Immunity: 1 Elsevier Items and Derived Items © 2009 by Saunders, An Imprint of Elsevier Inc

Chapter 3
Immunity
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
Outline

The Acquired Immune Response Antigens Cellular Involvement in the Immune Response Major Divisions of the Immune Response Memory and Immunity Types of Immunity Immunopathology Oral Diseases with Immunologic Pathogenesis Autoimmune Diseases that Affect the Oral Cavity
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc. 2
The Acquired Immune Response
(pg. 82) Has the capacity to remember and respond more quickly the second time a foreign material enters the body Works with the inflammatory response and a working repair process Involves white blood cells, especially lymphocytes and their products
Defends the body against injury
Antigens
(pg. 82) Mainly proteins, often microorganisms and their toxins May be tumor cells, or cells infected with viruses
Foreign substances
Human cells that have been transformed
Antigens (cont.)
Human tissue
Organ transplants, tissue grafts, incompatible blood types during a transfusion Tissue from the persons own body becomes an antigen
Autoimmune diseases
Cellular Involvement in the Immune Response

B lymphocytes T lymphocytes Macrophages Cytokines
Cellular Involvement in the Immune Response (cont.)
(pg. 83)
Cells that are able to recognize and respond to antigen
Derived from precursor cells in bone marrow (stem cells) 20% to 25% of the WBC (white blood cell) population
Two main types

B lymphocytes (B cells) T lymphocytes (T cells) Can destroy cells recognized as foreign without recognizing specific antigens
Also there are natural killer cells (NK cells)
Cellular Involvement in the Immune Response (cont.)
B Lymphocytes
(pgs. 83-84) Lymph nodes, tonsils, and other body tissue
Mature and reside in lymphoid tissue
B lymphocytes travel to the site of injury when stimulated by antigen
Two main types Plasma cells

B memory cell
Produce specific antibodies
Retains the memory of previously encountered antigen and will clone itself in the presence of antigen
B Lymphocytes (cont.)
10
Plasma Cells
Produce antibodies that are categorized into 5 classes of immunoglobulins, which are carried in blood serum
All have the same basic Y structure, but have an area with variable (V) structure at the tips of the Y The stem of the Y is constant (C) for all 5 types, and links the antibody to other components of the immune response Antigen combined with antibody
Immune complex
T Lymphocytes
(pgs. 83, 85) The thymus is large in an infant, shrinks as the child matures Memory cells T-helper cells Increase functioning of B lymphocytes T-suppressor cells Turn off functioning of B lymphocytes T-cytotoxic cells Attack virally infected cells or tumor cells
Travel to the thymus and mature
Several different types of T lymphocytes

T Lymphocytes (cont.)
13
Macrophages
(pg. 84) Produce cytokines called monokines After phagocytosis, they process and present antigen to lymphocytes This stimulates lymphocytes to travel from lymphoid tissue to the injury site
Active in phagocytosis of foreign material
Help both B and T lymphocytes

Amplify the immune response but do not remember the antigen like lymphocytes
14
Cytokines (Cont.)
15
Cytokines (Cont.)
(pgs. 84-85) (Table 3-2)
Proteins made by cells that are able to affect the behavior of other cells
Different cytokines have different functions.
16
Major Divisions of the Immune Response
(pgs. 85-86) B lymphocytes are the primary cells. Involves production of antibodies T lymphocytes are the primary cells. Lymphocytes may work alone or be assisted by
macrophages.
Humoral response

Cell-mediated response
The cell-mediated portion regulates both major responses.
17
Major Divisions of the Immune Response (cont.)
18
Memory and Immunity
(pg. 86)
The immune system has memory; the inflammatory system does not.

