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Perio Final > Sweep 2.1 > Flashcards

Sweep 2.1 Flashcards

1
Q

Iron can increase outer membrane protein expression in

A

P.gingivalis

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2
Q

S.cristatus can inhibit

A

fimA expression

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3
Q

• Critical probing depth (Lindhe) -

A

probe depths less than which root planing will cause attachment loss (2.9mm)

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4
Q 
Gram-negative
Anaerobic 
Helical-shaped
Highly motile microorganisms
1st identified in ANUG
Several different species, hard to distinguish
A

Treponema denticola

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5
Q 
Gram-negative
Short, round-ended rod
Anaerobic
Black pigmented Bacteriodes
Luxuriant growth in naphthoquinone
Associated with puberty/ pregnancy gingivitis (Kornman and Loesche)
Elevated in NUG
A

Prevotella intermedia/ nigrescens

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6
Q

CaH(PO4) x 2 H2O= Brushite (B)

A

Basis for supragingival calculus formation

Seen in recent (<2 week old) calculus

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7
Q

Ca4H(PO4)3 x2H2O= Octa calcium phosphate (OCP)

A

Predominant in exterior layers

Forms platelet like crystals

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8
Q

Ca5 (PO4)3 xOH= Hydroxyapatite (HA)

A

Predominant in inner layers of old calculus

Forms rod or sand-grain like crystals

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9
Q

-Ca3 (PO4)2 = Whitlockite (W)

A

Most common form in subgingival calculus

Hexagonal crystals

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10
Q 
Used primarily to detect serum antibodies to periodontal pathogens
Membrane immunoassay (EvalusiteTM): chairside use to detect Aa, Pg, and Pi (detection limit of 105 for Aa and 106 for Pg)
A

Enzyme-linked immunosorbent assay (ELISA)

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11
Q

Based on the binding of protein to latex: latex beads are coated with species-specific antibody
Currently these assays only for research purposes

A
  • Latex agglutination
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12
Q

released during tissue destruction (cell death)

A
  • Aspartate amino-transferase:
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13
Q

a membrane-bound glycoprotein involved in maintenance of alveolar bone

A
  • Alkaline phosphatase:
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14
Q

a lysosomal enzyme degrades proteoglycans and ground substance

A
  • β-glucuronidase:

β-glucuronidase (βG)
Elevated βG in GCF from sites with severe periodontal disease
High sensitivity and specificity when related to occurrence of clinical attachment loss
Good predictor for future periodontal breakdown

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15
Q

a proteolytic enzyme found in lysosomal granules of neutrophil

A
  • Elastase:
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16
Q

Peri-implantitis:

A

Inflammatory reactions associated with loss of supporting bone around an implant in function

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17
Q

Ulceration covered by a yellowish – white or grayish slough which is termed “Pseudo membrane”.

A sign of

A

NUG

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18
Q

Necrosis of epithelium and superficial layers of the connective tissue.
Hyperemic CT with engorged capillaries and dense infiltrations of PMNs.

A

Histopath of NPD

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19
Q

3 commonly used drug types that are associated with

gingival overgrowth:

A

Anticonvulsants (Phenytoin sodium or epinutin)
Immunosuppressant (Cyclosporin A)
Calcium channel blocking agents (Nifedipine).

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20
Q

Scores: 0 to 3; bleeding is considered.
Presence of bleeding automatically leads to a score ≥2
Frequently used index in clinical trials
First published by Löe (1961) and Löe & Silness (1963

A

Gingival Index (GI) Loe Silness:

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21
Q

Gingival index

A

0 -normal
1 - mild inflam, slight color change and edema, no bleeding
2 - moderate inflam, redness, edema, bleeds on probing
3 - severe inflam, marked redness and edema, ulceration, spontaneous bleeding
Spontaneous bleeding
Brushing
Eating
Blood on my pillow

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22
Q

Plaque index - 0

A

No plaque

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23
Q

Plaque index - 1

A

1- A film of plaque adhering to the free gingival margin and adjacent area of the tooth. The plaque may be seen only by using the probe on the tooth surface.

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24
Q

Plaque index - 2

A

2- Moderate accumulation of soft deposit s within the gingival pocket, or the tooth and gingival margin which can be seen with the naked eye.

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25
Q

Plaque index - 3

A

3- Abundance of soft matter within the gingival pocket and/or on the tooth and gingival margin.

