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NBDE II boards > Prosthodontics > Flashcards

Prosthodontics Flashcards

1
Q

Mobility classifications

Define: Mobility class I, II, III

A 
Mobility class I - horizontal movement between 0.2-1.0 mm 
Mobility class II - horizontal movement between 1.0 - 2.0 mm
Mobility class III - horizontal movement of greater than 2mm
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2
Q

Furcation classifications

Define: Grade I, II, III, IV

A

Grade I - incipient
Grade II - cul-de-sac with definite horizontal component
Grade III - complete bone loss in furcation
Grade IV - complete bone loss in the furcation and recession of the gingival tissues resulting in a furcation opening that is clinically visible

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3
Q

What are systemic factors that alter the magnitude or duration of the host response that impact the appearance of gingivitis?

A

endocrine changes during puberty

pregnancy, diabetes and blood dyscrasias

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4
Q

What are the medications that cause gingival enlargement

A

Anti-seizure - phenytoin
Immunosupressive - cyclosporine
Calcium channel blockers - nifedipine, verapamil, diltiazem, sodium valproate
Oral contraceptives

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5
Q

List of non-plaque induced gingival conditions

A 
Sexually transmitted diseases
Viral infections (herpes)
Fungal infections (candidiasis) 
Hereditary gingival fibromatosis 
Allergies to foods, restorative materials, toothpastes etc 
Traumatic lesions
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6
Q

What are the characteristics of necrotizing perio diseases?

A

ulcerations and necrosis of marginal gingiva; covered by white/yellow slough or pseudomembrane and have blunting of the papillae, bleeding on provocation or spontaneous bleeding, pain, and fetid breath.

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7
Q

What are the two classes of necrotizing perio diseases?

A

Necrotizing ulcerative periodontitis (bone loss and attachment loss)
Necrotizing ulcerative gingivitis (no attachment loss)

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8
Q

What are predisposing factors of necrotizing perio disease?

A

stress, smoking, and immunosuppression (ie HIV)

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9
Q

What are the characteristics of aggressive periodontitis?

A

Patients are typically healthy besides the gingival disease.

There is rapid bone loss and attachment loss.

Amount of microbial deposits are not consistent with disease severity.

Diseased sites infected with Actinobacillus actinomycetemcomitans (A.a)

Abnormalities in phagocyte function; hyperresponsive macrophages producing increased PGE2 and IL-1

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10
Q

What is the difference between localized and generalized aggressive periodontitis?

A

Localized:

  • circumpubertal onset
  • localized firm molar or incisor with proximal attachment loss on at least two permanent teeth, one of which is a first molar
  • ROBUST serum antibody response

Generalized:

  • affecting persons under the age of 30, but not always
  • affecting at least 3 teeth other than first molars and incisors
  • episodic nature of perio destruction
  • POOR serum antibody response to infecting agents
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11
Q

What systemic diseases manifest as periodontitis?

A

Hematologic disorders: acquired neutropenia and leukemia

Genetic disorders: neutropenia, down syndrome, leukocyte adhesion deficiency syndorme, papillion lefevre syndrome, chediak higashi syndrome, histiocytosis syndrome, glycogen storage disease, infantile genetic agranulotosis, ehlers-danlos syndrome, hypophosphatasia

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12
Q

What is the dental plaque composition of surpagingival plaque?

A

gram (+) cocci and short rods - tooth associated/closest to tooth

gram (-) rods and filaments and spirochetes - mature outersurface plaque

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13
Q

What is the dental plaque composition of cervical region plaque?

A

gram (+) cocci and short rods - tooth associated/closest to tooth

gram (-) rods, cocci, filaments, flagellated rods and spirochetes - tissue associated

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14
Q

What is the dental plaque composition of pocket plaque?

A

gram (-) rods - tooth associated

gram (-) rods and cocci, filaments, flagellated rods and spirochetes - tissue associated

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15
Q

What are the 4 phases of plaque formation?

A
  1. Pellicle
  2. initial adhesion and attachment of bacteria
  3. Colonization & plaque maturation
  4. Phases of specific bacteria
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16
Q

The pellicle phase

What consists of the pellicle?