Some lymphocytes retain memory of an antigen after an initial encounter. This means the immune response will be faster and stronger the next time an antigen enters the body. The retained memory is called immunity.
19
Types of Immunity

Passive Immunity Active Immunity
20
Passive Immunity
(pg. 86)
Using antibodies created by another person to prevent infectious disease
Natural When antibodies from the mother pass through the

placenta to the developing fetus
Acquired When antibodies are acquired through an injection Short lived but fast acting
21
Active Immunity
(pg. 86)
Antibodies created by the person themselves
Natural Protection conferred following survival from an

infectious disease
Acquired Injection or ingestion of either altered pathogenic

microorganisms or products of those microorganisms immunization with a vaccine
22
Immunopathology
(pg. 86)
The study of immune reactions involved in disease
The immune system can malfunction and cause tissue damage. Hypersensitivity Autoimmune diseases
23
Hypersensitivity (Cont.)
(pgs. 87-88) (Table 3-3) An exaggerated response Tissue destruction occurs as a result of the immune response. Four main types
An allergic reaction

24
Hypersensitivity (Cont.)
25
Type I Hypersensitivity
(pg. 87) The reaction occurs within minutes after exposure to an antigen. Plasma cells produce IgE. IgE causes mast cells to release histamine, causing
increased dilation and permeability of blood vessels and constricting smooth muscle in bronchioles of the lungs.
Immediate (anaphylactic type)

The reaction may range from hay fever to asthma and life-threatening anaphylaxis.
26
Type II Hypersensitivity
(pg. 87) Antibody combines with an antigen bound to the surface of tissue cells, usually a circulating RBC (red blood cell).
Cytotoxic type
Activated complement components, IgG and IgM antibodies in blood, participate in this type of hypersensitivity reaction.
This destroys the tissue that has the antigens on the surface of its cells (e.g., Rh incompatibility).
Type III Hypersensitivity
(pg. 87) Immune complexes are formed between microorganisms and antibody in circulating blood. These complexes leave the blood and are deposited
in body tissues, where they cause an acute inflammatory response.
Immune complex type (serum sickness)
Tissue destruction occurs following phagocytosis by neutrophils.
28
Type IV Hypersensitivity
(pg. 87) T lymphocytes that previously have been introduced to an antigen cause damage to tissue cells or recruit other cells. Responsible for the rejection of tissue grafts and transplanted organs
Cell-mediated type (delayed)
29
Hypersensitivity to Drugs
(pgs. 87-88) Topical administration may cause a greater number of reactions than oral or parenteral routes. But the parenteral route may cause a more widespread and severe reaction.
Drugs can act as antigens.
30
Autoimmune Diseases
(pg. 88) The body learns to determine self from nonself. The recognition mechanism breaks down; some body cells are not tolerated and are treated as foreign antigens.
Immunologic tolerance
Autoimmune disorder
31
Immunodeficiency
(pg. 88) A deficiency in number, function, or interrelationships of the involved WBCs and their products May be congenital or acquired Infections and tumors may occur as a result of the deficiency.
An immunopathologic condition
32
Oral Diseases with Immunologic Pathogenesis

Aphthous ulcers Urticaria and angioedema Contact mucositis and dermatitis Fixed drug eruptions Erythema multiforme Lichen planus Reactive arthritis (Reiter syndrome) Langerhans cell disease
33
Aphthous Ulcers
(pgs. 88-91)
Painful oral ulcers with an unclear cause

Occur in about 20% of the population Trauma is the most common precipitating factor. May be caused by emotional stress or certain food May be associated with certain systemic diseases Thought to have an immunologic pathogenesis Occur in three forms: minor, major, and herpetiform
34
Minor Aphthous Ulcers
(pg. 89) Occur on movable mucosa Up to 1 cm in diameter with a erythematous halo

surrounding a yellowish-white fibrin surface
Discrete, round or oval ulcers
May have single or multiple lesions May have a prodrome of 1 to 2 days
35
Minor Aphthous Ulcers (cont.)
36
Major Aphthous Ulcers
(pgs. 89-90)
Larger (>1 cm), deeper, and longer lasting than minor aphthous ulcers

Very painful Occur in the posterior of the mouth more often than minor aphthous ulcers May require several weeks to heal May require a biopsy
37
Major Aphthous Ulcers (cont.)
38
Herpetiform Aphthous Ulcers
(pgs. 89-90) Resemble herpes simplex ulcers Painful, generally occur in groups
Tiny (1 to 2 mm)

