Allergology final

General part (written)

1. Conditions to which patients must respond for conducting complex oral

diagnostics.
2. Allergy diagnostics – allergic history and physical examination.

1. Medical history
2. Objective examination
3. Clinical tests
4. Para clinical studies

Skin allergy test (in vivo)- direct and indirect. Used to confirm sensitisation to allergen.

Clinical tests: pulmonary function test and bronchodilation tests for asthma diagnosis and
severity.

Direct—> Patch test —> intradermal

Direct —> Prick-puncture —> scratch test —> prick test

Paraclinical studies:

Eosinophilia – abnormally increased number of eosinophils (Eo) in the bloodstream.

Normally in the peripheral blood is 1-4% (up to 400 - 450 cells per mm3).

• In children – 40-100 cells/μL higher

450-1500 cells/μL Atopy:

• atopic rhinitis/dermatitis/asthma

• asymptomatic atopy

1500-2000 cells/μL • Non-atopic bronchial asthma

• Allergic broncho-pulmonary
aspergillosis
Allergology final

2000 cells/μL • Helmiths infestation

• Vasculitis - panarteritis nodosa, Churg-

Strauss
vasculitis, Wegener's granulomatosis

• Bronchogenic carcinoma

• Pulmonary eosinophilic syndromes –

Loeff ler
syndrome, chronic eosinophilic
pneumonia,
tropical eosinophilia, hypereosinophilic
syndrome

• Hemopathy – chronic myelogenous

eosinophilic
leukemia, Hodgkins disease

Allergy specific in vitro tests:

- total serum IgE determination

- Allergen- specific IgE determination
- Eosinophil cationic protein determination
- IgG blocking antibodies determination

Treatment/management of allergic diseases

● Environmental control - patients removal or control from the sensitising

environment, or removal of allergen from the environment.
Allergology final
● Non specific immunotherapy (hyposensitization) - therapy for body reactivity
modification.
● Allergen specific immunotherapy ( hyposensitization)- use of vaccine for allergic
diseases. Vaccines contain the allergen. Patient is sensitised (proven through SATs
and other in vivo and in vitro methods.
● Drug treatment- H1 antihistamines, corticosteroids, cromones, decongestants,
antileukotrienes.

In vivo methods (by direct skin tests)

3 types of skin tests:

1.Epicutaneous - used to verify the presence of allergy to dental materials such as dental
alloys, materials for endodontic treatment, light curing filling materials, bonding agents.

2.Percutaneous - scratch and prick tests are used to confirm clinical sensitivity induced by
aeroallergens, foods, local anesthetics, latex, some drugs and a few chemicals.

3.Intradermal - bacterial allergens, foods, pollen, dust mites, cats, cockroaches, mice and
dogs.

3. Diagnostic procedures in allergology – patch test.

- Epicutaneous allergy tests

- Type IV hypersensitivity (cell-mediated)
- 72hours on the place of epithets with localised eczema
- Skin on the back is used, plaster containing allergens. Plaster is hypoallergenic.
Stays on skin for 48hours.
- Patient should not take any cortisone medication during the test and avoid the sun.

Contraindications: chemotherapy, inflammatory dermatoses of the back, pregnancy.

Positive skin tests confirm the presence of allergic sensitisation.

4. Diagnostic procedures in allergology – skin prick test and intradermal test.

Prick tests

Technique: placing a small drop of each test extract and control solution on the volar
surface of the forearm. The drops are placed 2.5 cm or more apart to avoid false-positive
reactions. A plastic lancet is passed through the drop perpendicular to the skin.

The patient's forearm must stay in a horizontal place.

Used to establish allergic reactions to local anesthetics.

Allergology final

The negative control is liquid without allergens, saline.

The positive control is 1:1000 solution of histamine.

Scratch Tests

Indications: hypersensitivity to local anaesthetic, antibiotics and latex.

Place: forearm

Technique: the volar surface of the forearm is cleaned. Lancet or a blunt hypodermic
needle is used to make a skin scratch 1-2cm in size. Allergen is applied. Reading after
20minutes and the next day.

Positive reaction (+) : halo of erythema, papule or vesicles around the allergen.

Negative reaction (-) : test should be repeated, combined with epicutaneous test and
allergen placed on scratch using a plaster.

5. Diagnostic procedures in allergology – specific tests, elimination, exposition and

provocation tests; indirect tests.

Indirect—> Specific tests on shock organ

Indirect—> Prausnitz küstner test

Allergology final
Prausnitz Kustner test

The test involves transferring serum from the test subject to another healthy person,
essentially using the second person as a mixing vessel for antibodies and antigen.

Specific tests on shock organs:

Elimination test – suspected allergen is removed and the patient for symptoms’ change.

Exposure test – the patient is in contact with the suspected allergen in a natural
environment.

Provocation test – the dosed suspected allergen is introduced to the patient under
observation in a controlled setting.

Provocation

-Digestive system test

-Conjuctival test
-Nasal test
-Inhaled bronchoprovocation
-Challenge tests in food allergy

6. Factors that hamper skin and mucosal testing and affect its results.

In a negative control in epicutaneous tests- is an empty chamber NOT filled with allergen,
while in prick and scratch test - saline solution or distilled water.

Skin testing should NOT be performed soon after allergy worsening or recent allergy
attack.

False negative tests are common in early stages of sensitisation when the skin doesn’t
have a large number of antibodies yet.

Desensitization -> Treatment can also make skin allergic reaction negative without
eliminating the general sensitisation of the organism .

In focal allergic disease patients skin testing should be done in the intervals between
attacks and aggravation. At least 2 weeks after.

Changes in the composition and storage of allergens:

- poor storage leads to dangerous and toxic reactions.

- Inappropriate solvent may lead to false positive or toxic reactions.
Allergology final

- Traces of formalin- false positive reactions.

- Negative skin tests: due to technical faults, fast evaporation of allergens from the skin
surface or plaster absorbing layer, not even contact between substance and skin, low
allergen concentrations.

- Patient should not have received cortisone or antihistamine for 3 days.

- For antiserotonin- 5 days.
- False negatives: hyperkeratosis, ichthyosis, poor turgor, poor blood supply, edema,
neurodermatitis, increased temp, hyperemia.

Complications:

Most frequent with intracutaneous tests. Sometimes with cutaneous tests. Least frequent
with epicutaneous tests.

Local : in or around an application site = erythema, edema, itchy, eczema, necrotic.

Focal : localised in a certain organ or system manifestations = Urticaria, anaphylactic

shock, migraine, rhinopathy, asthma.

Treatment:

- intravenous infusion of antihistamine and corticosteroid drug

- Anaphylactic shock : first aid.
- Asphyxia and hypoxia: tracheotomy, thoracotomy, cardiac massage.

7. Indications and contraindications for allergy testing. Complications after

skin and mucosal testing.

Contraindications
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Local • Acute and chronic eczema, neurodermitis.

• Secondary inflammatory or degenerative
disorders e.g ichthyosis, scleroderma.
• Dermographism, urticaria.
• Secondary skin infections.
• Blood circulation disorders.

General • Lung emphysema, cardiac asthma.

• Coronary sclerosis, heart attack, cardiac
decomposition, severe thyrotoxicosis,
acidosis, diabetes, renal insufficiency

NOT performed during the first 4 months of pregnancy -> bleeding and miscarriage.

Patch test : used for contact eczema and drug allergy diagnosis.

Undesired reactions in Prick test:

Disadvantage: early traumatic erythematous reactions, disappears during the first 10-
20mins and often mistaken for positive reactions.

Undesired reactions in Patch test:

- Organism sensitization following patch tests.

- Permanent depigmentation of the skin - contact vitiligo. Caused by undiluted dental
adhesives.
- False negative : due to lower concentrations of the ingredient when diluting it with
petroleum jelly.

Indications and contraindications for Epicutaneous Testing

- Epicutaneous : used for all lesions of the oral mucosa not related to any mechanical
trauma or physical factors.
- In vivo method. Testing unwanted reactions to dental materials.
- Restrictions in: immunosuppressive and corticosteroid medication (local or
systemic), chemotherapy, inflammatory dermatoses on the back and pregnancy.

8. Orofacial manifestations of drug intolerance.

Drug intolerance = adverse reaction to drugs including allergic reactions.

Allergology final
1. Pain killers(analgesic) e.g codeine, morphin, NSAIDS (ibuprofen), aspirin

2. Antibiotics e.g penicillin, sulphonamides, tetracycline

3. Antiepileptic e.g phenytoin, carbamazepine

Risk factors:

• Age (adults penicillin)

• Genetics

• Food allergies (soy, egg, crustaceans)

• Frequent intake of medications

• Drug overdose

• Route of administration (parenteral worst)

Orofacial manifestations of drug intolerance

Oral cavity most commonly affected due to lack of keratinising epithelium and fast cell
turnover of the oral mucosa.

Affected by type IV hypersensitivity, mediated by sensitised T cells.

Examples:

- Erythema fixum
- Drug induced stomatitis
- Ulcerative stomatitis
- Dry mouth
- Dysgeusia (altered taste, oral erosions, papillary changes on the oral mucosa or
gums, gingival hyperplasia, bisphosphonate induced osteonecrosis of the jaw)
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9. Drug induced variations in salivary secretion. Drugs.

Dry Mouth, Xerostomia -> Due to inhibition of salivation.

Accompanied by burning and pricking sensation, sore throat, difficulty swallowing,

hoarseness.

Drugs also alter the calcium and phosphate levels in saliva and change its buffer capacity.

Increased salivation (Ptyalism)

Saliva is watery. Lacking normal buffer capacity.

Saliva colour changes. Discolouration of saliva, red or orange, during treatment with
clofazimine, rifampicin or rifabutin in patients with Parkinson’s disease.

Salivary glands swelling (Painful or painless)

During treatment with aspirin, antihistamine, antihypertensives, doxycyclines, penicillin,

sulphonamides, NSAIDS, anti-psychotics, intravenous X-ray contrast media.

Mouth pain (stomatodynia)

10. Drug induced lesions in the oral cavity. Drugs.

1) Contact stomatitis
- antibiotics, aspirin, cinnamon containing chewing gums, iodine, mouth washes,
cosmetics.

- pain, sore mouth, burning and xerostomia.

2) Aphthous like lesions and ulcerations

- labial or buccal mucosa and heal within 10 to 14 days.

- lime, potassium tablets, local administration of aspirin, trichloroacetic acid, hydrogen
peroxide, sodium lauryl sulphate.

3) Oral candidiasis
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- corticosteroids, broad spectrum antibiotics, immunosuppressants, anti neoplastic drugs,
oral contraceptives.

4) Fixed erythema
- localised, with sharp borders, reddened and swollen
- 7 to 15days with post lesional hyperpigmentation
- Appear in mouth, on the extremities, palms and feet
- Not usually itchy

5) Vesiculobullous lesions
● Pemphigus
- Drugs containing sulfhydryl groups
- Non thiol drugs containing amide groups
● Lupus

- chlorpromazine, isoniazid, methyldopa, penicillamine, quinine, anticonvulsant, beta

blockers, sulphonamides.

● Lichen plants
- agents used to treat lichen plants (dapson, tetracycline and interferon) could actually
cause lichenoid lesions.

- Dental restoration materials can also cause oral lichenoid reactions e.g amalgam, gold
or cobalt.

● Erythema multiforme
- appear on lips, buccal mucosa or conjunctiva.
- In severe cases, genital and pharyngeal mucosa is infected ( Stevens-Johnsons
syndrome)

● Toxic epidermal necrolysis

- lesions on the skin and linings. In the oral cavity widespread painful vesicles.
- Xerostomia, esophageal strictures, eye complications.
Allergology final

- Caused by: antimicrobial agents, analgesics, anticonvulsants, allopurinol,

chlormezanone, rifampicin, fluconazole vancomycin.

11. Drug induced changes on lips and oral mucosa. Drugs.

1) Cheilitis
‣ Inflammation of the corner of the mouth angles due to fungal infection, hypovitaminosis
B, contact allergic reactions to cosmetics or intake of medications (protease inhibitors of
AIDS, antipsoriatic drugs, retinoids, cytotoxic medications, phenothiazine and
xerostomia inducing agents.

Swelling of the lips and oral mucosa

‣ penicillin, local anesthetics, cephalosporins, ACE inhibitors, aspirin, barbiturates.

‣ Latex cause angioedema

2) Glossitis
‣ Inflammation of the tongue

‣ Severe pain and swelling, dysarthria, dysphagia, fever and lymphadenopathy.

‣ penicillin, bleomycin, lansoprazole

3) Gingival hyperplasia
‣ Phenytoin, cyclosporine, calcium channel blockers.

‣ Develop within months after the initiation of the drug.

‣ Resolves after stopping or lowering dose.

12. Drug induced oral pigmentations. Drugs.

1) Dental discolouration
‣ due to intake of certain medication during tooth formation, the development of the
enamel and/or dentin.

‣ e.g tetracycline in children less than 12 years. Yellowish brown discolouration.

‣ Extrinsic causes: coffee, tea, chlorhexidine, smoking, betel, copper salts.
Allergology final

‣ Pinkish red discolouration develops during high doses of barbiturate treatment or carbon
oxide intoxication.

