5.2 Immunology & Hypersensitivity in the Oral Cavity

5.2 Immunology & Hypersensitivity in the Oral Cavity

Quick Answer: Innate defenses act first (epithelium, saliva, neutrophils, complement); adaptive defenses add specificity and memory via B cells (antibodies) and T cells. Saliva’s key adaptive molecule is secretory IgA (sIgA). Hypersensitivity is immune injury: Type I IgE (latex anaphylaxis), Type II antibody-cytotoxic, Type III immune complex, Type IV delayed T-cell (many contact allergies to metals/materials). Know the type, the mediator, and a dental example.

Immunology on the AFK sits inside applied biomedical sciences and reappears in oral medicine (vesiculobullous disease, lichen planus), periodontics (host response to biofilm), and medical emergencies (anaphylaxis). This section is the core vocabulary.

Innate Immunity

Innate immunity is immediate, uses germline-encoded pattern recognition, and has no classic immunologic memory (though trained innate immunity is an advanced nuance—not AFK focus).

Barriers and oral fluids

Cellular innate effectors

Pattern recognition: Toll-like receptors (TLRs) and related sensors detect PAMPs (LPS, peptidoglycan, viral nucleic acids) → NF-κB and interferon pathways → inflammation. Periodontal pathogenesis partly reflects chronic innate activation by biofilm products (LPS from Gram-negatives).

Complement pathways (names only for AFK): classical (antibody-triggered), alternative (surface recognition), lectin (MBL). Outcomes: C3b opsonization, C3a/C5a anaphylatoxins (inflammation), MAC (C5b–9) lysis of susceptible microbes.

Acute inflammation essentials

Cardinal signs (heat, redness, swelling, pain, loss of function) reflect vascular events: transient vasoconstriction → arteriolar dilation → increased permeability → leukocyte extravasation (selectins, integrins, chemokines). Neutrophil chemotaxis defects (e.g., some leukocyte adhesion issues, severe neutropenia) produce severe periodontal destruction—link immunology to periodontics later.

Adaptive Immunity

Adaptive responses are antigen-specific, improve on re-exposure (memory), and require clonal lymphocyte activation.

Antigen presentation and MHC

Without co-stimulation and cytokines, T-cell encounters can lead to anergy—exam-level idea: full activation needs more than peptide–MHC alone.

T lymphocytes

Oral relevance: periodontal tissue destruction is as much host inflammatory response as bacterial enzymes; immune dysregulation models (Th17/Treg balance) appear in advanced reading—AFK needs the principle that inflammation damages attachment apparatus.

B lymphocytes and antibodies

B cells recognize native antigen via surface Ig; with T help (for most protein antigens) they become plasma cells secreting antibody and generate memory B cells.

Secretory IgA pathway (high yield): plasma cells in salivary glands produce dimeric IgA; polymeric Ig receptor transports it across epithelium; secretory component protects sIgA in secretions. Low saliva flow → less delivery of sIgA and innate factors → infection/caries risk (ties to xerostomia physiology).

Primary vs secondary response

• Primary: lag, IgM first, then IgG; lower titer
• Secondary (memory): faster, higher titer, affinity maturation, IgG (or appropriate isotype) dominates

Vaccination logic rests on memory—relevant when discussing HBV vaccination for healthcare workers in infection-control contexts.

Hypersensitivity Reactions (Gell and Coombs)

Hypersensitivity = immune-mediated tissue injury. Classify by mechanism, then attach a dental example.

Type I — Immediate (dental focus)

Sequence: sensitization (IgE production, FcεRI binding) → re-exposure → cross-linking → degranulation.

Clinical spectrum: urticaria, angioedema, bronchospasm, hypotension/anaphylaxis, allergic rhinitis/asthma triggers.

Dental examples:

Chairside implication: allergy history, latex-safe protocols for at-risk patients/staff, emergency epinephrine readiness for anaphylaxis (emergency chapter expands doses/protocols).

