This document discusses hypersensitivity reactions and their classification. It begins by describing Type I reactions, which are immediate and antibody-mediated, including anaphylaxis and atopy. Type II are cytotoxic reactions mediated by IgG antibodies. Type III are immune complex diseases caused by antigen-antibody complexes. Type IV are delayed or cell-mediated hypersensitivity reactions. The document then discusses specific types of hypersensitivity reactions in more detail, including their mechanisms, clinical features, and importance in dentistry with certain materials, drugs, and allergens.

1. V.S.Rashmi Priyem
IIYear B.D.S.
ULTRA’S BEST Dental Science College, Madurai

2. ▪ Introduction
▪ Classification of Hypersensitivity Reactions
▪ Type I
▪ Anaphylaxis
▪ Atopy
▪ Type II
▪ Hypersensitivity in Dentistry

3. ▪ Allergic to Any Medications ?
▪ Have you Ever had a Reaction to a Anaesthetic ?
▪ IfYes, Describe what Happened ?
▪ Was Treatment Given ? If So,What ?

4. ▪ Hypersensitivity refers to the Undesirable Injurious
Consequences in the Sensitised Host, following
Contact with Specific Antigens.
▪ Result of Inappropriate Immune Reaction.
IMPortant 2M
Food
Allergy

5. ▪ The Host should have had Contact with the Antigen
(Allergen).
▪ Initial Contact Sensitises the Immune System,
Leading to Priming of the Appropriate B or T
Lymphocytes.
▪ Sensitising or Priming Dose.
▪ Subsequent Contact with the Allergen causes
Manifestations of Hypersensitivity.
▪ Shocking Dose.

6. TYPE I

7. ▪B Cell or Antibody Mediated
▪Occurs in :
▪Anaphylaxis
▪Atopy
▪Antibody – Mediated Cell
Damage
▪Arthus Phenomenon
▪Serum Sickness

8. ▪T Cell Mediated
▪Occurs in :
▪ Infection
▪ Contact Dermatitis

9. Immediate
Hypersensitivity
Delayed
Hypersensitivity
Action Appears and Recedes
Rapidly
Appears Slowly, Lasts
Longer
Induced by Antigens or Haptens by
any Route
Antigen or Hapten
Intradermally or by
Skin Contact
Circulating Antibodies Present
Antibody Mediated
Reaction
Absent
Cell Mediated Reaction
Transfer Passive Transfer via
Serum
Tranferred via T Cells
or Transfer Factor
Desensitisation Easy
Short Lived
Difficult
Long Lasting

10. ▪Based on Different Mechanisms of
Pathogenesis.
▪Now Widely Used Across the Globe.

11. ▪ Type I : Anaphylactic Reaction
▪ Type II : Cytotoxic Reaction
▪ Type III : Immune Complex Diseases
▪ Type IV : Delayed or Cell Mediated Hypersensitivity
▪ Type V : Stimulatory Hypersensitivity
ACID

12. ▪ Anaphylactic, IgE or Reagin Dependent
▪ Antibodies fixed on Surface of Tissue Cells – Cell
Fixed Ab.
▪ Mast Cells & Basophils
Antigen + Cell Fixed Ab.
Release of Pharmacologically Active Subs.
Produce Clinical Rxn.
IMPortant 5M

13. ▪ Cytotoxic, IgG( Rarely IgM ) Dependent
IgG (Rarely IgM) Antibodies + Cell Surf. Or Tissue
Antigens
Cause Stimulation or Damage
▪ Intermediate bet. Hypersensitivity & Autoimmunity
Presence of
Complement

14. ▪Immune Complex Diseases caused by Ag-Ab
Complexes
▪Precipitate in & around Small Blood Vessels
▪Causing Damage To Cells and Membranes,
Interfering the Function

15. ▪ Delayed or Cell Mediated
▪ It is a Cell Mediated Response
▪ Ag Activates Specifically Sensitised CD4 & CD8 T
Cells
▪ Leads to Secretion of Lymphokines and Phagocyte
Accumulation

16. ▪ A Collective Term for the Four Enzyme Cascades—
the Complement, Coagulation, Fibrinolytic, and Kinin
Systems
▪ The Pathology and Clinical Features of
Immunological Diseases would also be Influenced by
the Mechanisms such as Inflammation, Complement,
Coagulation, Fibrinolytic and Kininogenic Systems
IMPortant 2M

17. IMPortant 5M
IMPortant 10M

18. ▪lgE DEPENDENT
▪Two Forms :
▪ Acute, Potentially Fatal, Systemic Form called
Anaphylaxis
▪ Chronic, Recurrent, Non-Fatal,Typically Localised
Form called Atopy

19. ▪ Classical Immediate Hypersensitivity Reaction.
▪ Antigens and Haptens can Induce Anaphylaxis.
▪ Haptens – Primitive Molecule Which Elicit Prod. Of Ab
▪ Interval of atleast 2-3 weeks between the Sensitising
and Shocking Dose.

