Oral Path Exam 1

Front 1

Central self tolerance

Back 1

Deletion of T cell clones with high affinity for self antigens during T cell maturation in the thymus (neg. selection).

Front 2

Peripheral self tolerance

Back 2

Anergy or apoptosis of T-dependent B cells due to lack of co-stimulatory signal from T cell

Front 3

Three mechanisms of loss of self tolerance

Back 3

Molecular modification, molecular mimicry, and emergence of sequestered antigens

Front 4

molecular modification as a mechanism of self-tolerance loss

Back 4

This is when a self antigen is modified by an external agent (ie. drugs) and antibodies formed are cross reactive with original antigen.

Front 5

Example of disease caused by molecular modification

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Drug induced hemolytic anemia. Alpha-methyldopa and ibuprofen can modify the Rhesus antigen and antibodies destroy RBCs

Front 6

Molecular mimicry as a mechanism of loss of self-tolerance

Back 6

This is when foreign antigens share structural similarity with self-antigens

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Example of molecular mimicry

Back 7

Rheumatic fever caused by group A and B strep that have antigens similar to cardiac myosin. Antibodies to bacteria attack and damage heart

Front 8

Emergence of sequestered antigens

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Example is sympathetic opthalmia. Ocular antigens expressed intra-ocularly are released following eye trauma. T cells activated and return to the eyes and damage them

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Factors in induction of autoimmunity

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Genetics, age (most common at puberty and middle age), and sex (more common in females). Almost always T-dependent

Front 10

MHC and autoimmunity

Back 10

Many autoimmune diseases are associated with class II MHC alleles (HLA-DR 3 and 4 with type 1 diabetes). Few are associated with class I

Front 11

Ankylosing spondylitis

Back 11

Strongly associated with presence of HLA-B27 allele (>90%).

Front 12

Viruses implicated in induction of type 1 diabetes

Back 12

Coxsackie B, rotavirus, herpes, hep C

Front 13

Virus implicated in induction of rheumatic fever

Back 13

Streptococcus pyogenes

Front 14

Molecular mimicry as a mechanism of loss of self-tolerance

Back 14

This is when foreign antigens share structural similarity with self-antigens

Front 15

Example of molecular mimicry

Back 15

Rheumatic fever caused by group A and B strep that have antigens similar to cardiac myosin. Antibodies to bacteria attack and damage heart

Front 16

Emergence of sequestered antigens

Back 16

Example is sympathetic opthalmia. Ocular antigens expressed intra-ocularly are released following eye trauma. T cells activated and return to the eyes and damage them

Front 17

Factors in induction of autoimmunity

Back 17

Genetics, age (most common at puberty and middle age), and sex (more common in females). Almost always T-dependent

Front 18

MHC and autoimmunity

Back 18

Many autoimmune diseases are associated with class II MHC alleles (HLA-DR 3 and 4 with type 1 diabetes). Few are associated with class I

Front 19

Graves disease (hyperthyroidism)

Back 19

antibodies bind to TSH receptor (TSH agonist) and lots of thyroid hormone is produced

Front 20

Hashimoto's thyroiditis (hypothyroidism)

Back 20

chronic inflammatory disease of the thyroid caused by antibodies to thyroid peroxidase. Thyroid shows heavy lymphocytic infiltrates (fills with T cells and causes goiter)

Front 21

Pernicious (macrocytic) anemia

Back 21

Autoantibodies to intrinsic factor (which is needed in order to absorb vit B12) cause a B12 deficiency. RBCs get bigger

Front 22

Type 1 diabetes

Back 22

Antibodies to Islet cells and insulin (both self and foreign). Causes destruction of Islets and any insulin in circulation. Lymphocytic infiltrate of islets occurs

Front 23

Myasthenia gravis

Back 23

Anti-acetylcholine receptor antibodies act as an antagonist by blocking the receptor and inhibiting muscle activation

Front 24

Rheumatoid arthritis

Back 24

anti-IgG IgM's, anti-citrulline, anti-collagen, and anti-ssDNA. Causes immune complex deposition in joints

Front 25

Systemic lupus erythematosus (SLE)

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Anti-ssDNA, dsDNA, and other nuclear antigens. Immune complex formation with deposition in the kidneys. Pts die from kidney failure. Present with malar or butterfly rash and diagnose with stain for C3 in the kidney

Front 26

Oral manifestations of pernicious anemia

Back 26

Painful glossitis with dissapearance of majority of the papilla

Front 27

Oral manifestations of Addison's disease

Back 27

Adrenals shut down, many different causes. Causes pigmentation of the oral mucosa

Front 28

Oral manifestations of type 1 diabetes

Back 28

Hyperplastic (inflamed) gingivitis

Front 29

Sjogren's syndrome

Back 29

Salivary gland enlargement due to antibodies to nucleolar mitochondria (salivary and lachrymal glands affected). Causes xerostomia

