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Oral Disease for FINALS > Oral mucocutaneous allergies > Flashcards

Oral mucocutaneous allergies Flashcards

1
Q

Define allergy

A

When the immune system responds in an exaggerated or inappropriate way to an extrinsic (non-self) antigen

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2
Q

Define autoimmunity

A

When the immune system responds in an exaggerated or inappropriate way to an intrinsic (self) antigen

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3
Q

Define hypersensitivity

A

When the immune system responds in an exaggerated or inappropriate way resulting in harm
i.e. allergy & autoimmunity are both forms of hypersensitivity

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4
Q

When does hypersensitivity occur? (2)

A

Occurs on second exposure to the antigen

Hypersensitivity is a characteristic of the individual (genetic factors involved)

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5
Q

Hypersensitivity types (4)

A

Type I - Immediate/ anaphylaxis
Type II - Cytotoxic
Type III - Immune complex
Type IV - Delayed
Examples of all 4 may occur in the dental setting
Types 1-3 antibody mediated, type 4 cell mediated

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6
Q

Type I hypersensitivity (3)

A

Acute hypersensitivity/ anaphylaxis
Rapid onset
IgE mediated

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7
Q

Allergen - type I hypersensitivity (3)

A

Is an antigen (Ag) that give rise to Type 1 Hypersensitivity reactions
Most allergens are small (10-40 kDa) proteins
Examples:
-Der p 1&2 - dust mite faeces
-pollen - grass

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8
Q

Mast cell degranulation (1)

A

Histamine and enzyme release (Tryptase & Chymase)

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9
Q

Histamine release in type 1 hypersensitivity causes (5)

A 
Increased Vascular dilatation (vasodilation)
Vascular permeability i.e. oedema
Bronchospasm
Urticarial rash
Increased asal and lacrimal secretions
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10
Q

Type 1 hypersensitivity most commonly presents as (3)

A 
Hay fever
Asthma
Acute allergic responses:                 
Angio-oedema / Anaphylaxis e.g 
-penicillin allergy
-latex allergy
-local anaesthetic allergy
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11
Q

Diagnosis for type 1 hypersensitivity (5)

A

Wheel and flare skin test
Apply small amount of Allergen just under skin using prick test.

Skin response is fast (5 min)

WHEEL caused by extravasation of serum into skin due to histamine – angio-odema.

FLARE (erythematous red patch) caused by axon reflex.

Late Phase (6 h+) due to leukocyte infiltrate + more oedema

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12
Q

Management of type 1 hypersensitivity (4)

A

Adrenaline (epinephrine)
Anti-histamines
Corticosteroids (e.g. dexamethasone)
Avoidance of allergen

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13
Q

Type 2 hypersensitivity (4)

A

Antibody-mediated hypersensitivity
Antibodies target self antigens (auto-antibodies)
Usually IgG or IgM
The antibodies induce cell damage and inflammation

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14
Q

Type 2 hypersensitivity: what happens (3)

A

Antibodies target self antigen (auto-antibodies)
Autoantibodies activate either: ADCC (antibody-dependent cell cytotoxicity) or complement
Complement activation results in inflammation, cell death (membrane attack complex)

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15
Q

Type 2 hypersensitivity responses in (2)

A

Acute transplant rejection (Host vrs Graft)

Autoimmune diseases e.g. pemphigus, pemphigoid

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16
Q

What is type 3 hypersensitivity (1)

A

Immune complex mediated hypersensitivity

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17
Q

Type 3 hypersensitivity - immune complexes form between (2)

A

Antigen and antibodies

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18
Q

Type 3 hypersensitivity - immune complexes may deposit in (3) where they induce (2)

A

The lining of blood vessels
Glomeruli
Lung
Induce complement activation and neutrophil binding –> inflammation and vascular permeability

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19
Q

Immune complex mediated hypersensitivity is important in (3)

A

Immune complex mediated vasculitis e.g. erythema multiforme, systemic lupus erythematous (SLE)

20
Q

Type 4 hypersensitivity features (5)

A 
Cell mediated immunity/ delayed type hypersensitivity
Mediated by T cells
Cellular response, so usually:
-slow to develop
-slow to resolve
-localised
21
Q

Cell mediated immune responses are important in (4)

A

Delayed type hypersensitivity responses
Contact dermatitis
Lichenoid reactions to amalgam fillings and other materials
Oral Lichen Planus (OLP)

22
Q

Cells in oral lichen planus (3)

A

CD1
Langerhan’s cells
This stimulates the Langerhan’s cells to migrate to the draining lymph nodes
The antigen also stimulates the keratinocytes to release TNF
*****

23
Q

Draining lymph node (5)

A

The Langerhan’s cells process the antigen
And present parts of it to T cells circulating through the lymph node
Antigen specific T cells become activated
Proliferate (clonal expansion)
And preferentially re-circulate to the oral mucosa

24
Q

T cells and PMN pathway (8)

