Periodontics Part 2 Flashcards
Plaque Formation Steps
- Pellicle Formation
* seconds
* consists of glycoproteins & proline-rich proteins= attachment sites for bacteria - 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 - Colonization & plaque maturation
* 24-48 hrs
* Coadhesion: Primary colonizers provide new receptors for other bacteria to attach
* Shift from Facultative gram (+) to anaerobic gram (-)
Phases of Bacteria in plaque formation
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
Biofilm
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
Red Complex
Associated w/ BOP & deeper pockets
* P. Gingivalis
* T. Denticola
* T. Forsythia
Orange Complex
Before red complex
supports plaque maturation
- Fusobacterium
- Prevotella intermedia
- Campylobacter rectus
Plaque Hypotheses
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
A. Actinomycetemcomitans
- causes Aggressive Periodontitis
- Leukotoxin:
P. Gingivalis
- Cause Chronic Periodontitis
Red complex
Secondary/Late colonizer
T. Denticola
- Causes ANUG/ANUP
- Penetrate epithelium and Connective Tissue
- part of red complex
- secondary/Late colonizer
T. Forsythia
- Nonmotile, gram (-) rod
- part of red complex
- Protease that cleaves immunoglobulins and complement factors
P. Intermedia
- Causes pregnancy gingivitis
- part of orange complex
- Secondary/Late colonizer
C. Rectus
- part of orange complex
- motile, gram (-) rod
- Polar flagellum
F. Nucleatum
- Nonmotile, gram (-) rod
- part of orange complex
- The “Bridge” bacteria
- induces apoptosis of leukocytes and release of tissue-damaging substances from leukocytes
Actinomyes
- healthy gingiva
- causes root caries
S. mutans
- coronal/enamel caries
S. Salivarius
- most common oral bacteria
- found on tongue
Pseudomonas, Staph
- Implants
Calculus
LOCAL FACTOR
* Mineralized dental plaque 1-14 days
* NOT destructive but allows biofilm attachment (plaque)
Supragingival vs subgingiva calculus
Supragingival Calculus
* white/yellow
* mineralization via saliva
* occurs near salivary duct openings
Subgingival Calculus
* dark (Brown/Black)
* mineralization via GCF
Materia Alba
Soft white cheeselike
*easily displaced by water spray
unorganized accumulation of
* bacteria
* salivary proteins
* Food Debris
* desquamated epithelial cells, and food debris
Extrinsic Stains
primarily an esthetic concern
* Does not cause gingival inflammation
Orange Extrinsic Stain
- anterior teeth
- poor OH
Brown Extrinsic Stain
- Drinking dark-colored beverages
- Poor OH
Dark Brown and Black Extrinsic Stain
- Tobacco
Yellow-brown extrinsic stain
- Chlorhexidine (CHX)
- Stannous Fluoride
Black thin lines on cervical 1/3 extrinsic stain
Healthy Mouth–> Iron Consumption
Green and yellow extrinsic stain
- anterior teeth
- poor OH
- Chromogenic bacteria
Bluish-green extrinsic stain
- occupational exposure to metallic dust
Local factors contributing to Periodontal Disease
- Calculus
- Materia Alba
- Malocclusion
- Faulty Restorations
- Appliances
- Self inflicted injuries
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
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
Subgingival Margins
Even if not FAULTY, Associated with:
* plaque accumulation
* gingival inflmmation
* deeper pockets
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
Self-Inflicted injury
Aggressive horizontal brushing cause:
* tooth abrasion
* gingival recession
Improper use of tooth picks & fingernail biting can damage gingival tissues
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
Neutrophil Abnormalities
- 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
Proinflammatory Mediators
IL-1: Bone resorption
IL-6
PGE2
TNFa: Activate Macrophages
MMPs
* matrix metalloproteinase
* destroy collagen
* Protain-ase=eats proteins
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
Macrophages
Antigen-presenting cells (APCs)
* monocytes
* dendritic cells
Regulate immune response by releasing cytokines
* ex: IL-8
Mast Cells
Vascular Permeability & dilation
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
MMPs
MMPs
* matrix metalloproteinase
* destroy collagen
* Protain-ase=eats proteins
Anti-inflammatory Mediators
IL-4
IL-10
TIMPs
