection:

  • Asymmetry (glands, face, neck)
  • Diffuse or focal enlargement
  • Erythema extra-orally
  • Trismus
  • Medial displacement of structures intraorally
  • Examine external auditory canal (EAC)
  • Cranial nerve testing

2. Palpation:

  • Palpate for cervical lymphadenopathy
  • Bimanual palpation of floor of mouth in a posterior to anterior direction
    o Have patient close mouth slightly & relax oral musculature to aid in detection
    o Examine for duct purulence
  • Bimanual palpation of the gland (firm or spongy/elastic)


  • Prolonged obstruction – atrophy of the acini.
  • A sialolith is distinguished by its calcific lamellar appearance


  • Plain occlusal film
  • Nearly 50% of calcifications are diffuse/ radiolucent so if the obstruction cannot be
    visualized on a plain xray, a sialogram should be done


  • 80-90% of SMG calculi are radio-opaque
  • 50-80% of parotid calculi are radiolucent
  • 30% of SMG stones are multiple
  • 60% of Parotid stones are multiple

Other diagnostic approaches:

  1. CT Scan:
  2. Ultrasound: Can detect small stones (>2mm), inexpensive, non-invasive
  3. Sialography:
    • Opacification of the ducts – retrograde injection of a water-soluble dye.
    • Provides image of stones and duct morphological structure
    • Disadvantages:
      • i. Irradiation dose
      • ii. Pain with procedure
      • iii. Possibility of perforation
      • iv. Infection dye reaction
      • v. Push stone further
      • vi. Contraindicated in active infection
  4. Radionuclide studies:
    • Useful to image the parenchyma
    • T99 – artificial radioactive element that – used as a tracer in imaging studies
    • Half life of 6 hours
    • Shares the Na-K-Cl transport system on the BM of the parotid acinar cells
  5. MRI Sialography:
    • Advantage: No dye, no irradiation, no pain
    • Disadvantage: Cost, possible artifact
  6. Diagnostic sialendoscopy:
    • Allows complete exploration of the ductal system, direct visualization of duct
    • Success rate of >95%2
    • Disadvantage:
      • Technically challenging
      • Trauma could result in stenosis
      • Perforation


  • Duct dilatation – to milk out the sialolith/ calcifications.
  • None: antibiotics and anti-inflammatories
  • Stone excision:
    • Lithotripsy
    • Interventional sialendoscopy
    • Simple removal (20% recurrence)
  • Gland excision

If patients defer treatment, they need to know:
– Stones will enlarge over time
– Seek treatment early if infection develops
– Salivary gland massage and hyper-hydration when symptoms develop

Stone composition:

  • Organic – often predominate in the center
  • Glycoproteins
    • Mucopolysaccharides
    • Bacteria
    • Cellular debris
  • Inorganic – often in the periphery
    • Calcium carbonates & calcium phosphates in the form of hydroxyapatite



Salivary gland cysts

Etiology: Pooling of saliva in tissues – secondary to trauma to a salivary gland

Classification: Pooling of saliva occurs:

  • Within the gland – Retention cysts
    • Salivary duct blocked – expansion and formation of cysts
    • Epithelial lined
    • Adults
  • Outside the gland – Extravasation cysts
    • Trauma – saliva spills into the tissues
    • Not epithelial lined
    • Kids
    • Neck cyst – extravasation cyst



  • Cysts located on the floor of the mouth are called ranulas (Usually the
    extravasation type) Picture
  • Ranulas can be superficial or unilateral
  • Superficial ranulas: due to trauma to 1 or more excretory ducts of sublingual
    salivary gland
  • If they burrow through the mylohyoid muscle (weak muscle), they are termed
    plunging ranulas. Picture
  • The other common site is the lower lip.
  • If the upper lip is involved, consider neoplasia

Common site: Lower lip > Floor of mouth > Palate > Buccal mucosa


  • Compressed fibrous CT
  • Surrounding pooled, eosinophilic mucin
  • Containing macrophages that have ingested mucin (mucinages)
  • If retention cyst – epithelial lining and dilated duct
  • If extravasation – no epithelial lining, remnants of ruptured salivary gland

Management: Surgical resection, excision, recurrences are common


Inflammation of salivary gland

Risk factors:

  • Systemic dehydration (salivary stasis)
  • Chronic disease and/or immunocompromise
  • Neoplasms (pressure occlusion of duct)
  • Sialectasis (salivary duct dilation) increases the risk for retrograde contamination. Is associated with cystic fibrosis and pneumoparotitis
  • Extremes of age
  • Poor oral hygiene
  • Calculi, duct stricture
  • NPO status (stimulatory effect of mastication on salivary production is lost)
  • Sialolithiasis – mechanical obstruction of the duct resulting in salivary stasis and subsequent gland infection


  1. Retrograde contamination of the salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity.
  2. Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection

Acute suppurative infection

More common in parotid gland

  • Etiology: the retrograde infection from the mouth
  • 20% cases are bilateral
    • Suppurative parotitis
    • Surgical parotitis
    • Post-operative parotitis
    • Surgical mumps
    • Pyogenic parotitis
  • Predilection for parotid: Parotid is primarily serous
  • Differentials for parotid gland enlargement:
    • Lymphoma
    • Actinomycoses
    • Cat-scratch disease
    • Sjogren’s syndrome
    • Wegener’s granulomatosis
    • Viral infection

NB: Calculus formation is more likely to occur in submandibular gland duct (85-90% of salivary calculi are in the SMG duct) However, the parotid gland remains the most common site of acute suppurative infection