‣ Fluorides, iron, ACE inhibitors

2) Black hairy tongue ( Lingua villosa nigra)

- smoking, antibiotics, poor dental hygiene

3) Pigmentation of the oral cavity

- Intake of mercury, arsenic, gold, copper, zinc.
- Antimalarial drugs ( chloroquine), busulfan, clofazimine, cyclophosphamide,
estrogens, ketoconazole, tetracycline, phenolphthalein, tranquillisers,
zidovudine, oral contraceptives.
- Pigmentation, usually yellowish brown, can be caused by food or beverages,
cocaine, chewing tobacco.

13. Drugs in oral allergology. Antihistamines.

Antihistamines (H1 blockers, H1 receptor antagonists) counteract the effects of histamine

released during an allergic reaction by blocking histamine (H1) receptors.

Act as inverse agonists.

Used in acute and chronic inflammation.

● Classification

Chemical classification :

- Ethanolamines
- Ethylenediamines
- Alkylamines
- Piperazines
- Piperidines
Allergology final

- Phenothiazines
Functional classification:

Generation 1 (nonselective, classical): Azatadine, Azelastine, Callergin, Chlorpheniramine,

Cyproheptadine, Dimenhydrinate, Dithiaden, Synpramin, Promethazine -> They are
cheap, sedating and anticholinergic. Dosage several times a day.

Generation 2 (selective, non sedating) : Cetrizine, Ebastine, Loratadine, Levocabastine. ->

Don't cross the BB barrier. Peripheral selectivity. Low occurrence of side effects.

Generation 3 ( selective, non sedating) : Levocetrizine, Fexofenadine, Desloratidine. ->

Derivatives of 2nd generation intended to have increased efficacy with fewer side effects.

● Uses
- allergic rhinitis (hay fever)
- Airway disorders- upper respiratory tract infections, otitis media, sinusitis, non specific
coughs.

- Atopic dermatitis
- Urticaria
- Bronchospasm in early stage asthma
- Itchy skin
- Food allergy
- Serum disease
- Anaphylaxis
- CNS and vestibular system disorders - insomnia relief, akathisia, serotonin syndrome,
anxiety, motion sickness, vertigo.
● Effects
Anti-allergic

- suppress swelling and flare response (vasodilation) by blocking histamine binding to

receptors on nerves, vascular smooth muscle, glandular cells, endothelium and mast
cells.
Allergology final

- Anticholinergic effect
- Local anaesthetic effect - Promethazine
● Side effects
- Muscarinic effects
- A-adrenergic effects
- Serotonin effects
- Neurotransmitter effects
● Drug interaction

Fexofenadine is not administered within 15 min of ingestion of aluminium and magnesium

containing antacids, which decrease its absorption.

Rupatadine metabolized by hepatic chromosome P450.

● Drug forms and dosage

Forms: tablets, capsules, syrups, eye drops, nasal sprays and drops, creams, injection
solutions.

14. Drugs in oral allergology. Corticosteroids.

Corticosteroids (CS) are a group of natural and synthetic analogues of the hormones
secreted by the pituitary gland. They are anti-inflammatory and anti-allergic agents.

Induce immunosuppression.

- Glucocorticoids (GCS) - anti inflammatory agents

- Mineralocorticoids - control salt and water balance through action of kidneys
- Corticotropins - control secretion of hormones by the pituitary gland
● Classification

By chemical structure:

1.Hydrocortisone type (cortisone, hydrocortisone, prednisolone, methylprednisolone,

prednisone). Short to medium acting.
2.Acetonides (triamcinolone, mometasone, fluocinolone)
Allergology final
3.Betamethasone (betamesthasone, dexamethasone, fluocortolone).
4.Esters ( Halogenated and Labile)

- by route of administration: topical, inhaled, oral, systemic.

- By biological activity : mild, moderate, potent, very potent.
● Uses
- Autoimmune diseases (collagen)
- Severe allergic reactions
- Bronchial asthma (inhaled anti-asthmatic drugs)
- Skin disorders ( atopic dermatitis, contact dermatitis)
- Hepatitis
- Acute Leukemia
- Lymphogranulomatosis
- Hemolytic or aplastic anaemia
- Organ transplantations
- Addison's disease
● Effects
- carbohydrate, lipid and protein metabolism
- Mineral metabolism
- Inflammation
- Immune system- immunosuppression
- CNS
- Endocrine system
Allergology final

- Hematopoeisis
- GIT

● Side effects (systemic and local)

Systemic:

Local inhaled (including epistaxis, tooth

decay, palatal erosions) :

Local topical CS :

- thinning skin

- Bruising

- Hyperpigmentation
- Vascular changes
Allergology final

- Dermatitis
- Rosacea
- Impetigo
- Mycoses
- Open comedones (blackheads)

● Warning and contraindications

Including: heart disease, high cholesterol, thyroid problems, liver problems, cataract or
glaucoma, myasthenia gravis.

● Drug interactions
- metabolism of methylprednisolone inhibited by erythromycin
- Insulin dosage increased during CS treatment
- Antacids decrease absorption
- Patients should not be vaccinated with live attenuated vaccines as viral replication can
be stimulated

- Taking NSAIDS with CS increase risk of gastrointestinal ulcers

● Drug forms and dosage

Forms: tablets, ampoules, ointments, creams, lotions, eyedrops, nasal sprays and drops,
injection solutions.
Allergology final

15. Drugs in oral allergology. Leukotriene antagonists. Mast cell stabilizers.

Decongestants.

Antileukotrienes are eicosanoids derived from arachidonic acid, which is present in cell
membranes. Shown to mediate bronchoconstriction and hyperventilation.

Antileukotrienes (AL) are agents that interfere with leukotriene synthesis or antagonise
leukotriene receptors.

● Classification:

- inhibitors of leukotriene synthesis

- antagonists of leukotriene receptors
● Uses
- Chronic asthma
- Bronchial asthma and allergic rhinitis (hay fever)
- Asthma induced by exercise
- Aspirin induced asthma
- Bronchospasm/ Bronchoconstriction
- Urticaria
- Psoriasis

● Effect: anti-inflammatory, bronchodilation

Allergology final
● Side effect
● Drug interaction: with B2 agonists result in additive effect. Administration with GCS
is not suitable. Aspirin or NSAIDS is not recommended.
● Drug form: coated tablets, chewable tablets, oral granules/packet.

Dosage:

Mast Cell Stabilizers

cromone medications used to prevent or control allergic reactions. They block calcium
channels used for mast cell degranulation, stabilising the cell and preventing release of
histamine.

● Classification:

-Disodium cromoglycate

-Ketotifen

-Nedocromil

● Uses:
- Asthma
- Allergic rhinitis
- Allergic conjunctivitis
- Mastocytosis

● Effects:
- Stabilize cell membranes
- Inhibit neuronal reflexes and decrease sensor sensitivity to anti inflammatory stimuli
- Inhibition of T-cell cytokine release
- Inhibit PAF release
- Systemic administration results in
reduced bronchial reactivity.

● Side effects:
Allergology final

● Drug forms: nebuliser solution for aerosol administration, drops, suspension,

capsules for inhalation.
● Dosage:

Decongestants

Medicines used to relieve nasal congestion (stuffy nose), associated with colds and
allergies.

Nasal decongestants stimulate alpha-adrenergic receptors.

Oral decongestants used as drug combinations with antihistamines.

● Classification:
- Oral decongestants (tablets and liquids)
- Prolonged decongestant effect with delayed onset
- Relieve symptoms of stuffy nose and sinuses
- Should NOT be used for more than 7 days
- Nasal (topical) decongestants (nasal sprays and drops)
- Short term relief of nasal congestion
- Strong and prolonged effectiveness
- Topical decongestants (sprays) should not be used for more than 3 days.
● Uses
- Rhinitis
- Sinusitis
- Allergic rhinitis (hay fever)
- Allergies
- Common cold
- Upper respiratory tract disorders

● Side effects:
Allergology final

Including: hallucinations, shaking, convulsions (seizures), pale skin, painful urination

● Drug forms: oral (tablets, capsules, gel capsules, liquids) and topical (spray, drops,
liquid, nasal gel)

Dosage:

16. Premedication before local anesthesia.

Protocols.

Step 1 - Medical history

Step 2 - Skin allergy tests: the skin prick test results guide us to the appropriate choice of
local or general anaesthetic agent. Respectively iodinated contrast medium.

Step 3 - Premedication:

- H1 antihistamines, H2 antihistamines, corticosteroids and vitamins

- Premedication drugs depend on the status of the patient, contraindications, side effects
and drug interactions.
Allergology final

- Suitable for adults and children over 7 years

In non allergic patients

Allergic patients - avoid dental procedures requiring anaesthesia during pollen season, in
atopic individuals with severe allergic reactions.

In allergic patients
Allergology final

Specific part (oral)

1. Allergy. Immunologic mechanisms of allergic reactions.

Factors altering the reactivity of the skin can affect the results: patients age, condition of
the skin, chronic diseases, prolonged drug therapy.

Innate immunity : based on a pattern of recognition.

Adaptive immunity:

1. Cell mediated with T and B lymphocytes.

2. Humoral immunity- based on specific immunoglobulins.

Primary organs : bone marrow, liver, thymus. Maturation of T and B lymphocytes.

Maturation of B lymphocytes in bone marrow.

Secondary organs: lymph nodes, spleen, mucosa and skin, GALT, BALT. Development of
adaptive immunity.

T cells

B cells : immunoglobulins (Ig) or antibodies and the T cell receptor (TCR)

Antigen presenting cells:

- Monocytes and macrophages : Produce cytokines including IL-1, IL-12, and tumour
necrosis factor (TNF)
- NK cells They are a non-T and non-B descent of lymphocytes
- Neutrophils: Most common leukocytes. Phagocytic. Also called polymorphonuclear
cells. Circulate in the blood and migrate to tissues in response to cytokines-
chemotaxis.
- Eosinophils: Host defence against parasitic infections. Contain lysozymes,
peroxidases. Increased in inflammatory process.
- Basophils and mast cells: Recruited to sites of allergic inflammation. Activated after
IgE binding to their high affinity IgE receptors.
Allergology final
- Mast cells: present in skin and mucosal tissues with increased abundance when
there is a parasitic infection or atopic process. They also release histamine.
Histamine plays a central role in triggering manifestations of anaphylactic reactions.

Complement system

- 25 circulation and membrane linked proteins.

- Humoral immune system protects against infection.
- Classic pathway: requires IgM and IgG + its subclasses.
- Alternative pathway: provides early immune protection for the naive host.
- Lectin pathway: depends on protein mannan binding lectin.

Cytokines

- Involved in innate immunity, antigen presentation, bone marrow differentiation,

cellular activation and adhesion molecule expression.
- Determines whether an immune response is cytotoxic, humoral, cell mediated,
allergic or tolerogenic.

Immunoglobulins

- Glycoproteins that are produced by plasma cells in response to an immunogen.

- Have a 4 chain structure. Composed of 2 identical light chains 23kD and 2 identical
heavy chains 50-70kD.
- Classes:
1.IgG - gamma heavy chains ( has 4 subclasses, IgG1, IgG2, IgG3, IgG4)
2.IgM - Mu heavy chains
3.IgA - alpha heavy chains ( IgA1, IgA2)
4.IgD - delta heavy chains
5.IgE - epsilon heavy chains

IgE

Increases in:

- Atopic skin diseases e.g eczema

- Hay fever
- Asthma
- Anaphylactic shock
Allergology final
Gell and Coombs Classification

I : immediate IgE mediated (allergic reactions)

II : cytotoxic IgG/IgM mediated (antibody mediated)

III : immune IgG/IgM immune complex mediated

IV : delayed type T cell mediated

● Type I igE mediated

- Anaphylaxis
- Atopic asthma
- Rhinitis
- Angioedema
- Urticaria
- Latex allergy
- Local aesthetics

● Type II antibody mediated

Mechanism: opsonization (phagocytic cell destruction) , complement mediated lysis,

cytoxicity.

● Type III immune complex reactions

Antibody IgG binds to antigen forming a circulating immune complex. Initiates a local
inflammatory reaction.

● Type IV delayed reactions

- Caused by T cells, CD4+ helper cells. e.g contact dermatitis.
- Th1 type of response.
- Antibody-independent. (allergy to dental materials. )

Cell mediated cytotoxicity

- CD4+ T cells, CD8+ T cells, and NK cells.

Th1 vs Th2 responses

Th1 : inflammatory reactions

Th2 : antibody dependent allergic reactions.

Allergology final
T-lymphocytes suppress igE
mediated antibody synthesis
and stimulate higher levels of
blocking IgG antibodies. Their
activation is crucial for
overcoming atopic
sensibilisation, which results
in Th1 type immunologic
reactivity.

2. Classification of allergens. Diagnostic allergen extracts.

Exogenous allergens have their origin in the external environment ronment such as
bacteria, viruses, fungi.

Endogenous allergens originate in the macroorgasnim structures. Most often the result of
virus processes or the loss of immune tolerance to macromolecules in the body. They are
also allergens that are the roots of autoimmune diseases such as autoimmune thyroiditis,
rheumatoid arthritis.

