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PATIENT EXAMINATION BDS2 REFRESH > 15. Allergy To Dental Materials + Drugs > Flashcards

15. Allergy To Dental Materials + Drugs Flashcards

1
Q

LOs

A
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2
Q

allergen routes of entry

A

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
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3
Q

what is a allergic reaction vs toxic reaction?

  • specific immune response?
  • dose dependent?
A

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

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4
Q
  1. what is hypersensitivity
  2. classifications?
A

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

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5
Q

Type I hypersensitivity reaction

A
  1. Antigen binds to specific IgE
  2. IgE is bound to high affinity Fc receptors on mast cells
  3. Cross linking between IgE / Fc receptor complex causes degranulation
    - release of histamine , serotonin , proteases , cytokines , leukotrienes
  4. Chemical cascade attracts eosinophils , neutrophils and macrophages to site of antigen / antibody complex
  5. Leukotrienes and histamines induce vascular permeability
    - causes smooth muscle contraction and bronchoconstriction
  • extreme case = anaphylactic shock , wheezing
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6
Q

Type III hypersensitivity reaction

A
  • activation of complements
  • activation of polymorphs
  • antibody:antigen complex that occurs in circulation and settle down onto a cell membrane (particularly
    kidneys)
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7
Q

Type IV hypersensitivity

A
  • 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)

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8
Q

what are the types of hypersensitivity and what do they do?

A
  1. Type 1 – Immediate IgE mediated - Anaphylaxis
  2. Type 2 – Auto antibody mediated
  3. Type 3 – Immune complexes
  4. Type 4 – T cell mediated - Delayed hypersensitivity
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9
Q

Relevance of Allergy to Dentistry

A

Dental team
* Management + awareness of Anaphylaxis
* Contact dermatitis may affect staff

Patients
* Awareness of previous allergy
* Reduce exposure to potential allergens

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10
Q

Materials used in dentistry that could cause problems

A

*Drugs
~ Local anaesthetics
~ cortico-steroids
~ antibiotics
~ analgesics

  • Restorative materials
    ~ Amalgams
    ~ Ionomers
    ~ Composites
    ~ Metals & Porcelains
  • Clinical materials
    ~ Latex
    ~ Impression materials
  • Tooth paste/mouth washes
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11
Q

what side effects can drugs cause on the oral mucosa

  • Corticosteroids
  • Methotrexate
  • Gold
  • Penecillamine
  • Antimalarials
  • NSAID’s
A

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

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12
Q

what is this?
what drugs may cause it?

A

lichenoid reactions

  • nifedipine
    ~ used for hypertension
  • Salazopyrene
    ~ anti inflamm used in GI, reheumatology,
    dermatology
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13
Q

what is this?
what drugs may cause it?

A

burn

  • aspirin
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14
Q

what is this?
what drugs may cause it?

A

gingival hyperplasia

  • nifedipine
    ~ hypertensions
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15
Q

oral reactions to toothpaste and mouthwashes

A
  • Gingival desquamation (peeling)
  • Gingival swelling & granulomatous (formed by T cell reactions) reactions
  • Benign migratory glossitis
  • Epithelial desquamation, inflammation
  • Ulceration
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16
Q

oral reactions to Creams, Ointments, Impression materials

A
  • Contact stomatitis
  • Gingival desquamation, swelling & granulomatous
    reactions
  • Mucosal Swelling
  • Epithelial desquamation, inflammation
  • ulceration
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17
Q

Adverse reactions to Local Anaesthetics (LEARN???)

A
  • 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
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18
Q

Adverse reactions to Local Anaesthetics

reasons for referral to LA allergy testing clinics

(LEARN???)

A
  • Collapse after LA (immediate or 2 hours later) (25%)
  • Swelling of lips, eyes, cheeks, face (immediate and up to 2 hours later) (25%)
  • Rash on chest, limbs, or contact area (1-7 hours later) (15%)
  • Breathlessness, sweating, nausea, disorientation (10%)
  • Headaches, irregular pulse and low BP.(8%)
  • Swelling of throat, difficulty in breathing (8%)
  • Behavioural changes (minutes to hours later) (5%)
  • Sleepiness, dizzy (5%)
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19
Q

Skin tests for type 1 local anaesthetic allergy

A

Stage 1 : prick test
- small amount of LA dropped onto arm
- skin is pierced with a small needle to introduce a small dose
- helpful for highly sensitive patients
- not good discriminators of allergy alone

Stage 2 : intradermal
- 25 micrometres of LA introduced underneath the skin
- causes white area around test site caused by vasoconstriction of LA
- more positive outcomes

Stage 3: intrabuccal test

20
Q
A

Conclusions
* Scratch skin tests alone are not good discriminators of allergy, intradermal tests are better discriminators

