Oral/dental Pain/lesions
Oral/dental pain and lesions encompass a range of conditions affecting the teeth, gums, and oral mucosa—including caries, abscesses, gingivitis, aphthous ulcers, and mucosal lesions—that present with pain, swelling, or visible tissue changes.
Oral/Dental Pain and Lesions
Oral and dental pain/lesions is an umbrella term encompassing any pathological process that produces pain, discomfort, or visible mucosal/structural change within the oral cavity — including the teeth, gingivae (gums), tongue, floor of mouth, hard and soft palate, buccal mucosa, lips, and the alveolar ridges. The term bridges dental (odontogenic) causes and non-dental (non-odontogenic) causes, ranging from the mundane aphthous ulcer to life-threatening oral squamous cell carcinoma (SCC).
Breaking down the key terminology:
- Odontogenic = "odonto" (Greek: tooth) + "genic" (origin) → pain arising from the teeth or their supporting structures
- Stomatitis = "stoma" (Greek: mouth) + "itis" (inflammation) → inflammation of the oral mucosa
- Glossitis = "glossa" (Greek: tongue) + "itis" → inflammation of the tongue
- Gingivitis = "gingiva" (Latin: gum) + "itis" → inflammation of the gums
- Cheilitis = "cheilos" (Greek: lip) + "itis" → inflammation of the lip
This topic matters because the mouth is the gateway to the GI and respiratory tracts, and oral lesions can be the first presentation of systemic diseases (e.g., Behçet disease, Crohn's disease, haematological malignancies, HIV, nutritional deficiencies, autoimmune blistering diseases). A systematic approach prevents you from dismissing a "mouth ulcer" that is actually an SCC or pemphigus vulgaris.
2. Epidemiology and Risk Factors
| Condition | Prevalence / Incidence | Key Demographics |
|---|---|---|
| Aphthous ulcers | 20–25% of general population; most common oral ulcer [1][2] | Young adults, slight female preponderance |
| Dental caries | Global: ~2.3 billion people affected; most prevalent chronic disease worldwide | All ages; peaks in childhood and elderly |
| Periodontal disease | ~50% of adults > 30 y have some form | Increases with age; smoking is the strongest modifiable risk factor |
| Oral SCC | HK: ~600 new cases/year; 5S risk factors endemic in Southern China [3] | Male > Female; peaks > 50 y |
| Nasopharyngeal carcinoma (NPC) | Endemic in Southern China including Hong Kong; 10th most common cancer overall, 6th in males [4] | Male predominance (M:F = 2–3:1) |
| Oral candidiasis | Common in immunocompromised, neonates, denture wearers | HIV, diabetes, steroid inhaler users |
| Herpes simplex (HSV-1) | Seroprevalence 30–100% [5] | Primary infection often in childhood |
| Lichen planus | Prevalence < 1%, most commonly 30–60 y [6] | No sex predilection |
| Pemphigus vulgaris | Rare, incidence 0.1–0.5/100k/y [7] | 40–60 y, highest in Ashkenazi Jews, Indians, SE Asians |
| Behçet disease | Prevalence 13.5–35/100k along ancient Silk Road (Turkey, Middle East, China) [8] | Peaks 20–40 y, M:F ≈ 1:1, strongly associated with HLA-B51 |
Think of risk factors in categories:
Local / Dental:
- Poor oral hygiene → plaque → calculus → gingivitis → periodontitis
- Ill-fitting dentures → chronic trauma → leukoplakia → malignant transformation
- Sharp/broken teeth → chronic ulceration → field cancerisation
Lifestyle / Behavioural:
- Smoking — single most important modifiable risk factor for periodontal disease and oral cancer
- Alcohol ("Spirits") — synergistic with smoking for HNSCC [3]
- Betel nut (areca nut) chewing — extremely relevant in Hong Kong and Southern China; causes oral submucous fibrosis (a premalignant condition) [3]
- Spicy food — chronic mucosal irritation
Infectious:
- HPV 16/18 — drives oropharyngeal SCC (tonsils, base of tongue) via E6/E7 oncoproteins inactivating p53 and Rb [3]
- EBV — primary aetiological agent for NPC; also linked to oral hairy leukoplakia in HIV [4]
- HSV-1 — herpes labialis and herpetic gingivostomatitis [5]
- Candida albicans — thrush in immunocompromised
- Treponema pallidum — syphilitic chancre, mucous patches, gumma
Nutritional:
- Iron deficiency → angular stomatitis, glossitis, Plummer-Vinson syndrome
- Vitamin B12 / folate deficiency → glossitis, aphthous-like ulcers
- Vitamin B6 deficiency → angular stomatitis
- Vitamin C deficiency (scurvy) → spongy, red, swollen and irregular gums that bleed easily [1]
Immune / Systemic:
- HIV/AIDS → oral candidiasis, oral hairy leukoplakia, Kaposi sarcoma, aphthous-like ulcers
- Autoimmune → Behçet disease, pemphigus vulgaris, bullous pemphigoid, SLE, lichen planus
- Immunosuppressive drugs → opportunistic infections, drug-induced mucositis
Drug-related:
- Phenytoin, phenobarbital, cyclosporine → gum hypertrophy [1]
- Anticholinergics → decreased salivary flow → xerostomia → ↑ risk of caries, candidiasis, and sialolithiasis [9]
- Methotrexate, chemotherapy → mucositis
- Allopurinol, aromatic AEDs, sulphonamides → SJS/TEN with severe oral erosions [10]
Genetic / Familial:
- HLA-B51 → Behçet disease [8]
- HLA-B15:02* → carbamazepine-related SJS/TEN (prevalence 13% in HK Chinese → mandatory to check before prescription) [10]
- HLA-B58:01* → allopurinol-related SJS/TEN (prevalence 7.4% in HK Chinese) [10]
The 5Ss of Oral Cancer Risk Factors
Smoking + Spirits + Sharp teeth + Sex (male / oral sex → HPV) + Spicy food [3]. This mnemonic is high yield — it captures the major modifiable risk factors for HNSCC.
3. Anatomy and Function of the Oral Cavity
Understanding oral anatomy is essential for localising pathology and understanding spread patterns.
The oral cavity extends from the vermilion border of the lips anteriorly to the junction of hard and soft palate superiorly and the circumvallate papillae of the tongue inferiorly/posteriorly. Beyond this is the oropharynx.
Components of the oral cavity [3]:
- Lips (vermilion border)
- Buccal mucosa — inner lining of cheeks, from the commissure of the lips to the pterygomandibular raphe
- Upper and lower alveolar ridges (gingivae)
- Hard palate — bony roof of mouth (maxilla + palatine bones)
- Floor of mouth — horseshoe-shaped area beneath the tongue
- Oral tongue — anterior two-thirds (mobile tongue), from tip to circumvallate papillae
- Retromolar trigone — mucosa overlying the ascending ramus of the mandible posterior to the last molar
The oropharynx lies posterior:
Three major paired salivary glands drain into the oral cavity:
| Gland | Duct Name | Duct Opening | Saliva Type | Stone Frequency |
|---|---|---|---|---|
| Parotid | Stensen's duct | Buccal mucosa opposite upper 2nd molar (parotid papilla) [9] | Serous (watery) | 6–20% of sialolithiasis |
| Submandibular | Wharton's duct | Sublingual caruncle on floor of mouth [9] | Mixed (serous + mucous) | Most common (~80%) |
| Sublingual | Rivinus ducts (multiple) | Floor of mouth | Mucous | Rare |
Why does the submandibular gland get stones most frequently? [9]:
- Wharton's duct is long and large — more surface area for calcium deposition
- Flow of saliva is slow and against gravity — the duct courses superiorly from the gland to the floor of mouth
- Saliva is more alkaline with a high mucin and Ca²⁺ content — favours crystallisation
There are also ~600–1000 minor salivary glands scattered throughout the oral mucosa (palate, buccal mucosa, tongue, lips). These are clinically important because minor salivary gland tumours (e.g., adenoid cystic carcinoma, mucoepidermoid carcinoma) can present as submucosal masses in the palate or tongue base [3].
| Nerve | Function | Clinical Relevance |
|---|---|---|
| Trigeminal (V) — V2 (maxillary) and V3 (mandibular) | Sensory to oral cavity; V3 also motor to muscles of mastication | Dental pain referred along V2/V3 dermatomes; invasion by tumour → paraesthesia/numbness |
| Lingual nerve (branch of V3) | Sensory (general) to anterior 2/3 tongue | Invasion causes ipsilateral paraesthesia of tongue [3] |
| Hypoglossal nerve (XII) | Motor to intrinsic and extrinsic tongue muscles (except palatoglossus) | Invasion causes tongue deviation (towards the side of lesion), fasciculation and atrophy [3] |
| Facial nerve (VII) — chorda tympani | Taste to anterior 2/3 tongue; parasympathetic to submandibular and sublingual glands | Parotid surgery risks facial nerve branches |
| Glossopharyngeal (IX) | Sensory (general + taste) to posterior 1/3 tongue; motor to stylopharyngeus | Tonsillar/oropharyngeal pathology; referred otalgia |
| Mental nerve (terminal branch of inferior alveolar nerve, from V3) | Sensory to chin and lower lip | Paraesthesia in area adjacent to lip lesion indicates mental nerve involvement [3] |
This matters enormously for cancer staging:
- Lip, anterior floor of mouth, anterior tongue tip → Level I (submental, submandibular nodes)
- Lateral oral tongue, buccal mucosa → Levels I–III (submandibular, upper/mid jugular)
- Base of tongue, tonsils, soft palate (oropharynx) → Levels II–IV (jugulodigastric → mid/lower jugular) — often bilateral
- NPC → retropharyngeal and upper cervical nodes; commonly bilateral [4]
4. Aetiology and Pathophysiology
This section organises the causes of oral/dental pain and lesions by category, with the pathophysiology explained from first principles.
4.1 Odontogenic (Tooth-Related) Causes
- Pathophysiology: Oral bacteria (esp. Streptococcus mutans) metabolise dietary sugars → produce lactic acid → demineralisation of tooth enamel → cavity formation. If untreated, progresses through dentine → pulp (pulpitis) → periapical abscess → cellulitis / osteomyelitis
- Pain mechanism: Enamel is anodontic (no nerves). Pain begins when dentine is exposed (dentinal tubules transmit stimuli to pulp) or when pulp is inflamed (pulpitis). Reversible pulpitis = sharp, brief pain with stimuli; irreversible pulpitis = spontaneous, throbbing, prolonged pain (the pulp tissue is dying)
- Risk factors: High sugar diet, poor oral hygiene, dry mouth (xerostomia — from Sjögren's, drugs, radiotherapy), enamel defects
- Gingivitis → Periodontitis is a continuum
- Plaque/biofilm accumulation → bacterial products trigger local immune response → inflammatory cell infiltration of gingiva → destruction of periodontal ligament and alveolar bone → tooth loosening and loss
- Gum hypertrophy causes [1]:
- Gingivitis (smoking, calculus, plaque, Vincent's angina)
- Drugs: phenytoin, phenobarbital, cyclosporine — these stimulate gingival fibroblast proliferation via different mechanisms (e.g., phenytoin inhibits collagenase → excess collagen deposition)
- Scurvy — vitamin C is essential for collagen synthesis; deficiency → defective collagen in gingival connective tissue → spongy, red, swollen and irregular gums that bleed easily [1]
- Leukaemia (usually monocytic) — leukaemic cell infiltration of the gingiva
- Pregnancy — hormonal (progesterone) influence on gingival vascularity and inflammatory response
- Pulpitis → necrosis of dental pulp → bacteria enter periapical tissue → abscess
- Can spread along fascial planes → Ludwig's angina (bilateral sublingual + submandibular space infection → floor of mouth elevation → airway compromise — a surgical emergency)
- Can also spread to the parotid space, parapharyngeal space, or mediastinum
- Inflammation of the soft tissue (operculum) overlying a partially erupted tooth, classically the lower third molar (wisdom tooth)
- Food and bacteria become trapped under the operculum → acute infection
- Very common in young adults (18–25 y)
4.2 Mucosal Lesions — Ulcerative
Aphthous ulcers are the most common cause of oral ulceration [1].
-
Types:
- Minor (80%): < 1 cm, shallow, on non-keratinised mucosa (buccal, labial, floor of mouth), heal in 7–14 days without scarring
- Major (Sutton's disease) (10%): > 1 cm, deeper, can affect keratinised mucosa, heal over weeks to months, may scar
- Herpetiform (10%): clusters of tiny (1–3 mm) ulcers, can coalesce, resemble herpes but are NOT caused by HSV
-
Pathophysiology: Exact aetiology unknown. Likely multifactorial — genetic susceptibility + environmental triggers (stress, trauma, hormonal changes, food hypersensitivity) → T-cell mediated mucosal damage → localised epithelial destruction → ulcer formation
-
Usually does NOT indicate serious underlying disease [1]
-
May occur in Crohn's disease or coeliac disease [1] — always consider systemic associations if severe, recurrent, or atypical
Causes of Oral Ulcers
Common: Aphthous ulcer, Trauma, Drugs (e.g., steroids), CA oral cavity [1]. Less common: Infections (HSV, syphilis, TB), Behçet disease, inflammatory bowel disease, SLE, pemphigus, SJS/TEN, neutropenia, lichen planus.
- Most common cause after aphthous ulcers
- From sharp/broken teeth, ill-fitting dentures, cheek biting, hot food burns
- Key concern: chronic traumatic ulcer that doesn't heal → must exclude malignancy (biopsy any ulcer persisting > 3 weeks)
Viral:
-
Herpes simplex virus (HSV-1) [5]:
- Primary infection: majority asymptomatic (except in elderly) — when symptomatic, presents as primary herpetic gingivostomatitis: fever, malaise, painful vesicles on gingivae and oral mucosa that rupture to form shallow ulcers. Very painful, especially in children
- Recurrent infection: associated with medical illness, menstruation, trauma, immunocompromised states, stress → herpes labialis: prodromal hyperaesthesia followed by rapid vesiculation, pustulation and crusting of the oral mucosa and perioral skin*** [5]
- Pathophysiology: HSV-1 establishes latent infection in the trigeminal ganglion. Reactivation → virus travels down sensory nerves → vesicular eruption at mucocutaneous junction
- Diagnosis: vesicular fluid for PCR for HSV DNA (serology is of limited value as a substantial proportion of the population is seropositive) [5]
- Treatment: Acyclovir initiated ≤48h of clinical disease or if severe [5]
-
Varicella-zoster virus (VZV): Reactivation in V2/V3 → intraoral vesicles/ulcers along the nerve distribution, with unilateral dermatomal pain
-
Coxsackievirus: Hand-foot-and-mouth disease (vesicles on oral mucosa, palms, soles) — common in HK children; herpangina (vesicles on soft palate and tonsillar pillars)
Bacterial:
- Syphilis: Primary chancre (painless ulcer with indurated margin) on lip or tongue; secondary mucous patches; tertiary gumma
- Vincent's angina (acute necrotising ulcerative gingivitis / ANUG) — fusospirochetal infection (Fusobacterium + Borrelia vincentii). Presents with painful, bleeding gums with necrotic interdental papillae, foul breath. Associated with poor hygiene, smoking, stress, immunosuppression
Fungal:
- Oral candidiasis (Candida albicans):
- Pseudomembranous (thrush): white plaques that CAN be scraped off, revealing erythematous base
- Erythematous (atrophic): red, painful mucosa (common under dentures or with inhaled steroids)
- Chronic hyperplastic (candidal leukoplakia): white plaques that CANNOT be scraped off → premalignant
- Angular cheilitis: cracking at the corners of the mouth — can be due to Candida ± Staphylococcus, often in the context of denture wearing, iron/B-vitamin deficiency, or drooling
- Pathophysiology: Candida is a commensal organism. Overgrowth occurs when local or systemic defences are breached (xerostomia, antibiotics, immunosuppression, diabetes)
Behçet disease is a systemic vasculitis of unknown aetiology [8].
- Oral ulcers occur in almost all patients: deep, multiple, painful ulcers with well-defined borders and necrotic base [8]
- Course: generally heals spontaneously within 1–3 weeks, but usually recurrent [8]
- Urogenital ulcers (75%): most specific lesion for Behçet syndrome [8]
- Strongly associated with HLA-B51 in Asians with familial clustering [8]
- Pathophysiology: dysregulated innate and adaptive immunity → vasculitis affecting vessels of all sizes → mucosal ulceration, uveitis, skin lesions, vascular thrombosis
4.3 Mucosal Lesions — White Patches
Leukoplakia: white-coloured thickening of mucosa of tongue and mouth [1]
- A premalignant condition [1]
- Causes: '5S' [1]:
- Sore teeth (poor dental hygiene)
- Smoking
- Spirits
- Sepsis
- Syphilis
- No apparent cause
- Can also be found on larynx, anus and vulva [1]
Definition (WHO): A white patch or plaque that cannot be scraped off and cannot be characterised clinically or pathologically as any other disease. It is a clinical term — the diagnosis is one of exclusion (i.e., rule out candidiasis, lichen planus, etc., before labelling it leukoplakia).
- Leukoplakia on the floor of the mouth has a particularly high risk of malignant transformation [3]
- Overall malignant transformation rate: ~1–5% per year (varies by site, size, presence of dysplasia)
Defined as bright red plaque of oral mucosa that cannot be characterized clinically or pathologically [3]
- Much less common than leukoplakia but has a much higher malignant potential (up to 50% harbour invasive carcinoma or carcinoma in situ at biopsy)
Variation of leukoplakia arising on an erythematous base [3]
- Highest rate of malignant transformation of the oral precancerous lesions [3]
Premalignant Oral Lesions — Malignancy Risk Ranking
Speckled leukoplakia > Erythroplakia > Leukoplakia (floor of mouth) > Leukoplakia (other sites). Any persistent white or red oral patch must be biopsied.
Lichen planus [6]:
- Prevalence < 1% of population, most commonly 30–60 y with no sex predilection [6]
- Aetiology: unknown, postulated to be autoimmune in basis (T cell-related) [6]
- Associations: IBD, PBC, alopecia areata, MG, thymoma [6]
- Infections: especially HBV and HCV infections [6]
- Mucosal involvement (30–70%) [6]:
- Oral (commonest): Wickham's striae on buccal mucosa/tongue, often asymptomatic, can occur alone or together with skin disease [6]
- Oral lichen planus is considered a premalignant condition with ~1% risk of malignant transformation to SCC over 5 years
- Pathophysiology: T-cell mediated attack on basal keratinocytes → interface dermatitis → characteristic band-like lymphocytic infiltrate at dermoepidermal junction → saw-tooth pattern of rete ridges on histology
- White, corrugated ("hairy") patches on the lateral borders of the tongue that CANNOT be scraped off
- Caused by EBV replication in epithelial cells
- Almost exclusively seen in immunocompromised patients (HIV — may be the first clinical sign)
- Not considered premalignant (unlike true leukoplakia)
- See Section 4.2.3 above. Key differentiating feature: pseudomembranous candidiasis CAN be scraped off, whereas leukoplakia and lichen planus cannot.
4.4 Mucosal Lesions — Red Patches
Glossitis: smooth tongue surface ± erythema [1]
- May present with shallow ulceration in later stages [1]
- Indicates nutritional deficiencies, e.g., Fe, B9, B12 [1]
- Mechanism: rapid turnover of tongue mucosal cells → particularly sensitive to nutritional deficiencies [1]
Why does iron/B12/folate deficiency cause glossitis? These nutrients are essential for DNA synthesis and cell division. The tongue epithelium has one of the highest turnover rates in the body (~every 10–14 days). When these nutrients are deficient, the rapidly dividing lingual epithelial cells cannot replicate adequately → the filiform papillae atrophy → the tongue becomes smooth, shiny, and erythematous.
