Sweep 2.1 Flashcards
(92 cards)
1
Q
Iron can increase outer membrane protein expression in
A
P.gingivalis
2
Q
S.cristatus can inhibit
A
fimA expression
3
Q
• Critical probing depth (Lindhe) -
A
probe depths less than which root planing will cause attachment loss (2.9mm)
4
Q
Gram-negative Anaerobic Helical-shaped Highly motile microorganisms 1st identified in ANUG Several different species, hard to distinguish
A
Treponema denticola
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
6
Q
CaH(PO4) x 2 H2O= Brushite (B)
A
Basis for supragingival calculus formation
Seen in recent (<2 week old) calculus
7
Q
Ca4H(PO4)3 x2H2O= Octa calcium phosphate (OCP)
A
Predominant in exterior layers
Forms platelet like crystals
8
Q
Ca5 (PO4)3 xOH= Hydroxyapatite (HA)
A
Predominant in inner layers of old calculus
Forms rod or sand-grain like crystals
9
Q
-Ca3 (PO4)2 = Whitlockite (W)
A
Most common form in subgingival calculus
Hexagonal crystals
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)
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
12
Q
released during tissue destruction (cell death)
A
- Aspartate amino-transferase:
13
Q
a membrane-bound glycoprotein involved in maintenance of alveolar bone
A
- Alkaline phosphatase:
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
15
Q
a proteolytic enzyme found in lysosomal granules of neutrophil
A
- Elastase:
16
Q
Peri-implantitis:
A
Inflammatory reactions associated with loss of supporting bone around an implant in function
17
Q
Ulceration covered by a yellowish – white or grayish slough which is termed “Pseudo membrane”.
A sign of
A
NUG
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
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).
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:
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
22
Q
Plaque index - 0
A
No plaque
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.
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.
25
Plaque index - 3
3- Abundance of soft matter within the gingival pocket and/or on the tooth and gingival margin.
26
Periodontal Screening and Recording (PSR) - 1
- no calculus, BOP
Colored are avisible
27
PSR - 2
Calc, maybe BOP
| Colored are avisible
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PSR - 3
Colored are apartially visible
| w/or w/o BOP, Calc
29
PSR 4
colored area not visible
| w or w/o BOP, Calc
30
PSR
1 4, goes to full perio eval.
| 2 sectants get 3s, go full perio eval.
31
O'Leary index
Disclose, rinse, then count red surfaces
32
```
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
```
Recommend gingival grafts
33
Simplified Oral Hygiene Index (OHI-S)
| Purpose
To assess oral cleanlines by estimating the tooth surface covered with debris and/or calculus
34
Simplified Oral Hygiene Index (OHI-S)
| Components
Simplified Debris Index
| Simplified Calculus Index
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Simplified Oral Hygiene Index (OHI-S)
Tooth selection
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.
