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


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