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BOARDs > Periodontics Part 2 > Flashcards

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

A
  • Tobacco
25
Q

Yellow-brown extrinsic stain

A
  • Chlorhexidine (CHX)
  • Stannous Fluoride
26
Q

Black thin lines on cervical 1/3 extrinsic stain

A

Healthy Mouth–> Iron Consumption

27
Q

Green and yellow extrinsic stain

A
  • anterior teeth
  • poor OH
  • Chromogenic bacteria
28
Q

Bluish-green extrinsic stain

A
  • occupational exposure to metallic dust
29
Q

Local factors contributing to Periodontal Disease

A
  • Calculus
  • Materia Alba
  • Malocclusion
  • Faulty Restorations
  • Appliances
  • Self inflicted injuries
30
Q

Malocclusion

A
  • 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
Q

Faulty Restorations

A

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
Q

Subgingival Margins

A

Even if not FAULTY, Associated with:
* plaque accumulation
* gingival inflmmation
* deeper pockets

33
Q

Appliances

A

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
Q

Self-Inflicted injury

A

Aggressive horizontal brushing cause:
* tooth abrasion
* gingival recession

Improper use of tooth picks & fingernail biting can damage gingival tissues

35
Q

Neutrophils

A
  • 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
Q

Neutrophil Abnormalities

A
  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
Q

Proinflammatory Mediators

A

IL-1: Bone resorption
IL-6
PGE2
TNFa: Activate Macrophages

MMPs
* matrix metalloproteinase
* destroy collagen
* Protain-ase=eats proteins

38
Q

Pathogenesis of Gingivitis

A

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
Q

Macrophages

A

Antigen-presenting cells (APCs)
* monocytes
* dendritic cells

Regulate immune response by releasing cytokines
* ex: IL-8

40
Q

Mast Cells

A

Vascular Permeability & dilation

41
Q

Lymphocytes

A

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
Q

MMPs

A

MMPs
* matrix metalloproteinase
* destroy collagen
* Protain-ase=eats proteins

43
Q

Anti-inflammatory Mediators

A

IL-4
IL-10
TIMPs

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