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Immune Response

Defends body against injury
Responds after the inflammatory response
Works in background of an already activated inflammatory response

The Immune Response differs from inflammatory response

Differs in that it remembers and responds more quickly to foreign substances that enter the body a second time.

Antigens

Foreign substances against which the immune response defends the body. Autoimmune disease parts of an individuals own body become antigens.

Cells involved in the Immune Response

1. T lymphocytes 2. B lymphocytes 3. Natural killer cells 4. Macrophages 5. Cytokines

T lymphocytes

Originate in bone marrow and travel to thymus. Thymus gets small as get older (processed into mature cells). FIRST LINE OF DEFENSE AGAINST INTRACELLULAR BACTERIA.

B lymphocytes

Plasma cells derived from stem cells in bone marrow. 20-25% of WBC

Natural killer cells and Macrophages

Involved in phagocytosis

Cytokines (Interleukin)

Proteins (chemicals)

TCR

A T cell receptor located on surface of T cell. Linked to protein complex (CD3). Used to recognize antigens and fight them off. Inherited and is in all cells except natural kill cells.

TCR-CD3 complex

Essential for activity of T cells

Types of T lymphocytes

1. T-helper (T4) 2.T-suppressor and T-cytotoxic (T8)

T-helper cell

T4 cell marker - CD4. Enhance antibody response. Assists B cells in producing antibodies.

T-suppressor

T8 marker. Suppress or turn off the functioning B lymphocytes.

T-cytotoxic

T8 marker. Surveillance against or attacking tumor cells directly.

Normal blood ratio

CD4:CD8 ratio is 2:1

AIDS

CD4 cells are selectively lost and the CD4 and CD8 ratio is less than 1:0

Two groups of T-helper cells

T-helper-1 (Th1)
T-helper-2 (Th2)

T-helper-1 (Th1)

Cells that synthesize interleukin-2 (IL2) and interferon-gamma(IFN-y). Stimulate macrophages to become phagocytic and mediate the formation of granulomas to influence the immune system.

T-helper-2 (Th2)

Synthesizes IL-4, IL-5 and IL-13. Secretion of IgE and other immunoglobulins and activation of eosinophils which influence immune system.

Two types of B lymphocytes

Plasma cells
B memory cells

B lymphocytes become plasma cells...

When stimulated by antigen

Plasma cells

Produce specific antibody needed to fight the antigen. Produce proteins called antibodies (immunoglobulins - Ig)

Types of immunoglobulins carried in blood stream

1.IgG 2.IgM 3.IgE 4.IgA 5.IgD

IgG

Digestive tract, most common, can pass to baby.

IgM

Appears first usually, largest in number.

IgE

Allergic reaction, production of histamines.

IgA

Found in saliva.

IgD

Most often found in B cells.

B memory cells

Retains memory of a previously encountered antigen. Duplicate itself. Capacity to remember.

Natural killer cells

Cells do NOT have TCR gene rearrangement. React against virus-infected cells and kill tumor and foreign cells with our previous sensitization.

Macrophages

Response to antigen. Present in CT. Involved in Phagocytosis. Amplify the immune system (make stronger). Does NOT remember encountered antigen.

Macrophages assist

The B and T lymphocytes that produce cytokines.

Macrophages serve as the link between...

Inflammatory and Immune Responses

Cytokines

Proteins that assist in communication of lymphocytes. Activate macrophages and enhance their function.

Lymphokines

Produced by B and T cells. Cause cytokines to have different function.

Monokines

Produced by macrophages (Interferon is a common monokine).

Immune complex

Antibody-antigen reaction (when antibodies combine with antigen).

Antibody titer

Show levels of antibody in the blood stream.

Two major divisions of Immune Response

1. Humoral Response
2. Cell-mediated Response
(they are inter-related)

Humoral Response

Produces antibodies. B lymphocytes are primary cells. Defend against bacteria and viruses.

Cell-mediated Response

Lymphocytes working alone. T lymphocytes are assisted by macrophages.

Passive Immunity

Using antibodies produced by another person.
Natural = from mother to child
Acquired = immunization/injection

Active Immunity

Body produces antibodies to protect against antigens.
Natural = getting sick
Acquired = vaccine/immunization

Type I Hypersensitivity Reaction

Anaphylaxis. Occurs within mins. Plasma cells produce IgE. IgE causes mast cells to release histamine. Life threatening. ASTHMA ATTACK, ALLERGIC RXS TO MEDICINE.

