Oral Path Final

Front 1

What enzymes do obligate anaerobes lack?

Back 1

Superoxide dismutase, catalase, and peroxidase. Without these, O2 is toxic

Front 2

Toxic effects of O2 for anaerobes

Back 2

Directly toxic due to oxidation of proteins. Indirectly toxic due to H2O2 or oxygen radicals that are produced

Front 3

Effect of redox potential

Back 3

anaerobes require low redox potential of about -150 to -250mV which isn't possible in the presence of O2

Front 4

Redox potential of normal healthy tissue

Back 4

It is about +150mV. If it falls below this level, anaerobes can grow.

Front 5

Factors that contribute to reduction in redox potential

Back 5

Plaque formation, loss of vascular supply, acid production by aerobes, and tissue necrosis.

Front 6

Plaque induced gingival diseases

Back 6

plaque induced gingivitis, gingival diseases modified by systemic factors, medications, and malnutrition.

Front 7

Non-plaque induced gingival lesions

Back 7

Specific bacterial, viral, or fungal infections as well as genetic disorders (pemphigoid)

Front 8

What is the most common form of periodontitis?

Back 8

Chronic periodontitis (adult). Associated with P. gingivalis, T. forsythia, and T. denticola primarily.

Front 9

What is the most important independent risk factor for periodontal disease?

Back 9

Smoking

Front 10

Red complex bacteria

Back 10

P. gingivalis, T. forsythia, and T. denticola

Front 11

Green complex bacteria

Back 11

E. corrodens, C. gingivalis, C. sputigena, C. ochracea, C. concisus, A. actino

Front 12

What inhibits the growth of A. actino?

Back 12

Growth of S. sanguis and A. viscosus

Front 13

Which complex is considered the most significant in periodontal disease progression?

Back 13

Red complex

Front 14

Role of GRoEL?

Back 14

Heat shock protein expressed by most periodontopathogens. Human antibodies to it react with human HSP and cause atherosclerosis. (oral-systemic connection)

Front 15

What organism contributes over 50% of the anaerobes of the periodontal pockets?

Back 15

Eubacterium. Also involved in corn-cob formation

Front 16

Non-specific plaque hypothesis

Back 16

All plaque is bad, large amounts produce disease and thus must be controlled

Front 17

Specific palque hypothesis

Back 17

Only certain plaque is pathogenic and produce substances that cause the destruction of periodontal tissues.

Front 18

How long does it take for a mature or climax biofilm to form?

Back 18

10-14 days

Front 19

Population shift in gingivitis/periodontitis

Back 19

Begins with mostly gram+ cocci and shifts to gram- rods

Front 20

Bacteria involved in pregnancy gingivitis

Back 20

Prevotella intermedia

Front 21

Primary bacterial agent of acute periodontitis

Back 21

A. actino

Front 22

Primary bacterial agents in ANUG

Back 22

Fusobacterium, Treponema, and Prevotella

Front 23

Are dentoalveolar infections plaque related?

Back 23

Nope

Front 24

Typical development of pulpitis

Back 24

Bacteria spreads from a carious lesion to the pulp via dentinal tubules

Front 25

Secondary mechanisms of pulpitis development

Back 25

Tooth wear, fracture, gingival crevice, or blood supply

Front 26

In which demographic would you be more likely to see a pulp polyp?

Back 26

In permanent teeth of children. They need endo tx at this point

Front 27

Spread of pulpitis from maxillary teeth

Back 27

Purulent sinusitis, brain abscess, infraorbital cellulitis, or cavernous sinus thrombosis

Front 28

Spread of pulpitis from the mandibular teeth

Back 28

Ludwig's angina, parapharyngeal abscess, empyema, or osteomyelitis of mandible

Front 29

Cause of Ludwig's angina

Back 29

Mixed infection of Streptococci, Porphyromonas, Prevotella, and Fusobacteria in the sublingual, submental, and submandibular spaces.

Front 30

Pathogen responsible for lumpy jaw

Back 30

A. israelii

Front 31

What factors predispose to osteomyelitis of the jaw?

Back 31

Radiation, osteoporosis, Paget's disease, IDDM, malaria, malnutrition, AIDS, etc

Front 32

Most common cause of osteomyelitis of the jaw

Back 32

Derived from pulpal periapical infection usually. Anaerobes usually responsible (tannerella, prevotella, porphyromonas). S. aureus not common in jaw

Front 33

Causes of periodontal abscess

Back 33

Impaction of food, compression of the pocket wall by orthodontic tooth movement, spread of infection from pocket to supporting tissues.

Front 34

Tx of periodontal abscess

Back 34

Incision and drainage followed by curettage along the root or extraction. Antibiotics if systemic involvement

Front 35

Nocardia

Back 35

Branching bacteria found in soil. This is a pulmonary opportunist and can disseminate to lung and kidney. Can be treated with trimethoprim/sulfa and surgery.