39
Diagnosis of Minor Aphthous Ulcers (Cont.)
40
Diagnosis of Minor Aphthous Ulcers (Cont.)
(pgs. 89-91) (Table 3-4)
Clinical appearance Location
Herpetic lesions appear on mucosa fixed to bone, aphthous lesions appear on movable tissue Aphthous ulcers do not produce systemic signs or symptoms as do herpetic lesions
Clinical history
41
Treatment of Minor Aphthous Ulcers
(pg. 91) There are several OTC medications such as Orabase and Zilactin. Topical or systemic steroids may help. Topical anesthetic may help.
Treatment

42
Urticaria (Hives)
(pg. 91)
Appears as multiple areas of welldemarcated swelling of skin
May have itching (pruritis)
Lesions caused by localized areas of vascular permeability in superficial connective tissue
43
Angioedema
(pg. 91)
Lesions caused by diffuse swelling due to increased permeability of deeper blood vessels
The skin covering the swelling appears normal Usually do not have itching
44
Urticaria and Angioedema
(pgs. 91-92) May be due to infection, trauma, emotional stress, and certain systemic diseases May be due to ingested allergens
Often idiopathic cause

45
Contact Mucositis and Dermatitis
(pg. 92)
Lesions resulting from contact of an allergen with skin or mucosa Involves CMI (cell-mediated immunity)
The mucosa initially becomes erythematous and edematous. Often there is burning and pruritus Later, the area becomes white and scaly.
Topical and/or systemic corticosteroids
Treatment
46
Contact Mucositis and Dermatitis (cont.)
47
Fixed Drug Eruptions
(pgs. 92-93)
Lesions that appear in the same site each time a drug is introduced
Generally appear suddenly after a latent period and subside when the drug is discontinued
May be single or multiple slightly raised, reddish patches or clusters of macules on the skin, or sometimes the mucous membranes
May have pain or pruritis
48
Fixed Drug Eruptions (cont.)
A type of allergic reaction (Type III)

Immune complexes are deposited along the endothelial walls of blood vessels. Inflammation causes vasculitis with damage to the vessel wall. This creates erythema and edema in superficial layers of skin or mucosa.
Treatment
The drug causing the reaction should be identified and discontinued.
49
Erythema Multiforme
(pgs. 93-94)
Cause is not clear; may be a hypersensitivity reaction
Most commonly occurs in young adults, affects men more commonly than women Characteristic skin lesion with concentric erythematous rings alternating with normal skin color
Target lesion
50
Erythema Multiforme (cont.)
51
(pgs. 93-94)
Skin lesions can range from macules to papules to bullae. Oral lesions are usually ulcers

Frequently form on lateral borders of the tongue Crusted and bleeding lips are frequently seen. Gingival involvement is rare.
May be chronic or may have recurrent acute episodes

53
(pgs. 93-94)
Stevens-Johnson syndrome
The most severe form More extensive and

painful oral lesions Genital mucosa and mucosa of eyes may be involved. Lips generally are encrusted and bloody.
54
(pg. 93) Based on clinical features and by exclusion of other diseases Topical or systemic corticosteroids Eye lesions may lead to blindness.
Diagnosis
Treatment and prognosis

55
Lichen Planus
(pgs. 93-96)
A benign, chronic disease affecting skin and oral mucosa

Unknown cause Lesions have characteristic Wickham striae Lesions may be on the tongue, lips, floor of mouth, and gingiva. Most common in middle age Slightly more common in women
Most commonly on buccal mucosa
Present in about 1% of the U.S. population

Lichen Planus (cont.)
57
Types of Lichen Planus
(pgs. 95-96) Most common form Epithelium separates from connective tissue
Reticular lichen planus
Erosive and bullous lichen planus
Desquamative gingivitis can be caused by lichen planus. Skin lesions
2 to 4 mm papules most commonly in lumber region, flexor surfaces of the wrist, anterior ankle
Types of Lichen Planus (cont.)
59
Diagnosis of Lichen Planus
(pgs. 95-96)
Based on clinical appearance and possibly biopsy
Epithelial atypia and dysplasia may occur in lesions that clinically appear to be lichen planus. These lesions may be premalignant.
Treatment and Prognosis of Lichen Planus
(pg. 96) Treated when symptomatic Regular oral examination and biopsy of suspicious lesions are necessary as these patients may be at increased risk of development of squamous cell carcinoma.
A chronic disease

61
Reactive Arthritis (Reiter Syndrome)
(pgs. 96-97)
Classic syndrome includes arthritis, urethritis, and conjunctivitis, but all components may not be present.