● Classification
Allergology final

According to their nature allergens 1. Household : dust, mites, hairs, dander

2. Pollen : grasses, weed, trees, flowers
3. Bacterial, virus, chlamydia
4. Fungal : moulds
5. Food
6. Insect
7. Helminth
8. Chemical
9. Industrial
10. Physical
11. Auto Allergens

Bacterial allergens Strep

Staph
Saprophytes
Intestinal bacteria
TB
Drug allergens - Radiocontrast agents
- Antibiotics
- Vitamins
- Local anesthetics
- Cosmetics
- Analgesics, antipyretics, anti rheumatics

Exogenous allergens penetrate through • Skin and oral mucosa

• Digestive system
• Respiratory
Auto Allergen classification ● Natural (primary)
● Acquired (secondary) : non infectious
and infectious

Allergen extracts for diagnostic use

Allergens used in diagnosing allergic diseases (asthma, rhinitis, dermatitis, pollinosis) are
liquid extracts of the major sensitising substances of household, bacterial, fungal, pollen,
food, industrial and other origin.

Depending on their application allergens used in diagnostics are divided into allergens for
use in : Intradermal, percutaneous and epicutaneous tests.

Allergen extracts containing one component from a different dental material are used.

3 series of dental allergens - for the personnel, for patients and screening series.
Allergology final
A dental screening series includes 30 allergens. Allergens are made of substances found
in all dental materials.

The physical and mechanical properties of dental materials are known to differ from the
original products. To this effect we could expect differences in the sensitising potential of
finished.

Difficulty of diagnosing allergic reactions to dental materials results from the insufficient
information of the precise composition of materials.

Allergens used in treatment are intended for specific hyposensitisation of patients having
allergies.

Allergies (chemically modified allergens) are the most recent category of allergens used in
specific immunotherapy (hyposensitisation).

Allergenic extracts

* Liquid AE - the most widely used

* Lyophilized AE- their main disadvantage is that there is a risk of unpredictable changes
in the allergen molecule during lyophilization (freeze drying)

*Modified allergens (allergoid) - with reduced or eliminated allergenicity and preserved

immunogenicity

*Mixed AE- not recommended due to the risk of undesired interactions between them
resulting in lost allergenic activity

*Liposomal AE - included in liposomes allergenic extracts, more efficient effect on the

human body

3. Allergic reactions and diseases – etiology, classification, management.

● Classification
Allergology final

● How does an allergic reaction occur

1. Sensitisation to an allergen occurs after repeated exposure

2. In delayed type (cell mediated) hypersensitivity: T cell populations destroy target cells
on contact or activate macrophages that produce hydrolytic enzymes

3. In immediate hypersensitivity: B cells secrete antigen-specific IgE antibodies and bind

to IgE receptors on surface of mast cells and basophils

4. histamine, cytokines, interleukins, leukotrienes, prostaglandins released

5. Cause allergic reactions: vasodilation, mucous secretion, nerve stimulation, smooth

muscle contraction

6. Allergic reactions result in: rhinorrhea, itchiness, dyspnea and anaphylaxis.

Systemic: anaphylaxis

Local: asthma, rhinitis, urticaria

● Etiology of allergic diseases

Penetrate organisms through skin, respiratory system and digestive system.

Most common:
✦ House dust mites
✦ Cockroaches
✦ Lipocalins - respiratory allergens of mice, rats, cats, dogs, horses, cows (dandruff, hair,
urine, saliva)
✦ Profilins - pollen (birch, grass), fruits (apple, kiwi, peach, nuts) and vegetables (carrots,
potato, celery)
✦ Insect venom
✦ Mold
✦ Bacterial allergens
✦ Drugs

● Management
1. Environmental - allergen avoidance. Pet removal, bedding wash, elimination diet, drug
replacement

2. Non specific immunotherapy (hyposensitization)

Allergology final
3. Allergen specific immunotherapy (hyposensitization) - use of vaccines. Vaccine
contains the allergen/s to which patient is sensitised

4. Drug treatment

● Manifestation
- First grade: Mild allergic reactions - short term actions, subside without treatment.
Manifestations are skin and mucosal. Itching of the skin, lips, oral mucosa, edema,
polymorphic rash, anxiety, agitation. Management: discontinue allergen exposure;
H1 antihistamines for 4-days; local steroids.
- Second grade: Moderate allergic reactions - require medication. Manifestations are
severe itch of skin, oral mucosa, polymorphic rash, swelling, Quinkes edema,
erythema, oral mucosal lesions, systemic allergic reactions (shortness of breath,
heart attack symptoms, anxiety, agitation). Management: discontinue allergen
exposure; H1 antihistamines for 7-10days; systemic steroids.
- Third grade: Severe allergic reactions - require complex treatment. Manifestations -
all the above. Giant urticaria, petechiae, severe Quickes edema, strong salivation,
erosions, ulcers, allergic shock. Management: proper position of patient
(horizontally with raised lower jaw to prevent asphyxia; loose clothes, belts,
removed dentures). Parenteral administration of Adrenaline and H1 antihistamines.
- Fourth grade: Extremely severe - complex treatment and monitoring. Manifestations
are threatening respiratory distress, vascular collapse, urticaria, pruritus,
angioedema and shock. Management: resuscitation

4.Bronchial asthma.Dentist’s approach.

Bronchial asthma is a chronic inflammatory disorder of the airways.

Asthma is a complex clinical syndrome characterised by:
• Airway (cellular) inflammation and bronchial remodelling
• Bronchial hyper-responsiveness
• Variable airflow obstruction

The bronchial wall reacts strongly with spasm to substances that are allergens, airborne
irritants, viral respiratory infections, and occupational exposure.It is thicker and swollen
and secretes a lot of mucus. Wheezing,cough,chest tightness and shortness of breath
appear and worsen particularly at night and early in the morning.

There are 5 types of asthma according to ethology:

1.Atopic-increased IgE-response to antigen contact
2.Non atopic:
-Non allergic asthma-exercise induced asthma,aspirin-induced asthma, asthma related to
viral or bacterial infections.
-Idiopathic asthma
3.Combined forms ( combination of atopic and non-atopic asthma)
4.Occupational asthma
5.Symptomatic asthma-infectious or non-infectious
Allergology final

According to severity:
-intermittent
-mild persistent
-moderate persistent
-severe persistent

Can be also:
-controlled
-uncontrolled

Oral manifestation:

-There is no specific oral manifestation of the disease itself, but prolonged inhaled
glucocorticoid therapy in chronic asthma can induce pseudomembranous candidiasis
(thrush) as a result of fungal overgrowth in the areas of local immunosuppression.
-Candida albicans is usually located on the soft palate and oropharynx.
This condition is usually asymptomatic.
-Dysphonia (hoarseness) is a side effect observed in prolonged inhaled glucocorticoid
therapy
-Studies have shown an increased number of dental erosions and reduced dental caries
resistance due to this medication.

Clinical findings:

• Decreased salivary flow, usually due to beta-2- agonists administration

• Bigger plaque and tartar accumulation
• Gingivitis
• Aggravated periodontal diseases
• Increased risk for caries development due to the decreased salivary flow and the impact
of the cariogenic carbohydrates and sugar containing anti asthmatic drugs.

Diagnosis:

The clinician must examine the symptoms compatible with asthma, medical history, and
excluded alternative diagnosis.

Additional diagnostic methods:

• Physical examination
• CBC with white blood cell differential
• Spirometry-functional analysis of breathing,bronchodilation test, bronchial challenge
tests
• Induced sputum
• X Ray of lungs and maxillary sinuses
• Immunoallergic assays-skin allergy tests(SAT), challenge tests etc.

Management:

Includes:
-Customized treatment plan
Allergology final
-Patients and their families education
-Lifestyle modification
-Medication
-Regular follow up

Classification of medications:
• Bronchodilators
• Methylxanthines
• Glucocorticoids
• Mast cell stabilisers
• Anticholinergic medications

Dentist’s approach treatment:

• Fluoride supplements, especially in patients with beta-2- agonist therapy, mouthwashes
and topical remineralising solutions.Follow-up 3 times a year.
• Rinsing the mouth with water after using inhalers
• Improving oral hygiene to reduce the possibility of developing gingivitis and periodontitis
• Antifungal therapy administered if necessary

Patients should be instructed to:

-maintain good oral hygiene
-place mouthpieces on the inhalers
-rinse the mouth with antifungal solutions after inhalation
-use stress-reducing techniques
-avoid dental materials that can provoke an attack
-careful selection of the position of the saliva ejector tube
-oxygen and bronchodilators should be available in dental practices

During asthmatic attack:

• Stop the dental procedure
• Remove all intraorally placed tools and materials
• Put the patient into comfortable position , to ensure airway patency
• Administer oxygen and beta-2-agonists
• If there’s no improvement-SC administration of epinephrine 0.01 mg/kg weight to a
maximum of 0.3 mg
• Call the emergency

Additionally to drug therapy:

1. Anxiolytics are recommended as treatment of choice in patients with fear of dental
treatment
2. Patients who were on inhalation therapy should be close to the inhaler during dental
procedures
3. Aspirin,NSAIDs, barbiturates and anaesthesia can cause exacerbation of asthma
4. Patients should be asked about sensitivity to aspirin: Samter’s triad consists of aspirin
sensitivity,asthma,nasal polyps
5. Avoid antihistamines such as Promethazine and Diphenhydramine-have drying effect
on the oropharyngeal mucosa and may cause exacerbation of the condition with sticky
bronchial secretions
6. Asthmatic patients are sensitive to cardio stimulating effect of epinephrine and it's
better to avoid it
Allergology final
7. Erythromycin,Clarithromycin,Ciprofloxacin should be voided in patients treated with
Theophylline levels, as Macrolides increase serum Theophylline levels, whereas
Phenobarbital reduces them
8. The use of tetracycline together with Theophylline is not recommended
9. Patients on oral corticosteroids may need extra steroids- consultation with their doctor.

Risk classification:
• High risk patients-individuals with symptoms of asthma, which exhibit a strong whistle
tachypnea and also patients with tachycardia, irregular heartbeat etc. When there are
side effects of treatment-dental manipulations are contradicted
• Patients with significant risk-they are with history of common asthma attacks, irrespective
of the medication.The stress of dental procedures may include an asthma attack.Dentists
should approach carefully these patients, to choose a sniper treatment plan and to
assess the need for prior sedation with anxiolytics
• Patients with medium risk-individuals with infrequent asthma attacks and long term
therapy.

5.Allergic rhinitis and rhinosinusitis.Dentist’s approach.

-Allergic rhinitis is the most common form of noninfectious rhinitis.It is associated with IgE-
mediated immune response against airborne environmental allergens.

-It is often accompanied with ocular symptoms-conjunctival redness, itching, swelling and
excess lacrimation.The term then is allergic rhinoconjunctivitis.

-Allergic rhinitis is most common in school age children and 20% of adults.

-Asthma and rhinitis often coexist

Types of AR:

1.Seasonal AR: Occurs in spring, summer, and early fall and airborne pollen is at its
highest levels.
2.Perennial AR: House dust mites, cat and dog dander, occupational allergens

Clinical features:

• Paroxysmal (sudden) sneezing

• Itchy nose, eyes, palate, pharynx and ears
• Nasal congestion with partial or complete obstruction
• Rhinorrhea,often combined with post nasal drip

Orofacial manifestations:

• Paroxysmal sneezing
• Nasal congestion
• Rhinorrhea
• Pharyngeal (post-nasal) drip
• Nasal obstruction
Allergology final
• Itching nose, palate, pharynx
• Impaired smell-hyposmia,anosmia
• Rhino-sinusitis/chronic sinusitis, accompanying perennial rhinitis
• Open mouth breathing due to constant nasal obstruction
• Transverse nasal crease- patients rub their nose with their palm upwards-‘allergic salute’
• Lower eyelid Venous stasis due to nasal congestion
• Petechiae on the hard palate
• Nasal polyposis
• Orthodontic anomalies-due to long open mouth standing-in perennial rhinitis
• Xerostomia

Diagnosis

- based on medical history and examination

- Nasal swab from the anterior to the posterior part of the nasal cavity; typical 5-10%
eosinophilia is observed
- SPTs and specific IgE investigations are also helpful

Management

• Allergen elimination
• Pharmacotherapy-antihistamines,oral decongestants, antileukotrienes,local steroids
• Specific immunotherapy

Dentist’s treatment approach:

-First generation antihistamines and decongestants may induce xerostomia, which can
result in oral candidiasis.
-Long term local corticosteroid therapy causes the same complications

The recommendations for dental treatment of patients with allergic rhinitis:

1.Suitable season choice for complex dental treatments- not in pollen session
2.In patients with perennial rhinitis-dental visits are appointed in the early morning hours
3.Relieve the symptom of drug-induced xerostomia through:
• Fluid intake-about 2L a day
• Salivary secretion stimulation
• Use of wetting agent for the oral cavity
4.Cases of diagnosed candidiasis are treated with an appropriate antifungal therapy

6.Atopic dermatitis.Dentist’s approach.

Atopic dermatitis is a form of eczema,is a non-contagious disorder characterised by

chronically inflamed skin and sometimes itching.A genetic predisposition is suspected.
Allergology final
AD is characterised by an increase in immune response to an external stimulus resulting
most commonly in an inflammatory reaction of the skin.
AD is a chronic disease with remissions and exacerbations. In half of the cases it is
combined with allergic rhinitis and/or asthma.

