Periodontics Part 2 Flashcards

1
Q

Plaque Formation Steps

A
  1. Pellicle Formation
    * seconds
    * consists of glycoproteins & proline-rich proteins= attachment sites for bacteria
  2. Adhesion & Attachment of bacteria
    * Minutes
    * Initial adhesion: weak reversible Van Der Waals& electrostatic forces
    * Strong irreversible attachment of adhesin molecules on early colonizers and host pellicle receptors
  3. Colonization & plaque maturation
    * 24-48 hrs
    * Coadhesion: Primary colonizers provide new receptors for other bacteria to attach
    * Shift from Facultative gram (+) to anaerobic gram (-)
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2
Q

Phases of Bacteria in plaque formation

A

Pellicle:
* glycoproteins, proline-rich proteins
* attachment sites for initial bacteria

Primary (early) Colonizers:
* Streptococcus except salivarus & actinomyces
* Feed on sugar & carbon from saliva/food

Secondary (late) Colonizers:
* P. Intermedia, P. Gingivalis, T. Denticola, Capnocytophaga, Campylobacter
* Feed on amino acids

Fusobacterium Nucleatum:
* bridging microorganism
* bind to primary & secondary colonizers

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3
Q

Biofilm

A

Fluid Channels
* allows nutrients to pass through plaque

Quorum Sensing
* communication b/w bacteria in a biofilm
* encourage growth of beneficial species
* discourage growth of competing species

Biofilm bacteria more RESISTANT TO ANTIMICROBIALs than planktonic or free-swimming bacteria

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4
Q

Red Complex

A

Associated w/ BOP & deeper pockets
* P. Gingivalis
* T. Denticola
* T. Forsythia

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5
Q

Orange Complex

A

Before red complex
supports plaque maturation

  • Fusobacterium
  • Prevotella intermedia
  • Campylobacter rectus
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6
Q

Plaque Hypotheses

A

3:
Non-specific
* more plaque=more disease
* Any bacterial species

Specific
* Specific bacteria=Disease

Ecological (most accurate)
* certain bacteria + host factors (smoking, diabetes)=change environment->favor pathogenic

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7
Q

A. Actinomycetemcomitans

A
  • causes Aggressive Periodontitis
  • Leukotoxin:
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8
Q

P. Gingivalis

A
  • Cause Chronic Periodontitis

Red complex

Secondary/Late colonizer

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9
Q

T. Denticola

A
  • Causes ANUG/ANUP
  • Penetrate epithelium and Connective Tissue
  • part of red complex
  • secondary/Late colonizer
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10
Q

T. Forsythia

A
  • Nonmotile, gram (-) rod
  • part of red complex
  • Protease that cleaves immunoglobulins and complement factors
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11
Q

P. Intermedia

A
  • Causes pregnancy gingivitis
  • part of orange complex
  • Secondary/Late colonizer
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12
Q

C. Rectus

A
  • part of orange complex
  • motile, gram (-) rod
  • Polar flagellum
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13
Q

F. Nucleatum

A
  • Nonmotile, gram (-) rod
  • part of orange complex
  • The “Bridge” bacteria
  • induces apoptosis of leukocytes and release of tissue-damaging substances from leukocytes
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14
Q

Actinomyes

A
  • healthy gingiva
  • causes root caries
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15
Q

S. mutans

A
  • coronal/enamel caries
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16
Q

S. Salivarius

A
  • most common oral bacteria
  • found on tongue
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17
Q

Pseudomonas, Staph

A
  • Implants
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18
Q

Calculus

A

LOCAL FACTOR
* Mineralized dental plaque 1-14 days
* NOT destructive but allows biofilm attachment (plaque)

19
Q

Supragingival vs subgingiva calculus

A

Supragingival Calculus
* white/yellow
* mineralization via saliva
* occurs near salivary duct openings

Subgingival Calculus
* dark (Brown/Black)
* mineralization via GCF

20
Q

Materia Alba

A

Soft white cheeselike
*easily displaced by water spray

unorganized accumulation of
* bacteria
* salivary proteins
* Food Debris
* desquamated epithelial cells, and food debris