20. ▪ Clinical Features are same with any Antigen but vary
between Species.
▪ Clinical Effects are Due to Smooth Muscle
Contraction & Increased Vascular Permeability.

21. ▪Affected Organs are known as Shock Organs.
▪Changes seen are
▪ Edema
▪ Decreased Coagulability of Blood
▪ Fall in Blood Pressure and Temperature
▪ Leucopenia and Thrombocytopenia

23. Edema Formation in the
Dermis, Mostly Involving
Head and Neck.
IcatiBAnt –
Bradykinin
Antagonist
C1 Esterase Def.

24. ▪Human Anaphylaxis, Previously associated
with Heterologous Serum Therapy, is Now
seen mostly following Injection of Antibiotics
or other drugs.
▪Prompt Treatment with Adrenaline can be
Life-Saving.
▪ 0.5ml of a 1 in 1000 Soln. Subcutaneously or
Intramuscularly.

25. ▪Cutaneous Anaphylaxis
▪Passive Cutaneous Anaphylaxis
▪Anaphylaxis in vitro
For Detection of Antibodies
– Antigen is Introduced

26. ▪ Small Shocking Dose of an Antigen is Administed
Intradermally to a Sensitised Host ,there will be a Local
Wheal and Flare Response (Local Anaphylaxis).
▪ The Wheal is a Pale, Central Area of Puffiness due to
Edema, which is surrounded by a Flare caused by
Hyperemia and Subsequent Erythema.

27. ▪ Useful in Testing for Hypersensitivity and in
Identifying the Allergen Responsible Diseases.
▪ In Highly Sensitised Individuals, even the Skin Test
may lead to Fatal Reactions.
▪ A Syringe loaded with Adrenaline should always be
kept ready.

28. ▪ This Test is Extremely Sensitive Method for the
Detection of Antibodies.
▪ A Small Volume of Antibody is Injected
Intradermally into a Normal Animal.

29. Antigen + Evans blue Dye(Consider)
After 4-24 hours , Immediate Blueing
Due to Vasodilatation and Increased Capillary
Permeability (Wheal and Flare Reaction)
Injected Intravenously

30. ▪Used to Detect the Human IgG Antibody
which is Heterocytotropic but not lgE which
is Homocytotropic.
▪Homocytotropic - Capable of Fixing to Cells
of Homologous Species only
▪Heterocytotropic - Capable of Fixing to Cells
of other Species

31. ▪Isolated Tissues, such as Intestinal or Uterine
Muscle Strips from Sensitised Guinea Pigs,
held in a Bath of Ringer’s Solution will
Contract Vigorously on Addition of the
Specific Antigen to the Bath.
▪This is known as the Schultz-Dale
Phenomenon.

32. ▪ Primary
▪ Mast Cells & Basophils
▪ Histamine
▪ Serotonin
▪ Eosinophil Chemotactic Factor of Anaphylaxis
▪ Enzymatic Mediators
▪ PGs & Leukotrienes
▪ Platelet Activating Factor

33. ▪Preformed Contents of Mast Cells and
Basophils.

34. ▪ Most Important Vasoactive Amine in Human
Anaphylaxis.
Released into the Skin
Stimulates Sensory Nerves
Produce Burning and Itching Sensations
Vasodilatation and
Hyperemia by an Axon
Reflex(Flare Effect)
Edema by Increasing
Capillary Permeability
(Wheal Effect)
Induces Smooth Muscle
Contraction in Tissues
and Organs

35. ▪5-Hydroxy Tryptamine
▪Found in the Intestinal Mucosa, Brain Tissue
and Platelets.
▪Causes Smooth Muscle Contraction,
Increased Capillary Permeability and
Vasoconstriction.

36. ▪ Eosinophil Chemotactic
Factors of Anaphylaxis
(ECF-A) are Released from
Mast Cell Granules which
are Strongly Chemotactic for
Eosinophils.
▪ Contribute to the
Eosinophilia accompanying
many Hypersensitivity
States.

