Lecture 11-12 Periodontitis Flashcards
Define Periodontitis
Plaque-induced inflammation of gingival tissues that results in destruction of the periodontal ligament, loss of alveolar bone, and migration of the junctional epithelium.
Is periodontitis reversible?
No, it is irreversible damage which distinguishes it from gingivitis
Active periodontal disease causes destruction of tooth attachment leading to what?
Periodontal pocket formation; loss of collagen attachment fibers and loss of alveolar bone that persists after the active disease process has stopped.
T or F, Attachment loss indicates if disease is ongoing or occurred earlier
False, it does not indicate
Severe periodontitis occurs in what population of people
More commonly in older individuals. However msot periodontitis is largely due to loss over a lifetime becoming more obvious and easier to measure in older individuals.
Do genetic factors play a role in periodontitis
Yes a major role. Up to 18x over ‘normal’ patients
What causes periodontitis
It could be the result of a variety of disease mechanisms. Multiple factors may have to work in synergy to bring about attachment loss. It is not clear what specifically causes active periodontal disease.
3 Major hypotheses to what causes periodontitis
- A specific bacterium
- Specific mechanism, multiple bacteria
- Multiple mechanism, multiple bacteria ***
3 major hypotheses to periodontal cause can be restated into what two hypothesis?
- Nonspecific Plaque hypothesis
2. Specific Plaque Hypothesis
What is the nonspecific plaque hypothesis
- All plaque is bad (forget a specific bacterium). Small amounts of plaque are neutralized by host. Large amounts of plaque produce disease. Plaque control is treatment. Much clinical treatment is still based on this theory
What is the Specific plaque hypothesis
Only certain plaque is pathogenic. Certain bacteria within the plaque produce more substances that cause the destruction of periodontal tissues.
Major suspected periodontal pathogens include: (5)
- Prophyromonas gingivalis
- Tannerella forsythia
- Treponema denticola
- Prevotella intermedia
- Aggregatibacter actinomycetemcomitans
5 Socransky’s postualtes for oral lesion
- Association with disease
- Elimination: decrease disease
- Consistant correlation with disease
- Is animal pathogen
- Possesses virulence factors for man
T or F, Few active disease sites in a mouth full of inactive sites usually exemplify Periodontitis
True
Make up of bacteria when healthy
Mainly G+ cocci with few spirochaetes or motile G- rods
Make up of bacteria with chronic gingivitis
About 55% G+ with occasional spirochetes and G- motile rods
Make up of bacteria with Chronic periodontitis
About 75% G- (>90% anaerobes). Motile rods and spirochetes are prominant
Make up of bacteria with Aggressive periodontitis
About 70% G- rods. Few spirochetes or mobile rods present. Associated with immune or genetic defects
What are the “Perio Pathogens”
A. actinomycetemcomitans
P. gingivalis
A. Actinomycetemcomitans
- G+ or G-
- Capnophilic or Aerobic
- Microaerophilic or Facultative
- Optimum pH
- Saccharolytic or Asaccharolytic
- G-
- Capnophilic (Like’s CO2)
- Facultative
- pH 7-8, 7.5 optimum (inflammed pocket = 8!)
- Saccharolytic (odd)
T or F, A. actinomycetemcomitans increase growth with steroid hormones but do not have catalase activity
False, It does increase growth with steroid hormones and also has catalase activity (H2O2 - detoxify)
A. actinomycetemcomitans major virulence factors:
- Fimbrae bind:
- epithelial cells
- matrix protein
- salivary proteins
- F. nucleatum - LPS vesicles (Blebs)
- LPS activates Macrophages
- Bone resorp.
- **Filled with Leukotoxin = pore protein (Cytotoxic for PMNs and Macrophages)
How much of aggressive adult periodontitis is associated with A. a.
30-50%
P. gingivalis
- G+ or G-
- Capnophilic, Anaerobic or Anarobic
- Motile or non-motile
- Optimum pH
- Saccarolytic or Asaccharolytic
- G- Rod
- Anaerobic
- Non-motile
- pH 7.5-8.5
- Asaccharolytic
T or f, P. gingivalis needs Hemin - forms pigment
True
Major Virulence factors for P. gingivalis
- CHO Capsule
- Fimbrae
- Toxic Products
- LPS (Not very inflammatory!!)***
- LPS Blebs
- Secretes many enzymes (proteases)
T or F, P. gingivalis and a. actinomycetemcomitans are found in very small numbers in a healthy mouth
True, (<.05%)
T or F, A.A is associated with localized aggressive periodontitis and P.G. with generalized chronic periodontitis
True
- A.A. is found at few sites
- P.G., if present, found at most sites
What causes sulcular ecology to be an anaerobic environment
Whatever oxygen makes it to this area is rapidly removed by reaction with organic molecules
What causes sulcular ecology to have bacteria use protein as substrate?
Low levels of saliva and food residue to these areas require that most of the bacteria here use protein as substrate rather than sugars
Is bacterial adhesion an important colonization factor in gingival pockets
No, the slow flow of fluid and absence of salivary washing decrease the role of bacterial adhesion as an important colonization factor and may of the organisms here are highly motile
What is the major function of PMNs in the gingival pockets and sulcular ecology
Remove LPS, detoxifying this potent bacteriallyy-derived inflammatory endotoxin
Will the LPS concentration be high or low in gingival pockets
High, since most of the subgingival flora are G-
What controls the mechanism of attachment loss?
Under gingival Th cell direction. The slow maintenance, replacement, and repair gives way to the final strategy of removing the inflammatory site. Keep the infection from going systemic at all costs!
