Oral Immunopathology Basics
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Direct answer
Why does lichen planus kill basal keratinocytes while pemphigus tears the epithelium apart higher up? Immunology holds both answers, and Gell and Coombs organize them. Type I IgE-mediated mast cell degranulation explains the oral swelling of allergy; type II cytotoxic antibodies explain pemphigus and pemphigoid, whose targets sit at different epithelial levels; type III immune-complex disease underlies lupus erythematosus; and type IV delayed T-cell attack explains lichen planus, tuberculin reactions, contact allergy to dental materials and graft rejection. To these the BDS student adds the autoimmune antibody panels of Sjögren and lupus, the HIV-related oral diseases that flag immune collapse, and the immunosuppressed transplant patient whose drugs reshape the gingiva.
What you must remember
- Type I (immediate, IgE, mast cells): urticaria and angioedema of the lip, allergic stomatitis, anaphylaxis; note that hereditary angioedema mimics allergy but runs on bradykinin via C1-esterase-inhibitor deficiency and does not respond to antihistamines alone.
- Type II (cytotoxic, IgG with complement): pemphigus vulgaris (anti-desmoglein 3, suprabasal split) and mucous membrane pemphigoid (anti-BP180/laminin 332, subepithelial split); also autoimmune haemolysis.
- Type III (immune complex): systemic lupus erythematosus with oral ulceration, malar rash, photosensitivity, anti-nuclear and anti-dsDNA antibodies; the facial discoid lesions of chronic cutaneous lupus involve the lower lip vermilion.
- Type IV (delayed, cell-mediated): oral lichen planus (CD8 attack on basal keratinocytes), the tuberculin test, contact allergic reactions to dental metals and restorative materials, and transplant rejection.
- Local anaesthetic "allergy" is overwhelmingly vasovagal syncope, intravascular injection or sulphite sensitivity — true lignocaine IgE allergy is rare, and the accusation deserves testing rather than acceptance.
- HIV-related oral markers: erythematous and pseudomembranous candidiasis, oral hairy leukoplakia (EBV-driven, lateral tongue border), linear gingival erythema, necrotizing ulcerative periodontitis, Kaposi sarcoma (HHV-8) and major aphthae; national NACO guidelines guide testing and referral.
- Ciclosporin and other transplant immunosuppressants produce gingival overgrowth and herpesvirus reactivation; chronic graft-versus-host disease after allogeneic bone marrow transplant produces lichenoid oral lesions and xerostomia.
One disease per type, and why it looks that way
Anchor each mechanism to a face. Type I is the lip that swells within an hour of the antibiotic — mast cell histamine dilates vessels fast, so onset is minutes and the lesion is soft, evanescent and itchy. Type II is pemphigus: antibody glued between keratinocytes dissolves their adhesion, so skin and mucosa shear at the weakest suprabasal plane, blisters are flaccid, and the Nikolsky sign is positive; pemphigoid's antibody sits at the basement membrane, so the split is deeper, the blister tense, the erosion slower. Type III is lupus: circulating complexes deposit in vessel walls, complement fires, and the result is the fixed, sun-lit malar rash with oral ulceration and renal injury. Type IV is lichen planus: lymphocytes arrive over days, home to the basal layer, kill keratinocytes one by one, and the epithelium responds with hyperkeratosis — white striae, not blisters, because the attack is chronic and cellular rather than acute and humoral. Learn each disease through its timing, its target and its lesion, and the classification stops being a mnemonic.
Give an oral example
The viva question that separates memorizers from understanders is simply "give one oral example of each hypersensitivity type". Weak candidates recite penicillin and graft rejection from medicine; strong candidates answer from their own specialty — angioedema of the lip, pemphigus vulgaris, the oral ulcers of lupus, lichen planus — and can say why the lesion looks the way it does. One hedged footnote earns credit: erythema multiforme is variously classified as type III or immune-complex-like and cytotoxic mechanisms, so quote it as a mixed or controversial example rather than a clean one.
Frequently asked questions
Which hypersensitivity type is oral lichen planus?
Type IV, delayed cell-mediated — CD8-positive lymphocytes destroying basal keratinocytes over weeks, which is why the lesion is white and chronic rather than blistered and acute.
What distinguishes hereditary angioedema from allergic angioedema?
C1-esterase-inhibitor deficiency with bradykinin mediation — no urticaria, no response to antihistamines or adrenaline alone, and a family history; fresh frozen plasma or C1-inhibitor concentrate treats acute attacks.
Which antibodies define Sjögren syndrome and SLE?
Anti-Ro (SS-A) with anti-La (SS-B) in Sjögren syndrome; anti-nuclear antibodies with anti-dsDNA (and low complement) in systemic lupus erythematosus.
What is oral hairy leukoplakia?
A white, corrugated, non-wipeable lesion of the lateral tongue border driven by Epstein-Barr virus, marking significant immune compromise in HIV and answering to antiretroviral therapy.
Why is true local anaesthetic allergy rare?
Because most reactions are vasovagal, intravascular-injection or adjuvant (sulphite) events; genuine IgE-mediated lignocaine allergy is uncommon and warrants specialist allergy testing before lifelong labelling.
What oral changes follow bone marrow transplantation?
Chronic graft-versus-host disease with lichenoid streaks, xerostomia and ulceration, plus ciclosporin-type gingival effects and reactivation of herpesviruses during immunosuppression.