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PH-GI21

Stomatitis and sialadenitis

How the lining of the mouth and the salivary glands become inflamed: aphthous ulcers, herpes and Candida on the mucosa; mumps, bacteria, stones and autoimmunity in the glands; and why too little saliva links the two.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe the oral mucosa and the salivary glands, and how saliva protects the mouth.
  • Explain how recurrent aphthous ulcers, herpes simplex virus and Candida each injure the oral mucosa, and why their lesions look different.
  • Explain how viruses from the blood, bacteria climbing a duct, stones and autoimmunity inflame the salivary glands.
  • Relate reduced salivary flow to both stomatitis and bacterial sialadenitis.
  • Recognise the classic appearances, tests and differentials of the main forms, and explain how anti-inflammatory, antiviral, antifungal and antibacterial treatment and restoring saliva flow act on each mechanism.

What it is

Stomatitis is inflammation of the lining of the mouth (the oral mucosa), seen as redness, ulcers or white patches; it can be confined to the mouth or be a sign of systemic disease. Sialadenitis is inflammation of a salivary gland, most often the parotid (parotitis) or the submandibular gland, caused by a virus such as mumps, bacteria climbing the duct, obstruction by a stone, or autoimmune disease such as Sjögren’s disease. The two are linked because saliva protects both the lining and the ducts.

6 types to tell apart
Recurrent aphthous stomatitis
Round, painful ulcers that recur on the non-keratinised lining, caused by a T-cell attack on the epithelium rather than infection; minor, major and herpetiform types.
Herpetic stomatitis
Herpes simplex virus, usually type 1, destroys epithelial cells: primary gingivostomatitis, mostly in young children, then recurrent cold sores from virus that stays latent in a sensory ganglion.
Oral candidiasis
Overgrowth of Candida, normally a harmless commensal, when the bacteria, saliva or T-cell immunity that hold it back fail: pseudomembranous (thrush), erythematous, denture-related and angular cheilitis.
Viral sialadenitis (mumps)
A systemic paramyxovirus infection that reaches the glands through the blood, usually swelling both parotids, and can involve the testes, meninges and pancreas.
Acute bacterial sialadenitis
Bacteria from the mouth, most often Staphylococcus aureus, climb a duct whose saliva flow has slowed; usually one parotid, with pus at the duct opening.
Obstructive and autoimmune sialadenitis
A stone, usually in the submandibular duct, blocks saliva and invites recurrent infection; in Sjögren’s disease and IgG4-related disease lymphocytes and plasma cells replace the secretory tissue.

US spelling: litres → liters.

Normal function

A renewing lining, washed by saliva

The mouth is lined by stratified squamous epithelium over a vascular lamina propria. Where chewing rubs hardest (gums, hard palate, top of the tongue) the surface is keratinised; the inner lips, cheeks, floor of the mouth and underside of the tongue have a thinner, non-keratinised lining. Basal cells divide constantly, so the lining renews itself within days and small injuries heal quickly.

Saliva, about 1 to 1.5 litres a day, comes from hundreds of minor glands in the lining and three pairs of major glands. The makes watery (serous) saliva that drains through the , which opens inside the cheek opposite the upper second molar. The make mixed, thicker saliva that runs forwards and upwards through the to open beside the frenulum of the tongue; the make mostly mucus.

Saliva protects the mouth in several ways. Its constant flow washes food, cells and microbes away and keeps the ducts flushed from the gland outwards. Mucins lubricate the lining; bicarbonate and phosphate buffer acid; lysozyme, lactoferrin and secretory IgA limit microbes; growth factors help the lining heal. Parasympathetic nerves acting on M3 muscarinic receptors drive secretion, which rises sharply at meals.

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