09/05 - Periodontal Pathogens Flashcards
(41 cards)
What is the non-specific plaque hypothesis?
- plaque control important in periodontal treatment
- all plaque bacteria considered bad
- any accumulation of micro-organisms at or below the gingival margin causes inflammation
What is the specific plaque hypothesis?
- specific organisms in dental plaque are the etiological agents
- microbial composition of disease sites different from healthy sites
- local debridement and systemic antibioitcs could control LAP
What are the prerequisites for disease initiation and progression?
- VIRULENT PERIODONTAL PATHOGEN: P. gingivalis with type II and IV fimA genotypes; virulence factors; right location in the site (adjacent to epithelium, apical part of the pocket)
- LOCAL ENVIRONMENT: colonization by beneficial species dilutes and inhibits pathogens; effect of local “regulon”/subgingival environment (iron increases outer membrane protein expression in P. gingivalis and S. cristatus can inhibit fimA expression)
- HOST SUSCEPTIBILITY: HIV infection; diabetes; smoking
What are the 4 different ways through which pathogens colonize?
- ADHESINS ON BACTERIA BIND HOST RECEPTORS: type I or IV collagen, sialic acid, galactosyl residues; bacteria have fimbriae or outer membrane proteins
- COAGGREGATION
- NUTRIENT UTILIZATION: Veillonella uses lactate made by streptococci; Campylobacter uses formate made by Selenomonas; Porphyromonas uses hermin from blood in sulcus
- COMPETITIVE INHIBITION: bacteriocins; hydrogen perioxide production
What are the 3 ways through which pathogens overcome host defenses?
- DESQUAMATION OF EPITHELIUM: invade epithelium and bind to underlying cells
- PREVENT ANTIBODY-BINDING: IgG and IgA proteases; mimic host antigens
- PREVENT PHAGOCYTIC CELLS: leukotoxin; non-lethal suppression of immune cells
The World Workshop in 1996 designated 3 pathogens. What are they?
- P. gingivalis
- A. actinomycetemcomitans
- T. forsythia
Is Actinobacillus actinomycetemcomitans (AA) motile? Gram positive or negative? How does it get its energy? Aerobic or anaerobic? Shape of bacteria and colonies?
- non-motile
- gram-negative
- saccharolytic (breaks down carbs for energy)
- capnophlic (thrive in high CO2)
- round-ended rod; star-shaped colonies
What is the evidence of AA as a pathogen based on association?
- high numbers associated with agressive periodontisis
- detected in active sites
- detected in prospective studies
What is the evidence of AA as a pathogen based on elimination?
- elimination or suppression resulted in successful therapy
- recurrent lesions harbor the species
What is the evidence of AA as a pathogen based on host response? It also inhibits ___ and induces ___.
- high levels of systemic and local antibody response
- inhibits growth of commensals (S. sanguis)
- induces disease in animal models
What is the evidence of AA as a pathogen based on virulence factors?
- tissue invasive (epithelial and endothelial cells)
- leukotoxin
- fibroblast inhibiting factor
- endotoxin
- collagenase
What is the evidence AGAINST AA being a pathogen?
- not seen in all cases of aggressive periodontitis
- seen in periodontally healthy subjects
- genetic analysis of the leukotoxin gene (13 clusters identified; II seen in severe disease; XII and XIV associated with health)
- AA with 530 bp deletion is 23x more likely to be disease-associated than AA with full length promoter region
There are ___ serotypes of AA which are based on ___. ___ are the dominant antigens.
- 5
- polysaccharides on the surface of an organism
- serotype-specific surface antigens (SPA)
Serotype ___ of AA is most commonly associated with localized aggressive periodontitis in the USA. It has a role in resistance to ___.
- b
- resistance to phagocytosis and killing by PMNs
Serotype ___ of AA is health-associated in Finland and disease-associated in Japan.
a
For an AA infection, ___ and ___ approach is vital to treatment. ___ and ___ are effective in reducing bacterial load. ___ approach is required to eliminate tissue reservoirs.
- mechanical
- chemotherapeutic
- amoxicillin 500 mg
- metronidazole 250 mg
- surgical
Which of the following is not a virulence factor produced by A. actinomycetemcomitans?
a. leukotoxin
b. collagenase
c. lipoteichoic acid
d. lipopolysaccharide
c. lipoteichoic acid
Is Porphyromonas gingivalis gram positive or negative? Aerobic or anaerobic? Motile? What is the shape of the bacteria and the color of the colonies?
- gram-negative
- anaerobic
- non-motile
- asacharolytic rods; black pigmented Bacteriodes
What is produced by PG?
- collagenase
- proteases
- hemolysins
- endotoxin
- fatty acids
- NH3
- H2S
- indole
For PG, what are cysteine proteases important for?
- protein degradation
- the maturation of cell surface proteins such as fimA fimbrillin
What is the evidence (4) of PG as a pathogen based on association?
- elevated in lesions of periodontitis
- lower in healthy sites and subjects
- elevated in progressing lesions
- presence indicates increased risk for attachment loss
What is the evidence (3) of PG as a pathogen based on elimination?
- elimination results in successful therapy
- recurrent lesion harbor organisms
- successful therapy lowered antibody level
What is the evidence of PG as a pathogen based on host response?
elevated antibody in serum/saliva of subjects with periodontisis
What is the evidence of PG as a pathogen based on virulence factors?
- several factors
- invades epithelial cells in vitro