37. ▪Enzymatic Mediators such as Proteases and
Hydrolases are released from Mast Cell
Granules.

38. ▪ The Lipoxygenase Pathway leads to the Formation of
Leukotrienes.
▪ The Cyclo-oxygenase Pathway leads to the
Formation of Prostaglandins and Thromboxane.
▪ Prostaglandin F2α and Thromboxane A2 are
Powerful but Transient Bronchoconstrictors.
▪ PGs Affect Secretion by Mucous Glands, Platelet
Adhesion, Permeability and Dilatation of Capillaries
and the Pain Threshold.

39. ▪PAF is Released from Basophils which Causes
Aggregation of Platelets and Release of
Vasoactive Amines.

40. ▪Anaphylatoxins released by Complement
Activation
▪Bradykinin and other Kinins formed from
Plasma Kininogens.

41. ▪ Intravenous Inj. of Peptone,Trypsin
and other Subs. Provokes a Clinical
Reaction resembling Anaphylactic
Shock.
▪ This is termed ‘Anaphylactoid Reaction’.
▪ Only Difference is that Anaphylactoid
Shock has No Immunological Basis
and is a Non-Specific Mechanism
involving the Activation of
Complement and the Release of
Anaphylatoxins.

42. ▪Refers to Naturally occurring Familial
Hypersensitivities of Human Beings, typified
by Hayfever and Asthma.
▪ The Atopens are generally not good Antigens when
Injected Parenterally but Induce IgE Antibodies,
formerly termed ‘Reagin’ Antibodies.
▪ Reagin Mediated Hypersensitivity

43. ▪ IgE differs from other Immunoglobulins.
▪ Unlike other Antibodies, IgE is Heat Sensitive and is
Inactivated at 56°C in 2-4 hours.
▪ Heating appears to Damage the Fc part of the IgE
Molecule, which is necessary for Fixation to Cells.
▪ The Atopic Antibody does not pass through the
Placenta.

44. Guess The Personality ?
He is Related To _____ .

45. Prausnitz-Kustner
(PK) Reaction

46. ▪ IgE is Species Specific
▪ Only Human IgE can fix to the Surface of Human
Cells.
▪ The Basis of the Prausnitz-Kustner (PK) Reaction.
▪ Original method for Detecting Atopic
Antibodies.

47. ▪ Caused by Overproduction of IgE Antibodies.
▪ Associated with a deficiency of IgA.
▪ Inhalant and Ingestant Antigens are dealt by IgA
Lining the Respiratory and Intestinal Mucosa and
they Do Not come into Contact with Potential IgE
Producing Cells.
▪ When IgA is Deficient, the Antigens cause Massive
Stimulation of IgE Forming Cells, leading to
Overproduction of IgE.
IgE
IgA

48. ▪ Symptoms are caused by the Release of
Pharmacologically Active Substances following the
Combination of the Antigen and the Cell Fixed IgE.
▪ Clinical Expression is determined by the Entry of the
Antigen
▪ Conjunctivitis ,Rhinitis and Dermatitis, etc.
▪ Specific Desensitisation (Hyposensitisation) -
Treatment of Atopy.

49. CYTOLYTIC and CYTOTOXIC

50. ▪ Reactions involve Combination of IgG (or rarely
IgM) Antibodies with the Antigenic
Determinants on the Surface of Cells.
▪ Alternatively, a Free Antigen or Hapten may be
Absorbed on Cell Surfaces.
▪ Subsequent Reaction of the Combined Antigen
or Hapten with its corresponding Antibody leads
to Cell Damage.

51. ▪ Drugs like Cephalosporins may
Behave in this manner, Leading to
Complement-Mediated Lysis of RBCs,
Leucocytes and Platelets, causing
Hemolytic Anemia, Agranulocytosis
and Thrombocytopenic purpura

52. ▪Examples :
▪Lysis of RBCs
caused by Anti-
Erythrocyte
Antibodies in
Autoimmune
Anemias
▪Hemolytic Disease
of the Newborn

54. Exopthalmos
Diarrhoea
Tachycardia
Enlarged Thyroid

56. ▪Dermatitis of Hand (Eczema) → Most
Common Adverse Reaction.
▪Localized Rashes & Swelling to Wheezing &
Anaphylaxis.
▪Prevention: Use Vinyl Gloves or Synthetic
Polymer Gloves.