21
Q

Extrinsic Stains

A

primarily an esthetic concern
* Does not cause gingival inflammation

22
Q

Orange Extrinsic Stain

A
  • anterior teeth
  • poor OH
23
Q

Brown Extrinsic Stain

A
  • Drinking dark-colored beverages
  • Poor OH
24
Q

Dark Brown and Black Extrinsic Stain

25
Yellow-brown extrinsic stain
* Chlorhexidine (CHX) * Stannous Fluoride
26
Black thin lines on cervical 1/3 extrinsic stain
Healthy Mouth--> Iron Consumption
27
Green and yellow extrinsic stain
* anterior teeth * poor OH * **Chromogenic bacteria**
28
Bluish-green extrinsic stain
* occupational exposure to metallic dust
29
Local factors contributing to Periodontal Disease
* Calculus * Materia Alba * Malocclusion * Faulty Restorations * Appliances * Self inflicted injuries
30
Malocclusion
* Crowding- plaque retentive area * Prominent roots & teeth w/high frena-gingival recession * Mesial Drift or extrusion due to missing teeth-->food inmpaction & plaque retention
31
Faulty Restorations
Plaque Retention: * overhanging margins * open margins * rough surfaces * ope contacts **Overcontoured restorations** are WORSE for gingival health than undercontoured-->form plaque retention areas, hard to clean
32
Subgingival Margins
Even if not FAULTY, Associated with: * plaque accumulation * gingival inflmmation * deeper pockets
33
Appliances
RPDs * Increased mobility of abutment teeth * Increased plaque accumulation Orthodontic Therapy: * increase plaque retention * create excessive forces on the periodontium * Must establish Periodontal health before starting tx Oral Jewelry: can result in * recession * pocket formation * bone loss
34
Self-Inflicted injury
Aggressive horizontal brushing cause: * tooth abrasion * gingival recession Improper use of tooth picks & fingernail biting can damage gingival tissues
35
Neutrophils
* first line of defense * most important cells in controlling bacterial challenge & destroying periodontal tissue * Chemotaxis to periodontal pocket * Phaygocytosis MMP-8 (Neutrophil collagenase): * most important proteinase in destruction of periodontal tissues * tetracycline inhibits
36
Neutrophil Abnormalities
1. Defective Neutrophil Chemotaxis leads to aggressive periodontitis Has to be just right to prevent tissue destruction * to much neutrophil activity=self inflicted tissue destruction * To little-->unchecked microbial challenge=tissue destruction
37
Proinflammatory Mediators
IL-1: Bone resorption IL-6 PGE2 TNFa: Activate Macrophages **MMPs** * matrix metalloproteinase * destroy collagen * Protain-ase=eats proteins
38
Pathogenesis of Gingivitis
Stage 1: * Initial Leasion * 2-4 days after plaque formation * Neutrophil infiltration * Increased GCF * No Gingivitis Stage 2: * Early Lesion * 4-7 days * T lymphocyte infiltration * increased collagen loss * BOP * Clinical Signs of Gingivitis: Redness, bleeding, edema Stage 3: Chronic Gingivitis/reversible * Established lesion: 14-21 days * B lymphocyte (B Cells) infiltration including mature plasma cells * collagen loss * clinical changes in color, contour, and consistency Stage 4: Not reversible * Advanced lesion * transition to irreversible damage of periodontitis
39
Macrophages
Antigen-presenting cells (APCs) * monocytes * dendritic cells Regulate immune response by releasing cytokines * ex: IL-8
40
Mast Cells
Vascular Permeability & dilation
41
Lymphocytes
B cells * become plasma cells--> make antibodies T Helper cells (CD4) * communication T Cytotoxic Cells (CD8) * kill intracellular antigens NK Cells: * T cells * recognize and kill tumor and viral infected cells
42
MMPs
MMPs * matrix metalloproteinase * destroy collagen * Protain-ase=eats proteins
43
Anti-inflammatory Mediators
IL-4 IL-10 TIMPs