Oral Mucosal Lesions in Children
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Direct answer
Fever, drooling and painful gums in a preschooler point first to primary herpetic gingivostomatitis: HSV-1 vesicles rupture into ulcers across the gingiva, lips, tongue and palate, run a self-limiting 10-14 day course, and shorten with weight-based aciclovir started within 72 hours of onset, the real emergency being dehydration. Two coxsackievirus cousins divide by geography: herpangina punches small posterior ulcers on the soft palate and tonsillar pillars in summer, while hand-foot-mouth disease (classically coxsackie A16) adds vesicles on palms, soles and buttocks. Koplik spots opposite the lower molars are pathognomonic of measles. Recurrent aphthous ulceration on movable mucosa comes as minor (under 1 cm, heal without scarring), major or Sutton's (over 1 cm, scar) and herpetiform (crops of pinpoint ulcers). Mucocele of the lower lip (an extravasation phenomenon from a traumatised minor gland) is the commonest paediatric salivary lesion, the ranula its floor-of-mouth counterpart, and Kawasaki disease — red cracked lips, strawberry tongue and coronary aneurysm risk treated with IVIG 2 g/kg and aspirin — is the mucosal diagnosis a dentist cannot afford to miss.
What you must remember
- Primary herpetic gingivostomatitis: HSV-1, first infection usually under six years; fever, vesicles then ulcers on gingiva, tongue, lips and palate with tender lymphadenopathy; management is hydration, analgesia and soft diet, with aciclovir effective if begun within 72 hours; admit the dehydrated child.
- Herpangina versus hand-foot-mouth: both coxsackievirus (herpangina classically coxsackie A types, HFMD coxsackie A16); herpangina ulcers sit posteriorly on soft palate and pillars without gingivitis; HFMD adds vesicles on hands, feet and buttocks; both peak in summer and autumn.
- Measles: Koplik spots — bluish-white specks on buccal mucosa opposite the mandibular molars — precede the rash and are pathognomonic.
- Recurrent aphthous stomatitis: minor (most common, under 10 mm, no scarring), major/Sutton's (over 10 mm, weeks to heal, scars), herpetiform (many pinpoint ulcers); movable mucosa only; treatment with topical corticosteroids, benzydamine and chlorhexidine; rule out haematinic deficiency and coeliac disease in recurrent disease.
- Mucocele: lower lip the classic site, bluish fluctuant translucency from extravasation (trauma) rather than retention; excision or marsupialisation with the gland removed to prevent recurrence; the tongue-tip counterpart involves glands of Blandin-Nuhn.
- Ranula: sublingual gland retention or extravasation in the floor of mouth, a soft blue swelling beside the frenum; the plunging type herniates through mylohyoid into the neck.
- Candidiasis: neonatal thrush — creamy white plaques that bleed when wiped, distinguished from milk curds that wipe cleanly; treated with nystatin or miconazole oral gel.
- Kawasaki disease: cracked red lips, strawberry tongue, diffuse oral erythema with fever five days or more, conjunctival injection and rash; coronary artery aneurysms are the danger; IVIG 2 g/kg with aspirin is the treatment — refer immediately.
Sorting an acute ulcerative outbreak
The diagnostic pathway is a site-and-sign map. Start with site: anterior mouth — gingiva, tongue, lips — favours HSV; posterior soft palate and pillars favour herpangina; movable mucosa with spared gingiva favours aphthae. Then fever: high fever preceding ulcers suggests HSV, herpangina or HFMD; aphthae arrive without fever. Then look beyond the mouth: vesicles on hands and feet clinch HFMD; conjunctivitis, red lips and a strawberry tongue after five days of fever raise Kawasaki, and that suspicion ends the dental workup and starts a paediatric referral. A ten-month-old with white plaques that scrape off with bleeding points to thrush. Within HSV itself, dehydration is the judge: a child who has not passed urine or cannot drink needs intravenous fluids and admission, not a stronger mouthwash. Finally, the red flag: any oral ulcer persisting beyond two to three weeks earns a biopsy or specialist referral, because paediatric malignancy and chronic ulcerative disease announce themselves exactly that way.
Where students slip
The herpes-versus-aphthae discrimination is the classic: herpetic lesions begin as vesicles and strike keratinised gingiva with fever, while aphthae occur singly or in crops on movable mucosa without fever — candidates who place aphthae on the gingiva lose the mark. The herpangina-versus-HFMD pair is tested by site (posterior versus posterior plus extremities). The mucocele question asks for the mechanism, and the marks sit in the word extravasation, plus the lower lip as the commonest site. Koplik spots get mislocated to the tongue; they belong to the buccal mucosa opposite the lower molars. Finally, candidates forget the aciclovir window — 72 hours from onset — and the dehydration-first management priority.
Frequently asked questions
How do herpangina and hand-foot-mouth disease differ?
Both are coxsackieviral, but herpangina confines its ulcers to the posterior soft palate and tonsillar pillars, while HFMD (classically coxsackie A16) adds vesicles on hands, feet and sometimes buttocks.
What is the treatment window for aciclovir in primary herpetic gingivostomatitis?
Within about 72 hours of onset, weight-based dosing shortens the course; beyond supportive care, the priority is hydration, with admission for the dehydrated child.
Classify recurrent aphthous stomatitis.
Minor (under 10 mm, most common, heal without scarring), major or Sutton's (over 10 mm, slow healing, scarring) and herpetiform (crops of small ulcers), all on movable, non-keratinised mucosa.
What is the commonest site and mechanism of a paediatric mucocele?
The lower lip, from extravasation of saliva after minor trauma to a gland duct rather than simple retention; excision includes the offending gland to prevent recurrence.
Which oral features suggest Kawasaki disease and why does it matter?
Red cracked lips, strawberry tongue and diffuse oropharyngeal erythema with five days of fever suggest Kawasaki disease, where delayed treatment (IVIG 2 g/kg with aspirin) risks coronary artery aneurysms.