DBMB 711: Week 5 Lecture

Type I hypersensitivity is mediated by which antibody and effector cell?

IgE bound to mast cells (via Fc receptors) that cross-link and degranulate, releasing histamine, leukotrienes, prostaglandins; immediate onset after re-exposure

What is the sensitization step in Type I hypersensitivity?

Initial exposure to allergen induces IgE production; subsequent exposures trigger immediate mast cell degranulation

List common clinical examples of Type I hypersensitivity.

Anaphylaxis (life-threatening), allergic rhinitis, certain drug allergies, latex allergy

Define Type II hypersensitivity and give dental-relevant examples.

Antibody-mediated cytotoxicity targeting cell-bound antigens; examples: pemphigus vulgaris (oral blisters/erosions), Goodpasture syndrome (kidney), autoimmune hemolytic anemia (RBCs)

Pemphigus vulgaris vs mucous membrane pemphigoid—what is the target and where do lesions appear?

Pemphigus vulgaris: antibodies against desmosomes; skin and oral mucosa. Mucous membrane pemphigoid: antibodies against basement membrane; predominantly mucosal surfaces, less often skin

Define Type III hypersensitivity and list classic conditions.

Immune complex-mediated disease due to antigen-antibody complexes depositing in tissues and activating complement; examples: serum sickness, SLE (lupus), glomerulonephritis

Mechanism and timing overview for hypersensitivity types using "ACID."

A (Type I—Anaphylactic/allergy): IgE/mast cells, seconds-minutes. C (Type II—Cytotoxic): antibodies against cell antigens, hours-days. I (Type III—Immune complex): complexes deposit and activate complement, days-weeks. D (Type IV—Delayed): T-cell mediated, 48-72 hours

What defines Type IV (delayed) hypersensitivity, and what is a classic example?

T-cell mediated immune response with delayed onset (48-72 hours); classic example: poison ivy; oral lichenoid reactions can be similar in timing

Oral lichenoid reaction—what clinical timing and effector suggest the mechanism?

Perioral itching/rash appearing ~48 hours after new material exposure suggests Type IV (T-cell mediated) delayed hypersensitivity

Oral lichen planus vs candidiasis—how can you differentiate at chairside?

Oral lichen planus white lesions do not wipe off; candidal plaques typically wipe off with gauze

Define immunologic tolerance and its induction sites.

The state in which lymphocytes do not react to self antigens; induced in bone marrow (B cells) and thymus (T cells)

Autoimmunity—typical etiologic pattern?

Genetic susceptibility plus an environmental trigger (e.g., viral infection) leading to self-directed B- or T-cell responses

Example of autoimmune disease triggered by infection in a genetically susceptible host.

Type 1 diabetes mellitus: often follows viral infection leading to immune attack on pancreatic beta cells

Sjogren's syndrome—key oral and ocular clues and consequences.

Dry mouth (xerostomia), dry eyes; reduced saliva causes rampant caries and predisposes to oral candidiasis via impaired immune exclusion and dysbiosis

Beyond medications, what clinical cue points to Sjogren's rather than drug-induced xerostomia?

Concurrent dry eyes (keratoconjunctivitis sicca) indicating systemic exocrine gland involvement

As a dentist, how should you act upon suspected Sjogren's in a patient?

Recognize oral/ocular signs, manage caries/xerostomia symptoms, and refer to medical team for definitive evaluation and systemic management

If antibodies are deficient, which infections increase and why?

Extracellular bacterial infections increase; antibodies neutralize, opsonize, and target extracellular microbes without MHC presentation

If T cells are deficient, which infections increase and why?

Viral and opportunistic/fungal infections increase; T cells (especially CD8+) recognize infected cells via MHC I; T-cell help is needed for effective B-cell responses

If neutrophils are deficient, which infections increase?

Fungal infections and many bacterial infections; neutrophils are first responders critical for phagocytosis and killing

If complement is deficient, which infections are likely?

Bacterial infections, including risk for invasive Neisseria species due to impaired membrane attack complex and opsonization

Primary vs secondary immunodeficiency—key distinctions.

Primary: inherited defects (e.g., SCID) presenting early with severe/recurrent infections. Secondary: acquired (e.g., chemotherapy, immunosuppressive drugs, malnutrition, aging, chronic disease)

What classic primary immunodeficiency is associated with "boy in the bubble"?

Severe Combined Immunodeficiency (SCID)—profound deficiency of adaptive immunity leading to fatal infections without isolation/therapy

Recurrent oral candidiasis with weight loss and lymphadenopathy—what should a dentist consider and do?

Consider underlying immunodeficiency; order/coordinate referral for labs (CBC with differential, A1C if indicated) and medical evaluation; treat the fungus but also address root cause via referral

Transplant patients—what immune elements are matched and suppressed?

HLA/MHC matched; T-cell activation suppressed (e.g., tacrolimus) to prevent graft rejection

Dental management priorities for immunosuppressed transplant patients.

Review immunosuppressive meds and side effects (e.g., xerostomia), screen for infections, coordinate invasive care (extractions, periodontal surgery, crowns) with medical team, consider pertinent blood counts

Recognize-act safely framework in dental care for immune dysfunction—what are the steps?

Identify oral clues (lesions, dry mouth, meds), infer immune mechanism (infection risk, bleeding risk, airway risk in anaphylaxis), and coordinate/referral with the medical team before proceeding

Antibiotic allergy scenario—what is the appropriate action if you did not prescribe the antibiotic?

Do not change dose or class yourself; contact and refer back to the prescribing clinician; you may advise to stop pending medical guidance

Clinical vignette: wheezing and hypotension after taking an antibiotic—diagnosis and mechanism.

Type I anaphylactic reaction; IgE-mediated mast cell degranulation causing bronchospasm and vasodilation—medical emergency

Immediate chairside priority in suspected anaphylaxis.

Recognize airway/blood pressure risk; initiate emergency management and activate EMS; this is a life-threatening situation

Clinical vignette: severe dry mouth, dry eyes, many caries—category and action.

Misdirected (autoimmune) process consistent with Sjogren's; manage oral complications and refer for systemic evaluation

Clinical vignette: very itchy perioral reaction 2 days after exposure—type and treatment.

Type IV delayed hypersensitivity; symptomatic relief (e.g., topical corticosteroid) and avoid trigger; categorize as "too strong" hypersensitivity

Clinical vignette: new oral infection on tacrolimus after kidney transplant—interpretation.

Secondary immunodeficiency due to immunosuppression; heightened infection risk necessitating careful management and medical coordination