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NBDE II boards > Prosthodontics > Flashcards

Prosthodontics Flashcards

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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
What are the energy sources for anaerobic bacteria?
asaccharolytic, amino acids, and small peptides
26
___________ is a constituent of gram (-) microorganisms that's an important initiator of the inflammatory host response.
endotoxin
27
What are the three plaque hypothesis?
1. nonspecific plaque hypothesis 2. specific plaque hypothesis 3. ecological plaque hypothesis
28
Describe nonspecific plaque hypothesis?
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
Describe specific plaque hypothesis?
dependent on the presence of specific microorganisms
30
Describe specific plaque hypothesis?
dependent on the presence of specific microorganisms
31
Describe ecological plaque hypothesis?
a change in pocket environment (ie change in nutrient status) is the primary cause for the overgrowth of putative pathogens
32
What bacteria are seen in periodontal health?
gram (+) facultative cocci and rods Streptococcus Actinomyces
33
What bacteria are seen in gingivitis?
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
What bacteria are seen in chronic periodontitis?
``` predominantly gram (-) anaerobes P.gingivalis, T.forsythia, P.intermedia, Campylobacter, Eikenella, F. nucleatum, A.A, treponema, eubacterium, and peptostreptococcus ```
35
What bacteria are seen in aggressive periodontitis?
A.a, the primary etiological agent of localized aggressive periodontitis
36
List characteristics of A.a
non-motile gram (-) straight or curved Capnophilic (grows well in CO2) Closely associated with localized aggressive periodontitis
37
What are the specific virulence factors of 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
List characteristics of Tannerella forsythia
non-motile gram (-) pleomorphic rod | grows slowly in anaerobic conditions and requires specific growth factor N-acetylmuramic acid
39
What are the specific virulence factors of T.forsythia?
proteolytic enzymes that cleave immunoglobulins and complement components
40
List characteristics of Porphymonas gingivalis
non-motile gram (-) pleomorphic rod grows anaerobically invased epithelial and endothelial cells mostly associated with chronic periodontitis
41
What are the specific virulence factors of P.gingivalis?
``` fimbriae for adherence presence of a capsule proteases - cleaves immunoglobulins, complement and other proteins collagenase hemolysin ```
42
List characteristics of P. intermedia
non-motile gram (-) rod anaerobic most commonly associated with pregnancy gingivitis and necrotizing perio disease
43
List characteristics of Campylobacter rectus
``` motile gram (-) rod, polar flagellum anaerobic ```
44
List characteristics of Fusobacterium nucleatum
non-motile gram (-) bacillus anaerobic can be found in both healthy and diseased patients
45
What are the specific virulence factors of F.nucleatum?
Induces apoptic cell death in PMNs and mononuclear cells and release of tissue damaging leukocytes Important bridging bacteria between early and late colonizers
46
List characteristics of peptostreptococcus and Eubacterium species
``` Both gram (+) Anaerobic ```
47
Calculus composition supragingical and subgingival What is the difference between the two?
Phosphate 75% calcium carbonate 3% Main difference is the mineral source. Supragingival = saliva Subgingival= GCF
48
What are the cells of the innate immune response?
``` Neutrophils Macrophages Monocytes Mast cells Dendritic cells ```
49
What are the cells of the specific immune response
Lymphocytes: T cells, B cells, plasma cells
50
What is the function of neutrophils? (PMNs)
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
How do PMNs know where to be directed?
Chemotaxis | ie C5a, IL-8
52
What are Monocytes/macrophages
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
What are Mast cells
Important for immediate inflammation and responsible for creating vascular permeability and dialysis important cells in anaphylaxis and allergic rxns
54
What are Dendritic cells
important for antigen processing and presentation to cells of the specific immune response
55
What are Lymphocytes
B and T cells | these cells differentiate into plasma cells and responsible for production of antibodies
56
What are T cells
Derived from the thymus | Two types: T helper cells and T cytotoxic cells
57
What are T cytotoxic cells
CD8 | controls intracellular antigens such as bacteria, fungi and viruses
58
What are T helper cells
helps in the production of antigen specific antibodies by B cells and plasma cells and T-cytotoxic cells
59
What are NK cells
T cells that can recognize and kill tumor and virally infected cells
60
What is considered the most important proteinase involved in the destruction of periodontal tissues?
MMPs (metalloproteinases)
61
What are the two mechanisms responsible for tissue destruction in periodontal disease?
1. MMPs | 2. Oxygen radicals
62
Which is MMP is responsible for being produced in large amounts of PMNs, destroying collagen of PDL and perio connective tissue
MMP-8
63
Oxygen radicals are produced by what? How does it affect the periodontium?
produced by PMNs and macrophages Toxic to the periodontium and has direct effect on cell functions and DNA
64
Cytokines are important signaling molecules. IL-1 is responsible for what? IL-8 is responsible for what?
IL-1 = bone resorption IL-8 = attracts inflammatory cells TNF alpha = activates macrophages
65
What are the 3 phases on perio health to gingivitis?
Stage I - inital lesions stage II - early lesion Stage III - Established lesion Stage IV - Advanced stage
66
What is the first stage of transition from health to gingivitis?
2-4 days with vascular dilation, infiltration of PMNs, collagen loss, increased gingival crevicular fluid flow
67
What is the second stage of transition from health to gingivitis?
4-7 days with increase in vasculature, lymphocyte infiltration, increased collagen loss and redness and bleeding on probing
68
What is the third stage of transition from health to gingivitis?
14-21 days with increased vasculature, mature plasma cells in the tissues, collagen loss and clinical changes in color, contour and consistency.
69
What is the fourth stage of transition from health to gingivitis?
Where stage 3 moves into PDL and bone space resulting in periodontitis

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