4.4.2 Erythroplakia (see 4.3.2)
- Erythematous, smooth, rhombus-shaped area on the midline dorsal tongue, anterior to the circumvallate papillae
- Due to chronic atrophic candidiasis
- Usually asymptomatic; benign
Pigmentation of the oral mucosa may be due to [1]:
- Lead or bismuth poisoning → blue-black line on gingival margin (Burton's line for lead)
- Haemochromatosis → blue-grey pigmentation on hard palate [1]
- Drugs (antimalarials, OC pills) → brown or black areas of pigmentation anywhere in the mouth [1]
- Melanosis in Peutz-Jegher syndrome [1] — perioral and buccal melanotic macules; associated with hamartomatous GI polyps
- Addison's disease → blotches of dark brown pigment anywhere in the mouth [1] — due to excess ACTH (from loss of cortisol negative feedback) cross-reacting with melanocyte-stimulating hormone (MSH) receptors
- Malignant melanoma → raised, painless black lesions anywhere in the mouth [1]
- Amalgam tattoo — blue-grey macule at a site of previous dental restoration (trapped amalgam particles); most common cause of localised oral pigmentation; benign
4.6 Vesiculobullous Lesions
Pemphigus vulgaris [7]:
- Due to acantholysis induced by autoAb binding to epithelial cell surface antigens [7]
- Target antigen: desmoglein-3 for mucosal pemphigus vulgaris, desmoglein-1 (superficial) for pemphigus foliaceus, both for mucocutaneous pemphigus vulgaris [7]
- Cutaneous blisters: flaccid blisters that rupture easily ± erythematous base → painful erosions [7]
- Nikolsky sign positive: blistering can be induced by mechanical pressure [7]
- Mucosal erosion in almost all patients [7]:
- Oral: most common site of involvement, oral pain exacerbated by chewing or swallowing → poor nutrition, weight loss [7]
Why does pemphigus vulgaris cause oral lesions first? Desmoglein-3 (the primary target in mucosal-dominant PV) is heavily expressed in the oral mucosa. Autoantibodies disrupt desmoglein-3 → loss of intercellular adhesion (acantholysis) between keratinocytes → intraepidermal blisters that are so fragile they rupture almost immediately in the mouth (due to constant mechanical trauma from chewing/speaking) → painful erosions. The oral lesions often precede skin involvement by weeks to months.
SJS: systemic mucocutaneous allergic reaction [10]
- Definition: mucocutaneous bullous lesions involving < 10% TBSA [10]
- Causes: Delayed drug hypersensitivity (75%): allopurinol, aromatic AED, sulphonamides, lamotrigine, nevirapine [10]
- Mucosal lesions: painful haemorrhagic erosions involving oral, ocular, bronchial and urogenital mucosae [10]
- Ocular involvement occurs in 80% of patients [10]
- HLA-B15:02: prevalence 13% in HK Chinese, associated with SJS/TEN related to carbamazepine → mandatory to check before prescription* [10]
Macroglossia: enlargement of the tongue [1]
- Congenital conditions, e.g., Down syndrome [1]
- Endocrine diseases, e.g., acromegaly [1] (excess GH → soft tissue growth), hypothyroidism (mucopolysaccharide infiltration)
- Tumour infiltration, e.g., haemangioma, lymphangioma [1]
- Amyloidosis infiltration [1] — misfolded protein (amyloid) deposits in the tongue; pathognomonic for systemic amyloidosis (AL type)
Angular stomatitis: cracks at corners of mouth [1] Indicates nutritional deficiencies including B6, B9, B12, iron [1]
Also caused by:
- Candida ± Staphylococcus aureus infection (especially in denture wearers where overclosure of the mouth creates moist skin folds)
- Excessive drooling (e.g., in Parkinson's disease, developmental delay)
4.9 Salivary Gland Pathology Causing Oral Pain
Sialolithiasis refers to the presence of stones or calculi in salivary glands or ducts [9]
- Sialoadenitis refers to inflammation of salivary glands commonly caused by sialolithiasis and autoimmune disease (e.g., Sjögren's syndrome) [9]
- Submandibular gland most frequently affected [9]
- Clinical presentation: colicky pain and swelling of the affected gland, characteristically worsened by eating (because food stimulates saliva production → the duct is obstructed → pressure builds → pain)
- Risk factors: dehydration, hypercalcaemia, gout, chronic periodontal disease, nephrolithiasis, anticholinergics, diuretics, smoking [9]
Occurs in the setting of debilitation, dehydration and poor oral hygiene, particularly among the elderly, post-operative patients [12]
- Most common organism: Staphylococcus aureus [12]
- Risk factors: salivary duct obstruction by calculi, tumour of oral cavity, post-operative patients who are dehydrated or intubated, anticholinergics [12]
- Clinical presentation: unilateral (usually) parotid swelling with tenderness, erythema over the gland, trismus, purulent saliva expressed from Stensen's duct
- Pathophysiology: reduced salivary flow → stasis → retrograde migration of oral bacteria up Stensen's duct → infection of gland parenchyma
4.10 Oral Malignancy
This is the most important "must-not-miss" diagnosis when evaluating oral lesions.
Epidemiology [3]:
- Male preponderance
- Predominantly a disease of elderly (age > 60)
Risk factors (4 factors for H&N cancer = HPV + EBV + Smoking + Alcoholism) [3]:
- HPV 16/18 → oncoproteins E6 and E7 inactivate p53 and Rb [3]
- EBV → majority related to NPC [3]
- Smoking + Alcoholism → synergism is well established [3]
- 5Ss: Smoking + Spirits + Sharp teeth + Sex (male/oral) + Spicy food [3]
Premalignant conditions [3]:
- Erythroplakia
- Leukoplakia (especially floor of mouth)
- Speckled leukoplakia (highest malignant transformation rate)
- Plummer-Vinson syndrome (Paterson-Brown-Kelly syndrome): triad of iron deficiency anaemia, dysphagia and cervical oesophageal web → well-established relationship with the development of oral cancer [3]
- Oral submucous fibrosis (from betel nut chewing)
- Lichen planus (small but real risk)
Site-specific features [3]:
| Subsite | Key Features |
|---|---|
| Lip | 88–98% lower lip; UV exposure is main RF; LN mets < 10% (Level I); paraesthesia = mental nerve involvement [3] |
| Tongue | Most commonly lateral and ventral surfaces; paraesthesia = lingual nerve; deviation/fasciculation/atrophy = hypoglossal nerve [3] |
| Floor of mouth | Leukoplakia here = highest malignancy risk; invasion into sublingual/submandibular ducts |
| Alveolus/gingiva | Tight attachment to mandibular periosteum → early bone invasion [3] |
| Retromolar trigone | Early mandibular involvement due to lack of intervening soft tissue; trismus = muscles of mastication involvement / skull base spread [3] |
| Buccal mucosa | Propensity to spread locally and metastasize to regional lymphatics (facial and submandibular nodes — Level I) [3] |
| Hard palate | SCC and minor salivary gland tumours most common; periosteum acts as barrier to spread [3] |
NPC is the predominant tumour type arising in the nasopharynx [4]
- Frequently originates from pharyngeal recess known as fossa of Rosenmuller [4]
- Remains asymptomatic for a long period → patients present with locally or regionally advanced disease [4]
- Tendency for early metastasis: lymph node metastases usually present at diagnosis and commonly bilateral [4]
- Common sites of distant metastasis: Bone (75%) / Liver / Lung / Distant LN [4]
- Risk factors: EBV infection (primary aetiological agent), salted fish, preserved/fermented food (high nitrosamines), family history, HLA haplotypes, CYP2A6 polymorphism, smoking, alcoholism [4]
Red Flag: Non-Healing Oral Ulcer
Any oral ulcer that does not heal within 3 weeks must be biopsied to exclude malignancy. This is a critical exam point. Do not dismiss persistent oral lesions as "just an aphthous ulcer" — oral SCC can present as a painless or mildly painful non-healing ulcer, and early detection dramatically improves survival.
5. Classification of Oral/Dental Pain and Lesions
| Category | Examples |
|---|---|
| White patches | Leukoplakia, lichen planus, candidiasis (pseudomembranous), oral hairy leukoplakia, white sponge naevus, SCC (early keratotic) |
| Red patches | Erythroplakia, glossitis, denture stomatitis, median rhomboid glossitis, erythematous candidiasis |
| Ulcerative | Aphthous ulcers, traumatic, infective (HSV, syphilis, TB), malignant, Behçet, drug-induced |
| Vesiculobullous | HSV, VZV, pemphigus vulgaris, bullous pemphigoid, EM/SJS/TEN, hand-foot-mouth disease |
| Pigmented | Amalgam tattoo, racial pigmentation, Addison's, Peutz-Jeghers, melanoma, drug-induced, heavy metal |
| Swelling/mass | Epulis, mucocoele, ranula, salivary gland tumours, fibroma, SCC, minor salivary gland tumour |
6. Clinical Features — Symptoms and Signs
| Symptom | Pathophysiological Basis | Think Of... |
|---|---|---|
| Toothache (sharp, localised) | Exposed dentinal tubules or inflamed pulp → stimulation of A-delta and C fibres in dental pulp | Caries, pulpitis, cracked tooth |
| Throbbing pain (spontaneous, worsens at night, with lying down) | Irreversible pulpitis → increased blood flow when supine → increased intrapulpal pressure | Irreversible pulpitis, periapical abscess |
| Burning sensation in mouth | Mucosal inflammation, atrophic epithelium → exposure of nerve endings | Glossitis (nutritional deficiency), erythematous candidiasis, burning mouth syndrome |
| Pain on eating/swallowing | Mechanical trauma to inflamed/ulcerated mucosa; salivary duct obstruction → distension | Aphthous ulcers, pemphigus, sialolithiasis |
| Colicky pain worsened by eating | Salivary stimulation → increased flow against obstructed duct → distension | Sialolithiasis |
| Paraesthesia/numbness of lip/chin | Mental nerve involvement by tumour or infection [3] | Oral SCC (sinister sign), osteomyelitis |
| Paraesthesia of tongue | Lingual nerve invasion [3] | Tongue SCC |
| Trismus (difficulty opening mouth) | Involvement of muscles of mastication; may indicate spread to skull base [3] | Peritonsillar abscess, retromolar trigone SCC, TMJ disorder, tetanus |
| Halitosis (bad breath) | Bacterial metabolism of food debris and necrotic tissue → volatile sulphur compounds | Periodontal disease, ANUG, dental abscess, sinusitis |
| Dysphagia | Oropharyngeal mucosal involvement, mass effect, or oesophageal web | Pemphigus, SCC (advanced), Plummer-Vinson |
| Referred otalgia | Shared sensory innervation (CN V3, IX, X) between oral cavity/oropharynx and ear | Tongue base/tonsil SCC, peritonsillar abscess, TMJ dysfunction |
| Xerostomia (dry mouth) | Decreased salivary production (drugs, Sjögren's, radiation) or dehydration | Sjögren's syndrome, anticholinergics, post-RT head and neck |
| Bleeding gums | Inflamed gingival tissue with dilated capillaries and fragile connective tissue | Gingivitis, periodontitis, scurvy, leukaemia, thrombocytopenia |
| Sign | Description | Pathophysiological Basis | Condition |
|---|---|---|---|
| White patch (cannot scrape off) | Adherent white plaque on mucosa | Hyperkeratosis ± dysplasia of epithelium | Leukoplakia, lichen planus |
| White patch (can scrape off) | White pseudomembrane revealing erythematous base | Candidal hyphae + desquamated epithelial cells + fibrin | Pseudomembranous candidiasis |
| Wickham's striae | Fine white lacy network on buccal mucosa/tongue [6] | Band-like lymphocytic infiltrate at dermoepidermal junction → irregular epidermal hyperplasia | Oral lichen planus |
| Red plaque (erythroplakia) | Bright red, velvety plaque | Thin atrophic epithelium ± dysplasia/carcinoma in situ → submucosal vasculature visible | High malignant potential |
| Smooth, red tongue (glossitis) | Loss of filiform papillae, erythematous, ± painful | Papillary atrophy due to nutritional deficiency (Fe, B9, B12) [1] | Iron/B12/folate deficiency |
| Macroglossia | Enlarged tongue, may have teeth indentations | Tissue infiltration (amyloid, tumour) or soft tissue growth (acromegaly, hypothyroidism) | Amyloidosis, acromegaly, Down syndrome, hypothyroidism [1] |
| Gum hypertrophy | Swollen, enlarged gingivae | Drug-induced fibroblast proliferation; leukaemic infiltration; scurvy | Phenytoin, cyclosporine, leukaemia, scurvy [1] |
| Nikolsky sign positive | Blistering induced by lateral pressure on normal-appearing skin/mucosa | Acantholysis (pemphigus) or dermal-epidermal separation | Pemphigus vulgaris, SJS/TEN [7] |
| Non-healing ulcer (> 3 weeks) | Ulcer with indurated, rolled/everted edges, possible fixation to deeper structures | Malignant proliferation → tissue destruction + desmoplastic stromal reaction → firm edges | Oral SCC |
| Exophytic growth or non-healing ulcer | Raised, fungating mass or persistent ulcer on tongue/floor of mouth | Uncontrolled epithelial proliferation [3] | Oral SCC |
| Tongue deviation (towards lesion side) | Deviation + fasciculation + atrophy | Hypoglossal nerve (XII) invasion by tumour → LMN lesion → ipsilateral denervation [3] | Tongue SCC (advanced) |
| Purulent discharge from Stensen's duct | Pus expressed on bimanual palpation of parotid | Bacterial infection of parotid gland parenchyma | Suppurative parotitis |
| Floor of mouth elevation | Firm, tender sublingual/submandibular swelling | Bilateral submandibular and sublingual space infection → cellulitis | Ludwig's angina (airway emergency!) |
| Dendritic ulcer (on fluorescein stain) | Branching ulcer with terminal bulbs on cornea | HSV replication in corneal epithelium [13] | Herpes simplex keratitis (if eye involved) |
| Hutchinson's sign | Vesicles on the nose | Involvement of nasociliary branch of V1 → heralds ocular involvement [13] | Herpes zoster ophthalmicus |
| Oral pigmentation — dark brown blotches | Hyperpigmentation anywhere in mouth | Excess ACTH cross-reacts with MSH receptors on melanocytes | Addison's disease [1] |
| Blue-black gingival line | Line along gingival margin | Lead/bismuth sulphide deposition in gingival margin capillary bed | Lead or bismuth poisoning [1] |
| Target lesions | Round papules with dusky centre, pale ring, erythematous halo | Cytotoxic T-cell attack on keratinocytes in a zonal pattern | Erythema multiforme [11] |
Key Examination Points for Oral Lesions
When examining an oral lesion, document: (1) Site (anatomical subsite), (2) Size, (3) Shape (regular/irregular borders), (4) Surface (smooth/ulcerated/keratotic/papillomatous), (5) Colour (white/red/pigmented/mixed), (6) Base (indurated/soft), (7) Margins (rolled/everted/undermined), (8) Fixation (to underlying structures), (9) Can it be scraped off? (10) Associated lymphadenopathy (cervical node examination — always check!).
7. Approach to History and Examination
- Pain characteristics: SOCRATES (Site, Onset, Character, Radiation, Associated symptoms, Time course, Exacerbating/relieving factors, Severity)
- Odontogenic pain is usually well-localised, related to thermal/sweet stimuli
- Mucosal pain is often diffuse, burning, worsened by spicy/acidic food
- Colicky, meal-related → sialolithiasis
- Referred otalgia → oropharyngeal pathology
- Duration: < 3 weeks = likely benign; > 3 weeks = must exclude malignancy
- Associated features: Weight loss (malignancy, pemphigus), joint pain (Behçet, Reiter's), skin rash (lichen planus, SJS, pemphigus), genital ulcers (Behçet, syphilis), eye symptoms (Behçet — uveitis, SJS — keratitis), GI symptoms (Crohn's, coeliac)
- Past medical history: HIV, diabetes, autoimmune disease, previous malignancy, organ transplant
- Drug history: Anticholinergics, phenytoin, cyclosporine, methotrexate, chemotherapy, allopurinol, carbamazepine, inhalers (steroid)
- Social history: Smoking, alcohol, betel nut chewing, sexual history (HPV risk), occupation (outdoor sun exposure)
- Nutritional history: Diet quality, vegetarian/vegan (B12 risk), alcohol intake (B-vitamin deficiency)
- Extraoral: Facial asymmetry, skin lesions, parotid/submandibular swelling, cervical lymphadenopathy (systematically examine Levels I–V), cranial nerve assessment (especially V, VII, IX, XII)
- Intraoral (systematic): Lips → buccal mucosa → upper and lower gingivae → hard palate → soft palate → floor of mouth → dorsal tongue → lateral tongue → ventral tongue → retromolar trigone → tonsillar pillars → posterior pharyngeal wall
- Teeth: Caries, missing teeth, sharp/broken teeth, prostheses, occlusion
- Salivary glands: Bimanual palpation of submandibular glands; milking Stensen's and Wharton's ducts to express saliva (serous vs purulent)
- Special tests: TMJ palpation, maximal mouth opening (normal ≥ 35 mm; < 35 mm = trismus), percussion of teeth (periapical pathology)
High Yield Summary
Definition: Oral/dental pain and lesions encompass a broad spectrum from benign (aphthous ulcers, dental caries) to life-threatening (oral SCC, Ludwig's angina, SJS/TEN).
Epidemiology (HK Focus): NPC is endemic in Southern China (EBV-driven); oral SCC driven by the 5Ss (Smoking, Spirits, Sharp teeth, Sex/HPV, Spicy food); betel nut chewing is a major regional risk factor.
Key Anatomy: Oral cavity ends at circumvallate papillae/hard–soft palate junction. Submandibular gland → most common site for sialolithiasis (long duct, against gravity, alkaline mucin-rich saliva). Lingual nerve → tongue sensation; hypoglossal nerve → tongue movement; mental nerve → lip/chin sensation.
Classification: Odontogenic vs Non-odontogenic; Ulcerative vs White vs Red vs Vesiculobullous vs Pigmented vs Swelling.
Premalignant lesions: Speckled leukoplakia (highest transformation rate) > Erythroplakia > Leukoplakia (floor of mouth highest risk). Plummer-Vinson syndrome established association with oral cancer.
Red flags for malignancy: Non-healing ulcer > 3 weeks, indurated/rolled edges, fixation to deeper structures, lymphadenopathy, cranial nerve involvement (paraesthesia, tongue deviation), trismus, weight loss.
Critical "must-knows": HLA-B15:02 must be checked before prescribing carbamazepine in HK Chinese (13% prevalence → SJS/TEN risk)*. Pemphigus vulgaris: oral erosions are often the first manifestation (anti-desmoglein 3). Aphthous ulcers = most common oral ulcer; usually benign but exclude Crohn's/coeliac if recurrent. Leukoplakia = diagnosis of exclusion (5S causes); biopsy always needed.
Active Recall - Oral/Dental Pain and Lesions (Part 1)
[1] Senior notes: Ryan Ho GI.pdf (p10) and Ryan Ho Fundamentals.pdf (p62) — Oral examination findings, leukoplakia, glossitis, macroglossia, gum hypertrophy, pigmentation, aphthous ulcers, angular stomatitis [2] Standard clinical reference — Aphthous ulcer epidemiology [3] Senior notes: felixlai.md (sections 343, 350, 351, 354, 355, 369, 370) — Head and neck cancer risk factors, 5Ss, premalignant lesions, site-specific oral SCC features, oropharyngeal cancer [4] Senior notes: felixlai.md (section 357) — Nasopharyngeal carcinoma epidemiology, risk factors, pathophysiology [5] Senior notes: Ryan Ho Rheumatology.pdf (p137) — HSV infection epidemiology, clinical features, diagnosis, treatment [6] Senior notes: Ryan Ho Rheumatology.pdf (p143) — Lichen planus epidemiology, aetiology, mucosal involvement [7] Senior notes: Ryan Ho Rheumatology.pdf (p152–153) — Pemphigus vulgaris, bullous pemphigoid pathogenesis and clinical features [8] Senior notes: Ryan Ho Rheumatology.pdf (p98) — Behçet disease epidemiology, clinical features, diagnosis [9] Senior notes: felixlai.md (sections 321, 325) — Parotitis, sialolithiasis anatomy, risk factors, pathogenesis [10] Senior notes: Ryan Ho Rheumatology.pdf (p147, 149) and Ryan Ho Opthalmology.pdf (p133) — SJS/TEN risk factors, HLA associations, clinical features [11] Senior notes: Ryan Ho Rheumatology.pdf (p130) — Erythema multiforme causes and clinical features [12] Senior notes: felixlai.md (section 321) — Suppurative parotitis microbiology and risk factors [13] Senior notes: Ryan Ho Opthalmology.pdf (p24–25) — Herpes simplex keratitis, herpes zoster ophthalmicus
Differential Diagnosis of Oral/Dental Pain and Lesions
The differential diagnosis of oral/dental complaints is vast — the mouth sits at a crossroads of dental, ENT, dermatological, rheumatological, haematological, and neurological pathology. The skill lies in pattern recognition: What does the lesion look like? Where is it? How long has it been there? What company does it keep (systemic features)?
