Periodontitis Flashcards
periodontal disease
a group of distinct clinical entities that affect the periodontium, including the gingiva, gingival attachment, periodontal ligament, cementum and alveolar bone
include gingivitis and periodontitis
gingival crevice
different surfaces for biofilm to form - hard surface (tooth), soft tissue (epithelium)
exposed to the outside environment
low oxygen penetration
close apposition to immune cels
bathed in GCF - high protein
periodontal pockets
a distinct environment
anaerobic, with slightly alkaline pH
generally gram+ next to tooth and gram- interacting with the epithelium
progression of periodontitis
biofilm accumulation –> change in microbial composition –> chronic inflammation –> alveolar bone loss
change in any factor can influence the others such as
more plaque
failure of immune response
localized injury/inflammation increasing GCF flow
acquired periodontists
manifestation of systemic disease
neutropenia, leukaemia
genetic disorders
metabolic disorders
changing composition of subgingival microbiome
progressive increase in anaerobic environment
lower redox potential in the gingival crevice
increase in GCF flow, slightly alkaline pH
gram-negative rods are dominant species in periodontitis
primary pathogen
establish themselves in a niche normally occupied by commensal microbial populations
possess the inherent ability to cross anatomic barriers or overcome other host defenses that limit commensals
opportunistic infections
infection when normal host defenses are diminished
can be caused by primary pathogen or normal commensal bacteria
periodontal pathogens are all
gram-negative anaerobic bacteria
evidence for role in periodontal disease
the organisms are present in diseased sites and their numbers increased with disease
the organisms possess the ability to cause damage to periodontal tissue
virulence genes
adherence/colonization factors: fimbriae, capsule
exotoxins
enzymes: proteases, lipases
immune evasion
biofilm formation or survival genes
exotoxin in aggressive periodontitis
leukotoxinA binds to receptor LFA-1
ATP released from cells
K+ pumped out
K+ efflux stimulates inflammasome formation
inflammasomes are for cleavage and secretion
cells undergo pyroptosis
IL-1B
pro-inflammatory and stimulates osteoclasts
inflammasomes are required for
cleavage pro-IL-1B and secretion of IL-1B