  • Prilocaine produced more positive skin reactions than any other local anaesthetic agent tested
  • In 95 of the 100 patients referred with suspected
    anaphylactoid reactions to local anaesthetic agents, negative skin reactions to at least one of the agents allowed intrabuccal challenge and subsequent recommendation of an agent for future use
  • Skin testing, though not providing formal proof of allergy, provides a useful test to indicate local anaesthetics which may be used for future procedures
21
Q

Type IV - hypersensitivity - contact hypersensitivity EGs to LA

A
  • Contact sensitivity
  • Mantoux skin test
  • Homograft rejection
  • involved in Orofacial granulomatosis (OFG)
22
Q

how to find out what particular products / chem constitutions someone is allergic to

A

patch testing

using aluminium wells

Patches left in place for 48 hours

Results are read at 48 and 96 hours

Patches with immediate sensitivity are removed

23
Q

What causes a lichenoid reaction on buccal mucosa ?

A
  • lichenoid reaction to amalgam
24
Q

Reactions to Latex

A
  • Dental school staff and students at high risk of sensitisation (Tarbo et al 1997)
  • less common now as latex free gloves
  • Skin sensitisation
    Dentists about 10%
    General hospital staff 5-8%
    Nurses 9%
    Anaesthetists 16%
  • Sensitisation may worse in symptomatic asthmatics
  • Percentages of new staff being sensitized will be less as no longer using powdered gloves
25
Q

Latex allergy - Management

A

Non latex gloves
- plastic
- polyvinyl

Advise patients to carry non latex gloves with them

Polyurethane condoms

Latex policy in clinics

Specific RAST test
- skin scratch test with latex

Blood test
- check if IgE against latex is raised

Antihistamines

Epipen
- extreme , contains adrenaline for anaphylactic shock

26
Q

Summary – Materials used in dentistry

A
  • Medicines causing Anaphylaxis – covered in other lectures
  • Medicines causing Mucosal reactions
  • Local Anaesthetic reactions
  • Contact sensitivity to dental materials
    * Type 4 reaction
    * Patch testing
  • Latex
27
Q

causes of lip swelling

A
  • Urticaria & Angioedema (specific fluid build up)
  • Reactions to Foods
  • Granulomatous conditions affecting the lips & oral cavity
28
Q
  1. what is urticaria?
  2. signs and symptoms?
  3. how long does it clear away in?
A
  • It sometimes occurs together with angioedema

1
Hives

2
* Wheals - spots or patches of raised red or white skin
* Wheals are usually itchy, painful or cause a burning sensation

3
* Usually clear away in a few hours, and are then replaced by other fresh wheals.

29
Q

Angioedema

  1. signs and symptoms
  2. how long does it last?
A
  • Often associated with autoimmune disease

1
* Angioedema is the name given to deeper swelling affecting the skin over the arms, legs, torso or face

  • May also affect the tongue, mouth, throat and sometimes the upper airway

2
* Swellings commonly last for more than 24hrs, and usually there is no itching

30
Q

Causes of Chronic Angioedema

A
  • Food allergy (particularly nuts, shellfish, milk & eggs)
  • Oral Allergy Syndrome
  • Medicines
  • Antibiotics
  • Angiotensin –converting enzyme (ACE) Inhibitors -
    Enalopril, Lisinopril etc:)
  • Angiotensin-2- receptor blockers (ARBs) – Irbesartan, Losartan etc:)
  • Aspirin & NSAIDS
  • Beta blockers
  • Latex
  • Hereditary (C1 esterase inhibitor deficiency)
    ~ Attacks triggered by – stress / injury/ surgery
    / dental treatment / pregnancy / medications
    ~ Often not possible to identify cause of
    chronic angioedema
  • Associated with auto immune disease
31
Q

Oral Cavity Reactions to Foods

A
  • Usually type 1 sometimes type IV
  • Oral cavity less sensitive than skin or nose
  • Peanuts most common. (? Does cracking of nuts break through protective mucin coat)
  • Other agents have been identified as causing problems
  • Octyl gallate antioxidant preservative - sore tongue & erythema (Pemberton et al)
  • Pumpkin seed -> swelling and Asthma (Fritsch et al)
32
Q

Immediate Food Allergy

  1. what type of hypersensitivity reaction is it?
  2. small or large quantity of food?
  3. symptoms
  4. how long does it take for reaction to develop?
  5. diagnostic tests?
A

1
* Type I reaction - Anaphylaxis

2
* Small quantity food needed

3
* Perioral Erythema
* Lip Swelling
* Oral Itching
* Tongue + pharyngeal swelling
* Nausea + vomiting

4
* Reaction develops in minutes to hours

5
* Diagnostic skin tests available

33
Q

Food Allergy

A
  • Immediate - Type I
  • Delayed
    o Does it really exist? - Coeliac disease +
    dermatitis herpetiformis well established =
    delayed hypersensitivity
    o Large quantity of food needed
    o Develops in hours and weeks
    o No diagnostic test except withdrawal & re-
    challenge
34
Q

