Paediatric Oral Medicine Flashcards
What are the viral orofacial soft tissue infections?
– Primary herpes
– Herpangina
– Hand foot and mouth
What are the complete diagnostic criteria and epidemiological characteristics of Primary Herpetic Gingivostomatitis?
Caused by Herpes Simplex Virus I
- Common in children
- 7-day incubation period via droplet transmission
- Rare in first 12 months due to maternal antibodies
- Nearly 100% of adults are carriers
- Presents with fluid-filled vesicles that rupture into painful ulcers
- Affects gingivae, tongue, lips, buccal and palatal mucosa
- Accompanied by severe oedematous marginal gingivitis
What are the signs of symptoms of primary herpetic gingivostomatitis?
– Fluid filled vesicles – rupture to painful ragged ulcers on the gingivae, tongue, lips, buccal and palatal mucosa
– Severe oedematous marginal gingivitis
– Fever
– Headache
– Malaise
– Cervical lymphadenopathy
What is treatment, complication, duration and healing for PHG?
Treatment
– Bed rest
– Soft diet/hydration
– Paracetamol
– Antimicrobial gel or mouthwash
– Aciclovir for immunocompromised children
Most common complication
dehydration
Lasts 14 days
Heals with no scarring
List all triggers for recurrent herpes labialis and distinguish it from primary infection.
Recurrent disease (herpes labialis):
Occurs in 50-75% of cases
Triggers include:
Sunlight exposure
Psychological stress
Other illnesses
Differs from primary infection by:
Localized presentation (typically lips)
Less severe symptoms
Shorter duration
Responds to topical acyclovir
Compare and contrast Herpangina with Hand, Foot, and Mouth Disease (both caused by Coxsackie A virus).
Herpangina:
Vesicles confined to tonsillar/pharyngeal region
Duration: 7-10 days
Hand, Foot, and Mouth:
Ulceration on gingivae/tongue/cheeks/palate
Distinctive maculopapular rash on hands and feet
Duration: 7-10 days
What are the 10 essential historical factors to investigate in a patient presenting with oral ulceration?
- Onset timing
- Frequency of occurrence
- Number of ulcers
- Anatomical site
- Size of ulcers
- Duration of each episode
- Dietary factors that worsen condition
- Presence of lesions in other body areas
- Associated medical conditions
- Previous treatments and their effectiveness
What are the infectious causes of oral ulceration?
viral/bacterial
– Viral: Hand foot and mouth/ Coxsackie Virus/ Herpes Simplex/ Herpes Zoster, CMV, EBV, HIV
– Bacterial: TB, syphilis
What are the immune mediated causes of oral ulceration?
Crohns, behcets, SLE, Coeliac, Periodic fever syndromes
What are the vesticulobullous disorders that cause oral ulceration?
Bullous or mucous membrane pemphigoid, pemphigus vulgaris, linear IgA disease, erythema multiforme
What are the vitamin deficiencies that can cause oral ulceration?
Iron, B12, Folate
Differentiate between the three patterns of Recurrent Aphthous Ulceration (RAU) and list ALL possible etiological factors.
Minor: <10mm diameter
Major: >10mm diameter
Herpetiform: 1-2mm diameter
Etiological factors:
Hereditary predisposition (45% have family history)
Hematological deficiencies (iron deficiency in 20%)
Gastrointestinal disease (Celiac in 2-4%)
Minor trauma in susceptible individuals
Psychological stress
Allergic reactions (SLS in toothpaste, food preservatives)
Hormonal changes (menstruation)
In a pediatric patient presenting with recurrent oral ulceration, outline the complete diagnostic algorithm and management plan, including all necessary investigations and potential treatment options based on findings.
Initial Assessment:
Complete history (all 10 key points)
Diet diary
Physical examination
Initial Investigations:
Full Blood Count
Haematinics (Folate/B12/Ferritin)
Celiac screen (Anti-transglutaminase antibodies)
Management Based on Findings:
If low ferritin: 3 months iron supplementation
If low folate/B12 or positive celiac screen: pediatric referral
Identify and manage exacerbating factors:
Nutritional deficiencies
Traumatic factors
Dietary triggers
Allergic factors (try SLS-free toothpaste)
Symptomatic Treatment:
Prevention of superinfection: Corsodyl 0.2%
Protect healing: Gengigel or Gelclair
Pain relief: Difflam or local anesthetic spray
Follow-up and monitoring:
Assess response to treatment
Monitor for development of systemic conditions
Adjust management plan based on response
Compare the clinical features of OFG with oral manifestations of Crohn’s disease and explain why they’re clinically indistinguishable.