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26
Q

Periodontal Screening and Recording (PSR) - 1

A
  • no calculus, BOP

Colored are avisible

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27
Q

PSR - 2

A

Calc, maybe BOP

Colored are avisible

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28
Q

PSR - 3

A

Colored are apartially visible

w/or w/o BOP, Calc

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29
Q

PSR 4

A

colored area not visible

w or w/o BOP, Calc

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30
Q

PSR

A

1 4, goes to full perio eval.

2 sectants get 3s, go full perio eval.

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31
Q

O’Leary index

A

Disclose, rinse, then count red surfaces

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32
Q 
When recession causes symptoms
Caries
Esthetic concerns
Progressive recession
Sensitivity
Subgingival restoration margins on thin biotype
Pre-orthodontic therapy
Final tooth position will be buccal
A

Recommend gingival grafts

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33
Q

Simplified Oral Hygiene Index (OHI-S)

Purpose

A

To assess oral cleanlines by estimating the tooth surface covered with debris and/or calculus

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34
Q

Simplified Oral Hygiene Index (OHI-S)

Components

A

Simplified Debris Index

Simplified Calculus Index

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35
Q

Simplified Oral Hygiene Index (OHI-S)

Tooth selection

A

Facial surfaces of # 3, 8, 14, 24
Lingual surface of # 19, 30

Literally just measuring plaque - 0-3, going up the tooth in terms of plaque coverage.

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36
Q

Plaque Index (PlI)

A

The PlI assesses the amount of plaque at the gingival margin, examining the same anatomical units as the GI
Plaque scores range from {0} to {3}
A probe is used to distinguish between scores {0} and {1}. Visible plaque is scored a {2} or a {3}
The Pl-I is computed for a tooth, subject, or population
It parallels the Gingival Index (GI) of Löe & Silness
First published by Silness & Löe (1964

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37
Q

Turesky Modification of Quigley-Hein Plaque Index

A

Score 0: No plaque
Score 1: Spots of plaque at cervical margin
Score 2: Thin, continuous band of plaque,
£1 mm wide, at cervical margin
Score 3: A plaque band >1 mm but <1/3 of crown height
Score 4: Plaque covering ³ 1/3 but < 2/3 of crown height
Score 5: Plaque covering ³ 2/3 of crown height

38
Q

The Quigley-Hein index is biased toward the

A

gingival third of the tooth surface

39
Q

Turesky Modification of Quigley-Hein Plaque Index

A

Facial and lingual surfaces are examined
Plaque is made visible using a disclosing agent and scored using a {0} to {5} scoring system
Scores are computed for subject, population
It is the most frequently used plaque index in clinical trials
Quigley & Hein (1962); Turesky

40
Q

NIDR Calculus Index

A

0 Calculus is absent
1 Supragingival calculus, but no subgingival calculus is present
2 Supragingival and subgingival, or subgingival calculus only is present

41
Q

Volpe-Manhold Index

A

Determines the quantity of supragingival calculus
Lingual surfaces of lower anteriors (#22-27)
Quantity is determined in mm of calculus along the 2 diagonal and the central lines drawn over the lingual surface of each tooth
Index, expressed in mm, is computed for tooth, subject, population
Most frequently used calculus index in longitudinal studies
Published by Volpe & Manhold (1962)

Criss cross lines on tooth

42
Q

Papillary-Marginal-Attachment (PMA)-Index

A

Background: “The number of units affected correlates with the severity of gingival inflammation”
Facial gingival surface is divided in 3 scoring units P - M - A
Gingival units affected with gingivitis are counted. Presence or absence of inflammation is counted as {1} and {0}, respectively
Severity component can be considered
Score computed for tooth subject population
First published by Schour & Massler (1947)

43
Q

The Extent and Severity Index (ESI)

A

Agreement
Disease is defined as attachment loss >1mm
Extent
Proportion of tooth sites in a patient showing signs of destructive periodontitis
Severity
Amount of attachment loss at the diseased sites, expressed as a mean value

44
Q

The Periodontal Index System (PI)

A

Score 0: Negative.
Score 1, 2: Gingivitis
Score 6: Gingivitis with pocket formation
Score 8: Advanced destruction with loss of masticatory function
All teeth are examined. The circumference of each tooth is inspected visually, and given a score.
Index computed for subject, population.