Bacterial sialadenitis


  • Mucoid saliva contains lysozymes & IgA antibodies – protect against bacterial infection (therefore, parotid has ↓ bacteriostatic activity)
  • Mucins contain sialic acid – which agglutinates bacteria and prevents its adherence to host tissue
  • Specific glycoproteins in mucins bind epithelial cells competitively inhibiting bacterial attachment to these cells

Diagnosis: Purulent saliva sent for culture

a) Acute bacterial sialadenitis

  • Uncommon disorder
  • Usually involving the parotid gland as an ascending infection


  • Strep pyogenes
  • Staph aureus
  • Strep viridans
  • Haemophilus
  • Debilitated/ dehydrated patients
  • Sjogren syndrome
  • Immune compromised patients


  • Gland swelling
  • Pain, fever, malaise
  • Redness of overlying skin
  • pus discharge
  • Trismus/lockjaw
  • Cervical lymphadenopathy


  • Reverse the medical condition that may have contributed to formation
  • Discontinue anti-sialogogues
  • Warm compresses, maximize OH, give sialogogues (lemon drops)
  • External salivary gland massage if tolerated
  • Antibiotics:
    • 70% of organisms produce B-lactamase or penicillinas
    • Need B-lactamase inhibitor like Augmentin or Unasyn or 2nd gen cephalosporin
    • Can adding metronidazole or clindamycin to broaden coverage
  • Failure to respond:
    • After 48 hours the patient should respond
    • Add 3rd gen cephalosporine
    • Add aminoglycoside
    • MRSA in nursing homes and nosocomial environments – vancomycin
  • Surgery for acute parotitis:
    • Limited role for surgery
    • Discrete abscess – surgical drainage
    • Approach is anteriorly based facial flap with multiple superficial radial incisions created in the parotid fascia parallel to the facial nerve
    • Close over a drain


  • Hematogenous spread
  • Direct extension- Abscess ruptures into external auditory canal and TMJ
  • Fascial capsule around parotid deep surface is weak – it is adjacent to the loose areolar tissues of the lateral pharyngeal wall (Achilles ‘heel of parotid). Therefore extension of abscess- in parapharyngeal space may result in:
    • Airway obstruction
    • Mediastinitis
    • Internal jugular thrombosis
    • Carotid artery erosion
  • Dysfunction of one or more branches of the facial nerve – rare
  • Thrombophlebitis – retromandibular vein or facial veins – rare

b) Chronic bacterial sialadenitis

  • Non specific inflammation
  • Associated with long term diseases of the salivary gland
  • Parotid more common


  • Unilateral swelling
  • Tenderness
  • Inflamed duct orifice
  • Purulent or salty discharge


  • Duct dilatation
  • Hyperplasia of duct epithelium
  • Periductal fibrosis
  • Acinar atrophy
  • Chronic inflammatory infiltrate


  • Duct obstruction or stricture
  • Destruction of glandular tissue
  • Duct dilatation (sialectasia)


  • Treat predisposing factor – calculus or stricture
  • Initial mx should be conservative:
    • Sialagogues
    • Massage
    • Antibiotics for acute exacerbations.
  • Should conservative measures fail, consider removing the gland

Viral sialadenitis


  • Droplet spread, incubation 2 – 3 weeks
  • Mumps = acute, contagious infection mainly caused by paramyxovirus (RNA virus)
  • Others causes of acute viral parotitis: coxsackie a & b, echo virus, cytomegalovirus and adenovirus


  • Fever, malaise
  • Painful swelling affecting the parotids (only in 70% of patients)

Physical exam:

  • Glandular swelling (tense, firm) Parotid gland involved frequently, SMG & SLG
  • Displace ispilateral pinna
  • 75% cases involve bilateral parotids, may not begin bilaterally (within 1-5 days may
    become bilateral)….25% unilateral
  • Low grade fever


  • Orchitis in 20% adult males (ensuing infertility is rare)
  • Oophoritis – Ovary inflammation
  • Pancreatitis
  • Meningitis OR meneigoencephalitis
  • Deafness


  • IgM antibody titres
  • ↑ Serum amylase
  • ↑ Lipase
  • Leukocytopenia, with relative lymphocytosis


  • Antipyretics
  • Analgesics
  • Adequate hydration
  • Isolate the patient 6 – 10 days after the onset of symptoms because the virus is in the saliva at this time

Prevention: MMR Vaccine: measles, rubella, mumps vaccine is administered in a single subcutaneous dose after 12 months of age. Booster at 4-6yr

Post irradiation sialadenitis

  • Common dose-related complication of radiotherapy
  • Causes fibrous replacement of damaged acini & squamous metaplasia of ducts.
  • Sialoliths = calcification within salivary duct, involves salivary gland also occur in 70 – 90% cases


  • Pain & sudden enlargement of gland in relation to gustatory stimuli
  • It is complicated by ascending infection & chronic sialadenitis


  • Acinar destruction and in case of sialolithiasis
  • lamellated structure composed of CaPO4 & CaCO3

Necrotizing sialometaplasia

Etiology: Ischaemia → infarction of salivary lobules

  • Uncommon disorder, may be mistaken for malignancy
  • Iatrogenic origin, possibly a reaction to ischemia or injury

Clinical: Deep crater-like mucosal ulcer, commonly on hard palate, persist for upto 8 weeks


  • Histologically may be mistaken for SCC
  • Lobular necrosis of salivary glands
  • Squamous metaplasia of ducts
  • Mucous extravasation
  • Inflammatory infiltrate surrounded by pseudoepitheliomatous hyperplasia