Front 30

Systemic sclerosis (scleroderma)

Back 30

Anti-collagen, anti-DNA topoisomerase, and anti-centromere antibodies. Everything will fibrose (skin, lungs, etc) and death happens within a few years

Front 31

Oral manifestations of SLE

Back 31

atrophic erythematous lesions in the oral cavity

Front 32

Lichen planus

Back 32

Usually due to T cell activation from a local insult (habits, dental materials, etc). Results in destruction of basal cell layer and formation of lacey or confluent papules on dorsal tongue or buccal mucosa

Front 33

Eoidermolysis bullosa

Back 33

Antibodies to type VII procollagen. Causes dermis and epidermis to separate and blisters to form

Front 34

Linear IgA disease

Back 34

Deposits of IgA along the basement membrane that react with BM antigens. Causes vesicles, bullae, and ulcers.

Front 35

Pemphigoid

Back 35

Autoantibodies to basement membrane antigens of stratified squamous epithelium. Causes subepithelial blisters (oral, skin, ocular) and desquamitive gingivitis

Front 36

Two forms of pemphigoid

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Mucous membrane (cicatricial) and bullous pemphigoid. Oral lesions in most cases of cicatricial and 40% of bullous.

Front 37

Pemphigus

Back 37

Autoantibodies to desmoglein-3. Initial manifestation is intraepithelial blisters that are very fragile and pop easily. It is pathogenic so if you give pt IgG to another person they will develop the disease

Front 38

Oral manifestations of pemphigus

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Despuamative gingivitis, buccal and palatal lesions, and lesions of larynx and esophagus. Can look like pemphigoid, but its more serious

Front 39

Therapy for pemphigus

Back 39

Intralesional steroids as well as systemic steroids such as prednisone and cyclophosphamide. Works well but effect is temporary

Front 40

What is coaggregarion?

Back 40

When bacteria associate, either same species (homotypic) or different species (heterotypic ie. corn cob) to form biofilm

Front 41

How many oral bacterial species can be found in the adult?

Back 41

Approx. 500-700 (predominantly anaerobic gram negatives)

Front 42

What is the pioneer organism in the oral cavity a few hours after birth?

Back 42

Strep salivarius

Front 43

What is the first organism to colonize the tooth surface after teeth erupt?

Back 43

Strep sanguis colonize the teeth at about 6 months of age when they begin to erupt

Front 44

Changes in oral flora with age

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Initially most oral baceria are gram positive, then with age there is a switch to more gram negative anaerobes

Front 45

Sucrose-independent adhesion

Back 45

Strep mitis uses Ag I/II for initial adhesion to salivary pelicle. No sucrose is necessary

Front 46

Sucrose dependent adhesion

Back 46

Strep mutans use glucan binding proteins to bind glucans that are a byproduct of sucrose breakdown.

Front 47

What is the function of M cells?

Back 47

They are concentrated near OMALT and they function in transporting antigens into OMALT for sampling

Front 48

What is the structure of IgA?

Back 48

It is a homodimer

Front 49

Where is the J-chain made?

Back 49

It is made by plasma cells and it induces polymerization of sIgA

Front 50

What is the secretory component?

Back 50

It is synthesized by epithelial cells and is part of the poly-Ig receptor. It is responsible for transcytosis of IgA

Front 51

What Ig's can be recognized by the poly-Ig receptor?

Back 51

IgM (pentomer) and IgA (dimer)

Front 52

Which Ig is the most efficient agglutinator?

Back 52

IgM is the largerst Ig with the highest MW and is the most efficient agglutinator

Front 53

How soon after birth do oral Ig's appear?

Back 53

sIgA is detectable in mucosal secretion at 1 week to 2 months after birth

Front 54

IgA isotypes

Back 54

A1 isotype predominates early on and then is replaced by A2 during puberty. It works better because it lacks the hinge region so it can't be cleaved by bacterial proteases.

Front 55

Lymphocyte trafficking

Back 55

Tissues have vascular address (HEV addressins) that help the activated lymphocytes to return to a similar tissue to where it was initially excited (gut, mucous lined cavity, etc). This is what causes the common mucosal immune response

Front 56

Requirement for lymphocytes to exhibit trafficking

Back 56

They must be activated B or T cells, naive lymphocytes do not exhibit preferential trafficking

Front 57

Function of amylase in saliva

Back 57

Mainly involved with digestion of starch, but also is antibacterial in that it inhibits adhesion or oral bacterial species

Front 58

Function of lactoferrin

Back 58

It takes iron out of solution so it isn't available for microbes to use, so they die (it is bactericidal). Strep mutans is highly susceptible to this