45
Q

The Periodontal Disease Index System

A

Score 1, 2, 3: Severity of gingivitis
Score 4: Initial attachment loss (£3 mm)
Score 5: Moderate attachment loss (>3 mm and
£6 mm)
Score 6: Advanced attachment loss (>6 mm)

4 areas per tooth are examined using a probe. The most severe score is tabulated and used for the calculation of the subject’s PDI
Index computed for subject, population

46
Q

Phases of Therapy

A 
Systemic phase
Initial (hygiene) phase
Corrective phase
Maintenance phase
-Supportive periodontal therapy
47
Q

Systemic phase

A

Eliminate or decrease the influence of systemic conditions

Protection from infectious hazards

48
Q

Initial (hygiene) phase

A 
Cause-related therapy
Removal of hard and soft deposits
Removal of retentive factors
Patient motivation (OHI)
Concluded by re-evaluation
49
Q

Corrective phase

A

Periodontal surgery
Implant surgery
Endodontic, restorative, prosthetic therapy
Patient cooperation determines options

50
Q

Maintenance phase

A 
Prevention of re-infection &amp; recurrence
Assessment of deepened, BOP+ sites
Instrumentation of deepened, BOP+ sites
Caries control
Control of prosthetic restorations
51
Q

Initial therpay

A

emergency treatment if needed
patient education
explanation of disease process and relevant factors
oral hygiene instruction
occlusal analysis and treatment of localized trauma from occlusion
bacterial sampling of select sites

52
Q

Becker,Berg and Becker

A

Good
Questionnable
Hopeless

53
Q

McGuire and Nunn

A 
Very good
Good
Fair
Poor
Hopeless
54
Q

Becker, Berg and Becker

Good (two or more factors)

A

<50% bone loss
No furcation involvement
<2 mobility

55
Q

Becker, Berg and Becker

Questionable (two or more factors)

A

50% bone loss,
6- to 8-mm probing depth,
Class 2 furcation,
Anatomic variables such as a deep palatal groove on the maxillary incisors or a mesial furcation involvement of the maxillary first premolar

56
Q

Becker, Berg and Becker

Hopeless (two or more factors)

A 
More than 75% bone loss,
more than 8-mm probing depth, 
Class 3 furcation involvement, 
Class 3 mobility, 
poor crown-root ratio,
unfavorable root proximity, 
Repeated periodontal abscess formation
57
Q

McGuire and Nunn

Good prognosis:

A

25% attachment loss and/or class I furcation involvement
Adequate remaining bone support
Adequate possibilities to control etiologic factors and establish a maintainable dentition,
Adequate patient cooperation
No systemic environmental factors or well controlled systemic factors.

58
Q

McGuire and Nunn

Fair prognosis:

A

25-50% attachment loss
grade I or easily accessible Grade II furcation involvement,
adequate maintenance possible
Few systemic complications

59
Q

McGuire and Nunn

Poor prognosis:

A

> 50% attachment loss
Class 2 tooth mobility
Inaccessible grade II furcation involvements, grade III furcation
difficult-to-maintain areas and/or doubtful patient cooperation,
presence of systemic/environmental factors.

60
Q

McGuire and Nunn

Hopeless prognosis:

A

> 75% attachment loss
Tooth mobility 2+
grade II and III furcation involvements,
difficult-to-maintain areas and/or doubtful patient cooperation,
Root proximity

61
Q

The younger patient would be expected to have a greater reparative capacity, however
Observed destruction indicates that inflammation

A

overcomes repair for this patient, therefore expect poorer outcomes of therapy

62
Q

Disease Severity

2 parameters

A

level of clinical attachment (approximate extent of root surface that is devoid of periodontal ligament)
radiographic examination shows the amount of root surface still invested in bone.

63
Q

Pocket depth is less important than

A

level of attachment because it is not necessarily related to bone loss.

64
Q

In general, a tooth with deep pockets and little attachment and bone loss has a better prognosis than one with

A

shallow pockets and severe attachment and bone loss.

65
Q

When greater bone loss has occurred on one surface of a tooth, the bone height on the

A

less involved surfaces should be taken into consideration when determining the prognosis.

66
Q

In smokers prognosis of slight-to-moderate periodontitis is generally

A

fair to poor.

67
Q

In smoking patients with severe periodontitis, the prognosis may be

A

poor to hopeless.

68
Q

Patients with slight to moderate periodontitis who stop smoking can upgraded to a

A

good prognosis,

69
Q

Patients smoking

whereas those with severe periodontitis who stop smoking may be upgraded to a

A

fair prognosis.