36
Plaque Index (PlI)
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
37
Turesky Modification of Quigley-Hein Plaque Index
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
The Quigley-Hein index is biased toward the
gingival third of the tooth surface
39
Turesky Modification of Quigley-Hein Plaque Index
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
NIDR Calculus Index
0 Calculus is absent
1 Supragingival calculus, but no subgingival calculus is present
2 Supragingival and subgingival, or subgingival calculus only is present
41
Volpe-Manhold Index
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
Papillary-Marginal-Attachment (PMA)-Index
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
The Extent and Severity Index (ESI)
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
The Periodontal Index System (PI)
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
The Periodontal Disease Index System
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
Phases of Therapy
```
Systemic phase
Initial (hygiene) phase
Corrective phase
Maintenance phase
-Supportive periodontal therapy
```
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Systemic phase
Eliminate or decrease the influence of systemic conditions
| Protection from infectious hazards
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Initial (hygiene) phase
```
Cause-related therapy
Removal of hard and soft deposits
Removal of retentive factors
Patient motivation (OHI)
Concluded by re-evaluation
```
49
Corrective phase
Periodontal surgery
Implant surgery
Endodontic, restorative, prosthetic therapy
Patient cooperation determines options
50
Maintenance phase
```
Prevention of re-infection & recurrence
Assessment of deepened, BOP+ sites
Instrumentation of deepened, BOP+ sites
Caries control
Control of prosthetic restorations
```
51
Initial therpay
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
Becker,Berg and Becker
Good
Questionnable
Hopeless
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McGuire and Nunn
```
Very good
Good
Fair
Poor
Hopeless
```
54
Becker, Berg and Becker
| Good (two or more factors)
<50% bone loss
No furcation involvement
<2 mobility
55
Becker, Berg and Becker
| Questionable (two or more factors)
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
Becker, Berg and Becker
| Hopeless (two or more factors)
```
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
McGuire and Nunn
| Good prognosis:
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
McGuire and Nunn
| Fair prognosis:
25-50% attachment loss
grade I or easily accessible Grade II furcation involvement,
adequate maintenance possible
Few systemic complications
59
McGuire and Nunn
| Poor prognosis:
>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
McGuire and Nunn
| Hopeless prognosis:
>75% attachment loss
Tooth mobility 2+
grade II and III furcation involvements,
difficult-to-maintain areas and/or doubtful patient cooperation,
Root proximity
61
The younger patient would be expected to have a greater reparative capacity, however
Observed destruction indicates that inflammation
overcomes repair for this patient, therefore expect poorer outcomes of therapy
62
Disease Severity
| 2 parameters
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
Pocket depth is less important than
level of attachment because it is not necessarily related to bone loss.
64
In general, a tooth with deep pockets and little attachment and bone loss has a better prognosis than one with
shallow pockets and severe attachment and bone loss.
65
When greater bone loss has occurred on one surface of a tooth, the bone height on the
less involved surfaces should be taken into consideration when determining the prognosis.
66
In smokers prognosis of slight-to-moderate periodontitis is generally
fair to poor.
67
In smoking patients with severe periodontitis, the prognosis may be
poor to hopeless.
68
Patients with slight to moderate periodontitis who stop smoking can upgraded to a
good prognosis,
69
Patients smoking
| whereas those with severe periodontitis who stop smoking may be upgraded to a
fair prognosis.
70
Well-controlled diabetics with slight-to-moderate periodontitis who comply with their recommended periodontal treatment should have a ----- prognosis.
good
71
Prognosis is poor for teeth with
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
Root concavities appear more marked on
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
In drug-influenced gingival enlargement, plaque control alone does
not prevent development of the lesions, and surgical intervention is usually necessary to correct the alterations in gingival contour.
74
(slight-to-moderate periodontitis), the prognosis is generally ----- provided the inflammation can be controlled.
good
75
Aggressive periodontitis would have a ----- prognosis.
poor
76
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
fair to poor prognosis
77
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 -----
circulating alkaline phosphatase
fair to poor.
78
The prognosis for a patient with NUG is -----.
good
79
With repeated episodes of NUG, the prognosis may be downgraded to ------.
fair
80
Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 1
Slight horizontal bone loss with minimal peri-implant defects
81
Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 2
Moderate horizontal bone loss with isolated vertical defects
82
Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 3
Moderate to advanced horizontal bone loss with broad, circular bony defects
83
Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)
Class 4
Advanced horizontal bone loss with broad, circumferential vertical defects, as well as loss of the oral and/or vestibular bony wall
84
Class 1 treatment
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
Class 2 treatment
```
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
Class 3 and 4 treatment
In peri-implantitis class 3 and 4, the presence of vertical defects almost always requires the use of GTR techniques.
87
2 types of T-helper cells - differ in -----
cytokine profiles
88
Th-2 cytokines activate
B cells to plasma cells
89
Initial lesion summary
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
Early lesion summary
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
Established lesion summary
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
Advanced lesion summary
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