This section organises the differential by clinical presentation (the way you encounter it at the bedside), then provides a systematic framework for narrowing down.
The first-principles approach to any oral complaint is to ask three questions:
- Is this odontogenic (from the teeth) or non-odontogenic (from the mucosa, salivary glands, bone, nerves, or referred)?
- If non-odontogenic, what is the morphology of the lesion? — Ulcer, white patch, red patch, vesicle/blister, pigmented lesion, swelling/mass, or no visible lesion (pain only)?
- Is this dangerous? — The "must-not-miss" diagnoses: malignancy, deep space infection (Ludwig's angina, peritonsillar abscess), SJS/TEN, pemphigus, blood dyscrasia, and referred cardiac pain.
2. Differential Diagnosis by Presentation
This is the most common presenting morphology. The differential spans benign to life-threatening.
Common causes of oral ulcers: Aphthous ulcer, Trauma, Drugs (e.g., steroids), CA oral cavity [1].
| Diagnosis | Key Distinguishing Features | Why This Happens (Pathophysiology) |
|---|---|---|
| Aphthous ulcer (most common) [1] | Small painful mucosal vesicle → shallow ulceration that heals without scarring [1]; recurrent; minor (< 1 cm, non-keratinised mucosa), major (> 1 cm, may scar), herpetiform (clusters). Usually does NOT indicate serious underlying disease [1]. May occur in Crohn's disease or coeliac disease [1] | T-cell mediated mucosal destruction; exact trigger unknown (stress, trauma, hormonal, food). Crohn's = granulomatous inflammation extending to oral mucosa |
| Traumatic ulcer | History of mechanical injury (sharp tooth, denture, cheek bite, thermal burn); solitary; site corresponds to source of trauma; heals when cause removed | Direct epithelial disruption → inflammatory response → ulcer crater |
| Oral SCC | Non-healing ulcer > 3 weeks; indurated, rolled/everted edges; fixation to deeper tissues; lymphadenopathy; smoking/alcohol history; elderly male. Exophytic growth or non-healing ulcer [3]. Trismus = involvement of muscles of mastication, may indicate spread to skull base [3] | Malignant keratinocyte proliferation → tissue invasion and necrosis → ulcer with desmoplastic stroma forming the hard, rolled edges |
| Herpes simplex (HSV-1) [5] | Primary: multiple shallow ulcers on keratinised AND non-keratinised mucosa + gingivitis + fever (primary herpetic gingivostomatitis). Recurrent: herpes labialis — prodromal hyperaesthesia then vesicles → pustules → crusts at mucocutaneous junction [5]. Crops of vesicles that ulcerate | Latent infection in trigeminal ganglion → reactivation → virus travels down sensory nerves → epithelial cell lysis → vesicle → rupture → ulcer [5] |
| Behçet disease [8] | Deep, multiple, painful ulcers with well-defined borders and necrotic base; recurrent; heals in 1–3 weeks [8]. Look for urogenital ulcers (most specific) [8], skin lesions, bilateral panuveitis | Systemic vasculitis → mucosal ischaemia and immune-mediated epithelial destruction [8] |
| Syphilitic chancre (primary) | Painless, indurated ulcer with clean base; single; usually lip or tongue; resolves spontaneously in 3–6 weeks. Secondary: mucous patches (shallow, painless, "snail-track" ulcers) | Treponema pallidum invasion → local immune response → granulomatous inflammation → ulcer. Painless because spirochetes suppress local pain signalling mechanisms |
| Vincent's angina (ANUG) | Painful, bleeding gums with necrotic interdental papillae; punched-out ulcers at gingival margin; foul breath (fetor oris); young adults with poor hygiene + stress + smoking | Fusospirochetal synergistic infection (Fusobacterium + Borrelia vincentii) → necrotising destruction of interdental papillae |
| HIV-associated ulcers [1] | Large, deep, persistent aphthous-like ulcers; often oropharyngeal; poor response to standard therapy. May also have oral hairy leukoplakia, Kaposi sarcoma, candidiasis | Severe immune dysregulation → uncontrolled T-cell mediated mucosal destruction; also opportunistic infections |
| Drug-induced ulcers | Methotrexate, chemotherapy (mucositis), nicorandil (persistent perianal/oral ulcers), NSAIDs, bisphosphonates (jaw osteonecrosis → ulceration) | Cytotoxic drugs inhibit rapidly dividing mucosal epithelial cells → epithelial loss → ulceration. Nicorandil → unclear mechanism, possibly local vascular effect |
| SJS/TEN [10] | Painful haemorrhagic erosions involving oral, ocular, bronchial and urogenital mucosae [10]; widespread skin involvement (target-like lesions progressing to skin sloughing); prodrome: high fever, malaise, arthralgia [10]; drug history (allopurinol, aromatic AEDs, sulphonamides) [10] | Cytotoxic T cells + NK cells mediate keratinocyte apoptosis via granulysin [10] → full-thickness epidermal necrosis |
| Erythema multiforme (EM major) [11] | Oral mucosal involvement (70%): affect vermilion lip, mucosal surfaces [11]; target lesions on skin (dusky centre + pale ring + erythematous halo); usually triggered by HSV or Mycoplasma pneumoniae [11]; course: appear over 3–5 days then resolve ≤ 2 weeks [11] | Triggering of autoreactive T cells [11] → interface dermatitis → keratinocyte apoptosis in a zonal pattern → target morphology |
| Pemphigus vulgaris [7] | Oral erosions often the first manifestation; painful erosions on buccal mucosa, palate, gingivae; Nikolsky sign positive [7]; flaccid blisters that rupture easily [7]; middle-aged adults | Autoantibodies to desmoglein-3 → acantholysis → intraepidermal split → fragile blisters that rupture immediately in the mouth [7] |
| Tuberculosis (oral) | Rare; chronic, irregular, painful ulcer usually on tongue dorsum; undermined edges; associated with pulmonary TB (secondary inoculation from sputum) | Mycobacterial infection → caseating granulomatous inflammation → tissue necrosis → ulcer |
| Crohn's disease | Oral ulcers (aphthous-like), cobblestoning of buccal mucosa, lip swelling (orofacial granulomatosis); GI symptoms | Granulomatous inflammation → mucosal ulceration; oral involvement = extraintestinal manifestation |
The Red Flag Triad for Pharyngeal Cancer
The triad: hoarseness + pain on swallowing + referred ear pain → pharyngeal cancer [14]. This comes directly from the Murtagh's diagnostic tips and is extremely high yield. Referred otalgia occurs because the oropharynx and ear share sensory innervation via CN IX (tympanic branch — Jacobson's nerve) and CN X (auricular branch — Arnold's nerve). A tumour irritating these nerves causes the brain to misinterpret the signal as ear pain.
| Diagnosis | Key Distinguishing Features | Why (Pathophysiology) |
|---|---|---|
| Leukoplakia [1] | White-coloured thickening that cannot be scraped off; diagnosis of exclusion; causes: 5S (Sore teeth, Smoking, Spirits, Sepsis, Syphilis) [1]; floor of mouth = highest malignant transformation risk [3]; premalignant [1] | Chronic irritation → reactive hyperkeratosis of epithelium ± dysplasia. Dysplastic cells produce excess keratin → white appearance |
| Oral lichen planus [6] | Wickham's striae on buccal mucosa/tongue — fine white lacy network [6]; often bilateral and symmetrical; often asymptomatic [6]; associated with HBV and HCV infections [6] | T-cell mediated attack on basal keratinocytes [6] → interface dermatitis → irregular epithelial hyperplasia + hyperkeratosis → white striae |
| Oral candidiasis (pseudomembranous) | White plaques that CAN be scraped off revealing erythematous base; immunocompromised, denture wearers, steroid inhaler users, neonates | Candida hyphae penetrate superficial epithelium → desquamated epithelial cells + hyphae + fibrin = white pseudomembrane. It scrapes off because the pseudomembrane sits ON TOP of the epithelium rather than being a change within it |
| Oral hairy leukoplakia | White, corrugated ("hairy") patches on lateral tongue; CANNOT be scraped off; almost exclusively in immunocompromised (HIV); NOT premalignant | EBV replication in lingual epithelial cells → hyperplasia and hyperkeratosis of epithelium. Unlike true leukoplakia, has specific viral aetiology and is not considered premalignant |
| White sponge naevus | Bilateral, symmetrical, thick white plaques on buccal mucosa; present from birth/childhood; benign; autosomal dominant | Mutation in mucosal keratin genes (K4, K13) → abnormal keratin production → spongy white epithelium |
| Lichenoid drug eruption | Unilateral white striae resembling lichen planus; temporal association with drug (NSAIDs, ACE inhibitors, antimalarials, gold, methyldopa); resolves on drug withdrawal | Drug-induced T-cell activation → interface dermatitis mimicking lichen planus |
| Speckled leukoplakia [3] | Variation of leukoplakia arising on an erythematous base [3]; mixed white and red; highest rate of malignant transformation [3] | Combination of hyperkeratosis (white) and atrophic/dysplastic epithelium with visible submucosal vasculature (red) |
Can It Be Scraped Off?
This is the single most useful bedside test for white patches. Candidiasis (pseudomembranous) = scrapes off. Leukoplakia, lichen planus, hairy leukoplakia = do NOT scrape off. If it doesn't scrape off and the patient has risk factors, biopsy it.
| Diagnosis | Key Distinguishing Features | Pathophysiology |
|---|---|---|
| Erythroplakia [3] | Bright red velvety plaque that cannot be characterised clinically or pathologically [3]; often asymptomatic; up to 50% harbour carcinoma in situ or invasive SCC at biopsy | Thin, atrophic, dysplastic epithelium → submucosal vasculature shows through = red |
| Glossitis [1] | Smooth tongue surface ± erythema; indicates nutritional deficiencies (Fe, B9, B12) [1]; rapid turnover of tongue mucosal cells → particularly sensitive to nutritional deficiencies [1] | Impaired DNA synthesis in rapidly dividing lingual epithelium → papillary atrophy → smooth, shiny, erythematous tongue |
| Erythematous (atrophic) candidiasis | Diffuse red, painful mucosa; often under dentures ("denture stomatitis"); common with steroid inhalers | Candida-induced chronic inflammation → mucosal atrophy → erythema |
| Median rhomboid glossitis | Erythematous, smooth, rhomboid area on midline dorsal tongue; usually asymptomatic | Chronic atrophic candidiasis on dorsal tongue → localised papillary atrophy |
| Geographic tongue (erythema migrans) | Migrating areas of depapillation with white raised borders; benign; waxes and wanes | Unknown; possibly immune-mediated. Loss of filiform papillae in patches → red areas (exposed underlying tissue); margins = regenerating epithelium |
| Oral SCC (early) | Erythematous patch with irregular margins; may be mixed (speckled leukoplakia); non-healing | Dysplastic epithelium replacing normal mucosa → thin, atrophic surface |
This differential is critical because several of these conditions are systemic and life-threatening.
Differential diagnoses with mucosal involvement [7]:
- Pemphigus vulgaris (majority)
- Pemphigoid (some)
- Herpes simplex
- Erythema multiforme
- SJS/TEN (extensive)
| Diagnosis | Blister Character | Oral Features | Key Clue |
|---|---|---|---|
| Pemphigus vulgaris [7] | Flaccid, fragile, Nikolsky +ve | Painful erosions; oral = most common and often first site [7]; pain exacerbated by chewing/swallowing → poor nutrition [7] | Anti-desmoglein 3 (mucosal) ± 1 (cutaneous) [7]; middle-aged |
| Mucous membrane pemphigoid (cicatricial pemphigoid) | Tense blisters → scarring erosions | Desquamative gingivitis; progressive scarring; ocular involvement → symblepharon, blindness | Anti-BP180/laminin-332; predominantly elderly; scarring is the hallmark (unlike BP) |
| Bullous pemphigoid [7] | Tense blisters; mucosal involvement 10–30% [7] | Less prominent oral involvement than pemphigus; predominantly elderly (median age 80y) [7] | Anti-BP180/BP230; subepidermal split → tense blisters |
| HSV (primary gingivostomatitis) [5] | Clusters of small vesicles → shallow ulcers | Multiple vesicles on keratinised AND non-keratinised mucosa; fever, gingivitis; prodromal hyperaesthesia [5] | Vesicles in crops; usually children or young adults; PCR for HSV DNA from vesicular fluid [5] |
| VZV (shingles — V2/V3) | Unilateral dermatomal vesicles | Vesicles/ulcers on palate (V2) or tongue/lower lip (V3); STRICTLY unilateral | Dermatomal distribution; older/immunocompromised; severe pain preceding rash |
| Hand-foot-mouth disease | Small vesicles on oral mucosa, palms, soles | Vesicles on soft palate, buccal mucosa, tongue | Coxsackievirus A16 or Enterovirus A71; children; HK outbreaks common |
| EM major [11] | Target lesions on skin ± vesicles/bullae | Oral (70%): painful erosions on vermilion lip, mucosal surfaces [11] | Target lesions; HSV or Mycoplasma trigger [11] |
| SJS/TEN [10] | Widespread skin sloughing | Painful haemorrhagic erosions of oral, ocular, urogenital mucosae [10] | Drug history; prodrome of fever [10]; < 10% TBSA = SJS; > 30% = TEN |
Pigmentation may be due to [1]:
| Diagnosis | Colour/Pattern | Location | Pathophysiology |
|---|---|---|---|
| Amalgam tattoo | Blue-grey macule | Adjacent to dental restoration | Iatrogenic implantation of amalgam particles into mucosa; most common localised oral pigmentation |
| Racial/physiological melanosis | Brown/black, diffuse, bilateral | Gingivae, buccal mucosa | Constitutional melanin deposition; benign; common in darker-skinned individuals |
| Addison's disease [1] | Blotches of dark brown pigment [1] | Anywhere in the mouth [1] | Excess ACTH (from loss of cortisol feedback) cross-reacts with MSH receptors → ↑melanin |
| Peutz-Jeghers syndrome [1] | Brown-black melanotic macules | Perioral and buccal | Autosomal dominant (STK11 mutation); mucocutaneous melanocyte proliferation; associated hamartomatous GI polyps |
| Lead/bismuth poisoning [1] | Blue-black line on gingival margin [1] (Burton's line) | Gingival margin | Metal sulphide deposition in gingival capillary bed |
| Haemochromatosis [1] | Blue-grey pigmentation [1] | Hard palate [1] | Iron overload → haemosiderin deposition in mucosa |
| Drug-induced [1] | Brown or black [1] | Anywhere [1] | Antimalarials, OC pills [1]; drug/metabolite deposition in mucosa or stimulation of melanocytes |
| Malignant melanoma [1] | Raised, painless black lesion [1] | Anywhere [1] (hard palate and gingivae most common for oral melanoma) | Malignant melanocyte proliferation; rare in oral cavity but very aggressive |
| Kaposi sarcoma | Purple/violaceous macule or nodule | Palate (most common oral site), gingivae | HHV-8 driven endothelial-origin tumour; almost exclusively in HIV/AIDS or immunosuppressed |
| Diagnosis | Key Features | Pathophysiology |
|---|---|---|
| Mucocoele | Blue-translucent, dome-shaped, painless swelling; usually lower lip; fluctuant; may rupture and recur | Ruptured minor salivary gland duct → mucin extravasation into surrounding tissue → pseudocyst |
| Ranula | Large mucocoele in the floor of mouth (sublingual gland); bluish swelling; "frog belly" appearance | Same as mucocoele but specifically from sublingual gland/duct damage |
| Epulis (fibrous epulis) | Firm, pink, pedunculated gingival swelling; arises from periodontal ligament | Reactive fibrous hyperplasia in response to chronic irritation (calculus, plaque) |
| Pyogenic granuloma | Bright red, dome-shaped, friable, bleeds easily; preceded by trauma; rapid growth [15]; common in pregnancy | Lobular capillary haemangioma [15]; reactive vascular proliferation in response to trauma/hormones |
| Oral SCC [3] | Exophytic mass or non-healing ulcer; indurated; fixation to deeper structures; lymphadenopathy [3] | Malignant epithelial proliferation |
| Minor salivary gland tumour [3] | Submucosal mass in tongue base or soft palate [3]; firm, smooth, painless; adenoid cystic carcinoma or mucoepidermoid carcinoma | Neoplastic proliferation of salivary gland epithelium; adenoid cystic carcinoma has perineural invasion tendency → pain/paraesthesia |
| Lymphoma [3] | Tonsils and tongue base may be the presenting site for a lymphoma [3]; firm, painless tonsillar enlargement (usually unilateral); B symptoms | Malignant lymphoid proliferation in Waldeyer's ring |
| Torus palatinus / mandibularis | Bony hard, midline palatal swelling (torus palatinus) or lingual mandibular swelling; painless; common | Benign exostosis of bone; entirely normal variant; no treatment needed unless interfering with dentures |
| Denture-related fibrous hyperplasia (epulis fissuratum) | Redundant tissue folds along denture flange margins | Chronic irritation from ill-fitting denture → fibrous tissue hyperplasia |
This is a very important differential in clinical practice — patients present with oral or facial pain but examination of the mouth is normal.
| Diagnosis | Key Features | Pathophysiology |
|---|---|---|
| Trigeminal neuralgia (tic douloureux) [14] | Sudden severe shooting pain in one division of CN V [14]; lasts seconds to minutes; triggered by light touch to trigger zone (washing face, eating, brushing teeth); pain-free intervals between attacks; usually V2/V3 | Neurovascular compression of trigeminal nerve root (usually by superior cerebellar artery) → demyelination → ephaptic transmission between fibres → paroxysmal pain |
| Glossopharyngeal neuralgia [14] | Sudden shooting pain radiating from one side of throat to ear [16]; triggered by swallowing, talking, yawning; rare | Compression/irritation of CN IX → paroxysmal pain in tonsillar fossa, pharynx, ear (shared territory) |
| TMJ dysfunction (TMJ arthralgia) [14] | Pain over TMJ region, worsened by jaw movement/chewing; clicking/locking of jaw; limitation of mouth opening; tenderness over TMJ | Disc displacement, osteoarthritis, myofascial pain of masticatory muscles; stress-related bruxism → muscle fatigue and joint overload |
| Dental abscess (referred pain) [14] | Pain may be poorly localised or referred to ear; tooth tender to percussion; swelling over alveolus | Periapical infection → inflammation stimulates A-delta and C fibres → referred via V2/V3 divisions |
| Sinusitis (maxillary) [14][17] | Facial pain or pressure (increases with bending over) ± radiation to tooth [17]; nasal congestion/discharge; double sickening [17] | Inflammation of maxillary sinus → pain referred to ipsilateral upper teeth because the roots of upper premolars/molars lie in close proximity to (or project into) the maxillary sinus floor |
| Referred cardiac pain [14] | Angina or MI can present as sore throat or jaw pain [14]; exertional, with chest tightness, SOB; relieved by GTN | Visceral afferents from heart enter spinal cord at same segments (C3–T4) as somatic afferents from jaw/throat → convergence on second-order neurons → cortex misinterprets as jaw pain |
| Burning mouth syndrome | Chronic burning pain in tongue, palate, lips; NO visible mucosal abnormality; more common in postmenopausal women; taste disturbance; dry mouth sensation | Neuropathic pain likely involving small sensory nerve fibres; possible overlap with peripheral neuropathy; hormonal and psychological factors contribute |
| Herpes zoster (pre-eruptive phase) | Severe unilateral pain in V2/V3 distribution preceding rash by 1–5 days; may mimic toothache; vesicles appear later | VZV reactivation in trigeminal ganglion → neural inflammation → pain before cutaneous vesicles erupt |
| Post-herpetic neuralgia [14] | Persistent pain > 90 days after herpes zoster in same dermatome | Nerve fibre damage and central sensitisation from acute VZV infection → aberrant pain signalling |
Angina/MI Presenting as Sore Throat
Cardiovascular causes (angina, myocardial infarction) are listed as serious disorders not to be missed in sore throat [14]. This is a classic exam pitfall. Always ask about exertional jaw/throat tightness, cardiac risk factors, and associated chest pain. Missing this can be fatal.