Predilection sites for eruption are:

-In children-face,scalp,neck,extensor surfaces of the extremities.
-In adults-hands,eyelids,back,upper chest, genitals

Oral manifestations:
• Recurrent cheilitis
• Fissures under the ear shells
• Pityriasis alba-irregular plates with fine scaling and hypo pigmentation of the cheeks
• A Dennie-Morgan fold line in the skin below the lower eyelid
• Infantile eczema appear mostly on the cheeks-they are red with vesicles that quickly
evolve into this

Diagnosis :

Williams and al.propose as diagnostic criteria at least 3 of the following:

• Skin folds involvement-cubital and popliteal fossa, neck
• History of asthma or hay fever, family history
• History of dry skin in the last year
• Onset before the age of 2

Lab tests:
-CBC with absolute eosinophil count in the blood
-Total IgE level in the blood
-SAT with food and inhaled allergens

Management:

- Treatment includes-regimen,diet,hygiene and household habits, photo protection.

- The best food for atopic infants is breast milk, and for older children fresh organic
find products with easily digestible proteins.
- The most common food allergens-chocolate, nuts, bolts, tropical fruits
- AD is considered idiopathic, but a genetic component is also suspected.
- Treatment is focused on removal of the suspected triggers and administration of
drugs-antihistamines,glucocorticoids,antiviral agents,antibiotics,cytostatics,aromatic
retinoids,essential fatty acids and physical therapy.
- People with AD often have dry and scaly skin-they should clean it with special
products, also oils are recommended.

Dentist’s approach:

Is based on orofacial manifestations- recurrent cheilitis,considering the patient’s age too.

It is desirable dental treatments to comply with the general condition of the patient and a
more favourable period of the disease to be chosen.
Allergology final

7.Insect allergy.Dentist’s approach.

The decayed bodies of insects or their faces can cause inhalation allergies such as
bronchial asthma or allergic rhinitis and stings or bites by insects may induce local
cutaneous or systemic allergic reactions including life threatening anaphylaxis.
The generalised allergic reactions are most often IgE-mediated.

Biological effects of the stinging insects' venom can defines as an integral of 4 types of
toxic action:
-Hemorrhagic
-Hemolytic
-Neurotoxic
-Histamine-like

Clinical features:
• Painful,itchy and burning local reactions with swelling
• Contact dermatitis
• Generalised urticaria rash
• Nodular,rarely vesicular or bullies rash
• Erythema,pruritus and angioedema
• Inhalation allergies(rhinitis,conjunctivitis)
• Bronchial spasms
• Hypotension
• Allergic shock

Can be accompanied by: headache, nausea, sweating,xerostomia,insomnia

Oral manifestations:

• Swelling around the eyes, lips,ears

• Laryngeal edema
• Dyspnea
• Dysphagia
• Dysphonia

Diagnosis

-Skin prick test with Hymenoptera venom

-Estimation of venom-specific serum IgE antibodies- through RAST and other in vitro
immunoassays

Management:

For patients developing reactions to Hymenoptera venom, this measures should be taken:

1. Preventing measures, avoid activities of high risk, wearing black or colourful clothes
etc.
Allergology final
2. All patients with history of systemic reaction should carry an emergency kit for self
administration
3. VIT is indicated in children and adults with history of severe systemic reaction ,
sensitisation to the relevant venom is demonstrated either by skin test and/or serum
sIgE
4. Patients should wear insignia for insect allergies( bracelet etc)

Dentist’s approach:

• Insignia
• Patients should present to the dentist the allergic passport and phone number to the
closest relative
• The windows should be closed during dental procedures
• All patients with insect allergy should carry epinephrine auto-injection for emergency
• It should always be expected that patients with Kinect allergy could develop
sensitization to dental materials too-thats why patch tests and SPTs are recommended

If an incidence occurs in a dental practice:

• Remove the sting with the tweezers
• Clean the affected area with cotton swab soaked in hydrogen peroxide
• Cool the sting side to reduce poison absorption
• Call EMS for aggravated cases

8.Acute and chronic urticaria.Quincke’s edema.

-Urticaria(hives) is a pruritic skin eruption characterised by transient wheals of varying

shapes and sizes with well defined erythematous margins and pale centres. Biopsy of
acute urticaria lesion reveals dilation of small venues and capillaries located in the
superficial dermis with widening of the dermal papillae, flattening of the rate pegs, and
swelling of collagen fibres.Urticaria is associated with allergic reactions and histamine
release or defects in the complement of kinin systems.

Urticaria triggers are:

• Animal dander
• drugs/meds
• Emotional stress
• Food
• Immune-hereditary angioedema
• Infection-echinococcus infection
• Inflammation
• Insect bites
• Mastocytosis
• Mechanical stimulants
• Pollen
• Post-infection
• Other diseases-Autoimmune disease, systemic lupus erythematosus, Henoch-Sclonlein
purpura, Leukaemia etc.
Allergology final
-Acute urticaria is common, possibly affecting around 10-20% of the population.It is a self-
limited disorder caused by an allergic reaction to food or drugs.
-When urticaria is present for more than 6 weeks it is diagnosed as chronic.

Clinical features:
-Urticaria may occur on any part of the body, whereas angioedema often involves the
face,tongue,extremities,and genitalia.
-The wheals may be in very large numbers, mostly over the body,1.3-5 cm in diameter and
there is no discontinuity of the epithelium.
-In contrast , angio edematous swellings do not characteristically occur in dependent
areas, are asymmetrically distributed and transient.
-Urticaria and angioedema can coexist

Diagnosis:
• Medical history
• Physical examination
• Chest radiograph examination
• Skin allergy tests. SAT
• Blood tests-CBC and differential,sedimentation rate, antinuclear antibody
test,antithyroglobulin and antimicrosomal antibodies, autologous skin test; in vitro assay
of serum-induced histamine release from basophils.
• Stools for ova and parasites
• Skin biopsy,immunofluorescence

Management
Medication:
-Antihistamines
-Corticosteroids-systemic and local
-Antileukotrienes
-Dapsone
-Omalizumab

Food allergy(mentioned below)

Drug allergy (mentioned below)

Quincke’s edema:
This is angioneurotic edema (or angioedema), a form of localized swelling of the deeper
layers of the skin and fatty tissues beneath the skin. Hereditary angioneurotic
edema (or hereditary angioedema) is a genetic form of angioedema.

Symptoms: Persons with it are born lacking an inhibitor protein (called C1 esterase
inhibitor) that normally prevents activation of a cascade of proteins leading to the
swelling of angioedema. Patients can develop recurrent attacks of swollen tissues,
pain in the abdomen, and swelling of the voice box (larynx) which can compromise
breathing.

Diagnosis: is suspected with a history of recurrent angioedema. It is confirmed by finding

abnormally low levels of C1 esterase inhibitors in the blood.
Allergology final
Treatment: include antihistamines and male steroids (androgens) that can also prevent the
recurrent attacks.

9.Food allergy with oral manifestations.

Food intolerance ’non-allergic hypersensitivity’: Is a result of a variety of enzyme

deficiencies or mediator releasing( tyramine, histamine). It refers most often to
disaccharide deficiency-milk intolerance due to lactose deficiency in the intestine mucosa
etc.

True food allergy is defined as an immune response to allergens of foodstuff and their
additives, mediated most frequently by antigen-antibody humoral reactions.

- IgE dependent
- Non-IgE dependent

Etiology and pathogenesis: Specific food allergens are referred to the different age groups.

Class I: prevails in childhood and the allergens are milk, eggs, soya, peanuts, other nuts
and fish.

- Milk: due to casein and beta-lactoglobulin, tolerance usually appears till the age of 2
and in 90% of the cases it disappears.
Allergology final
- Eggs: allergens most in egg white, the sensitisation disappears in 50% of the cases
till the age of 5.

Class II: prevails in adults and frequently caused by fruits and veggies- apple, peach, kiwi,
banana, strawberry, celery, carrot.It results with specific reaction- oral allergen
syndrome (OAS).

The cross reactivity between latex and allergens of

chestnut,spinach,walnut,kiwi,banana,avocado,melon is very important for the
dentists.

The routes of sensitisation with food allergens are digestive tract mainly, skin and
respiratory tract.

The allergens ,passed through the physiological and immunological barriers of digestive
tract, provoke immune response.The majority of food allergies is characterised by a
rapid onset following exposure to the allergen and belongs to type I, IgE-mediated
hypersensitivity. The mediators of those reactions are histamine, leukotriene.

Symptoms: True food allergy is characterised by a rapid onset following exposure to the
food allergen, when IgE-mediated mechanism is involved- symptoms appear in a
time period of several minutes up to 4h.

- Skin and mucosal symptoms-urticaria, atopic and contact dermatitis, oral allergy
syndrome,angioedema.
- Digestive symptoms-nausea,vomiting,stomach ache and diarrhea
- Respiratory symptoms-rhinitis, conjunctivitis,laryngospasm,bronchospasm,asthma.

Systemic manifestations:

- Anaphylaxis and anaphylactic shock

- Peculiar form is anaphylaxis caused by physical exercise and the ingestion of food
- Symptoms like contact dermatitis and dermatitis herpetiformis are assigned to cell-
mediated hypersensitivity

Orofacial manifestations:

- Angioedema associated or not with urticaria, affects certain parts of the body:Face,
lips, tongue and larynx.
Allergology final
- Oral allergy syndrome
- Recurrent aphthous stomatitis- food allergy to certain fruits, milk,cheese,citric acid
and colouring agents.

Diagnosis: Clinical and laboratory.

- Anamnesis;History of allergies etc

- Eating habits
- SAT: Skin test-Prick and patch tests; Antihistamine therapy must be stopped at
least 3 days before skin test; prick tests are not carried out in areas of dermatitis or
in areas where dermal corticosteroids or immunomodulation creams have been
applied
- Oral challenge tests-can produce false positive results; are contraindicated in
patients with anaphylactic shock, asthma and individuals with inflammation
- Trial elimination diets
- Specific IgE assays-CAP system technique

Treatment: Is symptomatic and etiological

- Elimination diet-in case of identified allergen

- Antihistamines-oral allergy syndrome,skin pruritus, urticaria, rhinitis,rhino-
conjunctivitis, in anaphylactic shock as IV
- Corticosteroids-for cell mediated reactions
- bronchodilators -asthma
- Adrenaline-for anaphylactic shock

10.Immune diseases with maxillofacial manifestations.

1) Orofacial granulomatosis - Chronic recurrent painless swelling of the oral mucosa,

lips and perioral tissues as a result of granulomatous inflammatory infiltration.

Symptoms:

- Facial swelling
- Diffuse swelling of the lips-hyperplastic gingivitis
- Cobblestone appearance of buccal mucosa
- Swollen buccal sulcus
- Lymphadenopathy
- Ulcers
Allergology final
Diagnosis: Based on biopsy of the affected tissue

DD-Crohn’s disease, sarcoidosis,Melkersson-Rosenthal syndrome

Management

- Remove food triggers if suspected

- Corticosteroids
- NSAIDs
- Folic acid,Vitamin B12,Dapsone
- Surgical reconstruction

2) Scleroderma - Is an autoimmune disorder where there is overproduction of

abnormal collagen.This collagen accumulates through the body causing hardening
and scarring.

Clinical features

- Diffuse scleroderma-systemic disorder of connective tissue characterised by

hardening and thickening of the skin, with telangiectasias,Raynaud’s phenomenon
and fibrotic degenerative changes in organs such as heart, lungs, kidneys and GI
tract.It can also remain on the face or hands or may diffuse and spread.
- Localised scleroderma-confined to skin and subcutaneous tissue or secondarily
involving the musculoskeletal system.It occurs in 3 forms: Morphea, Linear
scleroderma, Coup de sabre or circumscribed scleroderma
- CREST syndrome (C=calcinosis, R=Raynaud’s disease, E=Esophageal dysmotility,
S=Sclerodactyly, T=Telangiectasias)

Oral manifestations of CREST:

- Dysphagia
- Microstomia
- Periodontal lesions
- Gingival recessions
- Xerostomia
Allergology final
Diagnosis

- Skin biopsy
- Lab testing:
• Anti-topoisomerase antibodies( anti-scl 70)

• Anti-centromere antibodies

Management

- Good oral hygiene

- Symptomatic treatment
- Antibiotics
- Steroids

3) Systemic lupus erythematosus - Is a chronic inflammatory autoimmune disease with

a wide spectrum of clinical forms, in which mucocutaneous manifestations may
occur with or without systemic manifestations.

Forms: Discoid (DLE) and Systemic (SLE) also subacute cutaneous LE.

Clinical features:

- Discoid form usually affects the face, but can occur on any body surface.
- The oral mucosa is involved in some cases 15-25% usually with skin lesions.
- Systemic form usually affects the skin and many organs, and the oral mucosa in 35-
40% of the cases.
- SLE is a multi-systemic disease characterised by 11 clinical criteria and laboratory
diagnostic criteria, if 4 or more of these criteria are present:
● Malar rash
● Discoid rash
● Photosensitivity
● Oral ulcers
● Arthritis
● Serositis
● Renal disorder
● Neurological disorder
● Haematological disorder
Allergology final
● Immunological disorders
● Antinuclear antibody

Oral manifestations:

- Painful erosions or ulcers

- Petechiae
- Edema
- Haemorrhages
- Xerostomia

Diagnosis

Lab tests:

- Histopathological examination:perivascular lymphocytic infiltration, vascular dilation

and edema in the upper CT, hydronic degeneration of the basal-cell layer and
atrophy of the epithelium
- Direct immunofluorescence shows granular or linear thick bands of IgG,IgM,IgA and
C3 deposition at the basal membrane zone of the epithelium and in the dermal
vessels
- Serological and other findings in the systematic form such as anti-ANA, anti-nDNA,
anti-SS-A and anti-Ro, anti-SS-B and anti-La , anti-nRNP,ESR

DD-Lichen planus,pemphigoid,pemphigus, erythema multiforme, Stevens-Johnson’s

disease

Management

- Avoid sun exposure

- Topical steroids, antimalarials, Dapsone,systemic steroids, Isotretinoin,
Azathioprine and other immunosuppressive drugs
Allergology final
4) Behçet's disease -Is a rare immune-mediated small-vessel systemic vasculitis that
often manifests with mucous membrane ulceration and ocular problems.
- Is a triple symptom complex-recurrent aphthous ulcers,genital ulcers and uveitis.
- A systemic disease can also involve- visceral organs: GI tract,
pulmonary,musculoskeletal,cardiovascular and neurological systems.