An antigenic marker called HLA-B27 is present in most patients, meaning there may be a genetic influence. Probably an abnormal immune response to a microbial antigen
Skin and mucous membrane lesions may be observed. May see aphthous ulcers, erythematous lesions, and geographic tonguelike lesions
Reactive Arthritis (Reiter Syndrome) (cont.)
63
Reactive Arthritis
Diagnosis

Clinical signs and symptoms HLA-B27 antigenic marker Disease lasts for weeks to months. Recurrent attacks are common.
Treatment and prognosis

64
Langerhans Cell Disease (Histiocytosis X)
(pgs. 97-98) Letterer-Siwe disease Hand-Schuller-Christian disease Solitary eosinophilic granuloma
Includes three entities

All have Langerhans cells and eosinophils.
65
Langerhans Cell Disease (Histiocytosis X) (cont.)
66
Langerhans Cell Disease
A type of macrophage
An immunocompetent cell of the mononuclear phagocyte series and participates in CMI Eosinophilic granuloma is treated by conservative surgical excision. Low-dose radiation may be used
Treatment

67
Autoimmune Diseases that Affect the Oral Cavity

Sjgren Syndrome Systemic Lupus Erythematosus Pemphigus Vulgaris Mucous Membrane Pemphigoid Bullous Pemphigoid Behet Syndrome
68
Autoimmune Diseases that Affect the Oral Cavity (cont.)
(pgs. 98-105) (Table 3-5) Several autoimmune diseases affect the oral cavity. The immune system treats the persons own cells and tissues as antigens.
69
Autoimmune Diseases that Affect the Oral Cavity (cont.)
70
Sjgren Syndrome
(pgs. 99-100) Results in a decrease in saliva and tears causing a dry mouth (xerostomia) and dry eyes (xerophthalmia) The combination may be called sicca syndrome.
Affects the salivary and lacrimal glands
71
Sjgren Syndrome (cont.)
(pg. 99)
May be associated with other autoimmune disorders

Primary Sjgren syndrome when it occurs alone Secondary Sjgren syndrome when it occurs with other autoimmune disorders
Patient may complain of oral discomfort due to dry mouth. May see loss of filiform and fungiform papillae on the dorsum of the tongue
(pg. 99)
Affects both major and minor salivary glands
Parotid gland enlargement occurs in about 50% of patients.
Biopsy reveals a characteristic appearance.

Major salivary glands Replacement with lymphocytes and the presence of

islands of epithelium called epimyoepithelial islands
Minor salivary glands Aggregates of lymphocytes surrounding the salivary

gland ducts
74
Patient may complain of burning and itching of eyes and photophobia.
Severe eye involvement may lead to ulceration and opacification of the eyes. 20% of these patients will have this disorder affecting fingers and toes Initial pallor and subsequent cyanosis of skin due to
cold or stress Hyperemia when blood vessels are warmed
Raynaud phenomenon
75
90% of these patients have a positive response to rheumatoid factor, an antibody to IgG present in serum
It is an antibody to an antibody.
Other autoantibodies, anti-Sjgren syndrome A, and anti-Sjgren syndrome B are also present.
76
Diagnosis and Management of Sjgren Syndrome
(pg. 100)
Diagnosis is made when two of three components are present.