3. Differential Diagnosis by Specific Presentations (Murtagh's Framework)
Probability diagnosis [14]:
- Viral pharyngitis
- Epstein-Barr mononucleosis (glandular fever)
- Streptococcal (GABHS) tonsillitis
- Chronic sinusitis with postnasal drip
- Oropharyngeal candidiasis
Serious disorders not to be missed [14]:
- Cardiovascular: angina, myocardial infarction
- Neoplasia/cancer: cancer of oropharynx, tongue
- Blood dyscrasias (e.g., agranulocytosis, acute leukaemia)
- Infection: acute epiglottitis (children and adults), peritonsillar abscess (quinsy), pharyngeal abscess, diphtheria (very rare), HIV/AIDS
Pitfalls (often missed) [14]:
- Foreign body (e.g., fish bone)
- Epstein-Barr mononucleosis (glandular fever)
- Candida: common in infants
Diagnostic tips [14]:
- Tonsillitis with a covering membrane may be caused by Epstein-Barr mononucleosis
- Admit if any suspicion of epiglottitis — and do NOT examine the throat
- The triad: hoarseness + pain on swallowing + referred ear pain → pharyngeal cancer
Many causes of ear pain are actually of oral/dental origin — referred via shared CN V3, IX, X innervation.
Probability diagnosis includes [14]:
- TMJ arthralgia
Pitfalls (often missed) with oral/dental relevance [14]:
- Dental abscess
- Referred pain: neck, throat (e.g., tonsillitis)
- Unerupted wisdom tooth and other dental causes
- TMJ arthralgia
- Facial neuralgias, especially glossopharyngeal
Serious disorders not to be missed [14]:
- Cancer of other sites (e.g., tongue, throat) — referred otalgia from oropharyngeal malignancy is an important cause of persistent unilateral ear pain with a normal otoscopic examination
When evaluating a suspected oropharyngeal malignancy, the differential includes:
- Squamous cell carcinoma — the overwhelmingly most common (> 90% of oral cavity malignancies)
- Minor salivary gland tumours — may present as submucosal masses in the tongue base and soft palate [3] (adenoid cystic carcinoma, mucoepidermoid carcinoma, polymorphous adenocarcinoma)
- Lymphoma — tonsils and tongue base may be the presenting site for a lymphoma [3] (diffuse large B-cell lymphoma most common in head and neck)
- Verrucous carcinoma — a well-differentiated, locally aggressive but rarely metastasising variant of SCC; exophytic, warty appearance
- Mucosal melanoma — very rare; hard palate and gingivae; pigmented or amelanotic; extremely aggressive
- Kaposi sarcoma — HIV/HHV-8 associated; purple/violaceous; palate
Why distinguishing these matters: Minor salivary gland tumours and lymphomas have entirely different treatment paradigms (surgery ± RT for salivary tumours; chemo-immunotherapy for lymphoma) compared to SCC (surgery ± chemoradiotherapy).
Differential diagnosis of salivary gland swelling [9]:
| Diagnosis | Key Features | Distinguishing Clue |
|---|---|---|
| Sialolithiasis [9] | Colicky pain + swelling worsened by eating; most commonly submandibular | Palpable stone in floor of mouth; visible on plain X-ray (80% of submandibular stones are radio-opaque) |
| Acute bacterial sialadenitis [9] | Sudden onset of firm, tender swelling; fever, chills, systemic toxicity; purulent discharge from duct [9]; dehydrated/post-operative/elderly | Commonly caused by S. aureus [9]; unilateral; expression of pus from duct orifice |
| Chronic bacterial sialadenitis [9] | Low-grade chronic infection → eventual destruction of salivary gland [9]; recurrent episodes | Decreased salivary secretion and increased mucus content predispose [9] |
| Viral sialadenitis (mumps) [9] | Acute pain and swelling of one or both parotid glands; non-specific prodrome (low-grade fever, malaise, headache, myalgia, anorexia) [9] | Bilateral parotid involvement classic; orchitis in post-pubertal males; vaccination history |
| Sjögren's syndrome [9] | Gradual swelling, typically bilateral parotid or submandibular; dry eyes and mouth (sicca complex) [9] | Autoimmune sialadenitis → parenchymal destruction and dilation of intraglandular ducts [9]; positive anti-Ro/anti-La antibodies |
| Sarcoidosis [9] | Bilateral painless parotid enlargement [9] | Granulomatous infiltration [9]; Heerfordt syndrome (parotid enlargement + uveitis + facial nerve palsy + fever) |
| Salivary gland tumours | Painless, progressive swelling; facial nerve palsy suggests malignant parotid tumour | The smaller the salivary gland, the higher the probability that a neoplasm is malignant [9] |
| HIV-associated salivary disease | Bilateral, cystic parotid swelling; lymphoepithelial cysts | HIV testing; bilateral cystic enlargement characteristic |
When evaluating any patient with oral/dental pain or lesions, always actively exclude:
| Category | "Must-Not-Miss" | Key Red Flag |
|---|---|---|
| Malignancy | Oral SCC, NPC, lymphoma, salivary gland carcinoma | Non-healing ulcer > 3 weeks; indurated mass; cranial nerve involvement; cervical lymphadenopathy; weight loss |
| Deep space infection | Ludwig's angina, peritonsillar abscess (quinsy), parapharyngeal abscess | Floor of mouth elevation; "hot potato" voice; trismus; drooling; stridor (airway compromise!) |
| Epiglottitis [14] | Acute swelling of epiglottis → airway obstruction | Admit if ANY suspicion; do NOT examine the throat [14]; drooling, stridor, tripod position |
| Blood dyscrasia | Agranulocytosis, acute leukaemia [14] | Severe oral ulceration/infection out of proportion to expected; gum hypertrophy (leukaemia, usually monocytic) [1]; pallor; petechiae; bleeding |
| SJS/TEN [10] | Severe drug reaction with mucosal involvement | Drug history; target lesions; skin sloughing; multiple mucosal sites involved (oral + ocular + urogenital) [10] |
| Pemphigus vulgaris [7] | Autoimmune blistering → severe erosions → dehydration, sepsis | Widespread oral erosions; Nikolsky positive [7]; pain exacerbated by eating/drinking → weight loss [7] |
| Cardiovascular [14] | Angina / MI presenting as sore throat or jaw pain [14] | Exertional symptoms; cardiac risk factors; diaphoresis |
High Yield Summary
Approach: Is it odontogenic or non-odontogenic? What is the morphology (ulcer / white / red / vesiculobullous / pigmented / swelling / no lesion)? Is it dangerous?
Most common oral ulcer: Aphthous ulcer [1]. Most dangerous mimic: Oral SCC — any ulcer > 3 weeks must be biopsied.
White patches: "Can it be scraped off?" → Yes = candidiasis; No = leukoplakia, lichen planus, hairy leukoplakia → biopsy.
Vesiculobullous with mucosal involvement: Pemphigus vulgaris (most, Nikolsky +ve), bullous pemphigoid (some), HSV, EM, SJS/TEN [7].
Pain without visible lesion: Trigeminal neuralgia, glossopharyngeal neuralgia, TMJ dysfunction, sinusitis, referred cardiac pain, burning mouth syndrome.
Murtagh's sore throat red flags: Cardiovascular (angina/MI), cancer of oropharynx/tongue, blood dyscrasias, epiglottitis, quinsy, HIV [14].
The cancer triad: Hoarseness + pain on swallowing + referred ear pain → pharyngeal cancer [14].
Oropharyngeal mass DDx: SCC (most common), minor salivary gland tumour (submucosal, tongue base/soft palate), lymphoma (tonsil/tongue base) [3].
Salivary gland DDx: Sialolithiasis (meal-related pain), sialadenitis (acute bacterial vs viral/mumps), Sjögren's (bilateral, sicca), sarcoidosis (bilateral, painless), tumour.
Active Recall - Differential Diagnosis of Oral/Dental Pain and Lesions
References
[1] Senior notes: Ryan Ho GI.pdf (p10) and Ryan Ho Fundamentals.pdf (p62) — Oral examination findings, leukoplakia, glossitis, gum hypertrophy, pigmentation, aphthous ulcers, angular stomatitis, causes of oral ulcers [3] Senior notes: felixlai.md (sections 350, 351, 354, 355, 369, 370, 371) — Oral SCC site-specific features, oropharyngeal cancer DDx (minor salivary gland tumour, lymphoma), premalignant lesions, clinical manifestations [5] Senior notes: Ryan Ho Rheumatology.pdf (p137) — HSV infection clinical features, diagnosis, treatment [6] Senior notes: Ryan Ho Rheumatology.pdf (p143) — Lichen planus aetiology, Wickham's striae, mucosal involvement [7] Senior notes: Ryan Ho Rheumatology.pdf (p147, p152) — Vesiculobullous disease DDx by distribution and mucosal involvement, pemphigus vulgaris, bullous pemphigoid [8] Senior notes: Ryan Ho Rheumatology.pdf (p98) — Behçet disease oral ulcers [9] Senior notes: felixlai.md (sections 325, 327) — Sialolithiasis, salivary gland swelling differential (sialadenitis, Sjögren's, sarcoidosis, tumours) [10] Senior notes: Ryan Ho Opthalmology.pdf (p133) and Ryan Ho Rheumatology.pdf (p149) — SJS/TEN clinical features, drug causes [11] Senior notes: Ryan Ho Rheumatology.pdf (p130) — Erythema multiforme causes, oral involvement, course [14] Lecture slides: murtagh merge.pdf (p43, p90, p92) — Murtagh's diagnostic strategies for ear pain and sore throat [15] Senior notes: Ryan Ho Rheumatology.pdf (p178) — Pyogenic granuloma clinical features [16] Senior notes: Ryan Ho Neurology.pdf (p22) — Glossopharyngeal nerve, glossopharyngeal neuralgia [17] Senior notes: Ryan Ho Respiratory.pdf (p54) — Rhinosinusitis symptoms and facial pain
Diagnostic Criteria, Diagnostic Algorithm, and Investigations for Oral/Dental Pain and Lesions
Unlike a single disease with one set of diagnostic criteria (e.g., SLE or rheumatic fever), "oral/dental pain and lesions" is an umbrella presentation. The diagnostic approach is therefore algorithmic — you start with the clinical presentation, triage urgency, identify the morphological category, and then deploy targeted investigations. Specific diagnostic criteria exist for individual conditions within this umbrella (e.g., Behçet disease, Sjögren's syndrome, GAS pharyngitis), and these will be detailed below.
The algorithm below captures the clinical reasoning process from the moment a patient presents with an oral complaint. Think of it as how a senior doctor on a ward round would approach this.
The 3-Week Rule
Any oral ulcer persisting for more than 3 weeks must be biopsied to exclude malignancy. This is the single most important principle in the diagnostic approach to oral lesions. Missing an early SCC because it was labelled "aphthous" is a disastrous and entirely preventable error.
2. Specific Diagnostic Criteria for Key Conditions
When a patient presents with sore throat, the key diagnostic question is: Is this GAS pharyngitis (which needs antibiotics to prevent rheumatic fever) or viral (which does not)?
Centor criteria [18]:
| Criterion | Points |
|---|---|
| History of fever | 1 |
| Tonsillar exudates | 1 |
| Tender anterior cervical adenopathy | 1 |
| Absence of cough | 1 |
Modified Centor (McIsaac) criteria add [18]:
- Age < 15 y → add 1 point
- Age > 44 y → subtract 1 point
Interpretation [18]:
| Score | Risk of Strep | Action |
|---|---|---|
| -1 to 1 | < 10% | No antibiotics or throat culture necessary |
| 2 to 3 | 15–32% | Antibiotics if throat culture positive |
| 4 to 5 | ~56% | Treat empirically with an antibiotic |
Why these criteria work from first principles: GAS pharyngitis is a bacterial infection, so it tends to produce exudative tonsillitis (pus), fever (systemic inflammatory response), and lymphadenopathy (regional immune activation). It does NOT typically cause cough (which is more characteristic of viral upper respiratory tract infection affecting the lower airway mucosa). The criteria effectively separate the bacterial phenotype from the viral phenotype.
Key investigations for sore throat [14]:
- Throat swab (for rapid antigen detection test or culture)
- FBE (full blood examination) — look for anaemic pallor of leukaemia [14], neutropenia (agranulocytosis), atypical lymphocytes (EBV)
- Mononucleosis test (heterophile antibody / Monospot) — for EBV infectious mononucleosis
- Blood sugar — diabetes predisposes to oral infections
- Biopsy of suspicious lesions [14]
Diagnostic tips from Murtagh [14]:
- Tonsillitis with a covering membrane may be caused by Epstein-Barr mononucleosis
- Admit if any suspicion of epiglottitis — and do not examine the throat
- The triad: hoarseness + pain on swallowing + referred ear pain → pharyngeal cancer
Diagnosis is predominantly clinical (AFP 2016) [17]:
- Criteria: sudden onset of ≥ 2 of (with ≥ 1 nasal symptom):
- Nasal blockage/congestion or nasal discharge PLUS
- Facial pain/pressure and/or decreased or loss of smell
Criteria for bacterial rhinosinusitis: ≥ 3 of [17]:
- Double sickening (initial improvement then deterioration)
- Discoloured, purulent nasal discharge
- Severe, localised pain
- Fever > 38°C or elevated ESR/CRP
Imaging: NOT indicated if uncomplicated [17]:
- Sinus XR: poor sensitivity and specificity → NOT recommended [17]
- Sinus CT: reserved for cases where complications are suspected [17]
This matters for the oral/dental differential because maxillary sinusitis commonly mimics or refers pain to the upper teeth. Understanding that sinusitis is a clinical diagnosis prevents unnecessary imaging in straightforward cases.
Recurrent oral ulceration (observed by physician or patient, recurring ≥ 3 times in 12 months) PLUS ≥ 2 of [8]:
- Recurrent genital ulceration
- Eye lesions (anterior/posterior uveitis, cells in vitreous on slit lamp, retinal vasculitis)
- Skin lesions (erythema nodosum, pseudofolliculitis, papulopustular lesions, acneiform nodules)
- Positive pathergy test
Pathergy test [8]:
- Procedure: skin prick with 20G needle
- Positive if pustule-like lesion/papules after 48 hours
- Performance: sensitivity 50–75% in endemic regions, 10–20% in the West
Why pathergy works: In Behçet disease, the innate immune system is hyper-reactive. Even minor trauma (a needle prick) triggers an exaggerated neutrophilic response → papule/pustule formation at the site. This does not happen in normal individuals.
When oral dryness (xerostomia) is a prominent feature, Sjögren's syndrome enters the differential. The ACR/EULAR 2016 criteria are used [19]:
Inclusion criteria: Any of: ≥ 1 symptom of ocular or oral dryness, glandular enlargement, characteristic extraglandular involvement [19].
Exclusion criteria (must be absent): History of head and neck radiotherapy, active HCV infection/AIDS, active sarcoidosis/amyloidosis/GvHD/IgG4 disease [19].
ACR/EULAR Classification Criteria (diagnostic = ≥ 4 points) [19]:
| Criterion | Points |
|---|---|
| Labial salivary gland biopsy: focal lymphocytic sialadenitis with ≥ 1 foci/4mm² | 3 |
| Anti-Ro positive | 3 |
| Ocular staining score ≥ 5 (or van Bijsterveld score ≥ 4) in at least 1 eye | 1 |
| Schirmer test ≤ 5mm/5min in at least 1 eye | 1 |
| Unstimulated whole saliva flow rate ≤ 0.1 mL/min | 1 |
Relevant investigations [19]:
- Schirmer's test: standard strip of filter paper placed on inside of lower eyelid → wetting of < 10mm in 5 min indicates defective tear production (< 5mm/5min for the classification criteria) [19]
- Labial salivary gland biopsy: biopsy of minor salivary glands from inner lower lip → focal lymphocytic sialadenitis indicates Sjögren's syndrome [19]
- Autoantibodies: ANA (80%), RF (> 90%), anti-Ro (60%), anti-La (40%) [19]
There are no formal "classification criteria" like SLE, but the diagnosis rests on a triad [7]:
- Clinical: Flaccid blisters/oral erosions + positive Nikolsky sign
- Histopathology (skin/mucosal biopsy): Suprabasilar acantholysis (intraepidermal split just above the basal layer — the "tombstone" appearance of basal cells remaining attached to the basement membrane)
- Immunological: Direct immunofluorescence (DIF) showing intercellular IgG and C3 deposition in a "chicken-wire" pattern; Indirect immunofluorescence (IIF) or ELISA detecting circulating anti-desmoglein 1 and/or anti-desmoglein 3 antibodies
For oral cavity SCC, the TNM staging system is the standard. Key points:
T staging (primary tumour) — based on tumour size AND depth of invasion (DOI):
| Stage | Size | Depth of Invasion |
|---|---|---|
| T1 | ≤ 2 cm | DOI ≤ 5 mm |
| T2 | ≤ 2 cm with DOI > 5 mm, OR > 2–4 cm with DOI ≤ 10 mm | |
| T3 | > 4 cm OR DOI > 10 mm | |
| T4a | Moderate advanced local disease (invasion of cortical bone of mandible/maxilla, maxillary sinus, skin of face) | |
| T4b | Very advanced local disease (invasion of masticator space, pterygoid plates, skull base, encases internal carotid artery) |
Why depth of invasion was added (AJCC 8th ed): DOI is the single strongest predictor of regional lymph node metastasis and survival, better than surface tumour size alone. A small but deeply invasive tumour is biologically more aggressive than a large but superficial one.
N staging (regional lymph nodes) — now includes extranodal extension (ENE):
- ENE positive = upstaged (e.g., a single node < 3 cm with ENE becomes N2a rather than N1)
For oropharyngeal SCC, the AJCC 8th edition introduced a separate staging system for HPV-positive (p16+) tumours, which have a much better prognosis. This is why p16 immunohistochemistry / HPV testing is mandatory.
