Pathogenesis of plaque associated periodontal disease Flashcards
(49 cards)
Pathogenesis means
“the origination and development of a disease
———–is the mechanism by which a causative factor (or factors) causes the disease
Pathogenesis
T/F Clinically healthy gingival tissues appear pink, are not swollen or inflamed, and are firmly attached to the underlying tooth and bone, with minimal bleeding on probing
T
Histological portions of gingiva are
- Epithelium( Gingival,Sulcular,Junctional)
2.CT
Gingival Epethelium
Stratified squamous keratinized and parakeratinized , continous with sulcular eptheliumat the crest of gingival margin,forms clinically visible gingival tissues by covering both free and attatched gingiva
Sulcular epithelium
Faces the tooth surface but is not attatched to it, lines periodontal pocket, Stratified squamous, non keratinized epithelium
This epithelium forms attatchment between tooth surface and gingival tissue
Junctional Epithelium
Key features of junctional epithelium
Semi permeable
Forms floor of sulcus
Non keratized
Wraps around the tooth in a collar fasion follow cemento enamel junction
Which stage of gingivitis marks the transition from Gingivitis to Periodontitis
Advanced LESION
Increased GCF flow is seen in which phase of gingivitis
Initial
A stage of gingivitis which occurs after 1 week of plaque accumulation
Early lesion
Stage of gingivitis which is reffered as Chronic gingivitis
Established lesion
Collagen destruction starts in ……stage of gingivitis and extends to PDL in …… stage of gingivitis?
Established, Advanced
The molecules that play a role in the pathogenesis of periodontitis can be broadly divided into two main groups:
A. sub gingival microbiota (i.e., microbial virulence factors.
B. the host immune–inflammatory response.
Name 5 Microbial Virulence Factors in causing periodontal diseases
1.Lipopolysaccharide.
2.Bacterial Enzymes and Noxious Products.
3.Microbial Invasion.
4.Fimbriae.
5.Bacterial Deoxyribonucleic Acid and Extracellular Deoxyribonucleic Acid
the host immune–inflammatory response is caused by 3….
1.MMPS
2.PG
3.CYTOKINES
LPSs composed of a lipid and a polysaccharide component, found in the
outer membrane of gram-negative bacteria, act as endotoxins
TLR-4 recognizes
LPS from gram-negative bacteria
Porphyromonas gingivalis has an atypical form of LPS that is recognized by both
tlr2 and tlr 4
A component of gram-positive cell walls, lip teichoic acid, also stimulates immune responses, although less potently than LPS. Inflammatory Responses in the Periodontium Lip teichoic acid signals through
TLR-2
T/F Both LPS and lip teichoic acid are released from the bacteria present in the biofilm and stimulate inflammatory responses in the tissues, thereby resulting in increased vasodilation and vascular permeability, the recruitment of inflammatory cells by chemotaxis, and the release of pro inflammatory mediators
T
Plaque bacteria produce several metabolic waste products that contribute directly to tissue damage.
These include 3 noxious agents such as
- ammonia (NH3).
2.hydrogen sulphide (H2S- short-chain carboxylic acids such as butyric acid and propionic acid.
these acids are detectable in GCF.
- short-chain carboxylic acids such as butyric acid and propionic acid.
——-induces apoptosis in T cells, B cells, fibroblasts, and gingival epithelial cells
Butyric acid
How noxious agents ‘‘Short chain fatty acids’’ aids in pathogenesis of periodontal disease?
1/Host Cell Effects – Butyric acid induces apoptosis in immune and epithelial cells.
2/Tissue Destruction – Short-chain fatty acids aid P. gingivalis infection by breaking down tissue.
3/Nutrient Supply – Increased bleeding in periodontal pockets provides nutrients for bacteria.
4/Inflammatory Response – Short-chain fatty acids enhance cytokine secretion and inflammation