Xerostomia Measurement of salivary flow and biopsy can help Keratoconjunctivitis sicca Confirmed with eye examination Rheumatoid arthritis
For most patients, the course of the disease is chronic and benign but these patients are at risk for the development of other more serious diseases.
Diagnosis and Management of Sjgren Syndrome (cont.)
78
Treatment of Sjgren Syndrome
(pg. 100) Nonsteroidal antiinflammatory agents for arthritis May need corticosteroids and immunosuppressive
drugs for severe cases
Symptomatic
Saliva substitutes for xerostomia Humidifier, sugarless gum, or lozenges Pilocarpine Glasses and/or artificial tears to protect eyes
79
Systemic Lupus Erythematosus (SLE)
(pgs. 100-102)
An acute and chronic inflammatory autoimmune disease
No known cause
Affects women 8 times more frequently than men, predominantly during childbearing years
Three times more frequent in black women than in white women
80
Systemic Lupus Erythematosus (SLE) (cont.)
A syndrome with a wide range of disease activity
Usually chronic and progressive Periods of remission and exacerbation
Autoantibodies to DNA are present in serum May have a genetic component
81
Clinical Features of Systemic Lupus Erythematosus (SLE)
(pgs. 101-102) Butterfly rash on bridge of nose May be erythematous lesions on fingertips Arthritis and arthralgia are common.
Skin lesions occur in 85% of individuals

Oral lesions accompany skin lesions in about 25% of patients with discoid LE.
Erythematous plaques or erosions May have white striae; resemble lichen planus but
are less symmetric
82
Clinical Features of Systemic Lupus Erythematosus (SLE) (cont.)
83
Diagnosis of Systemic Lupus Erythematosus (SLE)
(pgs. 101-102)
Usually based on multiorgan involvement and presence of antinuclear antibodies in serum
Inflammatory infiltrate is around blood vessels in connective tissue.
84
Treatment and Prognosis of Systemic Lupus Erythematosus (SLE)
Aspirin and antiinflammatory drugs for mild signs and symptoms
Hydroxychloroquine and corticosteroids along with immunosuppressive agents may be used.
The text recommends consultation with the patients physician before initiating dental treatment.
85
Pemphigus Vulgaris
(pgs. 102-104)
A severe, progressive autoimmune disease affecting skin and mucous membranes
Characterized by intraepithelial blister formation resulting from acantholysis, a breakdown of cellular adhesion between epithelial cells
Genetic and ethnic factors have been reported.
Often seen in Ashkenazic Jews

Pemphigus Vulgaris (cont.)
(pg. 103)
Oral lesions
The first signs of disease occur in the oral cavity in more than 50% of cases. May be shallow ulcers, to fragile vesicles, to bullae Nikolsky sign Rubbing with a finger can produce a bullae.
87
88
(pgs. 103-104) Erythema, bullae, erosions, ulcers
Skin lesions
Microscopic appearance
Acantholytic cells The loss of

attachment between epithelial cells leads to cells that appear rounded.
Tzanck cells
Diagnosis of Pemphigus Vulgaris
Made by biopsy and microscopic examination

Direct immunofluorescence Identifies autoantibodies present in tissue Indirect immunofluorecence The patients serum is used to detect circulating
autoantibodies.
90
Treatment and Prognosis of Pemphigus Vulgaris
High doses of corticosteroids

May include immunosuppressive drugs Mortality rate of 8% to 10% in 5 years is related to complications of corticosteroid treatment.
91
Mucous Membrane Pemphigoid (Cicatricial Pemphigoid) (BMMP)
(pgs. 104-105) Affects oral mucosa, conjunctiva, genital mucosa, and skin Gingival lesions have been called desquamative gingivitis, but this may be seen with lichen planus and pemphigus as well.
A chronic autoimmune disease
Not as severe as pemphigus vulgaris
Will see positive Nikolsky sign
92
Mucous Membrane Pemphigoid (Cicatricial Pemphigoid) (BMMP) (cont.)
93
Diagnosis of Mucous Membrane Pemphigoid
(pg. 104)
Made by biopsy and histologic examination

No degeneration of epithelium occurs An inflammatory infiltrate, usually with predominant plasma cells and eosinophils, is seen in connective tissue.
94
Treatment and Prognosis of Mucous Membrane Pemphigoid
A chronic disease with a benign course

