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Perio Final > Sweep 1.2 > Flashcards

Sweep 1.2 Flashcards

1
Q

Width of keratinized tissue <2mm prediposes to

A

recession

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2
Q

Narrow gingiva cannot protect from

A

friction

Cannot buffer against muscle pull

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3
Q

Facilitates subgingival plaque formation since

Mobile tissue causes

A

pocket to open
Facilitates food impaction
Impedes oral hygiene

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4
Q

When would you recommend gingival grafts?

A 
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
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5
Q

Epithelial mesenchymal interaction

A

The characteristics of the gingiva are genetically determined rather than being the result of functional adaptation to environmental stimuli.

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6
Q

Biofilm formation-attachment

A

Planktonic bacteria adhere to acquired pellicle
Salivary glycoproteins and antibodies in pellicle
Alteration in surface charge and free energy
Bacteria vary in attachment ability

Rapid attachers - specific attachment structures (fimbriae, extracellular polymers, glycocalyx)
Slow attachers- no specific mechanism
Bacterial characteristics change following attachment
Synthesis of new outer membrane proteins
Active cellular growth

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7
Q

Co-aggregation-

A

cell-to-cell recognition of genetically distinct cell types
Mediated by protein or glycoprotein receptors on one cell and carbohydrates on the other
All cells are suspended
‘clumps’ form, which then attach to pellicle

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8
Q

Co-adhesion -

A

interactions between suspended and already adhering micro-organisms
Influenced by
Temperature (no co-adhesion >37 degrees)
Lactose (increase lactose, decrease in co-adhesion)

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9
Q

Interbacterial matrix

A

highly variable

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10
Q

Gram-positive matrix-

A

very fibrillar

Due to dextrans and levans

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11
Q

Gram-negative matrix- very

A 
regular
Contains tri-laminar vesicles
Filled with endotoxins and proteolytic enzymes
Probably involved in adherence
Interbacterial carbohydrates
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12
Q

Skeleton of plaque -

A

mutans

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13
Q

Structure- subgingival plaque

Cuticle forms

A

primary attachment
Origin: epithelial attachment?, crevicular fluid?, secreted by adjacent epithelium?
Structure similar to supragingival plaque

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14
Q

Structure- subgingival plaque

Bacterial layers near sulcular epithelium

A

different from tooth-attached
No inter-bacterial matrix
More spirochetes and flagellated bacteria

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15
Q

Streptococcus cristatus

A

Facultative species, Can live w/ or w/o O2

Uses up O2 when available

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16
Q

Fusobacterium nucleatum

A

Robust anaerobe

Binding to strep improves survival when O2 is present

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17
Q

Porphyromonas gingivalis

A

Microaerophilic, obligate anaerobe

Coaggregation essential to survival when O2 is present

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18
Q

Tissue culture experiment

A

F. nucleatum invades epithelial cells
S. cristatus does not invade cells
After coaggregation, S. cristatus is carried inside by F. nucleatum

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19
Q

Quorum sensing

Auto-inducer (AI) 1 or 2 turns on in response to

A

cell density

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20
Q

Commensal bacteria produce and respond to low levels of

A

AI-2

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21
Q

Pathogens produce —— in high levels

A

AI-2 i

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22
Q

AI-2 may determine switch from

A

commensal to pathogenic community

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23
Q

Biofilm

Exo-polymers

A

retard diffusion

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24
Q

Biofilm

Ion-exchange mechanism prevents

A

highly charged molecules from reaching deeper zones – prevent diffusion.

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25
Q 
Biofilm
Extracellular enzymes (beta-lactamases, formaldehyde dehydrogenase, formaldehyde lyase) inactivate
A

antibiotics

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26
Q

P.gingivalis with type I and V fimA genotypes -

A

healthy, type II and IV in disease

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27
Q

Effect of local ‘regulon’ (subgingival environment)

Iron can increase

A

outer membrane protein expression in P.gingivalis

S.cristatus can inhibit fimA expression

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28
Q

Veillonella uses lactate made by

A

streptococci

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29
Q

Campylobacter uses formate made by

A

Selenomonas

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30
Q

Porphyromonas uses

A

hemin from blood in sulcus

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31
Q

Competitive inhibition

A

Bacteriocins

Hydrogen peroxide production (S.sanguinis inhibits A.A.)

