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Perio Final > Sweep 1.2 > Flashcards

Sweep 1.2 Flashcards

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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
``` Biofilm Extracellular enzymes (beta-lactamases, formaldehyde dehydrogenase, formaldehyde lyase) inactivate ```
antibiotics
26
P.gingivalis with type I and V fimA genotypes -
healthy, type II and IV in disease
27
Effect of local ‘regulon’ (subgingival environment) | Iron can increase
outer membrane protein expression in P.gingivalis | S.cristatus can inhibit fimA expression
28
Veillonella uses lactate made by
streptococci
29
Campylobacter uses formate made by
Selenomonas
30
Porphyromonas uses
hemin from blood in sulcus
31
Competitive inhibition
Bacteriocins | Hydrogen peroxide production (S.sanguinis inhibits A.A.)
32
Desquamation of epithelium
Invade epithelium | Bind to underlying cells
33
Antibody prevent binding
IgG and IgA proteases | Mimic host antigens
34
Phagocytic cells
Leukotoxin – powerful virulance factor. AA produces this. Can also cause…. Non-lethal suppression of immune cells
35
Actinobacillus actinomycetemcomitans (AA)
``` New name - Aggregatibacter actinomycetemcomitans (Still AA) non-motile, Gram-negative, saccharolytic, capnophilic, (requires Co2 to grow) round-ended rod. Characteristic star-shaped colonies ```
36
AA Inhibits growth of
commensals- Streptococcus sanguis
37
AA with 530 bp deletion is 23x more likely to be disease-associated than
AA with full length promoter region.
38
AA and disease
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
Virulence factors of A. actinomycemtemcomitans (read from text)
``` Leukotoxin (RTX) Induce apoptosis Cytolethal distending toxin (CDT) Chaperonin 60 LPS Apoptosis, bone resorption, etc OMP, vesicles Fimbriae Actinobacillin Collagenase Immunosuppressive factor ```
40
Porphyromonas gingivalis
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
Virulence factors of P. gingivalis (read from text)
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
Tannerella forsythia
``` 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
Treponema denticola
``` Gram-negative Anaerobic Helical-shaped Highly motile microorganisms 1st identified in ANUG Several different species, hard to distinguish ```
44
Prevotella intermedia/ nigrescens
``` 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
Fusobacterium nucleatum
``` 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
The organism that is found MOST often in both remission and progression of adult periodontitis is
Fusobacterium nucleatum
47
CaH(PO4) x 2 H2O= Brushite (B)
Basis for supragingival calculus formation | Seen in recent (<2 week old) calculus
48
Ca4H(PO4)3 x2H2O= Octa calcium phosphate (OCP)
Predominant in exterior layers | Forms platelet like crystals
49
Ca5 (PO4)3 xOH= Hydroxyapatite (HA)
Predominant in inner layers of old calculus | Forms rod or sand-grain like crystals
50
-Ca3 (PO4)2 = Whitlockite (W)
Most common form in subgingival calculus | Hexagonal crystals
51
Several putative periodontal pathogens such as Pg, Tf, and Aa possess in common a trypsin-like enzyme that hydrolyzes a substrate
N-benzoyl-DL-arginine-2-naphthylamide (BANA).
52
Aspartate amino-transferase:
released during tissue destruction (cell death) | -
53
Alkaline phosphatase:
a membrane-bound glycoprotein involved in maintenance of alveolar bone
54
- β-glucuronidase:
a lysosomal enzyme degrades proteoglycans and ground substance
55
- Elastase:
a proteolytic enzyme found in lysosomal granules of neutrophil
56
Extracellular destruction enzymes | Associated with the activity of
matrix metalloproteinases | Produced by inflammatory, epithelial and connective tissue cells
57
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
58
Elastase
Periocheck® (chair-side test kit) | Positive correlation of elastase in GCF with clinical attachment loss
59
``` Matrix metalloproteinases (MMPs) Secreted by ```
fibroblasts and macrophages
60
``` Matrix metalloproteinases (MMPs) Responsible for ```
remodeling and degradation of ECM components
61
Matrix metalloproteinases (MMPs) Regulated by tissue inhibitors of
MMPs (TIMPs)
62
Matrix metalloproteinases (MMPs) High MMP levels in GCF are at significantly greater risk for
progression of periodontitis
63
Matrix metalloproteinases (MMPs) GCF MMPs level reduces in
response to treatment
64
MMP-2 (gelatinase A), MMP-9 (gelatinase B), MMP-8 (collagenase 2), MMP-13 (collagenase 3), and MMP-3 (stromelysin-1) involve in the
initial destruction of | periodontal ECM
65
Dental plaque-induced gingivitis: | Characterized by
probing depth less than 3 mm and BoP. No gingival recession Red and edematous soft tissue.
66
Elimination of open furcations
Furcation involvement ≤3 mm
67
Phases of Therapy
``` Systemic phase Initial (hygiene) phase Corrective phase ----Additional therapeutic measures Maintenance phase -----Supportive periodontal therapy ```
68
Systemic phase
Eliminate or decrease the influence of systemic conditions | Protection from infectious hazards
69
Initial (hygiene) phase
``` Cause-related therapy Removal of hard and soft deposits Removal of retentive factors Patient motivation (OHI) Concluded by re-evaluation ```
70
Corrective phase
Periodontal surgery Implant surgery Endodontic, restorative, prosthetic therapy Patient cooperation determines options
71
Maintenance phase
``` Prevention of re-infection & recurrence Assessment of deepened, BOP+ sites Instrumentation of deepened, BOP+ sites Caries control Control of prosthetic restorations ```
72
Initial Phase of Therapy. III. | re-evaluation
re-assess prognosis (PD, CAL, BOP, furcations, mobility, sensitivity) re-assess need for consultations & tests assessment of risk factor modulation patient motivation
73
Maintenance Phase of Therapy. I. | frequency variable
``` 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
Maintenance Phase of Therapy.II.
prophylaxis, fluoride therapy subgingival scaling of deep pockets additional treatment if indicated SRP, antibiotics, host modulation therapy, strategic extractions
75
Gingival diseases modified by medications- 3 commonly used drug types that are associated with gingival overgrowth:
Anticonvulsants (Phenytoin sodium or epinutin) Immunosuppressant (Cyclosporin A) Calcium channel blocking agents (Nifedipine).
76
The acute-phase reaction cascade is a mechanism by which
periodontitis could potentially influence systemic diseases
77
Acute phase reaction cascade | Mediators (production and release of inflammatory cytokines)
TNF- IL-1 IL-6 IFN-
78
Acute phase reaction cascade Secondary systemic reaction
Fever and leukocytosis Complement activation Serum glucocorticoids increased Altered synthesis of acute phase proteins

Perio Final (8 decks)

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