Clinical features (identical in both conditions):
Lip/facial swelling
Cobblestone buccal mucosa
Linear ulcers
Mucosal tags
Angular cheilitis
Pathology: Non-caseating granulomas → lymphatic obstruction
What is the aetiology of OFG?
what are the associated allergens?
largey unknown
– Cinnamon Compounds
– Benzoates
– Much higher IgE mediated atopy rates compared to the general popn
Detail the complete diagnostic workup for OFG and explain the rationale for each investigation.
Diagnostic approach:
Clinical examination
Growth measurement using pediatric charts (monitor impact on development)
Laboratory tests:
Full Blood Count (assess overall health status)
Haematinics (identify nutritional deficiencies)
Faecal Calprotectin (screen for inflammatory bowel disease)
Serum Angiotensin Converting Enzyme (screen for sarcoidosis)
Specific testing:
Patch testing (identify potential allergens)
Diet diary (identify dietary triggers)
Note: Lip biopsy not essential for diagnosis
Endoscopy typically avoided in children due to risks
Describe the complete management strategy for OFG, including all therapeutic options and their indications.
Management approach:
Conservative measures:
Oral hygiene support
Symptomatic relief for ulceration
Dietary exclusion (reduces inflammation but not curative)
Management of nutritional deficiencies
Medical interventions:
Topical steroids (first-line)
Topical tacrolimus
Short-course oral steroids (severe cases or unresponsive to topical)
Intralesional corticosteroids
Surgical intervention:
Reserved for unresponsive cases
Consider for long-standing disfigurement
Last resort when other treatments fail
Detail all clinical characteristics and management principles of geographic tongue.
Clinical characteristics:
Idiopathic and non-contagious condition
Can present at young age
Shiny red areas with loss of filiform papillae
White margins surrounding affected areas
Causes intense discomfort in children
Triggers: spicy foods, tomatoes, citrus fruits/juices
Management:
Bland diet during flare-ups
Natural history: symptoms typically improve with age
Compare and contrast the clinical and histological features of all three types of epulides.
benign hyperplastic lesions
Fibrous Epulis
– Firm, pink lump
– Caused by irritation
– Doesn’t usually grow back
Pyogenic Granuloma
– Red/purple, bleeds easily
– Triggered by irritation or pregnancy
– Might come back
Peripheral Giant Cell Granuloma (PGCG)
– Dark red lump
– Contains giant cells
– Can damage bone
What are characteristics of congenital epulis?
*Rare lesion
*Occurs in neonates
*Most commonly affect the anterior maxilla
*F>M
*Granular cells covered with epithelium
*Benign
*Simple excision is curative
Differentiate between the two types of HPV-associated mucosal swellings and their characteristics.
Squamous papilloma
– Small, cauliflower-like lump
– Painless, often on tongue or palate
HPV 6, 11
Verruca vulgaris (common wart)
– Looks like a skin wart
– Rare in the mouth
HPV 2, 4
Compare and contrast mucocele variants and detail their complete management approach.
Mucous Extravasation Cyst:
Normal secretions rupture into adjacent tissue
Mucous Retention Cyst:
Secretions retained in expanded duct
Common characteristics:
Bluish, soft, transparent cystic swelling
Can affect minor or major salivary glands
Most common in minor glands of lower lip
Peak incidence in 2nd decade
Management considerations:
Most rupture spontaneously
Surgery indicated only if:
Lesion fixed in size
Note: Surgery risks damaging adjacent glands
Surgical approach must include:
Removal of cyst
Removal of adjacent damaged minor salivary gland
What is a ranula?
why is US or MRI needed?
Mucocele in floor of mouth (FOM)
Source: Sublingual or submandibular duct/glands
Use US/MRI to rule out plunging ranula
Differential: Lymphangioma
Differentiate between Bohn’s nodules and Epstein pearls in neonates.
Bohn’s Nodules:
Location: alveolar ridge
Origin: dental lamina remnants
Content: keratin
Timing: present in first 28 days
Resolution: early months of life
Epstein Pearls:
Location: palatal midline
Origin: trapped epithelium in palatal raphe
Prevalence: ~80% of neonates
Resolution: first few weeks of life