57. ▪ Irreversible Hydrocolloids :
▪ Inhaling Fine Airborne Particles can cause Silicosis &
Pulmonary Hypersensitivity.
▪ Dustless/Dustfree Alginate is preferred.
▪ Elastomers : Cellular Toxicity Levels
▪ Polyether > Addition Silicone > Polysulphide

58. ▪ Heavy Metals like Lead and Silica particles are
present in the Alginate powder.
▪ Have Potential Toxicity Risk for Both Practitioner and Patient.
▪ During the Impression Making , Alginate is left in
close Contact with the Oral Mucosa for 2 min, and the
Tissue is Highly Vascularised and has Great
Absorption Potential.

59. ▪ Large Amalgam Particles that are Embedded
Accidentally in the Gingiva during
Placement of a Restoration may Elicit Chronic
Inflammation.

60. ▪ Benign Pigmentation of the Mucosa can
occur from Embedded Amalgam Particles,
commonly referred to as “Amalgam Tattoo."

61. ▪Cause Inflammatory Reactions on Newly
Prepared Dentin.
▪The Blandness of GIC is Attributed to
Absence of Strong Acids of Toxic Monomers.
▪Irritancy :
Zinc Oxide < Zinc Polycarboxylate =Glass
Ionomer < Zinc Phosphate

62. ▪When Zinc Phosphate is used to Cement a
Crown or Inlay
The Phosphate Cement is forced into the
Dentinal Tubules
▪It creates a wide spread Three-Dimensional
Inflammatory Lesion involving all the Coronal
Pulp Tissue.

63. ▪ ZOE is considered the Least Damaging
Restorative Material.
▪ Sensitivity is manifested as Positive
Inflammatory Responses to Eugenol in certain
Root Canal Sealers.
▪ Eugenol causes Contact Dermatitis, because it
can React Directly with Proteins to form
Conjugate and Reactive Haptens.

64. ▪Small Amounts of the Metals can be Released
into the Oral Cavity.
▪Leached Metals can Potentially Trigger an
Allergic Reaction.

65. ▪Nickel in Dental Appliances is known to be a
Very Common cause of Contact Allergy and
Hypersensitivity Reactions.

66. ▪Patients developed Muscle and Joint Pain
after receiving Titanium Dental Implants,
Orthodontic Braces or Endoprostheses.
▪Titanium Allergy presents with Urticaria,
Eczema, Cheilitis, Redness of the Mucosa.
▪Patch Test is Ineffective. Instead MELISA Test
is done for Titanium Sensitisation.

67. ▪Formaldehyde is a common cause of Contact
Dermatitis.
▪Features : Anaphylactic Reaction or Shock
and Generalized Urticaria.
Acts as
Bactericidal

68. ▪Cause Denture stomatitis when used as
Denture Base Material.
▪Prevention : 7 hr Incubation in Water at 70°C
followed by a 1-h Incubation in Water at
100°C causes the Maximum Conversion of
the Monomer.

69. ▪ Penicillins & Sulfonamides
▪ Parenterally Administered Penicillin can Cause An
Anaphylactic Reaction.
▪ When Orally Administered – Delayed Reaction.

70. ▪ Aspirin, Codeine, NSAIDS
▪ Symptoms : Mild Urticaria to Anaphylaxis
▪ Bronchospasm : Most Common Reaction
▪ Alterantive to be Prescribed → Acetaminophen

71. ▪ Esters, Procaine, Benzocaine
▪ Injectable & Topical Ester Local Anaesthetic →
Primary Cause
▪ Allergic Rxn.in Amides – Due To Reactions to
Preservatives Such as Parabens & Sodium
Metabisulfate

73. ▪ Most Definitive Diagnostic Test – All are Prescribed.
▪ Suspected Allergen applied to Skin to produce small
area of Contact Dermatitis.
After 48 to 96 hrs
Hyperemia, Edema,Vesicle Formation & Itching
Positive Reaction

75. ▪Actions Include
▪Bronchodilation
▪Increased Heart Rate
▪Cutaneous, Mucosal Vasoconstriction
▪Reverses Rhinitis and Urticaria

76. ▪Benadryl (Chlorpheniramine) is Most Often
Used.
▪Inhibits Action of Histamine released during
Reaction to Allergen.

77. ▪Hydrocortisone is used Most Often.
▪Stablilizes Cell Membranes Against Actions
of Histamines, Bradykinins, and
Prostaglandins.

78. Always!