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32
Q

Desquamation of epithelium

A

Invade epithelium

Bind to underlying cells

33
Q

Antibody prevent binding

A

IgG and IgA proteases

Mimic host antigens

34
Q

Phagocytic cells

A

Leukotoxin – powerful virulance factor. AA produces this. Can also cause….
Non-lethal suppression of immune cells

35
Q

Actinobacillus actinomycetemcomitans (AA)

A 
New name - Aggregatibacter actinomycetemcomitans (Still AA)
non-motile, 
Gram-negative, 
saccharolytic,
capnophilic, (requires Co2 to grow)
round-ended rod.
Characteristic star-shaped colonies
36
Q

AA Inhibits growth of

A

commensals- Streptococcus sanguis

37
Q

AA with 530 bp deletion is 23x more likely to be disease-associated than

A

AA with full length promoter region.

38
Q

AA and disease

A

5 serotypes
Based on polysaccharides on surface of organism
Serotype specific surface antigens ( SPA) are dominant antigens
Patients infected with only one serotype
Serotypes are stable over time
Serotype b most commonly associated with localized aggressive periodontitis in USA
Has a role in resistance to phagocytosis and killing by PMNs
Serotype a health-associated in Finland, disease-associated in Japan

39
Q

Virulence factors of A. actinomycemtemcomitans (read from text)

A 
Leukotoxin (RTX)	
Induce apoptosis
Cytolethal distending toxin (CDT)
Chaperonin 60
LPS
Apoptosis, bone resorption, etc
OMP, vesicles
Fimbriae 
Actinobacillin
Collagenase
Immunosuppressive factor
40
Q

Porphyromonas gingivalis

A

Gram-negative
anaerobic
non-motile
asacharolytic rods
Black pigmented Bacteriodes (breaks down iron, forms black colonies.
Produce collagenase, proteases,hemolysins, endotoxin, fatty acids, NH3, H2S and indole.
Cysteine proteinases (ARG-gingipain and LYS-gingipain) important in protein degradation and in the maturation of cell surface proteins such as fimA fimbrillin.

41
Q

Virulence factors of P. gingivalis (read from text)

A

Involved in colonization and attachment
Fimbriae, hemagglutinins, OMPs, and vesicles
Involved in evading (modulating) host responses
Ig and complement proteases, LPS, capsule, other antiphagocytic products
Involved in multiplying
Proteinases, hemolysins
Involved in damaging host tissues and spreading
Proteinases (Arg-, Lys-gingipains), Collagenase, trypsin-like activity, fibrinolytic , keratinolytic, and other hydrolytic activities

42
Q

Tannerella forsythia

A 
A.k.a Bacteroides forsythus, Tannerella forsythensis
Gram-negative
Anaerobic
Spindle-shaped 
highly pleomorphic rod
Requires N-acetylmuramic acid (NAM)
Co-cultivates with F.nucleatum
Serrated S-layer on cell surface
Mediates adhesion
Hemagglutination
43
Q

Treponema denticola

A 
Gram-negative
Anaerobic 
Helical-shaped
Highly motile microorganisms
1st identified in ANUG
Several different species, hard to distinguish
44
Q

Prevotella intermedia/ nigrescens

A 
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
45
Q

Fusobacterium nucleatum

A 
Gram-negative
Anaerobic
Spindle-shaped rod.
Early colonizer in plaque
Bridging organism
Most common isolate cultured from subgingival microbiota in health and disease.
Can induce cell death in leukocytes 
Releases cytokines, elastase and oxygen radical from leukocytes.
Several subspecies
F.nucleatum ss nucleatum
F.nucleatum ss polymorphum
F.nucleatum ss vincentii
F. periodonticum
46
Q

The organism that is found MOST often in
both remission and progression of adult
periodontitis is

A

Fusobacterium nucleatum

47
Q

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

A

Basis for supragingival calculus formation

Seen in recent (<2 week old) calculus

48
Q

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

A

Predominant in exterior layers

Forms platelet like crystals

49
Q

Ca5 (PO4)3 xOH= Hydroxyapatite (HA)

A

Predominant in inner layers of old calculus

Forms rod or sand-grain like crystals

50
Q

-Ca3 (PO4)2 = Whitlockite (W)

A

Most common form in subgingival calculus

Hexagonal crystals

51
Q

Several putative periodontal pathogens such as Pg, Tf, and Aa possess in common a trypsin-like enzyme that hydrolyzes a substrate

A

N-benzoyl-DL-arginine-2-naphthylamide (BANA).