Clinical findings

- Skin and mucosa-aphthous stomatitis, inflammatory bowel disease,erythema

nodosum, lesions similar to pyoderma gangrenosum
- Ocular system-uveitis,retinal vasculitis etc
- Bowels- pain, nausea, diarrhoea,tenderness,bloating etc.
- Lungs- hemoptysis,pleuritis,cough, fever
- Musculoskeletal system-arthralgia
- Neurological system-chronic meningoencephalitis
- Cardiac-pericarditis

Diagnosis

The patient must have oral ulcers at least 3 times in 12 months along with 2 out of 4
‘hallmark’ symptoms:

- Genital ulcers
- Skin lesions
- Eye inflammation
- Pathergy reaction( papule >2 mm after 24-48h or more after needle-prick)

Management

- Colchicine
- Corticosteroids
- Immunosuppressive therapy- cyclosporine A, Azathioprine, Cyclophosphamide
- Anticoagulation and platelet antiaggregation
Allergology final
5) Erythema exudativum multiforme (EEM) - Erythema multiforme is a skin condition of
unknown cause, possibly mediated by deposition of immune complex (mostly IgM)
in the superficial microvasculature of the skin and oral mucous membrane that
usually follows an infection or drug exposure. It is an uncommon disorder, with peak
incidence in the second and third decades of life.

Clinical findings:

- The condition varies from mild,self-limited rash to severe.life threatening form

known as erythema multiforme major(Stevens-Johnson syndrome,SJS) that also
involves mucous membranes.
- SJS is characterised by the presence of target lesions, blistering and detachment of
the skin and mucous membranes.EM major also tends to follow herpes simplex
virus infections.
- Oral lesions are irregular and painful.

Diagnosis: The appearance of the rash can be visually identified but also viral and biopsy
can be applied.

Management: Depends on the etiology:

- Allergic cases-antihistamines and vitamin C

- Cases with recurrent HSV infection-Acyclovir
- Cases with bacterial infection-Erythromycin,Tetracycline
- Cases with oral manifestations only-topical adhesive bases
- Severe forms-systemic steroids in combination with wide-spectrum antibiotics

6) Linear IGA disease ( dermatosis) - Is an autoimmune,subepidermal vesiculobullous

disease that may be idiopathic, drug induced or triggered by preceding infection or
cancer.It is similar to bullous pemphigoid dermatitis herpetiformis, associated with
HLA-B8 and gluten sensitivity and linear deposition of IgA along the basement
membrane and often has circulating IgA antibodies. Remission occurs in children
after 2 years of onset usually and in adults within 5-6 years of onset usually.
Allergology final
Clinical findings

- Prolonged prodromal itching, transient pruritus or burning before lesions

appear,ocular manifestations are characterised by pain, grittiness or
discharge.Bullae may be chronic or appear acutely ,as seen in drug-induced
disease.Lesions in children are typically located over the lower abdomen and
anogenital region; in adults the lesions overlie the trunk and limbs.
- Oral manifestations are similar to bullous pemphigoid and dermatitis herpetiformis
lesions.

Diagnosis

- Direct immunofluorescence-linear IgA along the basement membrane

- Biopsy

Management: Leave bullae intact; cover ruptured lesions and erosions with sterile
dressings.

7) Pemphigus - Is a blistering autoimmune disease that affects the skin and mucous
membranes. In pemphigus autoantibodies against desmoglein(protein) are formed.
These autoantibodies attack desmogleins and destroy the desmosomes-a
phenomenon called acantholysis. This causes blisters on skin and mucous
membranes that slough off and turn into sores.

Clinical features:

- Clusters of blisters usually appear first in the mouth and then gradually spread over
the skin of the rest of the body.
- When blisters burst, they leave round patches of raw and tender skin.
- The skin itches, burns and gives off an odour.
- The patient loses appetite and weight, in the progressed stage it may cause
extreme weakness , prostration and shock accompanied by child sweating, fever
and often pneumonia.

Diagnosis: Histopathology and direct immunofluorescence, biopsy

Management

- Oral steroids-Prednisone
Allergology final
- Topical steroids
- Immunosuppressive agents( Cyclosporine A)
- Intravenous gamma globulin

11.Specific oral allergies.

1) Angioedema - Recurrent large circumscribed areas of subcutaneous or mucosal

edema of sudden onset, usually disappearing within 24h. Frequently as an allergic
reaction to food or drugs. Is a manifestation of immediate type of hypersensitivity

Acquires angioedema (AAE)-can be immunologic , non immunologic or idiopathic.It is

usually caused by allergy. It can also be caused as a side effect to certain medications ;
ACE inhibitors.

Hereditary angioedema(HAE)-exists in 3 forms, all of which are caused by a genetic

mutation inherited in an autosomal dominant form.

-TypeI and Type II are caused by mutations in the SERPING1 gene,which result in either
diminished levels of the C1-inhibitor protein( TYPE I) or dysfunctional forms of the
same protein(TYPE II)

-Type III has been linked with mutations in the F12 gene, which encodes the coagulation
protein factor XII.

Clinical findings

- Swelling usually around the mouth and the mucosa of the mouth and or throat as
well as the tongue for several minutes to hours.
- It can also appear in the hands or other parts
- HAE that involves the larynx, can cause asphyxiation
- It can be itchy or painful
Allergology final
- In severe cases, stridor of the airway occurs with gasping or wheezy inspiratory
breath sounds and decreasing O2 levels.
- Usually edema develops over 12-36h and subsides within 2-5 days

Diagnosis: Based upon clinical findings, Biopsy is not necessary

Management: Should visit specialists for complete evaluation

2) Oral lichen planus- Is associated with allergies to different metals, contained in the
metal alloys-mercury,gold,nickel,chromium,cobalt,copper,zinc, palladium, platinum.

Lichen planus is an autoimmune inflammatory much-cutaneous disease.It is characterised

by eruption of flat-topped,shiny, violaceous papules on flexor surfaces, male
genitalia and oral mucosa.

Clinical findings

- White or blue-white striae forming an interweaving lace like network of lines of

epithelial thickening
- OLLs are in complete or partial contact with restorations of precious or non-precious
metals and alloys.The are usually symptomless
- Toxic,irritant or allergic reactions to amalgam alloys are the most common reason
for OLLs
- Lichen planus is bilateral and symmetrical , and the contact with the metals is not
compulsory compared to the oral lichen planus.
- In OLLs the mucosal changes disappear after the irritant is removed.

Diagnosis

- Patch test with dental materials, which are present in the patient’s restorations
- Biopsy is NOT needed
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3) Allergic contact dermatitis - Is contact hypersensitivity in the oral cavity which is
triggered by antigens, comprising dentifrices(tooth pastes etc), local antimicrobial
drugs, systemic drugs etc.

Allergy to dental materials appears commonly through IV hypersensitivity reaction and less
often through type I. Oral mucosa is affected less than the skin.

Clinical findings

- Erythema
- Petechiae
- Papules
- Vesicles
- Bullas
- Erosions
- Ulcers

They are found on the mucosa mostly and rarely on the gingival.

-Medicamentous allergic stomatitis: Is a type IV allergic reaction to drugs.Pathologic

changes are diffusely visible on oral mucosa, usually affecting huge areas from 20-40
mm.They often begin as inflammation with deem, followed by huge confluent erosions with
pseudo-membranes.They can manifest in the form of bullas also

-Fixed drug reaction: Is a localised or fixed allergic reaction.It occurs on oral mucosa in the
form of localised, sharply demarcated erosion with thick pseudomembranes.Localised
lesions are to be expected on the hard palate mucosa,dorsum of the tongue or on the
lip.They always appear on the same spot after repeated contact with the allergen.

-Stomatitis(cheilitis) venenata-is a contact allergic reaction caused by different chemical

and cosmetic substances on the lips and oral mucosa.It is manifested as inflammation with
highly pronounced edema,followed by small erosions.With chronic local irritation on the
lips, exfoliative cheilitis with strong exudation can be expected.

-Contact allergic stomatitis-is due to different materials such as nickel sulphate, mercury
based, gold etc

Other reasons for oral mucosa allergic reactions can be;

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- Composites
- Ethereal oils
- Silicon and polyester impression materials etc

Patient’s complaints:

- Tingling
- Pruritus
- Burning
- Pain
- Swelling
- Xerostomia
- Dyspepsia

Diagnosis : Lab tests and patch test

Management:

- Removal of allergen
- Systemic antihistamines( Zyrtec,Xyzal,Claritin)
- local steroids

12.Dental materials with allergic potential – metals, acrylates, root canal filling
materials. Short characteristics.

1) Dental amalgam
- Oral lichenoid lesions are the most common clinical manifestation of
hypersensitivity to the components of dental amalgam.
- They are a result of cell mediated reaction (type 4) and are located on the oral
mucosa on contact with the amalgam restorations.
- There are reports of acute and generalised reactions occurring immediately after
the amalgam filling-bullas on oral mucosa in contact with the restored tooth and
ipsilateral itching rash of the facial skin; urticaria.
- Most of these reactions are self-limiting and will disappear after a few days.
- There is a contact (cell-mediated - type IV) reaction to the amalgam and a chronic
toxic reaction due to the repeated constant effect of the toxic agent in low
concentration for a long period of time.
- In acute cases there is a rapid development of local and distant symptoms, which
indicate type I hypersensitivity reaction.
- Dentist’s approach: use of alternative materials
Allergology final
2) Formaldehyde
- Used in cosmetics, endo filling materials etc
- Can induce delayed type 4 hypersensitivity( allergic cheilitis, stomatitis)
- IgE mediates sensitisation is very rare but can be life threatening
- It binds to proteins of periapical tissues and becomes a complete allergen.
- Symptoms- angioedema,asthma,CV reaction, urticaria ,dyspnea, rhinitis

3) Eugenol
- Reacts usually as a contact allergen and induces localised delayed type 4
hypersensitivity reaction.
- It can also provoke immediate allergy, including anaphylactic shock.Eugenol-
specific-IgE are determined in these patients.

4) Chlorhexidine
- Is an antiseptic
- Allergic reactions can be type I or IV

5) NSAIDs and Antibiotics

- xerostomia
- saliva color changes
- salivary glands swelling
- mouth pain
- contact stomatitis
- aphthous-like lesion and ulcerations
- oral candidiasis
- fixed erythema
- vesiculobullous lesions
- pemphigus
- lupus
- lichen planus
- erythema multiforme
- cheilitis
- glossitis
- swelling of the lips and oral mucosa
- dental discolouration etc
Allergology final
6) Metal allergy
- type IV hypersensitivity reaction
- can be on metals(precious/ non-precious), or metal alloys containing nickel
sulphate, cobalt etc
- can also cause oral lichenoid lesions and/or leukoplakia in the buccal mucosa and
tongue caused by metal alloys.

13. Allergy to dental materials – clinical features.

Dental materials and medications can cause all types of allergic reactions from I to IV.

Allergic reactions manifest:

- Asthma
- Urticaria and Quincke’s edema
- Allergic shock
- Immune hemolytic anemia
- Thrombocytopenia and agranulocytosis
- Serum sickness and vacuities
- Drug-induced lupus and contact hypersensitivity reactions

Non allergic reactions:

- Pseudo-allergic
- Toxic

Skin reactions

- Abnormal metabolism

Drugs commonly cause drug allergy:

Allergology final
- Antibiotics- beta-lactams (penicillins and cephalosporins), streptomycin, kanamycin
A, neomycin B, chloramphenicol, tetracyclines, aminoglycoside, macrolides.
- Chemotherapeutic agents – sulfonamide preparations
- X-ray contrast agents containing iodine.
- Analgesics and anti-inflammatory drugs – aspirin, antipyretics, NSAIDs.
- Anesthetics and neuroleptics – agents for general and local anesthesia (muscle
relaxants and local anesthetics).
- Corticosteroids.
- Polypeptide hormones – insulin.
- Other products-gold salts, hydralazine

Allergic reactions to acrylic dentures can be:

- Early – induced by some of their components or degradation products: monomer,

coloring agents, inhibitors, activators, formaldehyde.
- Later – due to the allergic potential acquisition by plastics in the oral environment
through saliva absorbing and microbial contamination.
- Late – triggered by aging plastic products after extended periods of use of acrylic
dentures – some of these are potent antigens – e.g. formaldehyde, which is
converted to paraformaldehyde.