3. Investigation Modalities — Detailed Guide
| Investigation | What It Tests | Key Findings | When to Use |
|---|---|---|---|
| Scraping test | Can the white patch be scraped off? | Candidiasis = yes (pseudomembrane); leukoplakia/LP = no | First step for any white oral patch |
| Pulp vitality testing (thermal, electric) | Whether dental pulp is alive | No response = pulp necrosis → periapical abscess likely | Suspected odontogenic pain |
| Percussion test (tooth tapping) | Periapical inflammation | Pain on percussion = periapical pathology | Suspected dental abscess |
| Nikolsky sign [7] | Epidermal cohesion | Positive = epidermis dislodged by lateral pressure → pemphigus vulgaris, SJS/TEN [7] | Vesiculobullous oral lesions |
| Pathergy test [8] | Innate immune hyper-reactivity | Pustule at needle prick site after 48h → Behçet disease [8] | Recurrent oral + genital ulcers |
| Schirmer's test [19] | Tear production (for Sjögren's) | < 10mm/5min = defective; ≤ 5mm/5min for ACR/EULAR criteria [19] | Oral dryness + dry eyes |
| Investigation | What It Tests | Key Findings / Interpretation | Condition |
|---|---|---|---|
| FBE (full blood examination) [14] | Haematological parameters | Anaemic pallor of leukaemia [14]; neutropenia → agranulocytosis (drug-induced — suspect carbimazole, clozapine, chemotherapy); atypical lymphocytes → EBV; pancytopenia → leukaemia, aplastic anaemia; thrombocytopenia → mucosal bleeding | Unexplained oral ulceration, gingival bleeding, gum hypertrophy |
| Blood film | Morphology of cells | Blast cells → acute leukaemia; atypical lymphocytes → EBV infectious mononucleosis | Suspected haematological malignancy |
| Mononucleosis test (Monospot / heterophile Ab) [14] | EBV infectious mononucleosis | Positive = confirms EBV mono (note: may be negative in first week) | Young adult with sore throat, membrane-covered tonsils, splenomegaly |
| Blood sugar [14] | Diabetes screening | Hyperglycaemia → predisposes to candidiasis, periodontal disease, poor healing | Recurrent oral candidiasis, poor wound healing |
| Iron studies, B12, folate | Nutritional deficiencies | Low iron / ferritin → glossitis, angular stomatitis [1]; Low B12 / folate → glossitis [1] | Glossitis, angular stomatitis, recurrent aphthous ulcers |
| Anti-desmoglein 1 and 3 antibodies (ELISA) | Pemphigus | Anti-DSG3 positive → mucosal pemphigus vulgaris; Anti-DSG1 + DSG3 → mucocutaneous PV [7] | Suspected pemphigus |
| Syphilis serology (RPR/VDRL + TPHA/FTA-Abs) | Treponema pallidum | Positive screening + confirmatory → primary (chancre), secondary (mucous patches), tertiary syphilis | Painless oral ulcer, mucous patches |
| HIV serology | HIV infection | Positive → oral candidiasis, hairy leukoplakia, Kaposi sarcoma, severe aphthous ulcers all become more likely | Unexplained oral candidiasis in young adult, oral hairy leukoplakia |
| EBV VCA IgA [4] | NPC screening | Elevated in NPC → supports diagnosis in right clinical context; used for screening in endemic areas (HK) | Suspected NPC; cervical lymphadenopathy of unknown primary |
| Plasma EBV DNA (quantitative PCR) | NPC diagnosis and monitoring | Elevated = suggestive of NPC (high sensitivity and specificity in endemic populations); used for screening, diagnosis, treatment monitoring, and surveillance for recurrence | NPC screening (HK programme), staging, post-treatment monitoring |
| ESR, CRP | Systemic inflammation | ↑ESR (> 50mm/h) + age ≥ 50 → consider giant cell arteritis [20]; elevated in any inflammatory/infective process | Temporal/facial pain in elderly; systemic features with oral ulceration |
| Autoantibodies: ANA, RF, anti-Ro, anti-La [19] | Autoimmune disease | ANA (80%), RF (> 90%), anti-Ro (60%), anti-La (40%) in Sjögren's [19] | Oral and ocular dryness (sicca symptoms) |
| HLA-B15:02* [10] | Pharmacogenomics | Prevalence 13% in HK Chinese; mandatory check before prescribing carbamazepine [10] → prevents SJS/TEN | Before prescribing carbamazepine or other aromatic AEDs |
| HLA-B58:01* [10] | Pharmacogenomics | Prevalence 7.4% in HK Chinese; associated with allopurinol-related SJS/TEN [10] → switch to febuxostat if positive | Before prescribing allopurinol (recommended but not mandatory) |
| Throat swab [14] | Identify pharyngeal pathogen | Rapid antigen detection test (RADT) for GAS (high specificity, moderate sensitivity); culture = gold standard | Sore throat with high Centor score |
| HSV PCR (from vesicular fluid) [5] | HSV DNA | Positive PCR confirms HSV-1 or HSV-2 infection | Vesicular oral lesions; note: serology is of limited value as a substantial proportion of the population is seropositive [5] |
Biopsy is the definitive diagnostic step for many oral lesions. The type of biopsy matters:
| Biopsy Type | Technique | When to Use |
|---|---|---|
| Incisional biopsy | Remove a representative portion of the lesion (including the margin with normal tissue) | Incisional biopsy should be performed in all cases of suspected oropharyngeal malignancy [3]; large lesions where excision would be mutilating; suspected leukoplakia/erythroplakia |
| Excisional biopsy | Remove the entire lesion | Small lesions (< 1 cm) that can be completely excised without significant morbidity; suspicious small mucosal lesions |
| Punch biopsy | Circular blade to obtain full-thickness skin/mucosa sample | Vesiculobullous lesions (need perilesional skin for DIF); lichen planus |
Key histopathological findings:
| Condition | Histopathology | Why This Pattern? |
|---|---|---|
| Leukoplakia | Hyperkeratosis ± epithelial dysplasia (mild/moderate/severe) | Chronic irritation → increased keratin production; dysplasia = disordered maturation indicating premalignant change |
| Erythroplakia | Usually severe dysplasia, carcinoma in situ, or invasive SCC | Thin atrophic epithelium without protective keratinisation; the redness IS the warning sign |
| Lichen planus | Band-like lymphocytic infiltrate at dermoepidermal junction; saw-tooth rete ridges; civatte bodies (apoptotic keratinocytes) | T-cell attack on basal keratinocytes → interface dermatitis |
| SCC | Islands/nests of malignant squamous epithelium invading stroma; keratin pearls (well-differentiated); intercellular bridges | Malignant keratinocyte proliferation breaking through basement membrane |
| Pemphigus vulgaris [7] | Suprabasilar acantholysis → intraepidermal blister; "tombstone" pattern of basal cells; DIF: intercellular IgG + C3 ("chicken-wire" pattern) | Autoantibodies to desmoglein-3 disrupt intercellular adhesion just above the basal layer [7] |
| Bullous pemphigoid | Subepidermal blister with eosinophilic infiltrate; DIF: linear IgG and C3 along basement membrane zone | Autoantibodies to BP180/BP230 at hemidesmosomes → complement-mediated damage to basement membrane zone |
| Minor salivary gland biopsy (Sjögren's) [19] | Focal lymphocytic sialadenitis with ≥ 1 foci/4mm² → indicates Sjögren's syndrome [19] | Autoimmune T-cell infiltration → destruction of salivary gland acini |
DIF vs IIF — What's the Difference?
Direct immunofluorescence (DIF) is performed on a tissue biopsy — it detects antibodies/complement already deposited in the tissue. Indirect immunofluorescence (IIF) is performed on patient serum — it detects circulating antibodies. For pemphigus, DIF shows the "chicken-wire" pattern of intercellular IgG; IIF detects circulating anti-desmoglein antibodies. Always take the DIF biopsy from perilesional, clinically normal-appearing mucosa/skin (not from the ulcer itself, which may be necrotic and give a false negative).
| Modality | Indication | Key Findings | Interpretation |
|---|---|---|---|
| Periapical X-ray | Dental pain; suspected periapical abscess | Radiolucency at tooth apex = periapical abscess/granuloma; loss of lamina dura = periodontal disease | Standard first-line dental investigation |
| Orthopantomogram (OPG / panoramic XR) | Overview of all teeth, mandible, TMJ; suspected dental pathology, mandibular lesions | Detects gross cortical invasion [3]; impacted wisdom teeth; jaw cysts; mandibular fractures | Screening for dental causes of pain; assessment of bony mandible in alveolar/gingival SCC |
| CT scan [3] | Suspected bony invasion; staging of H&N cancer; deep space neck infections; sinusitis complications | Useful to detect bony invasion [3]; detection of cervical lymph node metastasis [3]; CT thorax and abdomen to assess for distant metastasis [3]; air-fluid levels in sinuses [17] | CT is the best modality for demonstrating subtle cortical invasion [3] (e.g., alveolar SCC invading mandible). CT with contrast also excellent for defining abscess collections (rim-enhancing fluid collection) |
| MRI scan [3] | Soft tissue assessment of oral/oropharyngeal tumours; mandibular marrow invasion; perineural spread | Imaging modality of choice for cancer of the oral cavity and oropharynx [3]; provides optimal visualization of soft-tissue infiltration of the tumour [3]; detection of cervical lymph node metastasis [3] | MRI is the best modality for demonstrating invasion of medullary cavity of mandible [3] — because MRI has superior soft tissue contrast and can detect marrow replacement by tumour (loss of normal fatty marrow signal on T1) |
| MRI brain (with contrast) | Trigeminal neuralgia (to identify neurovascular compression or secondary causes) | Normal (idiopathic TN — neurovascular compression may be seen on high-resolution MRI); structural lesion (tumour, MS plaque, aneurysm) | Exclude secondary causes of trigeminal neuralgia; FIESTA/CISS sequences can show vascular loop compressing trigeminal nerve root |
| USG-guided FNAC [3] | Deeply seated cervical lymph node [3]; salivary gland mass | USG has limited use in oropharyngeal cancer but is a useful adjunct for FNAC to ensure accurate aspiration of a deeply seated lymph node swelling [3] | Cell aspirate for cytology → differentiate reactive vs metastatic vs lymphoma |
| Sialography | Salivary duct obstruction / chronic sialadenitis (less used now) | Filling defect in duct = stone; sialectasis (dilated ducts) = chronic sialadenitis/Sjögren's | Largely replaced by CT/MRI sialography; still occasionally used |
| CT sialography / MR sialography | Salivary duct pathology; sialolithiasis | Precise stone localisation; duct strictures; gland architecture | Non-invasive alternative to conventional sialography |
| PET-CT | H&N cancer staging; detection of unknown primary; surveillance for recurrence | Increased FDG uptake at primary tumour and metastatic sites | Used for staging advanced H&N cancer; particularly useful for detecting unknown primary when a patient presents with cervical metastasis (CUP — carcinoma of unknown primary) |
| Salivary gland scintigraphy (⁹⁹ᵐTc scan) [19] | Salivary gland function (for Sjögren's) | ⁹⁹ᵐTc scan for uptake at major salivary glands [19] — decreased uptake and excretion = hypofunction | Insensitive but objective measure of salivary function |
| Investigation | Indication | Rationale |
|---|---|---|
| Panendoscopy with biopsy [3] | Suspected H&N malignancy | Incisional biopsy should be performed in all cases; assess tumour extent and look for synchronous tumour [3]. Panendoscopy includes direct laryngoscopy, bronchoscopy and OGD [3] — this is based on the concept of field cancerisation: the entire upper aerodigestive tract mucosa is exposed to the same carcinogens (smoking/alcohol), so there is a 5–10% risk of a synchronous second primary tumour |
| p16 immunohistochemistry | Oropharyngeal SCC | Surrogate marker for HPV-driven tumours; p16 positive = HPV-associated → separate (better prognosis) staging system in AJCC 8th edition |
| HPV DNA testing (ISH/PCR) | Oropharyngeal SCC | Confirms HPV-driven tumour biology; may guide de-escalation of treatment |
| NPC screening (EBV DNA + nasopharyngoscopy) | HK population screening; clinical suspicion of NPC | Plasma EBV DNA as screening biomarker; positive → nasopharyngoscopy with biopsy of any suspicious nasopharyngeal lesion |
| Temporal artery biopsy [20] | Giant cell arteritis presenting with jaw claudication/facial pain | Must order urgently (< 24–48h) [20]; may be falsely negative due to patchy inflammation ("skip lesions") [20] → long segment biopsy (≥ 2 cm) reduces false negatives |
4. Diagnostic Approach by Common Scenario — Practical Synthesis
- History: Duration, risk factors (5Ss: Smoking, Spirits, Sharp teeth, Sex, Spicy food [3]), weight loss, otalgia, dysphagia
- Examination: Lesion characteristics (indurated? rolled edges? fixation?), cranial nerves (lingual nerve, hypoglossal nerve, mental nerve [3]), cervical lymph nodes
- Investigations:
- Apply Modified Centor criteria [18]
- Low score → reassure, symptomatic treatment
- Moderate score → throat swab (RADT ± culture)
- High score → empirical antibiotics
- If membrane-covered tonsils → consider EBV mononucleosis [14] → mononucleosis test [14]
Key examination points for sore throat [14]:
- On inspection note the general appearance, look for toxicity, the anaemic pallor of leukaemia, the nasal stuffiness of infectious mononucleosis, or the halitosis of a streptococcal throat
- Palpate the neck for soreness and lymphadenopathy and check the sinus area
- Then inspect the oral cavity and pharynx
Key history for sore throat [14]:
- First determine whether the patient has a sore throat, a deep pain in the throat or neck pain
- Enquire about relevant associated symptoms such as a metallic taste in the mouth, fever, upper respiratory infection, postnasal drip, sinusitis, cough and other pain such as ear pain
- Note whether the patient is an asthmatic and uses a steroid inhaler or is a smoker or exposed to environmental irritants
If an adult presents with ear pain but normal auroscopy, examine possible referral sites, namely TMJ, mouth, throat, teeth and cervical spine [14].
This is because the ear receives sensory innervation from CN V3 (auriculotemporal nerve), CN VII (sensory branch), CN IX (Jacobson's nerve), CN X (Arnold's nerve), and C2/C3 (great auricular nerve). Any pathology along these nerves' territories can cause referred otalgia.
| Presentation | First-Line Ix | Second-Line Ix | Definitive Ix |
|---|---|---|---|
| Persistent oral ulcer | Clinical exam; FBE | CT/MRI if suspicious | Incisional biopsy |
| White patch | Scraping test | Swab (if scraped off → Candida) | Biopsy (if cannot scrape off) |
| Red patch | Clinical exam | — | Biopsy (erythroplakia = high Ca risk) |
| Vesiculobullous | Nikolsky sign; vesicular fluid PCR (HSV) | Anti-DSG Ab (ELISA); drug Hx review | Biopsy + DIF (perilesional) |
| Sore throat | Modified Centor; RADT/throat swab; FBE | Monospot; blood sugar | Biopsy if suspicious lesion |
| Salivary gland swelling | Bimanual palpation; plain XR (OPG) | USG ± FNAC; CT/MRI | Biopsy if neoplasm suspected |
| Neck mass / lymphadenopathy | USG + FNAC | CT/MRI neck; PET-CT | Excisional biopsy if lymphoma suspected |
| Jaw/facial pain (no lesion) | Dental exam; TMJ palpation; sinus tenderness | MRI brain (TN); sinus CT | ECG/troponin if cardiac; temporal artery Bx if GCA |
| Oral dryness | Schirmer test; salivary flow | Anti-Ro/La, ANA, RF | Labial salivary gland biopsy |
High Yield Summary
Algorithm: Triage airway first → Hx + systematic intraoral/extraoral exam → Odontogenic vs non-odontogenic → Morphological categorisation → Targeted investigations → Biopsy any suspicious/persistent (> 3 weeks) lesion.
Diagnostic Criteria to Know:
- Modified Centor criteria for GAS pharyngitis [18]: Fever + Exudates + Anterior LAD + No cough (± age adjustment). Score -1 to 1 = no Abx; 2-3 = swab first; 4-5 = empirical Abx.
- ISG criteria for Behçet disease [8]: Recurrent oral ulcers (≥ 3/yr) + ≥ 2 of genital ulcers/eye lesions/skin lesions/positive pathergy.
- ACR/EULAR Sjögren's [19]: ≥ 4 points from labial biopsy (3), anti-Ro (3), ocular staining (1), Schirmer (1), saliva flow (1).
Imaging Hierarchy for Oral Cancer:
- MRI = imaging modality of choice for oral/oropharyngeal cancer (soft tissue) [3].
- CT = best for subtle cortical bone invasion [3].
- MRI = best for medullary cavity invasion of mandible [3].
- Panendoscopy = mandatory to look for synchronous tumour (field cancerisation) [3].
Must-Know Lab Tests: FBE (leukaemia screen), Monospot (EBV), HSV PCR (from vesicular fluid, not serology), anti-desmoglein Ab (pemphigus), anti-Ro/La (Sjögren's), EBV DNA (NPC), HLA-B15:02* (before carbamazepine in HK Chinese) [10].
Active Recall - Diagnosis and Investigations for Oral/Dental Pain and Lesions
References
[1] Senior notes: Ryan Ho GI.pdf (p10) and Ryan Ho Fundamentals.pdf (p62) — Oral examination findings, leukoplakia, glossitis, aphthous ulcers, angular stomatitis [3] Senior notes: felixlai.md (sections 351, 354, 355, 370, 371) — Oral/oropharyngeal cancer diagnosis: incisional biopsy, panendoscopy, CT, MRI, USG-guided FNAC, imaging modality of choice, field cancerisation [4] Senior notes: felixlai.md (section 357) — NPC: EBV VCA IgA [5] Senior notes: Ryan Ho Rheumatology.pdf (p137) — HSV: PCR from vesicular fluid, serology limitation [7] Senior notes: Ryan Ho Rheumatology.pdf (p152) — Pemphigus vulgaris: Nikolsky sign, histopathology, DIF [8] Senior notes: Ryan Ho Rheumatology.pdf (p98) — Behçet disease: ISG criteria, pathergy test [10] Senior notes: Ryan Ho Rheumatology.pdf (p149) and Ryan Ho Opthalmology.pdf (p133) — SJS/TEN: HLA-B15:02, HLA-B58:01 pharmacogenomics [14] Lecture slides: murtagh merge.pdf (p44, p90, p92) — Murtagh's sore throat and ear pain: key history, key examination, key investigations, diagnostic tips [17] Senior notes: Ryan Ho Respiratory.pdf (p54) — Rhinosinusitis diagnostic criteria (AFP 2016), imaging indications [18] Senior notes: Ryan Ho Respiratory.pdf (p51) — Centor and Modified Centor criteria for GAS pharyngitis [19] Senior notes: Ryan Ho Rheumatology.pdf (p89) — Sjögren's syndrome: ACR/EULAR criteria, Schirmer test, labial biopsy, autoantibodies [20] Senior notes: Ryan Ho Neurology.pdf (p65) — Giant cell arteritis: diagnostic criteria, temporal artery biopsy
Management Algorithm and Treatment Modalities for Oral/Dental Pain and Lesions
The management of oral/dental complaints follows a structured hierarchy: secure the airway → treat emergencies → address the specific aetiology → manage symptoms → prevent recurrence → rehabilitate function. Because this is an umbrella topic spanning dozens of conditions, I'll present a master management algorithm first, then drill down into treatment modalities by condition category.
2. Emergency Management
Ludwig's angina (bilateral sublingual + submandibular space infection):
- "Ludwig" — named after Wilhelm Friedrich von Ludwig; "angina" from Latin angere = to strangle. The name tells you the condition: a throat infection that strangles the airway.
- Management: Secure airway FIRST (may require fibreoptic intubation or surgical tracheostomy if intubation impossible due to floor of mouth swelling and trismus). IV broad-spectrum antibiotics covering oral flora (IV amoxicillin/clavulanate or IV benzylpenicillin + metronidazole; add clindamycin if penicillin-allergic). Urgent surgical drainage of abscess if fluctuant collection present. IV dexamethasone may help reduce oedema and buy time.
Peritonsillar abscess (quinsy):
- Needle aspiration or incision and drainage of the abscess. IV antibiotics (penicillin-based + metronidazole). IV fluids. Interval tonsillectomy may be considered if recurrent.
Epiglottitis [14]:
- Admit if any suspicion — do NOT examine the throat [14] (because direct visualization may trigger complete laryngospasm and airway obstruction)
- Secure airway in controlled environment (ideally operating theatre with ENT standby). IV ceftriaxone or cefotaxime. IV dexamethasone. Humidified oxygen.
- Immediate: Withdraw the causative drug — this is the single most important intervention
- Supportive care: ICU or burns unit admission for TEN; fluid resuscitation; wound care (non-adherent dressings, avoid skin shear); nutritional support (often requires NG/NJ tube due to severe oral erosions); temperature regulation; VTE prophylaxis
- Systemic immunosuppression: steroids, IVIg, cyclosporin, plasmapheresis (no consensus, controversial) [10]
- Ocular treatment [10]:
- Saline rinses to remove mucous and inflammatory debris
- Topical corticosteroids + broad-spectrum antibiotics
- Early amniotic membrane transplantation (AMT) if moderate-severe conjunctival involvement — can increase epithelialisation, decrease inflammation, neovascularisation, and scarring [10]
- Oral care: Gentle oral hygiene; chlorhexidine mouthwash (alcohol-free); topical anaesthetic gel (lidocaine 2%) before meals; soft/liquid diet
- Monitor with SCORTEN for prognostication [21]
3. Management by Condition Category
The medical student's role is to recognise odontogenic causes, provide emergency analgesia and antibiotics when indicated, and refer to dental services.
| Condition | Management | Rationale |
|---|---|---|
| Dental caries (early) | Dental referral for restoration (filling) | Remove carious dentine, seal with restorative material to prevent progression |
| Reversible pulpitis | Remove stimulus (e.g., repair caries); analgesics | Pulp is inflamed but still viable; removing the cause allows recovery |
| Irreversible pulpitis | Root canal treatment (RCT) or extraction | Pulp is necrotic/dying; RCT removes dead pulp, disinfects, and seals canals; extraction is alternative |
| Periapical abscess | Drainage (via RCT, incision, or extraction) + antibiotics if systemic signs | Abscess needs source control; antibiotics alone without drainage will not resolve it |
| Pericoronitis | Irrigation + chlorhexidine; antibiotics if systemic; wisdom tooth extraction (definitive) | Remove the nidus of infection under the operculum; extraction prevents recurrence |
| Periodontal disease | Scaling and root planing; oral hygiene instruction; smoking cessation | Remove calculus/biofilm mechanically; patient self-care prevents reaccumulation |
Analgesics for dental pain: Paracetamol 1g QDS + Ibuprofen 400mg TDS (if not contraindicated) — this combination provides synergistic analgesia via different mechanisms (central COX inhibition + peripheral COX-1/2 inhibition). Avoid aspirin in children (Reye syndrome risk). Opioids rarely needed and should be short-course only.