Front 36

Actinomyces

Back 36

A. israelii and A. viscosus are the primary pathogens. Over 50% of infections are lumpy jaw. Treat with surgery and penicillin

Front 37

Common location of abscess in lumpy jaw

Back 37

The angle of the mandible

Front 38

Origination of infection in lumpy jaw

Back 38

Mandibular first molars and anterior maxillary teeth most often involved. Usually associated with trauma, periodontal pocket or infected tonsil

Front 39

Which bacteria form sulfur granules?

Back 39

Actinomyces israelii

Front 40

Inflammatory response in gingivitis

Back 40

Enhanced expression of adhesion molecules, enhanced migration of neutrophils, and inflammatory infiltrate of neutrophils, B cells, and T cells

Front 41

When does the initial lesion of experimental gingivitis begin?

Back 41

2-4 days after cessation of oral hygeine practices

Front 42

Majority of lymphocytes in initial gingivitis lesion

Back 42

T cells (mostly TH-1)

Front 43

Early lesion in experimental gingivitis

Back 43

Evolves from initial lesion in 4-7 days. Marked increase in lymphocytic infiltrate, initially T cells predominate, then B cells later.

Front 44

Established lesion in experimental gingivitis

Back 44

Intense PMN infiltrate, pocket now formed. B cells transform to plasma cells and produce IgG. Increaseing B cell infiltrate correlates with disease progression. Increased T cell infiltrate correlates with stable lesion

Front 45

Advanced lesion in experimental gingivitis

Back 45

Bone destruction occurs, apical extension of junctional epithelium. Plasma cells predominate in CT and PMN's predominate in pocket.

Front 46

Effect of crevicular IgA levels on periodontal disease severity

Back 46

There is an inverse correlation...more IgA means less severe disease.

Front 47

T lymphocyte contribution in periodontitis

Back 47

20-30% of lymphocytes in are CD4+ T cells that produce Th2 cytokines (IL-6, IL-10, and IL-13. This contributes to high B cell response and increased bone loss.

Front 48

At what level of blood PMN is periodontitis risk increased?

Back 48

<1000/uL there is increased risk. <200/uL there is a 100% probability of infection

Front 49

Causes of PMN disfunction that can contribute to periodontal disease

Back 49

Agranulocytosis, neutropenia, leukocyte adhesion deficiency, IDDM, Downs syndrome

Front 50

PMN function in acute periodontitis

Back 50

Increased number of crevicular PMN's, but reduced chemotaxis, reduced chemotaxis, and reduced killing. (PMN dysfunction)

Front 51

PMN function in chronic periodontitis

Back 51

Increased number of crevicular PMN's, increased activity and level of enzymes.

Front 52

Signifigance of Il-1B and TNF-a

Back 52

They are pro-inflammatory cytokines produced by monocytes and PMN's that are bone resorptive. They stimualte fibroblast proliferation and production of PGE2 and matrix metalloproteinases

Front 53

Function of matrix metalloproteinases

Back 53

Stimulated by IL-1B and TNF-a. They cause destruction of extracellular matrix of gingiva and PDL

Front 54

Function of leukotriene B4 (LTB4)

Back 54

It brings more neutrophils into the area and keeps the inflammatory process going (chemoattractant, degranulation, and hyperalgesia)

Front 55

What initially stimulates release of pro-inflammatory mediators?

Back 55

LPS binds to CD14 on phagocytic cells and they release the cytokines.

Front 56

Gene polymorphism and periodontitis

Back 56

The rare allele of IL-B 3953 is significantly associated with severe chronic adult periodontitis

Front 57

What is the realtive risk of periodontitis in smokers?

Back 57

2.5-6 times more likely to develop periodontitis

Front 58

Possible mechanisms for smoking contributing to periodontitis

Back 58

Increased plaque formation, decreased gingival blood flow, impaired PMN chemotaxis, phagocytosis, and respiratory burst.

Front 59

IDDM and periodontitis

Back 59

Type 1 has 5x increased risk, type 2 has 3x increased risk. Increased severity with age and lack of control. Possibly due to PMN dysfunction from altered energy metabolism during periods of high glucose levels.

Front 60

Pre-term and low birth weight

Back 60

Periodontitis has the biggest correlation with pre-term and low birth weight babies

Front 61

Salivary gland infections (general)

Back 61

Usually viral and parotid gland is most often affected. Mostly seen in adults (except mumps)

Front 62

What is the most common cause of acute viral sialedenitis?

Back 62

Mumps followed by CMV. Coxsackie A, echovirus, and Influenza A are rare

Front 63

Complications of mumps

Back 63

Testicular atrophy (orchitis), meningoencephalitis, pancreatitis, and sensorineural hearing loss.

Front 64

Bacterial sialedenitis

Back 64

Relatively rare, mostly due to retrograde infection back through the duct. Commonly involves S. viridans and S. aureus. Mostly due to gland or duct abnormality causing obstruction.

Front 65

Tx for acute sialedenitis

Back 65

Antibiotics and algesics. Rehydrate and stimulate saliva. External gland massage and possible drainage via surgical opening.

Front 66

Most important predisposing factor in sialadenitis

Back 66

Xerostomia (caused by dehydration, drugs, irradiation, and Sjogren's)

Front 67

Oral manifestations of graft vs. host disease

Back 67

Salivary gland involvement with swelling and desquamitive gingivitis