70
Q

Well-controlled diabetics with slight-to-moderate periodontitis who comply with their recommended periodontal treatment should have a —– prognosis.

A

good

71
Q

Prognosis is poor for teeth with

A

short tapered roots and large crowns.

Disproportionate crown-to-root ratio
Reduced root surface available for periodontal support
Periodontium may be more susceptible to injury by occlusal forces.

72
Q

Root concavities appear more marked on

A

maxillary first premolars, the mesiobuccal root of the maxillary first molar.
These concavities increase the attachment area and produce a root shape that may be more resistant to torquing forces

73
Q

In drug-influenced gingival enlargement, plaque control alone does

A

not prevent development of the lesions, and surgical intervention is usually necessary to correct the alterations in gingival contour.

74
Q

(slight-to-moderate periodontitis), the prognosis is generally —– provided the inflammation can be controlled.

A

good

75
Q

Aggressive periodontitis would have a —– prognosis.

A

poor

76
Q

Periodontitis as a manifestation of systemic diseases can be divided into two categories.

those associated with hematologic disorders such as leukemia and acquired neutropenias.

those associated with genetic disorders such as familial and cyclic neutropenia, Down syndrome, Papillon-Lefevre syndrome, and hypophosphastasia.

Although the primary etiologic factor in periodontal diseases is bacterial plaque.

these patients present with

A

fair to poor prognosis

77
Q

Periodontitis as a MANIFESTATION OF SYSTEMIC DISEASES.

Include hypophosphatasia, where patients have decreased levels of ——, severe alveolar bone loss, premature loss of deciduous and permanent teeth and the connective tissue disorder.

The prognosis will be —–

A

circulating alkaline phosphatase

fair to poor.

78
Q

The prognosis for a patient with NUG is —–.

A

good

79
Q

With repeated episodes of NUG, the prognosis may be downgraded to ——.

A

fair

80
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 1

A

Slight horizontal bone loss with minimal peri-implant defects

81
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 2

A

Moderate horizontal bone loss with isolated vertical defects

82
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 3

A

Moderate to advanced horizontal bone loss with broad, circular bony defects

83
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 4

A

Advanced horizontal bone loss with broad, circumferential vertical defects, as well as loss of the oral and/or vestibular bony wall

84
Q

Class 1 treatment

A

Surgical reduction of pocket depth, thinning of mucosal flaps and apical repositioning of flaps at a bone edge level, using the corresponding suture technique.
The implant surface is cleaned and decontaminated.
Implantoplasty is only performed if threads are exposed.

85
Q

Class 2 treatment

A 
Similar to class 1, but repositioning is performed more apically, leaving more implant surface exposed, thus requiring an implantoplasty.
If local vertical resorption has three or more walls, this bone defect is restored using classical GTR techniques. 
In cases where the defect involves one or two walls, osteoplasty or bone leveling is performed to favor soft tissue repositioning, to fulfill self-cleaning criteria.
86
Q

Class 3 and 4 treatment

A

In peri-implantitis class 3 and 4, the presence of vertical defects almost always requires the use of GTR techniques.

87
Q

2 types of T-helper cells - differ in —–

A

cytokine profiles

88
Q

Th-2 cytokines activate

A

B cells to plasma cells

89
Q

Initial lesion summary

A

Vasculitis subjacent to JE
Exudation of fluid into tissue and gingival sulcus
Increased migration of leukocytes into JE and gingival sulcus
Serum proteins present extravascularly
Alteration of the most coronal portion of JE
Loss of perivascular collagen

90
Q

Early lesion summary

A

Accentuation of features of the initial lesion
Accumulation of lymphoid cells immediately subjacent to JE
Cytopathic alteration in resident fibroblasts
Further loss of collagen network
Early proliferation of basal cells of JE
Inflammatory changes are clinically evident

91
Q

Established lesion summary

A

Persistence of features of acute inflammation
Increased proportion of plasma cells
Presence of extravascular immunoglobulins in CT, JE and gingival sulcus
Continuing loss of collagen and matrix
Proliferation and lateral extension of JE
Early pocket formation may be evident
No apical migration of JE and no bone loss at this stage

92
Q

Advanced lesion summary

A

Persistence of established lesion features
Increased proportion of plasma cells (~50%)
Extension of lesion into alveolar bone and PL, with significant bone loss
Continued loss of collagen fibers and matrix subjacent to PE
Formation of periodontal pocketing and apical migration of JE from CEJ

Perio Final (8 decks)

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