Antibiotics for dental infections: Only indicated when there are systemic signs (fever, malaise, lymphadenopathy, facial swelling) or spreading infection. First-line: amoxicillin 500mg TDS (covers streptococci and most oral anaerobes). If penicillin-allergic: clindamycin 300mg QDS or metronidazole 400mg TDS (specifically targets anaerobes). If severe/spreading: IV amoxicillin/clavulanate or IV benzylpenicillin + metronidazole.
Antibiotics Are NOT a Substitute for Drainage
A periapical abscess or dental abscess will not resolve with antibiotics alone. The principle of source control applies: you must drain the pus (via extraction, RCT, or incision and drainage). Antibiotics are adjunctive, not definitive. Prescribing antibiotics without dental referral is a common error.
3.2 Infective Mucosal Conditions
Treatment [5]:
- Acyclovir: initiated ≤ 48h of clinical disease or if severe or associated with significant symptoms [5]
- Can be topical for oral lesions + not immunocompromised, otherwise systemic [5]
- Systemic dosing: Acyclovir 200mg PO 5 times daily (or 400mg TDS) for 7–10 days for primary; 5 days for recurrent [22]
- Alternatives: Valaciclovir 1g BD for 7–10 days (primary) or 500mg BD for 3–5 days (recurrent); Famciclovir 250mg TDS for 7–10 days (primary) [22]
- Foscarnet: treatment of choice if acyclovir resistance (occasionally in immunocompromised hosts) [5]
- Prophylaxis for recurrence if ≥ 6 significant relapses per year [22]:
- Acyclovir 400mg BD; or Valaciclovir 500mg–1g OD; or Famciclovir 250mg BD
Why acyclovir works: Acyclovir is a nucleoside analogue (guanosine analogue). It requires phosphorylation by viral thymidine kinase (only present in HSV-infected cells) to become active → selectively targets infected cells. The active triphosphate form inhibits viral DNA polymerase → chain termination → stops viral replication. This selectivity explains its excellent safety profile.
- First-line: Phenoxymethylpenicillin (Penicillin V) 500mg BD for 10 days [18]
- Alternative: Amoxicillin 500mg BD for 10 days (equally effective, better taste for children)
- Penicillin-allergic: Clarithromycin 250–500mg BD for 5 days; or Azithromycin 500mg OD for 5 days
- Why treat GAS: Not primarily to speed resolution (which only shortens symptoms by ~1 day), but to prevent rheumatic fever (an immune-mediated sequela). Rheumatic fever requires a preceding GAS infection and can cause permanent rheumatic heart disease. Treatment within 9 days of symptom onset prevents rheumatic fever.
| Type | First-Line | Alternative | Notes |
|---|---|---|---|
| Pseudomembranous (thrush) | Nystatin suspension 100,000 units/mL, swish and swallow QDS for 7–14 days | Miconazole oral gel 2.5mL QDS | Nystatin is a polyene antifungal that binds ergosterol in fungal cell membrane → pore formation → cell death. It is NOT absorbed systemically → topical effect only |
| Moderate/severe or immunocompromised | Fluconazole 100–200mg PO OD for 7–14 days | Itraconazole solution 200mg OD | Fluconazole inhibits lanosterol 14-alpha-demethylase (CYP51) → blocks ergosterol synthesis → fungal cell membrane destabilisation |
| Denture stomatitis | Nystatin + denture hygiene (soak in chlorhexidine or dilute sodium hypochlorite overnight) | Miconazole gel applied to denture fitting surface | Must treat the denture as a reservoir; antifungals alone without denture hygiene = recurrence |
| Angular cheilitis | Topical miconazole or combined miconazole/hydrocortisone cream | Nystatin cream | Often mixed Candida + S. aureus infection; miconazole has some anti-staphylococcal activity |
| Steroid inhaler-related | Spacer device + mouth rinse after inhaler use (prevention); topical antifungal if established | — | The steroid deposits on oropharyngeal mucosa → local immunosuppression → Candida overgrowth |
- Oral metronidazole 400mg TDS for 5 days (targets anaerobes — Fusobacterium, Borrelia)
- Chlorhexidine 0.2% mouthwash BD
- Gentle debridement by dentist once acute phase settles
- Address predisposing factors: oral hygiene, smoking cessation, stress management, HIV testing if risk factors
- IV antibiotics covering S. aureus (most common) [12]: IV flucloxacillin (or vancomycin if MRSA suspected) + metronidazole (for anaerobic cover)
- Aggressive IV hydration
- Warm compresses; gentle massage of gland towards duct orifice to express pus
- Sialogogues (lemon drops, sour sweets) to stimulate salivary flow
- Surgical drainage if abscess does not respond to antibiotics within 7–10 days
3.3 Autoimmune / Inflammatory Conditions
Management is largely symptomatic:
| Severity | Treatment | Mechanism / Rationale |
|---|---|---|
| Mild (minor RAS) | Topical corticosteroid paste (e.g., triamcinolone acetonide 0.1% in orabase) applied to ulcer BD–QDS | Suppresses local T-cell mediated inflammation → reduces pain and accelerates healing |
| Mild + pain | Analgesic mouthwash (benzydamine hydrochloride 0.15%) or topical lidocaine 2% gel | Benzydamine is a locally-acting NSAID + local anaesthetic; lidocaine blocks sodium channels in sensory nerve endings |
| Moderate (frequent recurrences) | Chlorhexidine 0.2% mouthwash (reduces secondary bacterial colonisation); topical steroid as above | Chlorhexidine is a broad-spectrum antiseptic; reduces bacterial load on ulcer surface → less pain and faster healing |
| Severe / major RAS | Systemic prednisolone short course (25–50mg tapering over 2 weeks); colchicine 0.5mg BD; dapsone 50–100mg daily | Systemic immunosuppression for refractory disease; colchicine inhibits neutrophil chemotaxis |
| Refractory | Thalidomide 100–200mg daily (strictly controlled — teratogenic); biologics (anti-TNF-alpha) in extreme cases | Thalidomide modulates TNF-alpha and T-cell function; very effective but severe teratogenicity and neuropathy risk |
Always investigate for underlying causes if severe/recurrent: FBE (exclude haematological disease), iron/B12/folate (exclude deficiency), anti-tTG (exclude coeliac disease), consider Behçet/Crohn's.
Management depends on organ involved [8]:
- Topical steroid for oral/genital ulcers [8] — first-line for mucocutaneous disease
- Colchicine for preventing recurrent ulcers and treating erythema nodosum and arthritis [8] — inhibits neutrophil chemotaxis and microtubule formation
- Thalidomide for resistant oral/genital ulcers [8] — modulates TNF-alpha; strictly controlled (pregnancy prevention programme mandatory)
- Systemic steroids and immunosuppressants for uveitis and neurological diseases [8] — azathioprine, ciclosporin, anti-TNF biologics (infliximab, adalimumab) for severe organ involvement
Management: treatment always indicated at disease onset even for mild disease to decrease complications [7]:
- Basic skin care: sterile puncture and drainage of large blisters, leave blister roof in situ to decrease infection risk, sterile wound dressing [7]
- Oral symptom management: avoid irritating food, apply topical local anaesthetic as needed, oral hygiene, consider topical steroid [7]
- Systemic corticosteroids: mainstay of initial treatment [7]:
- Regimen: 1–1.5mg/kg/day oral prednisone/prednisolone → begin tapering ≥ 1 week after last formation of new lesions [7]
- Alternative: upfront rituximab + prednisone gaining popularity recently [7]
- Monitoring: response assessed by cessation of new blister formation, absent Nikolsky sign, healing of old lesions and dropping ELISA titres [7]
- Steroid-sparing adjunct: azathioprine (preferred), MMF, cyclophosphamide (refractory only) [7]
- Other immunosuppressive therapy for refractory disease: rituximab, IVIg, immunoadsorption, plasmapheresis, cyclophosphamide, topical steroids [7]
Why rituximab is gaining traction: Rituximab is a monoclonal antibody against CD20 on B lymphocytes → depletes B cells → reduces autoantibody production (anti-desmoglein). The RITUX 3 trial showed that upfront rituximab + low-dose prednisone achieved complete remission off therapy in 90% at 2 years, compared to ~34% with prednisone alone. This is now considered first-line in many centres.
Management: no evidence for treatment of underlying cause [11] (i.e., the HSV or Mycoplasma has already triggered the immune response; treating the infection doesn't reverse the EM):
- Urgent consult ophthalmology for ocular involvement [11]
- Topical corticosteroids for symptomatic relief in mild cutaneous lesions [11]
- Topical corticosteroids + analgesic mouthwash for symptomatic relief in painful oral erosions [11]
- Systemic corticosteroids (controversial) in severe and/or associated with mucosal involvement [11]
Prevention [11]:
- Elimination of underlying cause: may not always be possible (e.g., HSV infection)
- Systemic prophylactic therapy for ≥ 6 recurrences/year or debilitating episodes [11]:
- Oral lichen planus is often asymptomatic [6] → may not require treatment
- Symptomatic erosive/ulcerative OLP: Topical corticosteroid (triamcinolone acetonide paste, fluocinonide gel, or betamethasone mouthwash) — mainstay of treatment
- Refractory: Topical tacrolimus 0.1% (calcineurin inhibitor — suppresses T-cell activation without steroid side effects); systemic immunosuppression rarely needed
- Long-term surveillance: ~1% risk of malignant transformation → regular follow-up (6–12 monthly) with biopsy of any suspicious change
The management principle is: remove the risk factor + treat the dysplasia + surveil for malignant transformation.
| Strategy | Details |
|---|---|
| Risk factor modification | Smoking cessation (most important); alcohol cessation; betel nut cessation; improve dental hygiene; remove chronic irritants (sharp teeth, ill-fitting dentures) |
| Biopsy and grading | Every leukoplakia/erythroplakia must be biopsied. Grade dysplasia: mild / moderate / severe / carcinoma in situ |
| No dysplasia or mild dysplasia | Observe with regular follow-up (3–6 monthly); risk factor modification; re-biopsy if change in appearance |
| Moderate–severe dysplasia or CIS | CO2 laser ablation can be used for excision or ablation of premalignant lesions [3]; surgical excision; cryotherapy. Ensure clear margins |
| Surveillance | Lifelong follow-up — these patients remain at risk (field cancerisation) |
3.5 Oral Cavity and Oropharyngeal Malignancy
This is a major surgical/oncological topic. The management is multidisciplinary (surgeon, radiation oncologist, medical oncologist, pathologist, radiologist, speech therapist, dietician, dental team).
Management of stage I and II (early) cancer — usually single modality [3]:
Management of stage III and IV (locoregionally advanced) cancer — usually combined modality [3]:
- Surgical resection of primary tumour is suggested as initial therapy rather than radiotherapy or chemotherapy [3]
- Modified radical neck dissection and post-operative radiotherapy with or without concurrent chemotherapy [3]
- Definitive radiotherapy or chemotherapy are options for patients who are medically inoperable or have unresectable disease [3]
- Concomitant chemoradiation is commonly utilized in advanced stage (III and IV) oropharyngeal carcinoma which effectively preserves function and is associated with survival comparable to surgery with postoperative radiation [3]
| Site | Surgical Approach | Reconstruction | Key Considerations |
|---|---|---|---|
| Lip [3] | Surgical excision with histological confirmation of tumour-free margin [3] | Wedge excision + primary closure; mucosal advancement flap for larger defects | Postoperative RT indicated for positive margins, tumour thickness > 4mm, perineural invasion, or LN metastasis [3] |
| Tongue [3] | Wide local excision for small T1–2 tumours [3]; partial glossectomy for larger tumours [3] | Fasciocutaneous free flaps for intraoral bulk and preservation of tongue mobility [3]; prosthetic augmentation for palatal contact [3] | Resection leading to decreased lingual contact with palate, lip and teeth → impaired articulation [3] |
| Floor of mouth [3] | Wide local excision for small mucosal lesions; marginal or segmental mandibulectomy for larger defects | Complex reconstruction with fasciocutaneous or vascularized osseous free flap [3] | Deep invasion into intrinsic muscles of tongue causes fixation and mandates partial glossectomy [3] |
| Alveolus/Gingiva [3] | Marginal resection of mandible for minimal bone invasion [3]; segmental mandibulectomy for medullary cavity invasion [3] | Osseous free flap (fibula) | Treatment frequently requires resection of underlying bone due to tight attachment of alveolar mucosa to periosteum [3] |
| Retromolar trigone [3] | Usually requires marginal or segmental mandibulectomy [3] | Soft tissue or osseous reconstruction | Ipsilateral neck dissection performed because of risk of metastasis to regional lymphatics [3] |
| Buccal mucosa [3] | Small lesions: surgical excision [3]; advanced lesions: combined surgical excision and postoperative radiotherapy [3] | Folded fasciocutaneous free flap or combination of pedicled and free tissue [3] | Local intraoral spread may necessitate resection of alveolar ridge of mandible or maxilla [3] |
| Hard palate [3] | Mucosal excision for very superficial lesions [3]; partial palatectomy or infrastructure maxillectomy for larger lesions [3] | Through-and-through defects require dental prosthesis for rehabilitation of swallowing and speech [3] | Periosteum of the palate acts as a barrier to spread of tumour [3] |
| Type | What Is Removed | Indication |
|---|---|---|
| Selective neck dissection [3] | Lymph nodes in areas with highest chance of nodal metastasis (e.g., Levels I–III) | Prophylactic: clinically N0 neck but high risk of occult metastasis (e.g., tongue cancer > 3mm) |
| Modified radical neck dissection [3] | Level I–V lymph nodes with preservation of one or more of: internal jugular vein, spinal accessory nerve, sternocleidomastoid muscle [3] | Clinically positive neck nodes |
| Radical neck dissection [3] | All Level I–V lymph nodes + internal jugular vein + spinal accessory nerve + sternocleidomastoid muscle [3] | Extensive nodal disease with extranodal extension involving these structures |
Sialolithiasis Management
| Severity | Management | Rationale |
|---|---|---|
| Acute obstruction | Conservative: hydration, warm compresses, sialogogues (lemon drops), gentle massage, analgesia | Stimulate salivary flow to flush out small stones; massage helps express the stone towards the duct orifice |
| Failed conservative / recurrent | Sialendoscopy (minimally invasive endoscopic stone retrieval) | Allows direct visualisation and basket extraction of stones; avoids gland excision; high success rate for stones < 7mm |
| Large stones / gland damage | Submandibular gland excision (for submandibular stones) or parotidectomy (for parotid stones) | Definitive removal of the stone factory; needed if gland is chronically damaged and non-functional |
| Condition | First-Line Treatment | Second-Line / Specialist | Mechanism |
|---|---|---|---|
| Trigeminal neuralgia | Carbamazepine 100mg BD, titrate up (check HLA-B15:02 before prescribing in HK Chinese* [10]) | Oxcarbazepine; microvascular decompression (MVD) surgery for refractory cases | Carbamazepine stabilises neuronal sodium channels → reduces aberrant firing in demyelinated trigeminal nerve. MVD physically separates the offending vessel from the nerve root |
| TMJ dysfunction | Conservative: jaw rest, soft diet, warm compresses, NSAIDs, physiotherapy, occlusal splint | Intra-articular steroid injection; arthroscopy; rarely open surgery | Most TMJ pain is myofascial → muscle relaxation and load reduction. Splints redistribute occlusal forces |
| Sinusitis (bacterial) [17] | Intranasal corticosteroid spray + saline irrigation. Antibiotics (amoxicillin or amoxicillin/clavulanate) if bacterial criteria met [17] | ENT referral for complications or chronic sinusitis; functional endoscopic sinus surgery (FESS) | Intranasal steroids reduce mucosal oedema → restore sinus drainage. Antibiotics target the bacterial pathogens. FESS widens the sinus ostia to improve drainage |
| Referred cardiac pain | Treat underlying ACS (aspirin, GTN, morphine, PCI as indicated) | — | Treating the myocardial ischaemia resolves the referred jaw/throat pain |
This is clinically important and frequently examined.
Indications: only in at-risk procedures in high-risk individuals (ESC guidelines) [23]:
High-risk individuals [23]:
- Any prosthetic valve (including transcatheter valve) or prosthetic materials used in valve repair
- Previous infective endocarditis
- Cyanotic congenital heart disease
- Any congenital heart disease repaired with prosthetic materials: up to 6 months post-op; lifelong if residual shunt or valvular regurgitation remains
At-risk dental procedures [23]:
- Requiring manipulation of gingival or periapical region of teeth
- Perforation of oral mucosa
Regimen [23]:
- No penicillin allergy: Amoxicillin 2g PO 1 hour before; or Ampicillin 2g IM/IV ≤ 30 min before
- Penicillin allergy: Clindamycin 600mg PO 1 hour before; or 600mg IM/IV ≤ 30 min before
- Alternative: Azithromycin/Clarithromycin 500mg PO 1 hour before [23]
Why prophylaxis: Dental procedures cause transient bacteraemia (oral streptococci enter the bloodstream). In patients with structurally abnormal cardiac valves or prosthetic material, these bacteria can adhere to the endocardium and establish vegetations → infective endocarditis. A single dose of antibiotic before the procedure kills bacteria during the transient bacteraemia window.