One of the most common allergens in allergic denture stomatitis is the monomer (released
or residual) which diffuses slowly and over a long period.

Allergic reactions are reported to all metals, as these induced by non-precious ones
prevail.

Management: Patch test, Prevention of occupational sensitization requires hazard-

reducing measures in the work environment and mandatory testing of dental
students (especially these in the risk groups).

14.Latex in dentistry. Dentist’s approach in cases of latex allergy.

-Immediate IgE-mediated allergy.

Latex protein
Allergology final
Natural rubber latex (NRL) is produced by the Hevea brasiliensis tree.

Latex allergy (LA) - Immune-mediated, non-localized. It is a result of type I hypersensitivity

reaction, and develops several minutes after exposure to the allergen.

Symptoms

- Redness and swelling of the lips and facial skin

- Itching
- General urticaria(seldom)
- Respiratory symptoms:Rhinorrhea,sneezing,wheezing,hoarse voice, asthma attack
- Anaphylactic shock (rarely)

-Symptoms vary from mild to severe, depending on the degree of sensibilisation and
weight exposure. They aggregate in repeated exposures, so the usual progression
is: Asymptomatic exposure->contact dermatitis->rhinitis,asthma-> anaphylaxis

There are 3 principles about latex reaction:

1.Severity of prior resections is not predictive of the future experience

2.Severe anaphylactic shock reactions can occur after any route of exposure

3.Mucosal exposure leads to more severe reactions

Latex allergy can be a manifestation of the latex-fruit syndrome, especially in patients

sensitised to avocado, banana, chestnut and kiwi

Diagnosis through medical history and testing-RAST (IgE) ,SPT

Allergic contact dermatitis

- Immune-mediated, localised
- It is a result of type IV hypersensitivity reaction to chemicals added to lates during
processing
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- Symptoms are: early -blistering, erythema, papules and chronic- dry skin with
vesicles, crusts, deep and painful fissures, pigmentation, itching
- Diagnosis-through medical history and patch testing

Irritant contact dermatitis

- Non-immunological, localised
- The most common reaction to latex
- Is due to sweating or rubbing under the gloves and from residual soaps and
detergents in prolonged contact with the gloved cutaneous skin
- Symptoms- chafing (rubbing) , patchy or dry, crusty, cracked skin

Populations at risk for latex allergy:

- Children with spina bifida or other diseases who have undergone multiple surgical
procedures, and patients with genitourinary abnormalities, requiring frequent
catheterisation
- Atopic individuals( asthma, rhinitis, eczema)
- Patients with food allergies especially to: banana, pinepale, avocado, chestnut, kiwi,
mango, passion fruit etc
- Industrial rubber workers, exposed for long periods to high amounts of latex
- Health care providers

Latex in practice: Latex gloves, Rubber dam, Rubber gaskets in the disposable syringes,
Rubber diaphragms and silicon rubber plungers in the anesthetic carpules, Endodontic file
stoppers, Face masks, Orthodontic elastic rubber bands and ties, Orthodontic headgears
and chin cups, Rubber polishers, Disposable saliva ejectors, Mouth gags and cheek
retractors, Tourniquets

Dental patient can be sensitised:

- Skin and mucosal- as mucosal contact implies bigger risk for anaphylaxis
- Respiratory- allergenic latex protein absorbed on the glove powder become
airborne ,when latex gloves are donned and taken off and can be directly inhaled

The following symptoms during dental procedures should not be neglected:

Allergology final
- Itching of the lips and skin
- Lips and tongue swelling
- Perioral or facial rash
- Chest tightness
- Tachycardia
- Hypotension

Dentist’s approach:

- Patients have experienced type I hypersensitivity reactions are in great risk for
anaphylaxis
- Patients at high risk should be identified
- Take a medical history
- All individuals with suspected LA (history) should get tested to identify if the allergy
is due to latex and/or rubber additives-SPT , RAST ,patch test

In cases of latex allergic patients the followings should be applied:

- Documentation of LA in patient’s record

- Placement of medical alert bracelet
- Supply with an epinephrine self injection kit
- Providing a latex free environment
- Early morning appointments
- Premedication with antihistamine and corticosteroids
- Readiness for immediate resuscitation

15.Occupational allergies in dental staff.

Dental products contain a number of allergens and irritants. Side effects can
be:Toxic ,irritant, allergic.

Chemical agents that cause allergic reactions, can be found in a number of dental
materials agents, adhesives, metals, medicines, dental antiseptics and disinfectants,
preservatives used in the manufacture of rubber chemicals (resins, binders, sealants,
vulcanization accelerators and stabilizers), and in medical gloves.

Repeated exposure to these chemical agents can cause occupational dermatitis in dental
professionals.
Allergology final
Main occupational allergens:

- Components in latex gloves

- (Meth)Acrylates
- Disinfectants
- Resin and eugenol materials
- Metals(cobalt, chromium, nickel)

Allergic reactions to disinfectants:

In medicine and in particular -in dental practice, there is a high risk of sensitization to some
biocides (thimerosal, glutaraldehyde, formaldehyde, glyoxal). In other antimicrobial agents,
which are potentially irritating or allergenic, cresol, mercury derivatives, quaternary
ammonium compounds, phenolics,chlorhexidine, alcohols are included.

Allergic reactions to acrylics and dental resin composites:The resins have good
mechanical and chemical properties and are widely used in dental materials. They are
included in the resin composites, bond systems, sealants, materials for orthodontic
appliances, crowns, bridges, dentures, in materials for relining and reparation, for
temporary restorations in prosthetic dentistry, cements and others.

Methacrylates are a widely recognized cause of allergic contact dermatitis.

Acrylates are plastic materials formed by polymerization of monomers derived from acrylic
or methacrylic acid. Polymerization can be accomplished at room temperature or with
heat.

Allergic reactions caused by gloves

The natural latex protein was used to make a variety of tools used in medicine, and
dentistry. The reason for this is the strength, elasticity, flexibility, resistance to tearing, and
good barrier properties.

Allergy to latex protein became highly relevant in the last three decades due to the
increased use of latex gloves and a reduction in production control, leading to a high
content of free latex protein. Exposure is through skin contact with the water soluble
proteins on the surface of medical gloves.
Allergology final
Allergy to latex gloves can occur as immediate reactions( contact urticaria, which is IgE-
mediated) or delayed reactions (contact dermatitis hypersensitivity mediated by T
lymphocytes)

Allergic reactions to eugenol and resin

Eugenol is an essential ingredient on the liquid of ZnO-eugenol pastes.It can be found in

impression materials, periodontal dressings, cements, liners, and temporary filling
materials.

Resin is a widespread flavour enhancer- it causes allergic contact dermatitis.

Allergic reactions to alloys

10/34 different metals are contact allergens.Some have toxic and carcinogenic effects.

The most important metal allergens are: Nickel, chromium, cobalt

Clinical characteristic of occupational allergy and/or atopic dermatitis in dental practice:

The above allergens or irritants can play a role in the clinical manifestation of type
hypersensitivity, allergic contact dermatitis or irritant contact dermatitis.

Contact urticaria-IgE based allergic reaction of immediate type with skin

symptoms ,accompanied sometimes by asthma and anaphylactic symptoms.

Allergic contact dermatitis-is a cell mediated hypersensitivity reaction (IV type),which is

almost always manifested in the area of contact with the skin localized mainly in those
areas (fingers).

Symptoms can range from dry skin to chronic eczema tic wetting or bleeding wounds.

Skin symptoms develop slowly and may persist for weeks or months.
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Irritant contact dermatitis(ICD)- may have a sharp, direct and immediate cytotoxic effect on
skin cells. More often, however, among dental personnel observed cumulative
dermatitis resulting from repeated contact with chemical subtoxic concentrations.
ICD is limited at site exposure and disappears soon after removal of the stimulus.

Diagnosis depends on the precise interpretation of the data from the history, symptoms
and results of SATs. In some cases, in addition blood tests are used to confirm allergy to
natural latex protein.

Full diagnostics include a detailed history, SAT or serological tests-they are necessary for
the proper distinction between irritant , allergic contact dermatitis and type I
hypersensitivity.

Prevention of occupational sensitizations in dental practice:

Once occupational allergy is diagnosed, it is necessary to take measures to reduce and

eliminate the symptoms. A major problem for effective coping with occupational allergies in
dental professionals is their low awareness.

On the other hand, not all allergists and dermatologists do the required comprehensive
testing to establish causal allergens and unfortunately corticosteroid therapy is still the only
way to treat occupational dermatitis.

Routinely used protective equipment in dental practice do not constitute adequate

protection against numerous professional allergens.

Creams after work provide some protection against developing irritant contact dermatitis.

Control of type I hypersensitivity:

Dental specialists with type I reaction to natural rubber proteins should avoid direct contact
and inhalation exposure.

People with allergies can use latex-free gloves and synthetic rubber products as well as
barrier creams that isolate direct contact with natural latex components.

Control of allergic contact dermatitis

Allergology final
In allergy thiurams (which function as accelerators in the vulcanization of rubber) and
carbamates of latex gloves it is necessary to choose the gloves of polyvinyl, polyurethane,
or styrene, those that do not pass through the curing process, and does not contain these
ingredients.

Exposure to glutaraldehyde can be reduced by changing the system for disinfection and
sterilization of instruments, use of hydrogen peroxide, peracetic acid or heat. Alternatively,
one can use chemical resistant gloves when handling the instrument as medical grade
gloves are not appropriate.

If you are allergic to methacrylates, it is necessary to avoid contact with bonding agents
and acrylic resins. Best protection is assured by 4H gloves, followed by nitrile ones.

Control of irritant contact dermatitis: It is based on the reduction or avoidance of exposure

to chemical agents.

16. Local anesthetics – allergenicity and allergic reactions. Dentist’s approach.

Allergic reactions:
Immune-mediated hypersensitivity reactions due to local aesthetics are rare, most side
effects are due to aesthetics’ toxicity or vasovagal effects.Allergic reactions can occur in
the following mechanisms:
• Type I hypersensitivity,IgE mediated reaction, characterized by massive release of
histamine,
serotonin, leukotriene and prostaglandin.
• Type IV hypersensitivity, cell-mediated response that develops within 2-3 days after the
administration.

Allergic reactions due to local anesthetics:

• Skin reactions(rashes,pruritus,edema and urticaria)
• Rhinorrhea
• Conjunctivitis
• Asthma like attack
• Anaphylactic shock

Anesthetics groups and allergenicity:

Immediate hypersensitivity reactions are mainly due to amides

And cell mediates ones due to esters

-Esters of para-aminobenzoic acid : Benzocaine, Procaine,

Chloroprocaine,Piperocaine,Tetracaine,Cocaine
Allergology final
- Amides: Articaine,Bupivacaine, Cinchocaine,Lidocaine, Mepivacaine,
Prilocaine,Ropivacaine

Adverse reactions due to additives:

• Parabens
• Sulfites- oral and nasal administration of sulphites may cause: bronchospasm,
rhinoconjunctivitis,urticaria,anaphylaxis
• Epinephrine

Local anaesthetic toxicity:

- if administered in excessive doses
- If administered improperly

In immune system-> anaphylaxis

In hematologic system->Methemoglobinemia
In the necrologic system -> tinnitus, tingling/numbness of mouth, tremor and blurred vision
etc.
In cardiovascular system->myocardial depression, bradycardia, CV collapse, cardiac
arrhythmia

Dentist’s approach to local aesthetics :

All individuals with suspected allergy to local aesthetics ,should be counselled by an
allergist and get tested to determine sensitisation to the anaesthetic agent or to the
additives-SPT and patch test.
In patients with allergy to local aesthetics the following precautions should be used:
• Documentation of this allergy in the patient's record.
• Placement of medical alert bracelet to indicate allergy to aesthetics
• If a patient is allergic to a certain anesthetic agent, a different one should be used. •
Premedication with antihistamines and corticosteroids
• Readiness for immediate resuscitation measures.

Premedication:

Premedication in non-allergic patients, with negative SPTs:

-H1-antihistamines:Zyrtec 10mg/d,Xyzal 5mg/d,Claritin 10 mg/d, Aerius 5mg/d etc; 3 days

before and 3 days after the procedure.
-H2-antihistamines: Zantac 300 mg/d, Quamatel 40mg/d; 3 days before and 3 days after
the procedure.
-Vitamines: Vitamin C 1000mg/d; 3 days before and 3 days after the procedure.

Premeditation in non-allergic patients, with positive SPTs:

-H1-antihistamines:Zyrtec 10mg/d,Xyzal 5mg/d,Claritin 10 mg/d, Aerius 5mg/d etc; 5 days

before and 5 days after the procedure.
-H2-antihistamines: Zantac 300 mg/d, Quamatel 40mg/d; 5 days before and 5 days after
the procedure.
-Vitamines: Vitamin C 1000mg/d; 5 days before and 5 days after the procedure.
-Steroids:Prednisolone 4x5 mg/d; 5 days before and 5 days after the procedure.
Allergology final
Premeditation to allergic patients, with negative SPTs:

-H1-antihistamines:Zyrtec 10mg/d,Xyzal 5mg/d,Claritin 10 mg/d, Aerius 5mg/d etc; 5 days

before and 5 days after the procedure.
-H2-antihistamines: Zantac 300 mg/d, Quamatel 40mg/d; 5 days before and 5 days after
the procedure.
-Vitamines: Vitamin C 1000mg/d; 5 days before and 5 days after the procedure.
-Steroids:Prednisolone 4x5 mg/d; 5 days before and 5 days after the procedure.