Front 59

Function of lysozyme

Back 59

It disrupts microbial cell walls by hydrolyzing bond between NAG and NAM. It is antibacterial

Front 60

Function of mucins

Back 60

It is a protein backbone with lots of sugars on it where bacteria can bind. It acts as a non-immunoglobulin agglutinin (NIA) to clump bacteria together. It is antibacterial

Front 61

Proline-rich proteins (PRP)

Back 61

They help to maintain calcium and phosphate saturation of saliva and are a major fraction of salivary proteins. Some PRP variants are associated with susceptibility to caries

Front 62

Function of defensins

Back 62

These are small proteins that form pores in microbial membranes (antimicrobial action)

Front 63

Function of histatins

Back 63

These are importnat salivary antifungal factors, woks very well on candida. It also forms pores in cell wall/membrane

Front 64

Describe corn cob formation

Back 64

Coaggregation of bacteria of different genus. Oral cocci attach and grow on the surface of filamentous bacteria such as Eubacterium or E.yurii.

Front 65

Function and composition of exopolysaccharides

Back 65

Composed mostly of glucans, mediates adhesion of secondary colonizers (S. mutans) and changes diffusion properties to trap acids

Front 66

Bacterial enzyme that synthesizes fructans and glucans from sucrose

Back 66

Glycosyltransferase. Facilitates sucrose-dependent adhesion

Front 67

Role of lipids in calculus formation

Back 67

Lipids derived from gram negative organisms attract and bind calcium and phosphate ions and start crystal formation (calculus)

Front 68

Why is pyrophosphate added to toothpaste?

Back 68

It chelates excess calcium ions so they can't be incorporated into calcium phosphate crystals that contribute to calculus formation

Front 69

Areas of heavy supragingival calculus deposits

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Lingual surfaces of mandibular incisors (Wharton's duct) and buccal surfaces of maxillary molars (Stenson's duct).

Front 70

Bacterial make-up of supragingival calculus

Back 70

Contains more gram positive organisms

Front 71

Bacterial make-up of subgingival calculus

Back 71

Contains more gram negative organisms

Front 72

Which serotypes of Strep mutans are human pathogens?

Back 72

Serotypes C, E, and F

Front 73

Mechanism of action of xylitol

Back 73

Xylitol disrupts the metabolism of Strep mutans by blocking the active site of glucosyltransferases. This doesn't kill the bacteria, just inhibits its growth.

Front 74

Glucan binding proteins (GBP) mediate what type of adhesion

Back 74

Sucrose denendent adhesion

Front 75

PRP's mediate what type of adhesion?

Back 75

Sucrose-independent adhesion. Type 1 pilli and fimbrae (Ag I/II) of bacteria bind to PRP's

Front 76

What are intracellular polysaccharides (IPS)?

Back 76

Storage product (similar to glycogen) made by bacteria during periods of carb excess, metabolized during fasting periods.

Front 77

Effect of IgA deficiency

Back 77

Mostly asymptomatic, no increased risk of caries unless IgM is absent as well

Front 78

Characterisitcs of parasitic infection

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Often chronic and over 90% of human parasites are single-celled protozoa

Front 79

What is a true oral parasite?

Back 79

One that can live its entire life cycle in the mouth

Front 80

What are the three true oral parasites?

Back 80

Entamoeba histolytica, Entamoeba gingivalis, and Trichomonas tenax

Front 81

E. histolytica

Back 81

Fecal-oral transmission, causes diarrhea. DIC is metronidazole

Front 82

E. gingivalis

Back 82

Oral-oral transmission, associated with periodontitis. Can manifest as furred tongue. No DOC, just get a cleaning

Front 83

Trichomonas

Back 83

Most common parasitic infection diagnosed in the USA. DOC is metronidazole

Front 84

G. lamblia

Back 84

aka beaver fever. Fecal-oral transmission. Causes diarrhea and DOC is metronidazole

Front 85

Plasmodium

Back 85

It is an obligate intracellular parasite that lives in RBC's. Causes anemia and pallor of oral mucosa. DOC is chloroquine

Front 86

What are the hosts for plasmodium?

Back 86

Humans and female anopheles mosquitos

Front 87

Toxoplasma gondii

Back 87

Obligate intracellular parasite, hosts are humans, cats, and pigs. Fecal-oral transmission as well as via pork chops (undercooked). Can cause birth defects. DOC is pyrimethamine

Front 88

What is the most common helminthic infection world wide?

Back 88

Ascaris lumbricoides (roundworm)

Front 89

What is the most common helminthic infection in Las Vegas?

Back 89

Enterobius vermicularis (pinworm), also called "day care itch". Anal-oral transmission

Front 90

What is the major oral manifestation/symptom of helminthic infection?

Back 90

Oral pallor (whiteness of lips and gingiva)