Topical corticosteroid for mild cases Systemic corticosteroids may be required for more severe cases. Eye lesions can lead to eye damage.
95
Bullous Pemphigoid
(pg. 105)
Some investigators believe bullous and mucous membrane pemphigoid are variants of a single disease, but 80% of these patients are older than 60.
Oral lesions are less common than in cicatricial pemphigoid.
Treatment
Systemic corticosteroids and nonsteroidal antiinflammatory drugs
96
Behet Syndrome
(pg. 105) Primarily oral ulcers, genital ulcers, ocular inflammation No sex predilection; mean onset is 30 years Autoantibodies to human mucosa may be found.
A chronic, recurrent autoimmune disease

Oral ulcers are similar in appearance to aphthous ulcers.
97
Behet Syndrome (cont.)
98
Diagnosis of Behet Syndrome
Requires that two of three types of lesions (oral, genital, and ocular) be present.
A pustular lesion after needle puncture suggests Behet syndrome.
99
Treatment and Prognosis of Behet Syndrome
(pg. 105) Chlorambucil is used for ocular lesions.
Systemic and topical corticosteroids
100
Discussion Questions
What is an autoimmune disorder? What is the difference between an antigen and an antibody? What are the differences between active and passive immunity? What oral diseases have an immunologic pathogenesis? What is an autoimmune disorder? What are the oral symptoms of Sjgren syndrome? What are differences between pemphigus and pemphigoid?

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Immunity: 1 Elsevier Items and Derived Items © 2009 by Saunders, An Imprint of Elsevier Inc

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Chapter 3

The Acquired Immune Response

Defends the body against injury

Human cells that have been transformed

Cellular Involvement in the Immune Response

B lymphocytes T lymphocytes Macrophages Cytokines

Cellular Involvement in the Immune Response (cont.)

Cells that are able to recognize and respond to antigen

Two main types

Also there are natural killer cells (NK cells)

Cellular Involvement in the Immune Response (cont.)

(pgs. 83-84) Lymph nodes, tonsils, and other body tissue

Mature and reside in lymphoid tissue

B lymphocytes travel to the site of injury when stimulated by antigen

Two main types Plasma cells

Produce specific antibodies

Travel to the thymus and mature

Several different types of T lymphocytes

Active in phagocytosis of foreign material

Help both B and T lymphocytes

(pgs. 84-85) (Table 3-2)

Different cytokines have different functions.

Major Divisions of the Immune Response

The cell-mediated portion regulates both major responses.

Major Divisions of the Immune Response (cont.)

Memory and Immunity

Passive Immunity Active Immunity

Using antibodies created by another person to prevent infectious disease

Natural When antibodies from the mother pass through the

Antibodies created by the person themselves

Natural Protection conferred following survival from an

Acquired Injection or ingestion of either altered pathogenic

The study of immune reactions involved in disease

Immediate (anaphylactic type)

Type III Hypersensitivity

Immune complex type (serum sickness)

Tissue destruction occurs following phagocytosis by neutrophils.

Cell-mediated type (delayed)

Drugs can act as antigens.

Oral Diseases with Immunologic Pathogenesis

Painful oral ulcers with an unclear cause

Minor Aphthous Ulcers

(pg. 89) Occur on movable mucosa Up to 1 cm in diameter with a erythematous halo

Discrete, round or oval ulcers

May have single or multiple lesions May have a prodrome of 1 to 2 days

Minor Aphthous Ulcers (cont.)

Major Aphthous Ulcers

Major Aphthous Ulcers (cont.)

Herpetiform Aphthous Ulcers

Diagnosis of Minor Aphthous Ulcers (Cont.)

Diagnosis of Minor Aphthous Ulcers (Cont.)

(pgs. 89-91) (Table 3-4)

Clinical appearance Location

Treatment of Minor Aphthous Ulcers

Appears as multiple areas of welldemarcated swelling of skin

May have itching (pruritis)

Lesions caused by localized areas of vascular permeability in superficial connective tissue

Urticaria and Angioedema

Often idiopathic cause

Contact Mucositis and Dermatitis

Contact Mucositis and Dermatitis (cont.)

Fixed Drug Eruptions

May have pain or pruritis