Oral Pathology Quiz 3

What does the immune response defend the body against?

Foreign substances, such as microorganisms.

What is an the acquired immune response?

Has the ability to remember. It responds very quickly when an antigen enters the body a second time.

What is an antigen?

A foreign substance the immune system defends against.

What are examples of things that can act as antigens?

Proteins, microbes/toxins, tumor cells, tissue grafts, organ transplants.

What happens in an autoimmune disease?

The body's own cells become treated as antigens.

What are lymphocytes, and where do they come from?

The primary immune WBCs; derived from bone marrow stem cells.

What are the three types of lymphocytes?

B lymphocytes, T lymphocytes, and Natural Killer (NK) cells.

Where do B lymphocytes mature and reside?

Mature from bone marrow stem cells; reside in lymph nodes.

What are the two main types of B lymphocytes?

Plasma cells and B memory cells.

What do plasma cells do?

Produce the specific antibody needed to fight an antigen.

What is the role of a B memory cell?

Retains memory of previously encountered antigens.

What are antibodies also called, and what are the five types?

Immunoglobulins — IgG, IgM, IgE, IgA, IgD.

What is formed when antibody binds antigen, and is the antigen still active?

An immune complex (antigen-antibody complex); the antigen becomes inactive.

What is antibody titer?

The level of an antibody in the blood.

Where do T lymphocytes develop and mature?

Develop from bone marrow stem cells; mature in the thymus.

What is the role of T memory cells?

Retain memory of previously encountered antigens, like B memory cells.

What do T-helper cells do, and what marker do they carry?

Boost the B-cell/antibody response; carry the CD4 marker.

What do T-suppressor cells do, and what marker do they carry?

Suppress B-cell function at the end of the immune response; carry the CD8 marker.

What do T-cytotoxic cells do, and what marker do they carry?

Kill virus- or tumor-infected cells (aka NK T-cells); carry the CD8 marker.

Are NK cells part of innate or acquired immunity?

Innate immunity, not acquired.

What do NK cells do?

Destroy foreign cells quickly without the need to recognize them by specific antigens.

Where are macrophages found?

In connective tissue during inflammation.

What do macrophages do?

Perform phagocytosis and present antigens to lymphocytes.

Do macrophages have memory?

No — they must be reactivated at every encounter.

What do dendritic cells do?

Act as antigen-presenting cells, along with macrophages and B cells.

Where are dendritic cells found, and what happens once activated?

Found in skin/mucosal tissue; migrate to lymphoid tissue to activate T and B cells.

What is a Langerhans cell?

A specialized dendritic cell found in skin and mucosal tissue.

What are cytokines?

Immune-cell signaling molecules (immunomodulators).

What are lymphokines, and what do they do?

Cytokines from lymphocytes; convert monocytes to macrophages, keep macrophages at the injury site, and activate them.

What are monokines?

Cytokines produced by macrophages.

What are interferons?

Produced by T cells and macrophages. Has antiviral properties.

What is the humoral response?

Antibody production, mainly by B lymphocytes.

What is the cell-mediated response?

Involves lymphocytes, T cells acting alone or with the help of macrophages.

Does the inflammatory response have memory?

No.

What is immunity?

Increased responsiveness from retained memory of a prior antigen.

What is active immunity?

Immunity from natural infection or immunization; a booster is sometimes needed to maintain it.

What is passive immunity?

Protection from antibodies produced by someone else, not the person's own immune system.

What is natural passive immunity?

Antibodies from mother pass through the placenta to the developing fetus.

What is acquired passive immunity?

Injection of antibodies against a microbe to which the person has not previously developed antibodies.

What is Type I hypersensitivity?

Anaphylaxis — IgE triggers mast cells to release histamine, causing vessel dilation/permeability and bronchoconstriction.

What is Type II hypersensitivity?

Cytotoxic — antibody attacks antigen on a cell surface, destroying that tissue.

What is Type III hypersensitivity, and what is a classic example?

Immune complexes deposit in tissues, causing inflammation and neutrophil-driven damage; classic example: systemic lupus erythematosus.

What is Type IV hypersensitivity, and what are examples?

Delayed, T-cell mediated damage; examples: the PPD (TB) skin test and graft/transplant rejection.

What does each type of drug allergy look like (Types I-IV)?

I: anaphylaxis/urticaria/angioedema.

II: hemolytic anemia.

III: serum sickness.

IV: contact dermatitis/mucositis.

Which route of drug administration causes more hypersensitivity reactions?

Topical administration, more than oral or parenteral.

What is an autoimmune disease?

When certain body cells are no longer tolerated and immune system treats them as antigens.

What is an immunodeficiency?

Immunopathologic condition that involves a deficiency in #, function, or interrelationships of the involved WBC and their products.

What is lichen planus?

A chronic mucocutaneous disease of skin and oral mucosa.

What is the classic appearance of lichen planus, and where is it most common?

Wickham's striae (white lacy lines) with papules; most common on the buccal mucosa.

What happens in erosive/bullous lichen planus?

The epithelium separates from the connective tissue, forming erosions, bullae, and ulcers.

What is the most common form of lichen planus?

The reticular form — Wickham's striae with white plaque-like areas.

What gingival finding can lichen planus cause?

Desquamative gingivitis — red, erosive, peeling gingiva.

What do the skin lesions of lichen planus look like, and where do they occur?

Purple, itchy (pruritic) papules on the wrists, elbows, ankles, and lumbar region.

How is lichen planus diagnosed?

Clinical appearance plus biopsy.

Is lichen planus considered premalignant?

It's controversial — there's a suggestion it may have premalignant potential.

How is lichen planus treated?