A

Occurs within seconds the surface is cleaned.
The pellicle consists of glycoproteins, proline-rich proteins, phosphoproteins, histidine rich proteins, enzymes (amylase) … these are attachment sites for bacteria

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17
Q

The initial adhesion and attachment of bacteria is governed by what forces?

A

Van der wasls and electrostatic forces

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18
Q

The colonization & plaque maturation

A

this occurs when the firmly attached bacteria start growing, resulting in the formation of microcolonies

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19
Q

Who are the primary colonizers that deposit on teeth?

A

streptococcal and A.a

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20
Q

Who are the late colonizers that deposit on teeth?

A 
Prevotella intermedia
Prevotella loescheii 
Capnocytophaga 
Porphyromonas gingivalis 
Treponema 
A,a
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21
Q

Who is the middle or bridging microorganisms that deposit on teeth?

A

fusobacterium nucleatum

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22
Q

What are bacteria in the red complex?

What is the red complex associated with?

A

Porphymonas gingivalis
Tannerella forsythia
Treponema denticola

These bacteria are associated with bleeding on probing and deeper pockets

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23
Q

What are bacteria in the orange complex?

What is the orange complex associated with?

A

fusobacterium
prevotella
campylobacter

This complex precedes the red complex, supporting the sequential of plaque formation and maturation.

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24
Q

What are the energy sources for gram (+) early colonizers?

A

sugars and saliva (carbon source)

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25
Q

What are the energy sources for anaerobic bacteria?

A

asaccharolytic, amino acids, and small peptides

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26
Q

___________ is a constituent of gram (-) microorganisms that’s an important initiator of the inflammatory host response.

A

endotoxin

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27
Q

What are the three plaque hypothesis?

A
  1. nonspecific plaque hypothesis
  2. specific plaque hypothesis
  3. ecological plaque hypothesis
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28
Q

Describe nonspecific plaque hypothesis?

A

perio disease comes from noxious products by the plaque biomass indicating that the quantity of plaque is of most importance in the initiation of disease

29
Q

Describe specific plaque hypothesis?

A

dependent on the presence of specific microorganisms

30
Q

Describe specific plaque hypothesis?

A

dependent on the presence of specific microorganisms

31
Q

Describe ecological plaque hypothesis?

A

a change in pocket environment (ie change in nutrient status) is the primary cause for the overgrowth of putative pathogens

32
Q

What bacteria are seen in periodontal health?

A

gram (+) facultative cocci and rods
Streptococcus
Actinomyces

33
Q

What bacteria are seen in gingivitis?

A

initial microbiota - gram (+) rods and cocci and gram (-) cocci
As it progresses to gingivitis, gram (-) rods and filaments appear followed by spirochites and motile

34
Q

What bacteria are seen in chronic periodontitis?

A 
predominantly gram (-) anaerobes 
P.gingivalis, T.forsythia, P.intermedia, Campylobacter, Eikenella, F. nucleatum, A.A, treponema, eubacterium, and peptostreptococcus
35
Q

What bacteria are seen in aggressive periodontitis?

A

A.a, the primary etiological agent of localized aggressive periodontitis

36
Q

List characteristics of A.a

A

non-motile
gram (-) straight or curved
Capnophilic (grows well in CO2)
Closely associated with localized aggressive periodontitis

37
Q

What are the specific virulence factors of A.a?

A

leukotoxin- kills human neutrophils, monocytes, lymphocytes
LPS
collagenase
protease that cleaves IgG (the most abundant type of antibody, is found in all body fluids and protects against bacterial and viral infections.)

38
Q

List characteristics of Tannerella forsythia

A

non-motile gram (-) pleomorphic rod

grows slowly in anaerobic conditions and requires specific growth factor N-acetylmuramic acid

39
Q

What are the specific virulence factors of T.forsythia?

A

proteolytic enzymes that cleave immunoglobulins and complement components

40
Q

List characteristics of Porphymonas gingivalis

A

non-motile gram (-) pleomorphic rod
grows anaerobically
invased epithelial and endothelial cells
mostly associated with chronic periodontitis

41
Q

What are the specific virulence factors of P.gingivalis?