Type II Hypersensitivity Reaction

Antibodies combine with antigen. ACTIVATE IgG and IgM. Destruction of tissue. Rhesus incompatibility (RH incompatibility) - mother with negative blood type, Graves disease.

Type III Hypersensitivity Reaction

Immune complexes are deposited in various tissues and cause acute inflammation. Neutrophils are attracted to tissues. Phagocytosis and death of neutrophil. Lysosomal enzymes are released and causes tissue destruction. Systemic Lupus.

Type IV Hypersensitivity Reaction (Delayed)

Drugs act as antigens and cause an immunologically induced inflammatory response. Involved a cell-mediated immune response. T lymphocytes cause damage to the tissue cells. Tuberculin test PPD. Rejection of tissue grafts and transplanted organisms.

Aphthous Ulcers

Canker sores. Affect about 20% of the population.

Etiology of Aphthous Ulcers

Varied, unclear. May be from foods, trauma, stress, depleted immune system, smoking, hormones, genetics, alcohol, etc.

Systemic Disease associated with Aphthous Ulcers

1. Behcets 2. Crohns 3.Ulcerative Colitis 4.Cyclic Neutropenia 5.Sprue 6.Periodic Fever Aphthous Stomatitis Pharyngitis Adentitis

Behcets

Multisystem disease. Affects CV system, GI system, muscular and sense of sight.

Crohn Disease

Multisystem disease. Irritable bowl syndrome, internal aphthous ulcers.

Ulcerative Colitis

Related to Crohns

Cyclic Neutropenia

Number of neutrophils vary.

Sprue

Ciliac disease. Sensitivity to gluten (wheat, rye, etc). Test for with blood test first and then biopsy intestines.

Periodic Fever Aphthous Stomatitis Pharyngitis Adentitis

Occurs in people who have fevers. Confused with herpes.

Histology of Aphthous Ulcers

CD4 to CD8 lymphocyte ratio decreases. Cell mediated immunity. Histocytes, PMNs and Macrophages present. T cytotoxicity ulcerations.

Types of Aphthous Ulcers

Minor
Major
Herpetiform

Minor Aphthous Ulcer

Most common. Discrete round to oval ulcers up to 1 cm in diameter. May be single or multiple. Surrounded by a erythematous halo. May have yellowish-white fibrinous membrane over top. Ulcers not preceded by vesicles.

Minor aphthous ulcers heal in

7-10 days. Prodomal burning for 1-2 days.

Minor aphthous ulcers occur on

Movable nonkeratinized mucosa

Major Aphthous Ulcer

More severe form. 1-3 cm in diameter, 1-10 in number. Heal with a scar. Resembles squamous cell carcinoma (biopsy to confirm). AIDS patients.

Major aphthous ulcers heal in

2-6 weeks

Major aphthous ulcers occur on

Labial mucosa, soft palate and tonsillare

Herpetiform aphthous ulcer

Greater number of lesions and more frequent recurrence. 1-3 mm in diameter and up to 100 lesions. Resemble primary herpes.

Herpetiform aphthous ulcers heal in

7-10 days

Herpetiform aphthous ulcers occur

Any location

Diagnosis of Aphthous Ulcers

Liquid tetracycline (herpes will not respond). Systemic disease may be associated.

Treatment of Aphthous Ulcers

Topical steroids, corticosteroids, topical tetracycline, topical anesthetics, Kenolog-orobase (1.5% cortisone acetate). Mouthwash: Tetracycline, Nystatin (candida) and Benedryl solution.

Uriticaria

Hives. Multiple areas of well demarcated swellings on skin. Pruritis (itching), Loc areas of vascular permeability. Release of histamine (IgE, IgG or IgM).

Angioedema

Soft, swollen areas under skin. Diffuse swelling of tissue caused by permeability of deeper BV's. Subcutaneous and submucosal CT. No pruritus (itching). Respiratory and GI. Histamine released (IgE, IgG or IgM).

Contact Mucositis

Red, burning pruritus. Smooth shiny appearance, firm to palpation. Small vesicles.

Fixed drug eruption

Single or multiple. Raised, red patches or cluster of macules on skin. Pain and pruritus. Related to Type III hypersensitivity - immune complexes are deposited along the endothelial wall of BV, causing vasculitis and damage, rise to erythema and edema.