52
Q

Aspartate amino-transferase:

A

released during tissue destruction (cell death)

-

53
Q

Alkaline phosphatase:

A

a membrane-bound glycoprotein involved in maintenance of alveolar bone

54
Q
  • β-glucuronidase:
A

a lysosomal enzyme degrades proteoglycans and ground substance

55
Q
  • Elastase:
A

a proteolytic enzyme found in lysosomal granules of neutrophil

56
Q

Extracellular destruction enzymes

Associated with the activity of

A

matrix metalloproteinases

Produced by inflammatory, epithelial and connective tissue cells

57
Q

β-glucuronidase (βG)

A

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

58
Q

Elastase

A

Periocheck® (chair-side test kit)

Positive correlation of elastase in GCF with clinical attachment loss

59
Q 
Matrix metalloproteinases (MMPs)
Secreted by
A

fibroblasts and macrophages

60
Q 
Matrix metalloproteinases (MMPs)
Responsible for
A

remodeling and degradation of ECM components

61
Q

Matrix metalloproteinases (MMPs)

Regulated by tissue inhibitors of

A

MMPs (TIMPs)

62
Q

Matrix metalloproteinases (MMPs)

High MMP levels in GCF are at significantly greater risk for

A

progression of periodontitis

63
Q

Matrix metalloproteinases (MMPs)

GCF MMPs level reduces in

A

response to treatment

64
Q

MMP-2 (gelatinase A), MMP-9 (gelatinase B), MMP-8 (collagenase 2), MMP-13 (collagenase 3), and MMP-3 (stromelysin-1) involve in
the

A

initial destruction of

periodontal ECM

65
Q

Dental plaque-induced gingivitis:

Characterized by

A

probing depth less than 3 mm and BoP.
No gingival recession
Red and edematous soft tissue.

66
Q

Elimination of open furcations

A

Furcation involvement ≤3 mm

67
Q

Phases of Therapy

A 
Systemic phase
Initial (hygiene) phase
Corrective phase
----Additional therapeutic measures
Maintenance phase
-----Supportive periodontal therapy
68
Q

Systemic phase

A

Eliminate or decrease the influence of systemic conditions

Protection from infectious hazards

69
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
70
Q

Corrective phase

A

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

71
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
72
Q

Initial Phase of Therapy. III.

re-evaluation

A

re-assess prognosis (PD, CAL, BOP, furcations, mobility, sensitivity)
re-assess need for consultations & tests
assessment of risk factor modulation
patient motivation

73
Q

Maintenance Phase of Therapy. I.

frequency variable

A 
more frequently initially
more frequently for patients at greater risk
assessment of PD, CAL
assessment of oral hygiene
assessment of risk factor modulation
radiographic assessment (at-risk-teeth)
74
Q

Maintenance Phase of Therapy.II.

A

prophylaxis, fluoride therapy
subgingival scaling of deep pockets
additional treatment if indicated
SRP, antibiotics, host modulation therapy, strategic extractions

75
Q

Gingival diseases modified by medications-

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).

76
Q

The acute-phase reaction cascade is a mechanism by which

A

periodontitis could potentially influence systemic diseases

77
Q

Acute phase reaction cascade

Mediators (production and release of inflammatory cytokines)

A

TNF-
IL-1
IL-6
IFN-

78
Q

Acute phase reaction cascade

Secondary systemic reaction

A

Fever and leukocytosis
Complement activation
Serum glucocorticoids increased
Altered synthesis of acute phase proteins

Perio Final (8 decks)

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