Premedication to allergic patients, with positive SPTs:

-H1-antihistamines:Zyrtec 10mg/d,Xyzal 5mg/d,Claritin 10 mg/d, Aerius 5mg/d etc; 7 days

before and 7 days after the procedure.
-H2-antihistamines: Zantac 300 mg/d, Quamatel 40mg/d; 7 days before and 7 days after
the procedure.
-Vitamines: Vitamin C 1000mg/d; 7 days before and 7 days after the procedure. -
Steroids:Prednisolone 4x5 mg/d; 5 days before and 5 days after the procedure,
Methylprednisolone 40-60 mg IM; 1 hour before the procedure.

17.Allergic reactions during local anesthesia. Anaphylactic shock. Management.

Emergency medical care in dentistry is most commonly in connection with local

anesthesia.
A major complication after local anesthesia is considered orthostatic cardiovascular
collapse, which is clinically demonstrated by loss of consciousness.
The main reason for this can be given to the fear of impending manipulation, the situation
in the dental office, hypotension, hormonal disorders.
The loss of consciousness is due to cerebral ischemia and is expressed clinically by the
collapsing of the patient, and loss of contact therewith.
Local anesthesia can be safe when provided properly (aspiration).
Allergy to local anesthetics is primarily to sulfites. Sulphates
Interactions between drugs and local anesthetics are rare.
Most deaths in dentistry are related to general anesthesia.
Before general anesthesia the patient should not take food for six hours, and liquids for
three hours in adults and up to two hours in children.
Premedication should be done by an anesthesiologist.
All patients should be monitored preoperatively clinically (pulse oximetry and blood
pressure).
Conditions caused by anesthetics:
- Respiratory failure;
Allergology final
- Respiratory obstruction;
- Reaction to drugs or overdose of anesthetic;
- Heart failure;
- Anaphylaxis;
- Failure in patients receiving corticosteroid therapy.
Allergic immediate reactions are responsible for emergencies in dentistry. They occur
immediately after exposure of the sensitized organism to the causative allergen –
they appear after several seconds to several hours.

Anaphylaxis:
General characteristics:
- it may be a consequence of the application of any drug, in particular penicillin and
different anesthetics placed i.v.
- more likely to occur after the patient has used drugs.
- can occur after a few to 30 minutes after taking the medication.
It is possible to show in the following patients:
-allergic to the accepted or similar type of medicine;
-with any type of allergy;
-with asthma, with eczema or a high temperature;
-without medical history of allergy or even in patients not taking drugs.
Prevention:
1. Prevention of potential allergens.
2. Allergy-oriented medical history.
3. When you administer any kind of injection, particularly i.m., the patient should be lying
on a hard, flat surface because of the possibility of seizure, if the injection is placed
on a standing patient may have difficulty differentiating between anaphylaxis from
simple fainting

Symptoms
- Fainting.
- Acute hypotension.
- Bronchospasm.
- Possible angioedema and / or urticaria

Dentist’s approach
1.Placing the patient lying down with raised legs;
2.Immediately give the necessary medication:
Allergology final
- Adrenalin 1:1000 in 1 mg / ml im or sc.
- Oxygen.
- Methylprednisolone - more efficient than Hydrocortisone, but more expensive – i.v.
solution of 500 mg.
- Hydrocortisone – i.v. 100-500 mg slow.
3. Providing airway patency.

Actions
- Setting the state of the patient.
- Calling the EMS.
- Immediate first aid.
- Set injection Epinephrine (adrenalin) 1:1000, 0.3 cc s.c. or i.m. every 3-5 minutes, if
necessary.
- Diphenhydramine 25-50 mg iv or im and Hydrocortisone 100 mg.
- Transporting the patient to the nearest hospital for medical emergencies.
- Tracheotomy at risk of constriction of the upper airways.

18. Burning mouth syndrome.

-Is a distinctive nosological entity characterised by unremitting oral burning or similar pain
in the absence of detectable mucosal changes and burning pain in the tongue or other oral
mucosal membranes.
-It most affects middle aged or elderly women
-Burning and pain is often accompanied by xerostomia, persethisia(tingling), and altered
taste or smell( dysgeusia, dysosmia)

● Classification: -can be idiopathic or linked with various conditions.

• Primary(real) BMS: subjective symptoms in the oral cavity that CANNOT be linked with
local or systemic cause
• Secondary BMS:burning sensation caused by local or systemic factors
-Type I:Symptoms present upon walking and increase throughout the day.Due to
SYSTEMIC DISEASES.
-Type II:Constant symptoms upon walking and through the day, but not at
night.PSYCHOGENIC FACTORS-depression and anxiety
Allergology final
-Type III:Alteration of days with symptoms and symptomless ones. DENTAL
MATERIALS,food,additives and preservatives
● Clinical features
Symptomatic triad:
-Constant burning pain on the oral mucosa(major)
-Dysgeusia (altered taste)
-Lack of oral lesions

● Diagnosis
-Medical history
-General health status: diabetes, thyroid disorders, allergies ,GERD etc.
-BMS is a diagnosis of exclusion
-BMS is difficult to diagnose due to several reason:
• BMS is defined by symptoms only-NO SPECIFIC CLINICAL FEATURES AND
ETIOLOGICAL FACTORS
• Symptomatic triad is rarely found in one
• Superimposed inflammation on oral mucosa can mask the clinical features

● Differential diagnosis - Oral allergy syndrome,Sjorgen syndrome,Lichen

planus,Denture stomatitis, Candidiasis, Leukoplakia,Contact stomatitis, GERD,
anemia, Vitamin deficiency, others

● Paraclinical studies:
- Salivary studies- sialometry,bacterial and fungal cultures
- Lab tests- CBC,serum blood glucose,electrolytes etc
- Psychologic screening

● Management
• Treatment is individual and based on the symptoms
• Variety of treatment plans and drugs
• Methods- cognitive behavioural therapy, acupuncture from stimulation of oral
microcirculation, low energy diode laser
• Secondary BMS treatment is directed to etiological factors removal
• In cases of primary BMS the patient is referred to neurologist and/or psychiatrist
Allergology final

19. Immunotherapy.
Is a medical term defined as ‘treatment of disease by inducing, enhancing or suppressing
an immune response ‘
The main goal of immunotherapy is to support the body’s natural defences to limit and
eradicate some of the listed diseases.
➔ The immunotherapeutic agents may be divided in:
• Immunostimulators- stimulating antibody-dependent and cell-mediated immune
responses
• Immunomodulators-regulating effect on immune response
• Immunosuppressants - agents that suppress the immune response
• Immune Correctors-impacting of certain elements of the immune system

➔ Approaches of immunotherapy:
• Active immunotherapy-agents for stimulation of the immune response
• Passive immunotherapy- immunoglobulin preparations
• Specific immunotherapy-directed towards certain antigens
• Non- specific immunotherapy-directed towards immune response as a whole

➔ Specific immunotherapy:
Long term therapeutic and immunomodulatory effects in treatment of diseases such as
allergic rhinitis, asthma, and hypersensitivity to poisons could be achieved only applying
specific immunotherapy
➔ Mechanism:
-They shift the patient’s immune response to an allergen from a predominantly “allergic” T-
lymphocyte response to a “non-allergic” T-lymphocyte response.
-After administration, the seasonal increase in allergen specific IgE is blunted while
protective allergen specific IgG4 production is increased.

➔ Indications for allergen immunotherapy:

-The diagnosis Is based on the history and physical examination findings , supported by
testing to confirm IgE sensitisation.
-Skin testing by prick or intradermal methods are preferred.
-In vitro tests such as CAP RASTs are an alternative
Allergology final
➔ Indications for immunotherapy :
• Allergic rhinitis
• Allergic asthma
• Venom allergy / poison
➔ Contraindications for immunotherapy:
• Atopic dermatitis
• Food allergy
• Chronic urticaria / angioedema
• Autoimmune disease
• Lack of response after previous specific immunotherapy
• Lack of relief in symptoms after a two-years long therapy
➔ Relative contraindications:
• Unstable asthma
• Severe coronary/ ischemic disease
• Malignancy
• Children younger than 5

➔ Possible problems:
-The β-blocker therapy (including eye drops) may hamper the immunotherapy. However,
specific immunotherapy is applied in patients receiving β-blockers in cases with life-
threatening hypersensitivity to insect venom, as the risk of systemic reactions to insect
stings is greater than the risk of the immunotherapy.
-Pregnancy is not a contraindication, but immunotherapy is usually not initiated during
pregnancy If a patient becomes pregnant while performing immunotherapy, the dose is
maintained at the previous level to avoid anaphylaxis.

➔ Allergen extracts for specific immunotherapy:

• Liquid-most widely used
• Lyophilized- risk of unpredictable changes in the allergen molecule during lyophilisation
• Modified allergens- reduced or removed allergenicity and preserved immunogenicity
• Mixed allergen extracts
• Liposome extracts

➔ The control, efficacy and outcomes of specific immunotherapy/hyposensitisation are

based on:
Allergology final
• Symptoms and general status, respiratory function and amount of medicine accepted
• Exposure and provocation testing, skin tests
• Respiratory infections, days of temporary work disability or spent in hospital setting
• Laboratory testing-allergen-specific IgE,IgG and other classes of antibodies,
determination of mediators and cells of allergic inflammation

➔ Alternative routes of immunotherapy

-Sublingual-swallow route: involving the administration of drops or rapid-dissolving tablets
under the tongue for 2-3 minutes, usually followed by swallowing.There is efficacy for
seasonal and perennial rhinitis, but is less effective than sublingual-swallow route.
-Intranasal route: Is effective, but local side effects may require pre-treatment with
antihistamines or cromoglycate.
-Oral route: is not recommended
-Inhaled route: is not recommended due to risks of side effects.

• The introduction of modified-synthetic and recombinant allergens allows better

standardisation of allergen extracts and opportunity for individualised treatment
according to individual sensitivity.
• The opportunity to use novel adjuvants to modify T lymphocyte responses is under
investigation.

➔ Practical approaches of specific immunotherapy/hyposensitization.

• Standard allergen immunotherapy is administered as a subcutaneous injection in the
upper part of the external surface of the upper arm.
• The allergologist chooses relevant allergen extracts based on the patient's clinical
history, data available about exposure to allergens, and the results of allergen-
specific IgE-antibodies testing.
• Only clinically relevant allergens should be applied using standardised allergen extract
solutions.
• When preparing the mixtures of allergen extracts, the physician should take into
consideration a possible cross-reactivity between allergens.
• Allergen specific immunotherapy/hyposensitization consists of 2 treatment phases: The
buildup phase and the maintenance phase
• The starting dose is 1000-10,000-fold less than the maintenance dose. For patients
highly sensitive, the starting dose may be even less.
• The maintenance phase begins when the effective therapeutic dose is achieved.
Allergology final
• Immunotherapy protocols involve injections 8-16 weeks during an updating phase,
followed by monthly maintenance injections, according to the individual protocol,
for a period of 3-5 years.
• The efficiency of immunotherapy depends on obtaining the optimal therapeutic dose of
each allergen extract.
• Clinical improvement can be observed shortly after the patient reaches the maintenance
dose.
• If no improvements, reassessment should be done.
• Immunotherapy must be performed by an allergologist and the vaccines should be
stored at 4 degrees Celsius.

20.Disturbance fields and chronic focal infection. Focal problem in oral medicine.
-Disturbance field (DF) is an energetically non-integrated area of the organism that turns
into a source of functional disturbances that may, but not necessarily, have material
fixations.
-The disturbance field constantly affects the ground regulation system of the organism and
induces certain structural changes.
Disturbance fields classification:
- Active are those that have overcome the reactive barrier and as a result there is an
impact of distance on the organism's general reactivity. They can be in a
compensation period with no clearly expressed clinical manifestation and their
presence can only be established from different test data or in a single symptom
and exposed clinical posture decompensation period.
- Dormant ones are restocked chronic pathological disorders whose local protective
barrier is still intact and therefore there is no distant disturbance.
During diagnostics of disturbance fields (DF) it is of great importance to specify the
dominant ones. Dominant is any field that has the greatest infuse on the pathogenesis of
the focal disease.
- Exogenous (environmental harms, energy DF and electrosmog) and
endogenous(80% are found in the oral cavity).

Disturbance fields-Focal diseases:

- Alopecia areata
- Otitis media
- Sinusitis chronica
- Lichen planus
- Neurodermatitis
- Glomerulonephritis chronica
- Acute arthritis, rheumatoid arthritis
- Heart rhythm disorders
- Subfebrile temperature
Allergology final
- Severe systemic diseases

Disturbance fields diagnostics:

-General reactivity tests
-Local reactivity tests: Electro-skin test of Gehlen, Local thermometry test, Thermography,
Corrosion potential measurement, Pulp vitality tests, Skin allergy tests

23.Prevention and treatment of maxillo-facial disturbance fields. Treatment plan.