Topical corticosteroids, good oral hygiene, regular soft tissue examination, and biopsy of any atypical-looking lesions.

What is pemphigus vulgaris?

A severe autoimmune blistering disease caused by autoantibodies against epithelial cell attachment (acantholysis).

Where do PV lesions often appear first, and what do they look like?

The mouth as ulcers, bullae, erosions, and vesicles.

What is Nikolsky's sign?

Pressure on normal-looking mucosa causes the epithelium to split into a blister.

What are Tzanck cells?

Rounded, detached acantholytic cells seen on microscopy.

How is pemphigus vulgaris diagnosed and treated?

Diagnosed by biopsy plus immunofluorescence; treated with high-dose corticosteroids and immunosuppressants.

What other diseases is pemphigus vulgaris associated with?

Systemic lupus erythematosus, Rheumatoid Arthritis, and Sjögren syndrome.

What is a mucous membrane pemphigoid?

A chronic autoimmune disease of the mouth, eyes, genital mucosa, and skin.

What is the most common site of a mucous membrane pemphigoid?

The gingiva, with erythema and ulceration.

What is the most serious complication of a mucous membrane pemphigoid?

Conjunctival scarring, which can lead to blindness.

How is a mucous membrane pemphigoid diagnosed and treated?

Diagnosed with direct immunofluorescence; treated with topical and systemic corticosteroids.

Why should MMP patients see an eye specialist?

Eye lesions can cause corneal and eyelid damage, so periodic evaluation is needed.

What are aphthous ulcers?

Aphthous ulcers are painful sores in the mouth, commonly triggered by trauma or emotional stress.

Where do aphthous ulcers ONLY occur?

Only on nonkeratinized mucosa; never on gingiva, hard palate, or tissue bound to bone.

What are minor aphthous ulcers like?

The most common type; under 1cm, heal in 7-10 days, usually in the anterior mouth.

What are major aphthous ulcers like?

Also called Sutton's disease; over 1cm, deeper, in the posterior mouth, can take weeks to heal and may scar.

What are herpetiform aphthous ulcers like?

Very tiny (1-2mm), painful, and the least common type; resemble herpes simplex ulcers.

When might a biopsy be needed for an aphthous ulcer?

For major aphthae, to rule out squamous cell carcinoma or fungal infection.

How are aphthous ulcers treated?

Topical steroids (most effective early) and topical anesthetics; systemic steroids for major ulcers.

Should topical steroids be used for a viral ulcer?

No, they are contraindicated for viral ulcers.

How do urticaria and angioedema differ?

Hives: multiple, well-demarcated areas of swelling accompanied by itching.

What is angioedema?

Diffuse swelling of the tissue caused by permeability of the deeper B.V.

What are their causes?

Infection, trauma, emotional stress, certain systemic diseases, and ingested allergens.

What mechanisms cause typical vs. hereditary angioedema?

Typical: histamine release (Type I).

Hereditary: uncontrolled complement cascade activation.

What medications can cause angioedema?

ACE inhibitors and angiotensin receptor blockers (ARBs).

How is urticaria/angioedema treated?

Avoid the trigger and use antihistamines; epinephrine for severe, breathing-threatening angioedema.

What causes allergic contact mucositis/dermatitis, and what hypersensitivity type is it?

Direct allergen contact with skin/mucosa; Type IV hypersensitivity.

What are common causes of contact mucositis/dermatitis in dentistry?

Latex gloves, dental materials, acrylics, LA preservatives, and cinnamon flavoring.

How is contact mucositis/dermatitis treated?

Skin testing, removing the allergen, and topical/systemic corticosteroids if needed.

What is a fixed drug eruption?

A lesion that recurs at the same site every time a particular drug is taken. Come after a latent period of several days.

What hypersensitivity type is a fixed drug eruption, and how is it treated?

Type III (immune complex); treated by identifying and discontinuing the causative drug.

What is erythema multiforme?

An acute, self-limited hypersensitivity-type reaction, often triggered by HSV, Mycoplasma infection, or a drug reaction.

What is the characteristic skin lesion of erythema multiforme, and what are the oral findings?

A target/bull's-eye skin lesion; oral ulcers and crusted, bleeding lips.

How is erythema multiforme treated?

Topical corticosteroids for mild cases, systemic corticosteroids for severe cases.

What is Stevens-Johnson Syndrome?

A variant of TEN (not a severe form of EM) affecting oral, genital, ocular, and skin surfaces; eye lesions can cause scarring and blindness.

What is the classic triad of Reactive Arthritis (Reiter's syndrome)?

Conjunctivitis, urethritis, and arthritis. (Can't see, can't pee, can't climb a tree).

Who does Reactive Arthritis typically affect, and what genetic marker is linked to it?

Much more common in men; linked to HLA-B27, usually after a venereal or GI infection.

What oral and skin lesions can occur with Reactive Arthritis?

Aphthous-like ulcers, erythematous lesions, and geographic-tongue-like lesions.

How is Reactive Arthritis treated?

Aspirin/NSAIDs; systemic corticosteroids if needed.

What is Sjögren syndrome?

An autoimmune disease that decreases saliva and tear production.

What is sicca syndrome?

Dry eyes + dry mouth.

What is the difference between primary and secondary Sjögren syndrome?

Primary = glands only.

Secondary = plus another autoimmune disease, like SLE or RA.

Who is most commonly affected by Sjögren syndrome?

Females, much more commonly than males.

What oral findings occur in Sjögren syndrome?

Xerostomia, sticky mouth, cracked lips, and increased caries, periodontal disease, and fungal infections.

What gland finding is common in Sjögren syndrome?

Bilateral parotid gland enlargement, in about half of patients.