15. Allergy To Dental Materials + Drugs Flashcards
LOs
allergen routes of entry
4 ROUTES OF ENTRY
- percutaneous/ mucosa
~ eg. plants / pet scratch - injection
~ eg. bee stings - inhalation
~ eg. hay fever (pollen) / asthma (dust) - ingestion
~ eg. food (nuts) / medicine
what is a allergic reaction vs toxic reaction?
- specific immune response?
- dose dependent?
ALLERGY
- an immunologically based sensitivity
* Specific immune response to the allergen
* Not dose dependent
* Reaction will change on subsequent exposure
TOXICITY
- a non-immunologically based reaction
* Non - specific, not immune
* Dose dependent
* May be accumulative
* Reaction will be similar on subsequent exposure
- what is hypersensitivity
- classifications?
1
* state of altered reactivity
* body reacts with an exaggerated immune
response to a foreign substance
2
* Hypersensitivity reactions classified as:
~ immediate type I
~ delayed IV
Type I hypersensitivity reaction
- Antigen binds to specific IgE
- IgE is bound to high affinity Fc receptors on mast cells
- Cross linking between IgE / Fc receptor complex causes degranulation
- release of histamine , serotonin , proteases , cytokines , leukotrienes - Chemical cascade attracts eosinophils , neutrophils and macrophages to site of antigen / antibody complex
- Leukotrienes and histamines induce vascular permeability
- causes smooth muscle contraction and bronchoconstriction
- extreme case = anaphylactic shock , wheezing
Type II hypersensitivity reaction
- mediated by IgG binding to antigen on cell or tissue surface
- IgG Fc binds to Fcy receptors of macrophages, NK (natural killer) cells
- IgG Fc also activates complement - opsonisation and activation of phagocytic cells
- degranulation or phagocytosis induces tissue damage
- mechanism in organ-specific disease (self-antigen or tissue)
Type III hypersensitivity reaction
- activation of complements
- activation of polymorphs
- antibody:antigen complex that occurs in circulation and settle down onto a cell membrane (particularly
kidneys)
Type IV hypersensitivity
- delayed type
- mediated by T cells (Th1, Th17, Tc)
- activated T cells secrete chemokines, cytokines
(IFN-y, TNF)to recruit and activate macrophages - activated macrophages secrete further proinflammatory cytokines (IL-12, TNF), tissue damage from degranulation
- formulation of granuloma: macrophages/ multinucleated giant cells, eosinophils, T cells, fibroblasts
- mechanism in organ-specific autoimmune disease
- not instantaneous
(TNF = tumour necrosing factor)
what are the types of hypersensitivity and what do they do?
- Type 1 – Immediate IgE mediated - Anaphylaxis
- Type 2 – Auto antibody mediated
- Type 3 – Immune complexes
- Type 4 – T cell mediated - Delayed hypersensitivity
Relevance of Allergy to Dentistry
Dental team
* Management + awareness of Anaphylaxis
* Contact dermatitis may affect staff
Patients
* Awareness of previous allergy
* Reduce exposure to potential allergens
Materials used in dentistry that could cause problems
*Drugs
~ Local anaesthetics
~ cortico-steroids
~ antibiotics
~ analgesics
- Restorative materials
~ Amalgams
~ Ionomers
~ Composites
~ Metals & Porcelains - Clinical materials
~ Latex
~ Impression materials - Tooth paste/mouth washes
what side effects can drugs cause on the oral mucosa
- Corticosteroids
- Methotrexate
- Gold
- Penecillamine
- Antimalarials
- NSAID’s
DRUGS SIDE EFFECTS
Corticosteroids candidosis
Methotrexate ulceration
Gold lichenoid reactions
Penecillamine loss of taste
Antimalarials lichenoid reactions
NSAID’s lichenoid reactions
(rarely), oral ulceration
Lichenoid reactions = white patches within the mouth that look like lichen planus
what is this?
what drugs may cause it?
lichenoid reactions
- nifedipine
~ used for hypertension - Salazopyrene
~ anti inflamm used in GI, reheumatology,
dermatology
what is this?
what drugs may cause it?
burn
- aspirin
what is this?
what drugs may cause it?
gingival hyperplasia
- nifedipine
~ hypertensions
oral reactions to toothpaste and mouthwashes
- Gingival desquamation (peeling)
- Gingival swelling & granulomatous (formed by T cell reactions) reactions
- Benign migratory glossitis
- Epithelial desquamation, inflammation
- Ulceration
oral reactions to Creams, Ointments, Impression materials
- Contact stomatitis
- Gingival desquamation, swelling & granulomatous
reactions - Mucosal Swelling
- Epithelial desquamation, inflammation
- ulceration
Adverse reactions to Local Anaesthetics (LEARN???)
- True allergy rare and accounts for <1% adverse
reactions - True allergy may be delayed as well as immediate
type - In UK 70 million dental LA given annually
- Adverse reactions to lignocaine & prilocaine
preparations reported to CSM over 25 year period
was 249 and included 9 deaths - LA account for 5-10% of adverse reactions to
anaesthetics drugs - Adverse effects are
- Associated with blocking ion channels in cell
membranes (CVS and CNS toxicity) - Due to other effects of drug or vehicle (mainly
peripheral nerve complications - Allergic reactions (often a mistaken diagnosis)
- Mechanical or other effects of technique such as
needle trauma or introduction of infection - need to work out if was truly an allergic reaction or caused by something else