Preventions: Due to the nature of the occurrence and development, the prevention of oral
disturbance fields and focal disease is primary or secondary.
Oral DFs are heavily dependent on the oral health state and the general reactivity of the
organism.The oral cavity is an entrance to numerous microorganisms.
Bacterial flora is rich and varied due to the existence of many retentive areas. Root canals
with their macro- and micro-branches systems do not allow mechanical removal of
bacterial invasion, which creates an opportunity for teeth to easily become DFs.
So first of all primary prevention is aimed to maintain the vitality of the dental pulp and
periodontal integrity. Vitality of discolored teeth or those which were the subject of
prosthetic treatment should be followed-up.
When impacted or semi-impacted teeth are detected at prophylactic examinations, it
should be carefully assessed whether they should stay in mouth or be extracted, because
they break the local reactivity of the body and often are determined as active DFs.
Periodontal tissues’ current state or their inflammatory and destructive changes,
associated with dental or medical reasons, should always be considered as the most
serious and difficult to treat DF.
Another important preventive measure is detection and removal of all allergenic factors in
the oral cavity.
Secondary prevention of focal infections is aimed at preventing activation of potential DFs
and early diagnostics of active DFs in the period of decompensation.
Measures to prevent activation and decompensation are actually actions against the terms
for activation and decompensation of potential DFs.

Treatment
1.First stage is guided by a physician with the aim to overcome the symptoms of DF-
induced disease.
2.Second stage is also guided by a physician, following the individual treatment plan, and
the aim is the patient's preparation for DF removal. At this stage dentists may also
participate actively.
Allergology final
3.Third stage is guided by the dentist and the main task is healing dental treatment. In this
stage the physician is also actively involved.
4.Fourth stage is guided by both dentist and physician and its purpose is recovery of
normal reactivity of the organism in the period after radical removal of the focal
infection. This stage is often decisive for the outcome of the disease.

-The second stage of the treatment plan includes preparation of the patient for radical
removal of the disturbance fields.
-Preparation depends on the chosen approach for DF removal (conservative or radical-
operative). For a period of 15 days the patient is given immunostimulators
(Dentavaks, Isoprinosine), antibiotics (7-10 days after antibiogram), antihistamines,
and Pyramidion (in streptococcal infection).
-Radical-operative method involves extraction of teeth determined as active odontogenic
DFs, and thorough curettage and drilling of the adjacent bone area (Türk method).
-Compilation of individual treatment plans for each patient is an extremely important and
responsible step in the complex oral treatment. It’s possible just after a
comprehensive oral diagnostic process and establishing the diagnosis.
-Patient’s reparative capabilities, based on age, overall reactivity, background pathology,
and cooperation, should be considered also in the implementation of the optimal
plan.
-Patient should be informed about the team of professionals who will work for the duration
of treatment and have to sign an informed consent form.

Treatment of “dental-focal” infection:

1.Treatment of caries
1.Endodontic treatment and retreatment if needed
2.Periodontal treatment of the entire dentition
3.Extraction of all teeth that cannot be saved
4.Follow-ups 1,6,12 months after treatment

Elimination of active DFs:

By endodontic treatment. Most authors challenge it, and some even deny it as a
therapeutic method, considering that it is a source of iatrogenic factors.
Active odontogenic and oral DFs are removed surgically, and in a symptomless period.
Mastication is then prosthetically restored. In patients, allergic to acrylics, patch test is
performed and polymers with low sensitising effect chosen.
Immunotherapy
Allergology final
The action of Imudon and other similar products is based on the included bacterial
lipopolysaccharide. These agents act as vaccines also, due to their immunostimulating
and immunomodulating effect, and stimulate the formation of homologous antibodies to
particular bacterial ingredients which assist the healing of the immunological inflammation.
As a result of their experience in the production, study and clinical application of the first
bacterial Immune Stimulator in the country, Petrunov et al. created and explored
experimentally polybacterial immune booster (vaccine) "Dentavax" – it is aimed at oral
immunotherapy and immunoprophylaxis of nonspecific inflammatory diseases of the oral
mucosa and periodontal tissues. It is based on several bacterial species: L. Acidophilus, C.
Albicans, Streptococcus pyogenes, Klebsiella pneumoniae, Staphylococcus aureus.

Dentavax is administered for the treatment of:

- Chronic catarrhal gingivitis
- Chronic periodontitis in adults
- Necrotizing ulcerative gingivitis
- Specific infections (herpes, aphthae, candidiasis, deep vertical bone pockets,
pericoronaritis with catchy breakthrough, after extractions, after tonsillectomy, in
trismus and abscesses in the maxillofacial region)
- Allergy

Instructions given to patient after surgical treatment include a diet rich in cereals, legumen,
milk, eggs, fish, fruits and vegetables in an appropriate form and combination.
Acupuncture, acupressure, climate therapy, physical therapy, and specific
hyposensitisation are also recommended.

It should be in mind that each focal treatment represents a risk which is expressed by:
- moments of worsening of disease;
- nonspecific regulatory interferences and hence - subsequential improper treatment
of secondary disease;
- possibility of temporary worsening of the clinical picture of secondary disease;
- allergic reactions;
- dysbiosis in the gastrointestinal tract as secondary DF
It is necessary to be provided:
- avoidance of surgical intervention in the acute phase of the disease;
- sufficient supply of minerals and elements in the body (particularly the shortage of
zinc and selenium, may lead to regulatory disorders);
- supply of enzymes and replacement therapy (in combination with vitamin C.)

24.Maxillofacial disturbance fields – reasons for the treatment failure.

Allergology final
Reasons for the failure of focal treatment in the maxillo-facial area are mainly associated
with misdiagnosed "allergic or focal disease" and thus making incorrect treatment plans.
Mistakes can be made during history taking, in clinical examination, and due to incorrect,
incomplete or inaccurate differential diagnosis, due to incorrect, incomplete or incorrect
diagnosis, and due to incorrect and incomplete treatment plan.
Much important are the errors of incomplete or incorrectly prescribed medication and
physical therapy, as well as determination of number and frequency of the examinations.

There are defined 4 stages in the course of focal diseases:

1.First stage: nonspecific symptoms without organ findings – reversible;
2.Second stage: nonspecific symptoms, manifested organ findings, permanent joint
complaints without significant bone changes – reversible;
3.Third stage: manifested organ findings with initial destruction – irreversible,
compensated;
4.Fourth stage:continuing irreversible organ changes.

Correctly carried focal treatment is meaningful primarily in the first and in the second stage
of the course of focal disease. The third stage has to be carefully evaluated since initial
organ destruction is present. This requires, above all, specialized therapeutic care to
unstoppable progressive course of the disease. In the fourth stage focal treatment does
not work and is rejected.

22. Thermovisional diagnostics.

Any object with a temperature higher than 0 emits infrared rays. -> The higher an object’s
T is, the more infrared radiation is emitted as black-body radiation.
Thermovision is a non-invasive contactless diagnostic method for the body, through which
temperature fluctuations can be shown on display. It is a precise and reliable method that
objectively reports changes in temperature at different points with an accuracy of tenths of
degree.

Medical analysis of the thermogram is based on the assessment of two major factors:
1) Temperature gradient-this is the value of the temperature difference between two
elements of the studied object.
The distribution of thermal emissions in the human body is uneven.There is physiological
asymmetry caused by the non-homogenous structure of the vascular system elements on
skin. The physiological asymmetry value is not bigger than 0.4 degrees.
2) Qualitative characteristics of the temperature field of the object or of a separate
fragment of the object.
Allergology final

There are 3 qualitative evaluation versions:

• Isothermia-when all or the majority of the elements of the tested object have identical or
similar temperature.
• Hypothermia-detection,within the temperature field of the objection an area with
temperature lower than the one of its surrounding elements; in terms of intensity
level hypothermia can be moderate(T gradient not higher than 1.0 degrees)
marked (T gradient 1.0-2.0 degrees) and well marked (T gradient higher than 2.0
degrees).
• Hyperthermia- detection,within the temperature field of the objector an area with a T
higher than the one of its surrounding elements; in terms of intensity level
hyperthermia is graded in the same way.
Thermovison test protocol:
• Distance between the camera and the patient-from 0.3-2 m
• Room temperature of 22 +/- 2 degrees
• No movement of air of more than 1 m/s; this is the reason why operation of fans and AC
is not allowed
• No thermal radiation open sources
• Patients or thermovision systems must not be exposed to direct sunlight or powerful
artificial lighting radiation.

The patients must remove tight and warm clothing and be isolated from any additional heat
sources, radiation etc.
Simultaneous pics of the face,right and left profiles, neck, abdomen, back are taken from
the infrared camera
T gradient greater than 0.4 degrees reveals the presence of a pathological process.

21. Local reactivity tests, applied in maxillofacial areas.

Gehlen test

Several locations were commonly claimed as foci—teeth (healthy and endodontically

treated), appendix, bladder, gallbladder, kidney, liver, prostate, and sinuses.

Recommendations concerning teeth as focus – therapy, consistent with EST and

thermography

Requirements to the patients:

Allergology final
1.No crème and make-up on the face.

2.For males – not to shave 12 hours prior to the procedure.

3.Patients should not take pain relievers, anti- inflammatory and anti-allergic drugs for at
least 1 week prior to the procedure.

Technique:

• The assay is carried out using a DC device, equipped with two electrodes. The cathode,
which is a metal cylinder, is held by the patient, and testing is performed with the anode
that ends with a soft brush. Brush is immersed in saline for closing the circuit.

The individual irritation threshold of the patient is determined initially.

Advantages:

- Non invasive
- Painless
- Easily applicable
- Highly reliable

Disadvantages:

- Counter-indicated for patients with skin diseases, pacemakers and heart valve
prostheses.
- It can’t be applied in patients with darker complexions.
- When the positive reaction is spread over an area of several teeth, the test doesn’t
alloy differentiation and gradation of activity of the foci.
- EST registers local reactivity at determined static moment – static test.
- A “blockade” is possible at first testing.
- Reading of the test is subjective and requires certain clinical experience. —
>Hyperalgesia and hyperaemia in the focal area

Thermovision(mentioned above)

Local thermometry:

• In cases when EST is inapplicable.

• When the positive reaction is spread over an area of several non-vital teeth, the test
doesn’t allow differentiation and gradation of activity of the foci.

Local thermometry test fully covers the EST

Principles

• LTT belongs to the so-called thermal diagnostics.

Allergology final
• LTT is a procedure of intraoral local measurement of the temperature of the periapical
area of teeth. Electronic thermometer with 1.5 mm sensor size and 0.01°С allowance is
used.

• A test is considered positive when the difference of temperatures of two adjacent or

symmetrical peri-apical areas is more than 0.4oC.

Advantages:

1. LTT fully covers the EST and may complement it. In cases when EST is
inapplicable – LTT substitutes it.
2. When the positive reaction of EST is spread over an area of several non-vital teeth,
LTT allows differentiation and gradation of activity of the foci.
3. Highly reliable.
4. Safe method.
5. Easily applicable.

Disadvantages

1. LTT registers the current picture – it is a static test.

2. The conical shape of the sensor allows sliding of the thermometer when the patient
closes the mouth, which leads to inaccuracy in the reading.

Thermography : Digital Infrared Thermal Imaging (DITI) is a diagnostic technique that is

non-invasive, non-contact and involves no exposure to radiation. During an exam, a DITI
camera is used to capture images, called thermograms. DITI is more widely applied in
focal diagnostics due to its safety and objectivity.

All objects emit a certain amount of black body radiation as a function of their
temperatures. The higher an object's temperature is, the more infrared radiation is emitted
as black- body radiation.

Thermographic camera (also called an infrared camera or thermal imaging camera).

Thermography -advantages:
1. Non-invasive and painless.

2. Non-contact method.
Allergology final
3. Saves time.

4. The risk of false positive results in patients with skin inflammations is reduced.

5. Good informativeness and an opportunity to compare.

6. Direct electronic data transfer.

7. Possibility for a precise software analysis of the recorded data.

Thermography-disadvantages:

1.Expensive equipment.
2.Static test.
3.It doesn’t register the altered general reactivity.
4.Infrared energy from the emitted body heat is the only registered energy.

Requirements:
• Patients should discontinue drug therapy.

• Patients should not consume coffee, black tea, alcohol, cigarettes or fatty foods on the
day of the exam.

• No crème and make-up on the face and body.

• Male patients should not shave on the day of the exam.

• Patients should bring current OPG

Thermography stages:

1. Acclimatization

2. Infrared capture

Pathogalvanism:

-Measurement is carried out as one electrode of the device is placed on the metal object,
and the other electrode on the oral mucosa.
-Each metal object’s values are registered. Normal values range from 0 to -150mV for non-
precious metals and from 0 to +150mV for precious metals.
- The total value of all metal objects in the oral cavity should not exceed 800 mV.
- If higher values are recorded, polishing of metal restorations is required and another
measurement a week later. In individuals with prominent clinical findings or positive patch
test removal of metal restorations is compulsory.

Electric pulp testing:

Technique:
Allergology final
The patient holds the device's passive electrode in the right hand, while the active one
(cathode) is placed on the typical RUBIN spot of a dried tooth that is to be tested.

Pressing the START button triggers the automatic increase in the micro electrical
monopoly impulse.

Upon the patient’s reaction the active electrode is removed from the tooth.

Then the recordings on the display are checked and reported.

Results:

- 2-6-10 mA-normal pulp response

- Up to 20 mA acute caries
- Up to 30 mA chronic caries
- Up to 35 mA dental pulp hyperaemia and partial pulpits
- From 40-60 mA coronal pulp necrosis
- Between 100-200 mA dental root pulp necrosis