Erythema Multiforme

Vesticulobubous disease. Skin and mucous membranes affected. Acute or chronic. Etiology unknown (hypersensitivity).

Precipitating Factors of Erythema Multiforme

Bacterial, Fungal, Viral, Infections, Stress and Allergies (drugs)

Three types of Erythema Multiforme

Oral Erythema Multiforme
Classic Erythema Multiforme
Stevens-Johnson

Histology of Erythema Multiforme

Intradermal edema of the spinous layer and edema of the superficial CT. Increase thickness of prickle layer. Acanthosis (dissolution of intercellular bridges of prickle layer).

Oral Erythema Multiforme

Oral Lesions: limited to gingiva, fiery red (desquamative), tongue, lips and palate may be affected, red borders, seldom bleed.

Classical Erythema Multiforme

Oral Lesions: resemble aphthous ulcers, hemorrhagic crusted lips, mucosal lesions are macular red erosive leaving necrotic slough, buccal and labial mucosa, tongue and gingiva, halitosis.

Classical Erythema Multiforme can have

Skin lesions also: appear like macules, papules or bulla that are red-white in color, ring like in appearance, called "target bulls eye". LOCATED ON HANDS

Treatment of Erythema Multiforme

Self limiting (2 weeks - 3 months)
Low dose steroid

Stevens-Johnson Syndrome

More severe form of Erythema Multiforme. Similar skin and oral lesions, more widespread and more severe. May lead to blindness.

Stevens-Johnson Syndrome Classic traid

Eye lesions (conjunctivitis)
Genital lesion
Lips (encrusted and bleed)

All types of Erythema Multiforme may be mistaken for

ANUG

Treatment of Stevens-Johnson Syndrome

Hospitalization, resolves in 6 weeks, systemic corticosteroid, systemic antiviral medications.

Lichen Planus

Common, chronic dermatologic disease that affects oral mucosa. Exacerbation and remission. Wickham striae (interconnecting white lines and circles). Small, papular, pinhead sized doomed or hemispheric glistening white nodules.

Most common location of Lichen Planus

Buccal mucosa

Etiology of Lichen Planus

Unknown (stress, drugs or chemicals)

Types of Lichen Planus

Reticular
Erosive/Bullous

Reticular Lichen Planus

Most common. Has gingival and skin lesions.

Gingival lesions of Reticular Lichen Planus

Wickham striae along with white slighty raised white plaque areas. Desquamative gingivitis (gingiva slough away in layers). Can be asymptomatic.

Skins lesions of Reticular Lichen Planus

2-4 mm papules. Wickham Striae. Affects lumbar region, flexor wrist and anterior surface of the ankles.

Erosive/Bullous Lichen Planus

Epithelium separates from the CT and erosions, bullae or ulcers form. Most common site is buccal mucosa. GIngival lesions look like desquamative gingivitis.

Histology of Lichen Planus

Chronic, orthokeratosis and parakeratosis, thickness of spinous layer can vary, rete ridges may be absent or hyperplastic or saw toothed, destruction of the basal cell layer, T lymphocytes.

Treatment of Lichen Planus

Corticosteroid, topical cyclosporin, may have increased risk of squamous cell carcinoma.

Reiter's Syndrome (Reactive Arthritis)

Abnormal immune response. Benign and self-limiting.

Triad of Reiter's Syndrome

Arthritis (inflammation/destruction of joints)
Urethritis (inflammation of urethra)
Conjunctivitis (inflammation of eye covering)

Etiology of Reiter's Syndrome

Unclear, maybe genetic. Antigenic marker (HLA-B27). Develop in 1-4 weeks after venereal or GI.

Reiter's Syndrome oral lesions

Aphthous like ulcers
Red lesions
Geographic tongue like lesions

Treatment of Reiter's Syndrome

Non steroidal anti inflammatory drugs

Langerhan Cell Disease (Histiocytosis X)

Eosinophils abundance, Langerhan cells (related to macrophages and histocytes), Etiology unknown.

Types of Langerhan Cell Disease

Letterer-Siwe (acute disseminated form)
Hand-Schuller-Christian (chronic disseminated)
Eosinophilic granuloma of bone (solitary or chronic)

Letterer-Siwe (acute disseminated form)

Acute, affects children younger than 3 years old, seldom have oral lesions, resembles lymphoma, fatal-rapid, responds to chemo therapy.