A 
fimbriae for adherence
presence of a capsule
proteases - cleaves immunoglobulins, complement and other proteins
collagenase
hemolysin
42
Q

List characteristics of P. intermedia

A

non-motile gram (-) rod
anaerobic
most commonly associated with pregnancy gingivitis and necrotizing perio disease

43
Q

List characteristics of Campylobacter rectus

A 
motile gram (-) rod, polar flagellum
anaerobic
44
Q

List characteristics of Fusobacterium nucleatum

A

non-motile gram (-) bacillus
anaerobic
can be found in both healthy and diseased patients

45
Q

What are the specific virulence factors of F.nucleatum?

A

Induces apoptic cell death in PMNs and mononuclear cells and release of tissue damaging leukocytes

Important bridging bacteria between early and late colonizers

46
Q

List characteristics of peptostreptococcus and Eubacterium species

A 
Both gram (+)
Anaerobic
47
Q

Calculus composition supragingical and subgingival

What is the difference between the two?

A

Phosphate 75%
calcium carbonate 3%

Main difference is the mineral source.
Supragingival = saliva
Subgingival= GCF

48
Q

What are the cells of the innate immune response?

A 
Neutrophils
Macrophages
Monocytes
Mast cells
Dendritic cells
49
Q

What are the cells of the specific immune response

A

Lymphocytes: T cells, B cells, plasma cells

50
Q

What is the function of neutrophils? (PMNs)

A

to protect the body from infection but also plays a part in destroying periodontal tissues

Protects by internalizing microorganisms by phagocytosis, can kill and digest microorganisms by a mix of oxygen radicals and enzymes

51
Q

How do PMNs know where to be directed?

A

Chemotaxis

ie C5a, IL-8

52
Q

What are Monocytes/macrophages

A

Responsible for ingesting antigens such as bacteria and presenting them to the cells of the specific immune response

Regulate immune response through the release of chemical signals called chemokines

53
Q

What are Mast cells

A

Important for immediate inflammation and responsible for creating vascular permeability and dialysis

important cells in anaphylaxis and allergic rxns

54
Q

What are Dendritic cells

A

important for antigen processing and presentation to cells of the specific immune response

55
Q

What are Lymphocytes

A

B and T cells

these cells differentiate into plasma cells and responsible for production of antibodies

56
Q

What are T cells

A

Derived from the thymus

Two types: T helper cells and T cytotoxic cells

57
Q

What are T cytotoxic cells

A

CD8

controls intracellular antigens such as bacteria, fungi and viruses

58
Q

What are T helper cells

A

helps in the production of antigen specific antibodies by B cells and plasma cells and T-cytotoxic cells

59
Q

What are NK cells

A

T cells that can recognize and kill tumor and virally infected cells

60
Q

What is considered the most important proteinase involved in the destruction of periodontal tissues?

A

MMPs (metalloproteinases)

61
Q

What are the two mechanisms responsible for tissue destruction in periodontal disease?

A
  1. MMPs

2. Oxygen radicals

62
Q

Which is MMP is responsible for being produced in large amounts of PMNs, destroying collagen of PDL and perio connective tissue

A

MMP-8

63
Q

Oxygen radicals are produced by what? How does it affect the periodontium?

A

produced by PMNs and macrophages

Toxic to the periodontium and has direct effect on cell functions and DNA

64
Q

Cytokines are important signaling molecules.
IL-1 is responsible for what?
IL-8 is responsible for what?

A

IL-1 = bone resorption
IL-8 = attracts inflammatory cells
TNF alpha = activates macrophages

65
Q

What are the 3 phases on perio health to gingivitis?

A

Stage I - inital lesions
stage II - early lesion
Stage III - Established lesion
Stage IV - Advanced stage

66
Q

What is the first stage of transition from health to gingivitis?

A

2-4 days with vascular dilation, infiltration of PMNs, collagen loss, increased gingival crevicular fluid flow

67
Q

What is the second stage of transition from health to gingivitis?

A

4-7 days with increase in vasculature, lymphocyte infiltration, increased collagen loss and redness and bleeding on probing

68
Q

What is the third stage of transition from health to gingivitis?

A

14-21 days with increased vasculature, mature plasma cells in the tissues, collagen loss and clinical changes in color, contour and consistency.

69
Q

What is the fourth stage of transition from health to gingivitis?

A

Where stage 3 moves into PDL and bone space resulting in periodontitis

NBDE II boards (5 decks)

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