Type II — Cytotoxic

Antibody binds fixed antigen on cell surfaces → complement or phagocyte destruction.

Examples (general medicine): transfusion reactions, autoimmune hemolytic anemia, Goodpasture (basement membrane), hyperacute transplant rejection.

Dental-adjacent: some drug-induced cytopenias; pemphigus/pemphigoid are better framed as autoantibody-mediated mucocutaneous disease (Type II-like attack on desmosomes/hemidesmosomes)—oral medicine depth later, mechanism kinship now.

Type III — Immune complex

Soluble antigen–antibody complexes deposit in vessels/tissues → complement → neutrophils → vasculitis-like injury.

Examples: serum sickness, Arthus reaction, SLE nephritis patterns.

Dental relevance: less common as “material allergy” than Type IV; systemic immune-complex diseases can show oral ulcers or petechiae when vasculitic or thrombocytopenic—recognize the mechanism class.

Type IV — Delayed (very high dental yield)

No antibody as the primary driver—sensitized T cells recruit macrophages; peak often 48–72 hours after challenge.

Dental / contact examples:

Latex note: latex can cause Type I (IgE, immediate, anaphylaxis risk) and also Type IV reactions to rubber accelerators (delayed contact dermatitis). Do not collapse all “latex allergy” into one mechanism—history of immediate systemic symptoms vs delayed rash guides risk.

Amalgam: true Type I allergy to amalgam components is uncommon; delayed lichenoid contact reactions and galvanic/irritant issues are the usual teaching distinctions. Mercury panic is not a substitute for immunologic classification.

Tolerance, Autoimmunity, and Oral Disease Bridges

Central and peripheral tolerance prevent self-reactivity. Failure → autoimmunity.

Oral medicine will detail:

• Pemphigus vulgaris — autoantibodies to desmogleins → acantholysis, flaccid bullae, positive Nikolsky conceptually
• Mucous membrane pemphigoid — basement membrane antibodies → tense bullae, desquamative gingivitis patterns
• Lichen planus — T-cell–mediated basal cell damage (Type IV–like interface process)
• Aphthous ulcers — multifactorial immune dysregulation, not simple infection

For this chapter, retain: autoantibodies vs T-cell injury map onto Type II-like vs Type IV-like mechanisms.

Periodontal Host Response (Immunology Link)

Biofilm antigens → GCF influx of neutrophils, complement, antibodies → if unresolved, chronic lymphocyte/macrophage lesions, cytokines (IL-1, TNF-α, IL-6, RANKL axis) → osteoclastic bone resorption and collagenolysis. Smoking and diabetes impair neutrophil function and wound healing—host modifiers of immune effectiveness. This is why plaque control and risk-factor control both matter.

AFK Integration Scenarios

1. Patient reports immediate urticaria and wheeze after rubber dam contact historically → treat as Type I latex risk until cleared; latex-free setup; emergency prep.
2. Rash under a new metal clasp 2 days later → Type IV contact until proven otherwise.
3. Lichenoid patch only on mucosa touching an old amalgam → consider contact (Type IV) contribution.
4. Child with recurrent oral candidiasis and infections → think innate/adaptive defects or local factors (steroids, xerostomia), not only “poor brushing.”
5. High caries after radiotherapy → loss of saliva’s innate and sIgA delivery, not a primary antibody subclass quiz—but connects immunity to environment.

Rapid review list

• Innate = fast, barriers, PMNs, complement, cytokines
• Adaptive = B/T specificity + memory; MHC I–CD8, MHC II–CD4
• Salivary hero antibody = sIgA
• Type I IgE immediate (latex anaphylaxis); Type IV T-cell delayed (nickel, many materials, amalgam lichenoid)
• Latex: Type I and/or Type IV—history timing matters
• Periodontitis = biofilm + destructive host inflammation

Carry these mechanisms into emergencies, materials selection, and oral medicine without memorizing every cytokine synonym.