Hand-Schuller-Christian (chronic disseminated)

Affects children less than 5 years old. Triad occurs in 25% of patients.

Hand-Schuller-Christian Traid

Radiolucent area in skull (punched out)
Unilateral or bilateral exophthalmus
Diabetes with gradual onset (collection macrophages in sella turcica affecting the pituitary gland)

Eosinophilic granuloma of bone (solitary or chronic)

Affects older children and young adults. Involves skull and mandible. Radiographically may resemble widened PDL; circumscribed radiolucency, perapical inflammation.

Sjogren Syndrome

Autoimmune disease, chronic progressive lymphocytic infiltration, affects salivary and lacrimal glands.

Primary Sjogren Syndrome

Sicca syndrome. Limited to salivary and lacrimal glands. Xerophthalmia (dry eyes), Xerostomia, Keratoconjunctivitis (thickening of conjunctive layer).

Secondary Sjogren Syndrome

Lacrimal and salivary gland involvement with the presence of another autoimmune disease. Rheumatoid arthritis may occur with this.

Oral Manifestations of Sjogren Syndrome

Xerostomia, Erythematous mucosa, Oral discomfort, Sticky, Gen. loss of filiform and fungiform papillae, Caries, Perio disease, Candida, Parotid enlargement and Lymphadenopathy.

Sjogren Syndrome may also exhibit

Burning and itching of the eyes and photophobia - extreme sensitivity to light.

Diagnosis of Sjogren Syndrome

2-3 component must be present (Xerostomia, Keratoconjunctivitis or Rheumatoid arthritis).

Lupus Erythematous

Autoimmune disease with unknown cause. Production of antinuclear antibodies (ANA) and anti DNA antibodies.

Lupud Erythematous affects

Women 8x more likely than men and black women 3x more than white women. SKIN, HEART, LUNGS, KIDNEYS, JOINT and NERVOUS SYSTEM.

Types of Lupus Erythematous

Systemic lupus erythematous
Chronic cutaneous lupus erythematous

Systemic Lupus Erythematous

Multisystem disease with skin and oral manifestation (heart and kidneys).

Signs and symptoms of Systemic lupus erythematous

Clinical: fever, weight loss, arthritis and fatigue
Gen. malaise, BUTTERFLY RASH on bridge of nose, kidney failure is most significant aspect of disease. Cardiac involvement, heptomegaly, splenomegaly. RENAL FAILURE is MOST COMMON CAUSE OF DEATH. Need medical consult.

Most common initial complaint of Systemic Lupus

Arthritis and Arthralgia (pain)

Skin lesions of Systemic Lupus

Telangiectasias (red papules that look like can have black heads occurring).

Oral lesions of Systemic Lupus

Resemble lichen planus
Erythema
Hyperkeratosis

Chronic Cutaneous Lupus

Few or no systemic signs or symptoms. Lesions limited to skin or mucosa. Scaly, erythematous patches that increase with sun exposure. Oral lesions may be identical to erosive lichen planus.

Histology of Lupus

Increase in B lymphocyte activity and abnormal T lymphocyte function. Hyperkeratosis. Degeneration of basal cell layer.

Pemphigus Vulgaris

Serious skin disease. Chronic. Autoimmune disease that affects adults from Mediterranean, South Asia or Jewish.

Oral lesions of Pemphigus Vulgaris

Ulcerations, vesicle or bullae may be first to appear. Halatosis. Vesicle or bullae that rupture and bleed leaving a denuded surface. Bulla are fragile (difficult to see). Nikolsky's sign (Bulla appear with firm pressure, desquamative gingivitis).

Skins lesions of Pemphigus Vulgaris

Erythema
Vesicles
Bulla
Erosions
Ulcers
Crusted lips that bleed

Pemphigus Vulgaris vs Pemphigus Vegetans

Vulgaris is most common
Vegetans is very rare

Histology of Pemphigus Vulgaris

Intracellular separation (basal layer)
Acantholysis (Epithelial cell separation, desmosomal attachment disappear, producing Tzanck cells (degenerating epithelial cells).

Cicatricial Pemphigoid (Mucous Membrane Pemphigoid)

Occular, oval vaginal and pharyngeal mucosa lesions. Gingiva is most common oral site. Erythematous and ulcerative gingiva (desquamative gingivitis). Nikolksy's sign. Bulla (less fragile then Pemphigus vulgaris). More serious occular involvement (scarring, symblepharons - adhesions).

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