IE Prophylaxis — Know the Indication AND Regimen
This is one of the most commonly examined topics linking cardiology and dental care. Know: (1) WHICH patients need it (prosthetic valve, prior IE, cyanotic CHD, repaired CHD with prosthetic material), (2) WHICH procedures (gingival manipulation, periapical procedures, oral mucosal perforation), (3) THE DRUG (amoxicillin 2g PO 1h before; clindamycin if allergic).
| Deficiency | Oral Manifestation | Treatment |
|---|---|---|
| Iron deficiency [1] | Glossitis, angular stomatitis, Plummer-Vinson syndrome | Oral ferrous sulphate 200mg BD–TDS; investigate and treat underlying cause (menorrhagia, GI blood loss, coeliac) |
| Vitamin B12 deficiency [1] | Glossitis, aphthous-like ulcers | IM hydroxocobalamin 1mg on alternate days for 2 weeks then every 3 months (if pernicious anaemia); oral supplementation if dietary |
| Folate deficiency [1] | Glossitis | Folic acid 5mg daily for 4 months; ALWAYS exclude B12 deficiency first (treating folate alone in B12 deficiency may precipitate subacute combined degeneration of the cord) |
| Vitamin C deficiency (scurvy) [1] | Spongy, red, swollen and irregular gums that bleed easily [1] | Vitamin C 250mg QDS until 4g given then 100mg daily maintenance |
| Drug | Indication | Mechanism | Key Contraindications / Cautions |
|---|---|---|---|
| Acyclovir | HSV, VZV | Guanosine analogue; requires viral thymidine kinase for activation → inhibits viral DNA polymerase | Renal impairment (dose adjust); adequate hydration (crystalluria risk) |
| Valacyclovir | HSV, VZV (prodrug of acyclovir) | L-valyl ester of acyclovir; better oral bioavailability | Same as acyclovir; thrombotic microangiopathy in immunocompromised at high doses |
| Nystatin | Oral candidiasis | Polyene; binds ergosterol → fungal membrane disruption | Very few (not absorbed systemically); unpleasant taste |
| Fluconazole | Moderate–severe oral candidiasis | Triazole; inhibits CYP51 (lanosterol 14α-demethylase) → blocks ergosterol synthesis | Hepatotoxicity; QT prolongation; multiple drug interactions (CYP3A4/2C9 inhibitor); pregnancy (teratogenic) |
| Carbamazepine | Trigeminal neuralgia | Voltage-gated sodium channel blocker → stabilises neuronal membrane | Mandatory HLA-B15:02 screening in HK Chinese before prescribing* [10]; hyponatraemia (SIADH); aplastic anaemia; hepatotoxicity; enzyme inducer |
| Prednisolone | Pemphigus, EM, Behçet (systemic), severe RAS | Glucocorticoid → genomic suppression of pro-inflammatory transcription factors (NFκB) | Long-term side effects: osteoporosis, diabetes, adrenal suppression, cataracts, infections, cushingoid features |
| Rituximab | Pemphigus vulgaris (refractory or upfront) | Anti-CD20 monoclonal Ab → B-cell depletion → reduced autoantibody production | Hepatitis B reactivation (mandatory HBsAg/anti-HBc screen); PML risk (very rare); infusion reactions; hypogammaglobulinaemia |
| Colchicine | Behçet disease, recurrent aphthous ulcers | Disrupts microtubule polymerisation → inhibits neutrophil chemotaxis and NLRP3 inflammasome | GI side effects (diarrhoea); narrow therapeutic index; dose reduction in renal/hepatic impairment; fatal in overdose |
| Thalidomide | Resistant oral/genital ulcers (Behçet) | Immunomodulatory (TNF-α modulation, anti-angiogenic, T-cell co-stimulation modulation) | Absolute contraindication in pregnancy (teratogenic — phocomelia); peripheral neuropathy; VTE risk; mandatory pregnancy prevention programme |
| Metronidazole | ANUG, anaerobic dental infections | Prodrug; reduced by anaerobic bacteria → toxic metabolites damage bacterial DNA | Disulfiram reaction with alcohol; peripheral neuropathy with prolonged use; metallic taste |
| Amoxicillin | Dental infections, GAS pharyngitis, IE prophylaxis | β-lactam; inhibits transpeptidase (PBP) → disrupts bacterial cell wall synthesis | Penicillin allergy; maculopapular rash in EBV infection (non-allergic but avoid in suspected EBV) |
| Clindamycin | Dental infections (penicillin-allergic), IE prophylaxis | Binds 50S ribosomal subunit → inhibits bacterial protein synthesis | C. difficile colitis (most important); hepatotoxicity |
| Cisplatin | Concurrent chemoradiation for advanced H&N SCC | Platinum cross-links DNA → prevents replication/transcription → apoptosis | Nephrotoxicity (mandatory aggressive hydration); ototoxicity; peripheral neuropathy; severe nausea |
These apply across almost all oral/dental conditions and are frequently under-emphasised:
- Smoking cessation — reduces risk of oral cancer, periodontal disease, poor wound healing, candidiasis recurrence. This is the single most impactful lifestyle intervention.
- Alcohol moderation — synergistic carcinogen with tobacco
- Betel nut cessation — prevents oral submucous fibrosis (HK/Southern China relevance)
- Oral hygiene — twice daily brushing, flossing, regular dental check-ups (every 6–12 months)
- HPV vaccination — the 9-valent HPV vaccine (Gardasil 9) covers HPV 16/18 → reduces risk of HPV-related oropharyngeal SCC. Gender-neutral vaccination is now recommended in many countries.
- Sun protection for lip — sunscreen lip balm for outdoor workers (prevents lip SCC)
- Dietary modification — reduce salt-preserved foods (HK: salted fish → NPC risk [4]); balanced diet with adequate vitamins and minerals
High Yield Summary
Emergency: Airway first (Ludwig's angina, epiglottitis — do NOT examine throat if epiglottitis suspected [14]). SJS/TEN → withdraw causative drug immediately + ICU/burns unit care.
Dental infections: Source control (drainage/extraction) is definitive; antibiotics are adjunctive. First-line: amoxicillin; penicillin-allergic: clindamycin or metronidazole.
HSV: Acyclovir initiated ≤ 48h [5]; topical if mild and immunocompetent, systemic if severe/immunocompromised. Foscarnet for acyclovir resistance [5].
Pemphigus vulgaris: Systemic corticosteroid (1–1.5mg/kg/day prednisolone) as mainstay [7]; rituximab + prednisone gaining popularity upfront [7]; steroid-sparing agents (azathioprine preferred) [7].
Behçet: Topical steroid for oral ulcers; colchicine for prevention; thalidomide for resistant ulcers; systemic immunosuppressants for uveitis/neuro [8].
Oral cancer (early): Surgery preferred; selective neck dissection for tongue cancer > 3mm [3]; post-op RT if thickness > 4mm or LVI/PNI [3].
Oral cancer (advanced): Combined modality — surgery + post-op chemoRT; or definitive chemoRT if unresectable [3]; TORS = less morbid for oropharyngeal tumours [3].
IE prophylaxis: Amoxicillin 2g PO 1h before dental procedures in high-risk patients (prosthetic valve, prior IE, cyanotic CHD) [23]. Clindamycin 600mg if penicillin-allergic [23].
Carbamazepine for TN: Mandatory HLA-B15:02 screening in HK Chinese (13% prevalence)* [10].
Active Recall - Management of Oral/Dental Pain and Lesions
References
[1] Senior notes: Ryan Ho GI.pdf (p10) and Ryan Ho Fundamentals.pdf (p62) — Glossitis, gum hypertrophy, aphthous ulcers, angular stomatitis, scurvy, pigmentation, nutritional deficiencies [3] Senior notes: felixlai.md (sections 350, 351, 353, 354, 355, 372) — Oral and oropharyngeal cancer management: site-specific surgery, neck dissection types, reconstruction, adjuvant RT/chemoRT, TORS, stage-based approach, CO2 laser for premalignant lesions [4] Senior notes: felixlai.md (section 357) — NPC risk factors (salted fish) [5] Senior notes: Ryan Ho Rheumatology.pdf (p137) — HSV treatment: acyclovir, foscarnet [6] Senior notes: Ryan Ho Rheumatology.pdf (p143) — Lichen planus: often asymptomatic oral involvement [7] Senior notes: Ryan Ho Rheumatology.pdf (p153) — Pemphigus vulgaris management: systemic corticosteroids, rituximab, steroid-sparing agents, monitoring [8] Senior notes: Ryan Ho Rheumatology.pdf (p98) — Behçet disease management: topical steroid, colchicine, thalidomide, systemic immunosuppressants [10] Senior notes: Ryan Ho Rheumatology.pdf (p149) and Ryan Ho Opthalmology.pdf (p133) — SJS/TEN management, HLA-B15:02 and HLA-B58:01 pharmacogenomics, amniotic membrane transplantation [11] Senior notes: Ryan Ho Rheumatology.pdf (p131) — Erythema multiforme management and prevention [12] Senior notes: felixlai.md (section 321) — Suppurative parotitis: S. aureus [14] Lecture slides: murtagh merge.pdf (p90, p92) — Epiglottitis: do not examine throat; sore throat diagnostic tips [17] Senior notes: Ryan Ho Respiratory.pdf (p54) — Bacterial rhinosinusitis treatment [18] Senior notes: Ryan Ho Respiratory.pdf (p51) — GAS pharyngitis: Centor criteria and treatment [21] Senior notes: Ryan Ho Rheumatology.pdf (p150) — SJS/TEN SCORTEN prognostication [22] Senior notes: Ryan Ho Urogenital.pdf (p247) — HSV antiviral dosing regimens, prophylaxis indications [23] Senior notes: Ryan Ho Cardiology.pdf (p150–151) — IE prophylaxis: indications, high-risk patients, at-risk procedures, antibiotic regimens
Complications of Oral/Dental Pain and Lesions
Complications arise when oral/dental conditions progress beyond the initial pathology — either because the disease itself is inherently aggressive (malignancy, deep space infection), because treatment carries iatrogenic risks (surgery, radiotherapy, immunosuppression), or because an apparently benign condition is not recognised or treated in time. This section covers complications organised by the category of the primary condition, with the pathophysiological "why" explained from first principles.
1. Complications of Dental Infections
The fundamental problem with dental infections is that bacteria reside in a confined, avascular space (the necrotic pulp chamber or periodontal pocket). Once infection breaches the periapical region, it enters the soft tissue planes of the head and neck — and the anatomy dictates where it spreads.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Periapical abscess | Pulp necrosis → bacteria enter periapical tissue → walled-off abscess | Throbbing toothache, localised swelling over alveolus, tender to percussion, may develop draining sinus (fistula) on gingiva or skin |
| Facial cellulitis | Abscess breaches periosteum → spreads into overlying facial soft tissue | Diffuse facial swelling, erythema, warmth, tenderness; no fluctuance (cellulitis = not yet localised) |
| Ludwig's angina | Bilateral infection of sublingual + submandibular spaces (classically from lower molar infection breaching the lingual cortex of the mandible below the mylohyoid line) | Floor of mouth elevation, "woody" induration of submandibular region, drooling, dysphagia, stridor — airway emergency. Why bilateral? The sublingual spaces communicate freely across the midline |
| Parapharyngeal / retropharyngeal abscess | Spread along fascial planes from submandibular or peritonsillar space into the parapharyngeal or retropharyngeal space | Trismus, torticollis, "hot potato" voice, neck swelling, dysphagia. Retropharyngeal abscess may cause posterior pharyngeal wall bulging on lateral neck X-ray |
| Mediastinitis | Descending necrotising infection tracking along the deep cervical fascial planes into the superior mediastinum | Chest pain, sepsis, high mortality (40–50%). This is the most feared complication — the "danger space" (between alar and prevertebral fascia) extends continuously from the skull base to the posterior mediastinum at the level of the diaphragm |
| Cavernous sinus thrombosis | Infection from upper face (particularly nasolabial/"danger triangle of the face") or maxillary teeth spreads via valveless facial veins → ophthalmic veins → cavernous sinus | Headache, proptosis, chemosis, ophthalmoplegia (CN III/IV/VI within cavernous sinus), V1/V2 sensory loss, high fever, rapid deterioration. Bilateral involvement is classic |
| Osteomyelitis of the mandible/maxilla | Chronic or severe dental infection → spread to medullary bone | Persistent pain, swelling, fistula, sequestrum formation on imaging; more common in mandible (less vascular than maxilla) |
The 'Danger Triangle of the Face'
The area bounded by the bridge of the nose and the corners of the mouth is drained by the anterior facial vein, which communicates via valveless veins with the pterygoid venous plexus and cavernous sinus. Squeezing a "pimple" or failing to treat an infection in this zone can lead to cavernous sinus thrombosis — a life-threatening intracranial complication. This is why mid-face infections demand aggressive antibiotic treatment.
| Complication | Mechanism |
|---|---|
| Bacteraemia / Sepsis | Dental infections (especially extraction, scaling, or spontaneous bacteraemia from periodontitis) allow oral bacteria (viridans streptococci, anaerobes) to enter the bloodstream → systemic inflammatory response → sepsis if uncontrolled |
| Infective endocarditis | Transient bacteraemia following dental procedures → bacteria adhere to damaged/prosthetic endocardium → vegetations [23]. This is precisely why IE prophylaxis exists for high-risk patients: prosthetic valve, previous IE, cyanotic CHD [23] |
- Tooth loss — progressive alveolar bone destruction → loosening → eventual loss of teeth. Periodontitis is the leading cause of tooth loss in adults
- Systemic inflammatory burden — chronic periodontitis is associated with increased cardiovascular risk, poorer glycaemic control in diabetes, and adverse pregnancy outcomes (preterm birth). The proposed mechanism is chronic low-grade bacteraemia and systemic inflammation from the periodontal pocket
- Aspiration pneumonia — oral bacteria from periodontal disease can be aspirated into the lower respiratory tract, particularly in elderly, debilitated, or neurologically impaired patients
2. Complications of Oral Infections
Complications of HSV [5]:
- Herpes keratitis: pain, blurring of vision [5] — HSV replicates in corneal epithelium → dendritic ulcer → if untreated, progresses to stromal keratitis → corneal scarring → one of the commonest causes for corneal transplant
- CNS involvement: meningitis (usually HSV-2), encephalitis (usually HSV-1) [5] — HSV-1 encephalitis has a predilection for the temporal lobes; carries high mortality if untreated (70%)
- Systemic involvement (if immunocompromised): oesophagitis, hepatitis, pneumonitis, encephalitis, retinitis [5]
- Other manifestations: erythema multiforme, eczema herpeticum [5]
- Erythema multiforme: HSV is the most common trigger (90% of EM cases) [11]; the immune response against HSV-infected keratinocytes causes collateral damage to normal skin
- Eczema herpeticum: widespread HSV infection in patients with pre-existing atopic dermatitis — can be life-threatening
| Complication | Timing | Mechanism |
|---|---|---|
| Peritonsillar abscess (quinsy) | During or shortly after acute infection | Direct spread of infection through tonsillar capsule into peritonsillar space → abscess collection between capsule and pharyngeal constrictor muscle. Presents with severe unilateral throat pain, trismus, "hot potato" voice, uvular deviation |
| Rheumatic fever | 2–4 weeks after untreated GAS pharyngitis | Molecular mimicry: antibodies against GAS M protein cross-react with cardiac myosin, valvular glycoproteins, and neuronal tissue → immune-mediated inflammation of heart (carditis), joints (migratory polyarthritis), CNS (Sydenham's chorea), skin (erythema marginatum, subcutaneous nodules) |
| Post-streptococcal glomerulonephritis | 1–3 weeks after pharyngitis or skin infection | Immune complex deposition in glomerular basement membrane → complement activation → glomerular inflammation |
| Scarlet fever | During acute GAS infection | Erythrogenic toxin (streptococcal pyrogenic exotoxin) → diffuse erythematous "sandpaper" rash with circumoral pallor, "strawberry tongue", Pastia's lines |
- Airway obstruction — the abscess pushes the tonsil medially and inferiorly, narrowing the oropharyngeal airway
- Aspiration — spontaneous rupture of abscess → pus drains into the airway
- Lemierre syndrome — septic thrombophlebitis of the internal jugular vein, classically caused by Fusobacterium necrophorum. Complicates pharyngeal infection → septic emboli to lungs (cavitating pneumonia), joints, liver. Presents as persistent fever + neck swelling/tenderness after pharyngitis ("postanginal sepsis")
3. Complications of Autoimmune / Vesiculobullous Oral Diseases
- Poor nutrition and weight loss — oral pain exacerbated by chewing or swallowing [7] → patients avoid eating → malnutrition, dehydration, muscle wasting
- Secondary infection — denuded mucosal and skin surfaces are a portal of entry for bacteria → cellulitis, sepsis. This is the most common cause of death in severe pemphigus
- Complications of immunosuppressive treatment — long-term systemic steroids cause osteoporosis, diabetes, cataracts, opportunistic infections, avascular necrosis. Rituximab carries risks of hepatitis B reactivation, progressive multifocal leukoencephalopathy (PML), hypogammaglobulinaemia. Azathioprine causes myelosuppression, hepatotoxicity
- Oesophageal involvement — pemphigus can extend to the oesophageal mucosa → painful dysphagia, oesophageal stricture
SJS/TEN complications [10][21]:
Acute complications:
- Acute skin failure: dehydration, electrolyte imbalance, hypovolaemic shock, hypercatabolic state, multi-organ failure [21] — the denuded skin loses its barrier function (just like a burn), leading to massive transepidermal fluid loss
- Infections: 27% bacteremia; sepsis and septic shock as the main cause of death [21]
- Most commonly S. aureus, P. aeruginosa, Enterobacteriaceae [21]
- Pulmonary: pneumonia, interstitial pneumonitis, acute respiratory failure (~25%) [21] — bronchial epithelial sloughing can cause airway obstruction and pseudomembrane formation
- GI: due to epithelial necrosis of oesophagus, small bowel, colon (uncommon) [21]
Late ocular complications (60%) [10]:
- Symblepharon: adhesion of palpebral and bulbar conjunctivae — complicates conjunctival ulceration in acute phase; can lead to dry eye due to disruption of tear film dynamics [10]
- Conjunctival scarring: may cause chronic microtrauma to cornea [10]
- Ankyloblepharon: fusion of eyelid margins [10]
- Conjunctivalisation of cornea due to loss of limbal stem cells → conjunctiva grows over cornea [10]
- Corneal neovascularisation [10]
Late mucosal sequelae:
- Urogenital: vaginal adhesion, labial stenosis [21] (from scarring of genital erosions)
- Oral: mucosal scarring, sicca-like symptoms
- Oesophageal stricture (rare but disabling)
Prognostication: SCORTEN scoring system [21]:
- Factors (1 point each): age > 40y, HR > 120, cancer/haematologic malignancy, BSA > 10%, serum urea > 10mmol/L, HCO₃⁻ > 20mmol/L, glucose > 14mmol/L [21]
- Mortality: 3.2% (0–1), 12.1% (2), 35.8% (3), 58.3% (4), 90% (5) [21]
SJS/TEN — Ocular Complications Are the Most Disabling Long-Term Sequelae
Even after the skin has healed, 60% of SJS/TEN patients have late ocular complications [10]. Symblepharon, corneal scarring, and limbal stem cell loss can cause progressive visual impairment and even blindness. This is why early ophthalmology involvement and amniotic membrane transplantation [10] in the acute phase are so critical — they reduce the severity of long-term scarring.