Food intolerance

A
  • Food intolerance (non-allergic hypersensitivity) is much more common
    o Onset of symptoms is usually slower and may
    be delayed by many hours after eating the
    offending food
    o Symptoms may also last for many hours, even
    into the next day
    o Intolerance to several foods or a group of
    foods is not uncommon, and it can be much
    more difficult to decide whether food
    intolerance is the cause of chronic illness, and
    which foods or substances may be responsible
35
Q

Symptoms of Delayed Food Allergy

A
  • Eczema
  • Arthralgia
  • Poor concentration / headaches / depression
  • Irritable bowel syndrome / Crohn’s disease
  • Urinary frequency
  • Arthritis + rhinitis
36
Q

Oral Allergy Syndrome / Pollen Food Syndrome

  1. cause?
  2. who develops
  3. type of hypersensitivity reaction
A

1
* Pollen allergens
* Birch most common

2
* Adults develop > children
* Usually occurs in people allergic to pollen from trees, grasses, weeds

  • Proteins of similar structure in fruit

3
* Distinctive type 1 reaction following direct contact of food and oral mucosa

  • Link to Orofacial granulomatosis patients?
37
Q

Oral Allergy Syndrome (OAS)

A
  • Oral allergy syndrome (OAS) is a common food-related allergic condition that develops in adults. OAS is connected to environmental allergies, such as hay fever
  • Features of oral allergy include swelling of mouth, periorbital tissues, pharynx
  • Birch allergy strongest association
  • 20% of patients with OAS may be scratch positive to
    apples, peaches, kiwifruit, and rarely chestnut, salami
  • Specific allergen Bet vI identified in birch and apples
  • Most common foods usually apples, peaches, kiwi,
    hazelnuts & almonds
  • Antigens inactivated by cooking
  • Other pollen – food cross reactions
  • Latex – Fruit Syndrome (Avacado, Banana, Mango)
38
Q

oral facial granulomatosis causes

A
39
Q

SUMMARY

A

Urticaria & Angioedema
* Causes of swelling around the face and mouth after dental treatment

Food allergy
* Immediate & Delayed
* Oral Allergy syndrome

40
Q

Guidelines for the Management of these reactions

A

Establish provisional diagnosis:
~ Allergy, toxicity or physiological reaction
~ local anaesthetics, dental materials, food
additives, mouthwash, toothpastes, etc

  • Previous history of reaction - mild/severe
  • Onset - rapid/delayed -how soon after contact
  • Type of symptoms - rash, oedema, conscious level,
    breathing difficulties, oral ulcers
  • Previous management of reaction -
    none/medication/hospitalisation
41
Q

how to test for hypersensitivity reactions?

A

Immediate (Type I) reactions
* Allergy testing- scratch tests / intradermal /
intrabuccal challenges
* Serology
~ Mast Cell Tryptase Levels
~ Complement/C1 Esterase Inhibitor
~ Total IgE + Specific IgE (RAST tests)
* Other Routine blood tests
~ FBP / B12 / Folate / Ferritin

Delayed hypersensitivity (Type IV)
* Allergy testing - Patch tests

42
Q

Complementary & Alternative Testing

A
  • Leukocytotoxic Test
  • IgG Elisa Test (not IgE RAST test)
  • Applied kinesiology
  • VEGA testing (Electrodermal testing)
  • Hair analysis
  • Auriculo-cardiac reflex
  • Stools analysis for yeast & parasites
43
Q

Management of patients

A
  • If allergy not proven with allergy testing, clear typed letter to referrer of findings and diagnosis. Always copy to GP
  • If allergy proven, give information to patient on proven allergens identified. Discharge from clinic with letter to referring GP/GDP
  • Consider advice such as avoidance of precipitating allergen (suggest alternatives if possible, for LA)
  • Use of MedicAlert badge
  • Prophylactic antihistamines/corticosteroids
  • Second generation non sedating – eg: Fexafenadine
  • Prednisolone 10mg for severe acute attacks
  • Availability of adrenaline (Epipen)/ emergency support services
44
Q

SUMMARY

A

*Mechanisms present in oral cavity for all types of
allergic (hypersensitivity reactions)

  • Established examples in oral cavity
    ~ Type 1 (Peanut)
    ~ Type 2 (Pemphigus)
    ~ Type 3 (Herpes & Erythema Multiforme)
    ~ Type 4 (Lichenoid)

*How to distinguish between allergy, toxicity and
pharmacological reactions

*What clinical / laboratory tests are helpfu

45
Q

Type II hypersensitivity reaction

A
  • 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)

PATIENT EXAMINATION BDS2 REFRESH (7 decks)

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