Oral Allergies and Immunologic Diseases Flashcards
Type I HS
Ab
Ag
Response time
Appearance
Cells involved
- Allergic or immediate HS rxn
- Allergen specific IgE triggers release of histamine
- Ab: IgE
- Ag: exogenous
- Wheal and flare
- Basophils, mast cells, eosinophils activated
Type II HS
Results from IgG/ IgM Ab binding to self Ag developing cytotoxic reactions
Type III HS
Resuslts from non-clearance and deposition of immune complex and inflammation
Type IV HS
CD4 T cell mediated cutaneous contact reactions to nickel, latex or skin responses to leprosy and TB
Appears as erythema and induration
Macrophages and T cells are activated
Mechanism of Type I
- First exposure to allergen
- B cell activation and allergen-specific IgE production
- IgE binds to IgE specific Fc receptors on mast cells/basophils
- Second exposure
- IgE on mast cells and basophils bind to allergen
- Mast cells and basophils are activated to release
- Histamine, leukotrienes, prostaglandins cytokines
- Causes Smooth muscle contraction, increased vascular permeability, vasodilation, increased mucus secretion, inflammation
Mast cell Commpounds
- Preformed mediators : immediate
- Histamine
- bronchoconstriction and vasodilation
- Newly synthesized mediators: late phase
- Leukotrienes, Prostaglandin D2: Bronchoconstriction and vasodilation
- Cytokines- inflammation
- Histamine
Reaction to Type I HS
Local allergic
Systemic (Anaphylaxis)
Chronic inflammation
Diagnosis of Type I
- History and signs
- family history, genetics (atopic)
- Detection of IgE Ab in patient
- Evidence of the IgE
- In vivo: Prick test and intradermal test
- In vitro: RAST or ELISA
- determines amt of IgE
Drugs and small molecules in Allergic Rxns
- Drugs bind to proteins in the body
- Penicillin core causes Type I
- Drug-protein conjugate develops Th2 type of immune response and production of of IgE
- Repeat exposure to drug triggers allergic reaction via mast cells
How can patients with penicillin alllergies be treated?
With cephalosporin
Drug- related Type I Allergies
Beta lactam antibiotics
Sulfonamides
Chemotherapy agents
HIV drug abacavir
Cross reactivity
- Latex causes cross reactivity to fruits and vegtables
- Called Oral Allergy SYndrome
Type IV DTH is encountered in
- Allergic contact dermatitis from sensitization to chemicals including dental chemicals
- Allergic reaction to many bacteria viruses and fungi
- Tuberculin type HS
- Granulomatous formation- TB leprosy
- Rejection of transplants
Mechanism of Type IV
- Sensitization
- DC take up small molecule modified with protein Ag
- Present molecule-protein conjugate to CD4 T cells
- T cell activation and memory T cells
- Elicitation
- subsequent exposure
- rapid secretion of proinflammatory cytokines: TNF and IL-1
- Recruitment of effector cells, monocytes, MO and site inflammation
Granuloma Formation
Examples
- DTH triggered via CD4 T cells response to pathogen
- Failure to kill and clear
- persistent antigenic stimuli prdoces chronic DTH- Chronic Granuloma
- Body tries to wall it off
- Leprosy, TB, measels mumps and herpes
Contact Dermatitis
- Small molecules like nickel
- Often lipophilic and cojugate with self proteins
- Langerhans DC take up conjugate and present to Th cells
- Th cells activate–> Allergic Contact Dermatitis
- Observed in periodontal disease with nickel
- TLR4 binds nickel –> inflammation
Antihistamines
- H1 receptor antagonists block binding of histamine to cells
Adrenergic agents
Beta receptor agonists, bronchiole smooth muscle relaxant, elevation of cAMP (einephrine)
Corticosteroids
Potent anti-inflammatory, prednisone, hydrocortisone
3 Allergic Oral Mucosal Reactions
RAS RAU/ Canker sores
Orofacial Granulomatosis
Wegeners Granulomatosis
RAS RAU Canker Sores
Prevelance
- Most common
- Triggered by a variety of causative agents with no single agent
- Numerous pathophysiology hypothesis
- Diff people have diff agents
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Ras RAU Canker Sores Mech
- Mucosal Mucosal destruction thru T cell mediated reaction
- Decreased ratio of CD4 and CD8 T cells
- Increased TNF–> Inflammation
- Process may involve ADCC (Ab Dependent Cellular Cytotoxicity)
- Genetic predisposition: HLA types, associated with RAU
- Stress, vacation, travel
- AIDS patients bc low CD4
Orofacial Granulomatosis
Cause and presentation
- Analogous to RAU
- Cause is unknown and abnormal immune response
- Gingiva swells, reythemia, pain, erosions, oral lesions
- Non tender persistent swelling of lips
Management of Orofacial Granulomatosis
- Goal to discover initiating cause
- Local measures to resolve