A

Oral mucosa
TNF incduces VCAM-1 expression on endothelium
Chemokines recruit T cells to oral epithelium (CCL5 [rantes])
ICAM-1 expression on oral keratinocytes allows T cells to bind to basal keratinocytes
This stimulates keratinocyte ICAM-1 (and MHC class II) expression
And then migrate between them
ICAM-1 & HLA II enables the keratinocytes to present antigen to the T cells, resulting in local
-activation of antigen specific T cells
-proliferation of antigen specific T cells
Cytotoxic T cells (CD8) kill basal keratinocytes (apoptosis)

25
Q

T cells and PMN histology (2)

A

Dense T cell banding in CT below epithelium

T cell infiltration into epithelium

26
Q

T cell mediated killing mechanisms (3)

A

Probably 2 mechanisms by which T cells induce apoptosis

  • fas/ fas-ligand mediated apoptosis
  • perforin/ granzyme B
27
Q

Fas-mediated apoptosis (4)

A

All cells express Fas
Only T cells and NK cells express Fas-L
T cells can only dock with target cells presenting T cell recognises
This allows Fas-L to engage Fas and induce apoptosis

28
Q

Perforin/ Granzyme B (1)

A

T cells have been identified secreting perforin and Granzyme B into dermal keratinocytes in skin LP

29
Q

Steps of type IV hypersensitivity (7)

A
  1. Langerhans cells move from epidermis to lymph nodes
  2. They present Ag to memory CD4+ T cells
  3. These go back to mucosa are activated and secrete TNFα & IFNγ.
  4. This increases expression of ICAM-1 and MHCII on Keratinocytes
  5. And causes secretion of pro-inflammatory cytokines
  6. More leukocytes are attracted to site
  7. T cells secrete tissue damaging cytokines
    Tissue damage seen at post 12h (delayed)

Tissue damage resolved if Ag removed

30
Q

Allergy appears to be a growing problem (4)

A

In the general population:
Large increase in children suffering from asthma
Large increase in allergic diseases among adults
In the dental surgery
-dentists and nurses becoming increasingly sensitised to latex and dental materials
-pts increasingly sensitised to latex, materials and drugs used in surgery

31
Q

Allergy - issues in dentistry (3)

A

Drug Allergies
Dental Materials Allergy
Latex Allergy

32
Q

Type I hypersensitivity reactions in dentistry (3)

A

Penicillin and other antibiotics
Local anesthetics
Non-steroid anti-inflammatory drugs (NSAIDs)

33
Q

Local anaesthetic allergy (4)

A

True allergy to LA very rare since preservatives removed from dental cartridges
Most reactions are vasovagal, due to IV injection
Some reaction due to latex allergy
LA allergy testing (wheel and flare)

34
Q

Ortho allergies (3)

A

Nickel containing wires
Bracket adhesives - Bis GMA
Acrylic materials

35
Q

Restorative dentistry allergies (4)

A

Amalgam
Composite filling materials - Bis GMA
Denture bases - acrylics
Rarely metals in crowns and denture bases

36
Q

Dental material allergies usually present as what type of response (3)

A

Usually present as type IV responses
Responses usually chronic and localised
Skin patch testing can be very helpful

37
Q

Skin patch testing (2)

A

Tests for type IV cell mediated delayed hypersensitivity responses
Samples applied to skin on back of arm for 72-96 hours

38
Q

Denture acrylic hypersensitivity (5)

A 
Polymethyl methacrylate (Mainly)
Methyl methacrylate monomer
Stabiliser (e.g. hydroquinone)
Initiator (e.g. benzoyl peroxide)
Chemicals released during polymerisation (e.g. formaldehyde)
39
Q

Cold cure acrylics (3)

A 
Less polymerisation
More free:
monomer
stabiliser
initiator
Activator (e.g: tertiary amine)
40
Q

Composite filling materials contain (5)

A 
Quartz or borosilicate fillers
Bis-GMA
Low MW monomers 			
e.g. TEG-DMA or EG-DMA
Coupling agents
Stabilisers, activators and initiators
41
Q

Bonding agents contain (2)

A

More resin and less filler than composite filling materials

More likely to cause problems

42
Q

Metal hypersensitivity: mainly what type of response? (3)

A

Delayed type IV
Nickel: ortho wires etc
Mercury: lichenoid reactions to amalgam fillings

43
Q

Latex protein allergy (Type I reaction) (5)

A

Skin contact

  • Urticaria
  • Angioedema
  • Rarely anaphylaxis

Air dispersal on glove powder particles

  • Asthma, cough, wheeze, rhinitis, conjunctivitis
  • Rarely anaphylaxis
44
Q

Chemical allergy - type 4 reaction (4)

A

Accelerators and antioxidants used during manufacture
Chemicals produced during manufacture
Allergic contact dermatitis
75% of work related glove allergies

45
Q

Powder irritancy (irritant reaction) (3)

A

Continual rubbing and contact with glove powder
Irritant contact dermatitis
-enhances skin penetration of allergens
-increases chance of sensitization

46
Q

Avoiding occupatiotional glove allergy problems (6)

A 
Use powder free gloves
Use hypoallergenic latex gloves
Use latex free gloves
Gloves provided here are powder and latex free (usually nitrile)
Using latex free also protects patients
Many other places still use latex gloves

Oral Disease for FINALS (34 decks)

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