Complications reflect the systemic nature of this vasculitis [8]:
- Ocular (25–75%): bilateral panuveitis (± hypopyon), retinal vasculitis, optic neuritis [8] — recurrent uveitis can lead to blindness if inadequately treated. Behçet disease is one of the few conditions that causes hypopyon uveitis
- Vascular disease: VTE common and occurs early (53%) [8]; arterial aneurysms (especially pulmonary artery — risk of fatal haemoptysis)
- Neurological (< 10%) [8]: parenchymal CNS disease (meningoencephalitis) or cerebral venous sinus thrombosis
- Relapsing/remitting course, increased severity in young male Asians [8]
The primary complication is malignant transformation — this is why these lesions matter.
| Premalignant Lesion | Transformation Rate | Highest Risk Subtype/Location |
|---|---|---|
| Leukoplakia [1] | ~1–5% per year overall | Floor of mouth has highest risk [3]; speckled leukoplakia has the highest rate of malignant transformation [3] |
| Erythroplakia [3] | Up to 50% harbour invasive SCC or CIS at biopsy | Any location; the red colour IS the danger sign (thin dysplastic epithelium) |
| Oral lichen planus | ~1% over 5 years | Erosive/atrophic forms higher risk than reticular |
| Oral submucous fibrosis | 7–13% | Progressive fibrosis → trismus → limits surgical access if SCC develops |
| Plummer-Vinson syndrome [3] | Well-established relationship with the development of oral cancer [3] | Postcricoid region; oral cavity |
5. Complications of Oral Malignancy
Complications of oral SCC arise from the disease itself, its treatment, or both.
| Complication | Mechanism | Clinical Significance |
|---|---|---|
| Local tissue destruction | Tumour invades adjacent structures — bone, muscle, nerves, blood vessels | Trismus (pterygoid muscle involvement, may indicate skull base spread) [3]; tongue deviation/fasciculation/atrophy (hypoglossal nerve invasion) [3]; paraesthesia (lingual/mental nerve invasion) [3]; pathological fracture of mandible |
| Regional lymph node metastasis | Oral SCC spreads via lymphatics to cervical nodes | Present at diagnosis in a high proportion of oropharyngeal cancers [3]; enlarging neck mass; may compromise carotid artery (carotid blowout syndrome — catastrophic haemorrhage) |
| Distant metastasis | Haematogenous spread to lungs, liver, bone | Less common than regional spread for oral cavity SCC; more common for NPC — bone (75%), liver, lung, distant LN [4] |
| Airway obstruction | Large oropharyngeal or tongue base tumours obstruct the airway | May require emergency tracheostomy |
| Malnutrition and cachexia | Dysphagia + odynophagia → reduced oral intake; cancer-related cachexia (cytokine-mediated wasting) | Weight loss is a major negative prognostic factor in H&N cancer |
| Aspiration pneumonia | Impaired swallowing (tumour bulk, nerve involvement) → aspiration of food/secretions | Common cause of morbidity in advanced H&N cancer |
| Complication | Mechanism | Prevention/Management |
|---|---|---|
| Impaired articulation [3] | Resection of large tumours of tongue leading to decreased lingual contact with palate, lip and teeth [3] | Reconstruction using soft pliable fasciocutaneous free flaps for intraoral bulk and preservation of tongue mobility [3]; prosthetic augmentation [3]; speech therapy |
| Impaired swallowing [3] | Loss of tongue bulk and mobility; palatal defects; pharyngeal resection | Dental prosthesis for through-and-through palatal defects [3]; swallowing rehabilitation; may require gastrostomy for nutritional support |
| Facial nerve injury (parotid surgery) [24] | The facial nerve (CN VII) runs through the parotid gland, dividing it into superficial and deep lobes. Parotid surgery risks damage to any of its five branches | Intraoperative nerve monitoring; meticulous surgical technique; temporary weakness (neuropraxia) common, permanent damage uncommon with experienced surgeon |
| Frey syndrome [24] | Characterised by sweating and flushing of facial skin over parotid bed and neck during mastication [24]. Results from aberrant regeneration of cut parasympathetic fibres between the otic ganglion and salivary tissues which leads to innervation of sweat glands and subcutaneous vessels [24] | Botulinum toxin injection; antiperspirant application; interposition of tissue flap (e.g., SCM muscle flap or dermis fat graft) between parotid bed and skin |
| Shoulder dysfunction (radical neck dissection) | Radical neck dissection removes the spinal accessory nerve (CN XI) [3] → denervation of trapezius → shoulder drop, winged scapula, inability to abduct shoulder above 90° | Modified radical neck dissection preserves CN XI when possible; physiotherapy post-op |
| Flap failure | Vascular compromise (thrombosis of anastomosed vessels) of free flap reconstruction | Close post-operative monitoring of flap (colour, temperature, capillary refill, Doppler); early return to theatre if compromise detected |
| Orocutaneous fistula | Breakdown of surgical wound → communication between oral cavity and skin | Wound care; may require secondary surgical closure; risk increased with prior radiation |
Radiotherapy is a mainstay treatment for H&N cancer but carries significant acute and long-term side effects, many of which directly affect the oral cavity.
| Complication | Timing | Mechanism | Clinical Features |
|---|---|---|---|
| Oral mucositis | Acute (during RT, peaks week 3–5) | Radiation damages rapidly dividing mucosal epithelial cells → ulceration, inflammation | Severe pain, difficulty eating/drinking → malnutrition, dehydration; may require treatment breaks, opioid analgesia, NG/PEG feeding |
| Radiation dermatitis | Acute | Radiation damages skin epithelium and dermis | Erythema → dry desquamation → moist desquamation in severe cases |
| Xerostomia | Acute onset, often permanent | Radiation destroys salivary gland acinar cells (serous acini are exquisitely radiosensitive) → irreversible gland atrophy | Dry mouth → impaired taste → difficulty chewing/swallowing → dramatically increased dental caries risk → poor quality of life. This is one of the most distressing long-term sequelae |
| Radiation caries | Late (months–years) | Xerostomia → loss of salivary buffering, antimicrobial and remineralising functions → rampant dental decay, characteristically affecting the cervical (neck) region of teeth and incisal edges | Rapidly progressive, diffuse caries pattern unlike typical caries; requires aggressive preventive dentistry (fluoride trays, frequent dental review) |
| Osteoradionecrosis (ORN) | Late (months–years) | Radiation damages blood vessels in bone → hypovascular, hypocellular, hypoxic tissue → bone cannot heal after trauma (e.g., tooth extraction) → necrosis, secondary infection | Exposed necrotic mandible, pain, fistula, pathological fracture. Prevention: comprehensive dental assessment BEFORE RT → extract all teeth with poor prognosis before RT begins (and wait ≥ 2 weeks for healing before starting RT). Why mandible > maxilla? The mandible has a poorer blood supply (single inferior alveolar artery) compared to the maxilla (rich collateral supply from multiple branches of the maxillary artery) |
| Trismus (radiation-induced fibrosis) | Late | Fibrosis of masticatory muscles (masseter, medial/lateral pterygoids) and TMJ capsule | Progressive limitation of mouth opening; interferes with eating, dental care, oral hygiene. Prevention: jaw exercises during and after RT |
| Dysphagia (radiation-related) | Acute and late | Acute: mucositis → pain on swallowing. Late: fibrosis of pharyngeal constrictors → impaired peristalsis → chronic dysphagia | May require long-term gastrostomy; aspiration risk |
| Hypothyroidism | Late (months–years) | Radiation to neck includes the thyroid gland → thyroid follicular cell damage → insufficient hormone production | Screen with TSH every 6–12 months post-RT; treat with levothyroxine if hypothyroid |
| Second primary malignancy | Very late (years–decades) | Radiation-induced DNA damage in surrounding tissues → field cancerisation + radiation carcinogenesis | Increased risk of SCC, sarcoma, or thyroid cancer in the irradiated field |
Pre-RT Dental Assessment Is Mandatory
All patients about to undergo head and neck radiotherapy MUST have a comprehensive dental assessment beforehand. Teeth with a hopeless prognosis are extracted BEFORE RT begins, and fluoride trays are fitted. This prevents the devastating complication of osteoradionecrosis, which can occur if a tooth in an irradiated field requires extraction later. ORN is extremely difficult to treat once established.
- Oral mucositis — cytotoxic agents (cisplatin, 5-FU, methotrexate) damage rapidly dividing oral mucosal cells → painful ulceration, secondary infection, poor nutrition. Ice chips during infusion (cryotherapy) can reduce mucositis by causing local vasoconstriction
- Neutropenic sepsis — chemotherapy-induced myelosuppression → neutropenia → oral bacteria gain systemic access via mucosal breaks → sepsis
- Candidiasis — immunosuppression from chemotherapy predisposes to oral candidiasis
6. Complications of Salivary Gland Pathology
- Recurrent infections — obstructed ducts → stasis → repeated bacterial sialadenitis → progressive gland destruction → chronically damaged, fibrotic gland
- Abscess formation — untreated sialadenitis → parotid or submandibular abscess requiring surgical drainage
- Ranula — obstruction of sublingual gland duct → mucous extravasation → floor of mouth swelling. A "plunging ranula" extends through the mylohyoid muscle into the neck
- Facial nerve injury [24] — see Section 5.2 above
- Frey syndrome (gustatory sweating) [24] — aberrant regeneration of cut parasympathetic fibres → innervation of sweat glands and subcutaneous vessels [24]
- Salivary fistula — leakage of saliva from the surgical wound; usually self-limiting
- First bite syndrome — intense pain in the parotid region with the first bite of each meal, due to loss of sympathetic innervation to the parotid; parasympathetic stimulation during eating causes unopposed contraction of myoepithelial cells
- Aesthetic deformity — concavity in the parotid region after superficial parotidectomy
Endotracheal intubation, commonly performed in the context of H&N surgery or any general anaesthesia, can damage oral structures [25]:
Complications of intubation [25]:
- Dental damage — the most common medicolegal claim related to anaesthesia. The laryngoscope blade can chip or avulse upper incisors, particularly if they are already loose, crowned, or have periodontitis
- Lacerations of lips, gums, tongue, pharynx, oesophagus [25]
- Laryngeal trauma [25] — arytenoid dislocation, vocal cord haematoma
- Oesophageal or endobronchial intubation [25]
| Primary Condition | Key Complications |
|---|---|
| Dental caries / abscess | Periapical abscess → cellulitis → Ludwig's angina → mediastinitis → sepsis; cavernous sinus thrombosis; osteomyelitis; IE (in susceptible patients) |
| Periodontal disease | Tooth loss; aspiration pneumonia; cardiovascular association |
| HSV | Herpes keratitis, encephalitis, EM, eczema herpeticum |
| GAS pharyngitis | Quinsy, rheumatic fever, PSGN, scarlet fever, Lemierre syndrome |
| Pemphigus vulgaris | Malnutrition, secondary infection/sepsis, treatment complications (steroid/immunosuppressant side effects) |
| SJS/TEN | Acute skin failure, sepsis, pulmonary complications, late ocular scarring (symblepharon, ankyloblepharon, corneal opacification), urogenital strictures |
| EM | Poor intake, ocular damage, recurrence |
| Behçet disease | Blindness (panuveitis), VTE/arterial aneurysm, neuro-Behçet |
| Leukoplakia / erythroplakia | Malignant transformation to SCC |
| Oral SCC | Local destruction (nerve invasion, bone invasion), LN metastasis, distant metastasis; treatment-related: impaired speech/swallowing, ORN, xerostomia, radiation caries, hypothyroidism |
| Salivary gland disease | Recurrent infection, abscess, facial nerve injury (post-surgery), Frey syndrome |
| Intubation | Dental damage, soft tissue laceration, laryngeal trauma |
High Yield Summary
Dental infection spread: Follows fascial planes — periapical abscess → cellulitis → Ludwig's angina (airway emergency) → mediastinitis (40–50% mortality). The "danger triangle of the face" connects mid-face infections to the cavernous sinus via valveless veins.
HSV complications: Herpes keratitis (commonest cause for corneal transplant), encephalitis (HSV-1, temporal lobe), erythema multiforme (most common trigger) [5].
GAS complications: Rheumatic fever (molecular mimicry — 2–4 weeks post-infection) and PSGN (immune complex — 1–3 weeks). Peritonsillar abscess → Lemierre syndrome (septic IJV thrombophlebitis).
SJS/TEN: Acute skin failure → sepsis (27% bacteraemia, main cause of death) [21]. Late ocular complications in 60% — symblepharon, ankyloblepharon, corneal neovascularisation [10]. SCORTEN predicts mortality [21].
Pemphigus: Malnutrition from oral pain; secondary sepsis from denuded mucosa; steroid/immunosuppressant toxicity.
Oral cancer treatment: Key surgical complications = impaired speech/swallowing (glossectomy), shoulder drop (radical neck dissection — CN XI sacrifice), Frey syndrome (parotidectomy). Key RT complications = xerostomia (irreversible), osteoradionecrosis (mandible — prevent with pre-RT dental assessment), radiation caries, trismus, hypothyroidism.
Premalignant lesion risk: Speckled leukoplakia > erythroplakia > floor-of-mouth leukoplakia [3]. Oral lichen planus ~1% over 5 years. Regular surveillance is mandatory.
Active Recall - Complications of Oral/Dental Pain and Lesions
References
[1] Senior notes: Ryan Ho GI.pdf (p10) and Ryan Ho Fundamentals.pdf (p62) — Leukoplakia as premalignant condition [3] Senior notes: felixlai.md (sections 351, 354, 355, 370) — Oral SCC complications: impaired articulation post-glossectomy, tongue nerve invasion, trismus, reconstruction needs; premalignant lesion transformation rates [4] Senior notes: felixlai.md (section 357) — NPC distant metastasis sites [5] Senior notes: Ryan Ho Rheumatology.pdf (p137) — HSV complications: herpes keratitis, CNS involvement, systemic involvement, EM, eczema herpeticum [7] Senior notes: Ryan Ho Rheumatology.pdf (p152–153) — Pemphigus vulgaris: oral pain leading to poor nutrition and weight loss [8] Senior notes: Ryan Ho Rheumatology.pdf (p98) — Behçet disease: ocular complications, vascular disease, neurological involvement, prognosis [10] Senior notes: Ryan Ho Opthalmology.pdf (p133) — SJS/TEN late ocular complications: symblepharon, ankyloblepharon, conjunctivalisation, corneal neovascularisation, amniotic membrane transplantation [11] Senior notes: Ryan Ho Rheumatology.pdf (p130–131) — EM complications: poor intake, ocular involvement [21] Senior notes: Ryan Ho Rheumatology.pdf (p149–150) — SJS/TEN acute complications: skin failure, sepsis, pulmonary involvement, GI involvement; SCORTEN scoring [23] Senior notes: Ryan Ho Cardiology.pdf (p150–151) — IE from dental procedures: rationale for prophylaxis [24] Senior notes: felixlai.md (section 338) — Post-parotidectomy complications: facial nerve injury, Frey syndrome [25] Senior notes: Ryan Ho Critical Care.pdf (p10) — Complications of intubation: dental damage, lacerations, laryngeal trauma
High Yield Summary
Definition: Oral/dental pain and lesions encompass a broad spectrum from benign (aphthous ulcers, dental caries) to life-threatening (oral SCC, Ludwig's angina, SJS/TEN).
Epidemiology (HK Focus): NPC is endemic in Southern China (EBV-driven); oral SCC driven by the 5Ss (Smoking, Spirits, Sharp teeth, Sex/HPV, Spicy food); betel nut chewing is a major regional risk factor.
Key Anatomy: Oral cavity ends at circumvallate papillae/hard–soft palate junction. Submandibular gland → most common site for sialolithiasis (long duct, against gravity, alkaline mucin-rich saliva). Lingual nerve → tongue sensation; hypoglossal nerve → tongue movement; mental nerve → lip/chin sensation.
Classification: Odontogenic vs Non-odontogenic; Ulcerative vs White vs Red vs Vesiculobullous vs Pigmented vs Swelling.
Premalignant lesions: Speckled leukoplakia (highest transformation rate) > Erythroplakia > Leukoplakia (floor of mouth highest risk). Plummer-Vinson syndrome established association with oral cancer.
Red flags for malignancy: Non-healing ulcer > 3 weeks, indurated/rolled edges, fixation to deeper structures, lymphadenopathy, cranial nerve involvement (paraesthesia, tongue deviation), trismus, weight loss.
Critical "must-knows": HLA-B15:02 must be checked before prescribing carbamazepine in HK Chinese (13% prevalence → SJS/TEN risk)*. Pemphigus vulgaris: oral erosions are often the first manifestation (anti-desmoglein 3). Aphthous ulcers = most common oral ulcer; usually benign but exclude Crohn's/coeliac if recurrent. Leukoplakia = diagnosis of exclusion (5S causes); biopsy always needed.
High Yield Summary
Approach: Is it odontogenic or non-odontogenic? What is the morphology (ulcer / white / red / vesiculobullous / pigmented / swelling / no lesion)? Is it dangerous?
Most common oral ulcer: Aphthous ulcer [1]. Most dangerous mimic: Oral SCC — any ulcer > 3 weeks must be biopsied.
White patches: "Can it be scraped off?" → Yes = candidiasis; No = leukoplakia, lichen planus, hairy leukoplakia → biopsy.
Vesiculobullous with mucosal involvement: Pemphigus vulgaris (most, Nikolsky +ve), bullous pemphigoid (some), HSV, EM, SJS/TEN [7].
Pain without visible lesion: Trigeminal neuralgia, glossopharyngeal neuralgia, TMJ dysfunction, sinusitis, referred cardiac pain, burning mouth syndrome.
Murtagh's sore throat red flags: Cardiovascular (angina/MI), cancer of oropharynx/tongue, blood dyscrasias, epiglottitis, quinsy, HIV [14].
The cancer triad: Hoarseness + pain on swallowing + referred ear pain → pharyngeal cancer [14].
Oropharyngeal mass DDx: SCC (most common), minor salivary gland tumour (submucosal, tongue base/soft palate), lymphoma (tonsil/tongue base) [3].
Salivary gland DDx: Sialolithiasis (meal-related pain), sialadenitis (acute bacterial vs viral/mumps), Sjögren's (bilateral, sicca), sarcoidosis (bilateral, painless), tumour.
High Yield Summary
Algorithm: Triage airway first → Hx + systematic intraoral/extraoral exam → Odontogenic vs non-odontogenic → Morphological categorisation → Targeted investigations → Biopsy any suspicious/persistent (> 3 weeks) lesion.
Diagnostic Criteria to Know:
- Modified Centor criteria for GAS pharyngitis [18]: Fever + Exudates + Anterior LAD + No cough (± age adjustment). Score -1 to 1 = no Abx; 2-3 = swab first; 4-5 = empirical Abx.
- ISG criteria for Behçet disease [8]: Recurrent oral ulcers (≥ 3/yr) + ≥ 2 of genital ulcers/eye lesions/skin lesions/positive pathergy.
- ACR/EULAR Sjögren's [19]: ≥ 4 points from labial biopsy (3), anti-Ro (3), ocular staining (1), Schirmer (1), saliva flow (1).
Imaging Hierarchy for Oral Cancer:
- MRI = imaging modality of choice for oral/oropharyngeal cancer (soft tissue) [3].
- CT = best for subtle cortical bone invasion [3].
- MRI = best for medullary cavity invasion of mandible [3].
- Panendoscopy = mandatory to look for synchronous tumour (field cancerisation) [3].
Must-Know Lab Tests: FBE (leukaemia screen), Monospot (EBV), HSV PCR (from vesicular fluid, not serology), anti-desmoglein Ab (pemphigus), anti-Ro/La (Sjögren's), EBV DNA (NPC), HLA-B15:02* (before carbamazepine in HK Chinese) [10].
High Yield Summary
Emergency: Airway first (Ludwig's angina, epiglottitis — do NOT examine throat if epiglottitis suspected [14]). SJS/TEN → withdraw causative drug immediately + ICU/burns unit care.
Dental infections: Source control (drainage/extraction) is definitive; antibiotics are adjunctive. First-line: amoxicillin; penicillin-allergic: clindamycin or metronidazole.
HSV: Acyclovir initiated ≤ 48h [5]; topical if mild and immunocompetent, systemic if severe/immunocompromised. Foscarnet for acyclovir resistance [5].
Pemphigus vulgaris: Systemic corticosteroid (1–1.5mg/kg/day prednisolone) as mainstay [7]; rituximab + prednisone gaining popularity upfront [7]; steroid-sparing agents (azathioprine preferred) [7].
Behçet: Topical steroid for oral ulcers; colchicine for prevention; thalidomide for resistant ulcers; systemic immunosuppressants for uveitis/neuro [8].
Oral cancer (early): Surgery preferred; selective neck dissection for tongue cancer > 3mm [3]; post-op RT if thickness > 4mm or LVI/PNI [3].
Oral cancer (advanced): Combined modality — surgery + post-op chemoRT; or definitive chemoRT if unresectable [3]; TORS = less morbid for oropharyngeal tumours [3].
IE prophylaxis: Amoxicillin 2g PO 1h before dental procedures in high-risk patients (prosthetic valve, prior IE, cyanotic CHD) [23]. Clindamycin 600mg if penicillin-allergic [23].
Carbamazepine for TN: Mandatory HLA-B15:02 screening in HK Chinese (13% prevalence)* [10].
High Yield Summary
Dental infection spread: Follows fascial planes — periapical abscess → cellulitis → Ludwig's angina (airway emergency) → mediastinitis (40–50% mortality). The "danger triangle of the face" connects mid-face infections to the cavernous sinus via valveless veins.
HSV complications: Herpes keratitis (commonest cause for corneal transplant), encephalitis (HSV-1, temporal lobe), erythema multiforme (most common trigger) [5].
GAS complications: Rheumatic fever (molecular mimicry — 2–4 weeks post-infection) and PSGN (immune complex — 1–3 weeks). Peritonsillar abscess → Lemierre syndrome (septic IJV thrombophlebitis).
SJS/TEN: Acute skin failure → sepsis (27% bacteraemia, main cause of death) [21]. Late ocular complications in 60% — symblepharon, ankyloblepharon, corneal neovascularisation [10]. SCORTEN predicts mortality [21].
Pemphigus: Malnutrition from oral pain; secondary sepsis from denuded mucosa; steroid/immunosuppressant toxicity.
Oral cancer treatment: Key surgical complications = impaired speech/swallowing (glossectomy), shoulder drop (radical neck dissection — CN XI sacrifice), Frey syndrome (parotidectomy). Key RT complications = xerostomia (irreversible), osteoradionecrosis (mandible — prevent with pre-RT dental assessment), radiation caries, trismus, hypothyroidism.
Premalignant lesion risk: Speckled leukoplakia > erythroplakia > floor-of-mouth leukoplakia [3]. Oral lichen planus ~1% over 5 years. Regular surveillance is mandatory.
Numbness, Tingling
Numbness and tingling (paresthesia) are abnormal sensations resulting from dysfunction or irritation of peripheral nerves, nerve roots, or central sensory pathways, often indicating neuropathy, compression, or ischemia.
Palpitations
Palpitations are the subjective awareness of one's own heartbeat, often perceived as rapid, irregular, or forceful cardiac contractions.