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
keystone pathogens
microbial species that remodel the microbial community in ways that promote the pathogenesis
drive dysbiosis
dysbiosis
an imbalance in the relative abundance of microbial species in an ecosystem or a community that is associated with a disease
pathobionts
the resident species that are normally harmless become pathogenic under certain conditions
a low-abundance or keystone pathogen can orchestrate a
disease by remodeling the healthy microbiota into a dysbiotic microbiota
P. gingivalis as a keystone pathogen
low-level colonization of the periodontium by P. gingivalis
secretes gingipain that cleaves C5
impaired leukocyte killing
dysbiosis due to loss of normal immune surveillance
more inflammation contributing to bone resorption
C5 blockade promotes the clearance of P. gingivalis
PAMPs
molecular signatures that are not present in normal mammals
recognized by pattern recognition receptors
PAMPs stimulate
an innate immune response, including cytokine and chemokine production
neutrophils
short-lived with high turnover rate
early responders
phagocytes
granules contain lytic enzymes antimicrobial peptide
reactive oxygen and nitrogen species generated
can form NETs
chronic inflammation causes periodontal damage
neutrophils fail to control dysbiotic microbiota
microbes invade connective tissue and interact with immune cells, dendritic cells, T cells
inflammatory mediators stimulate bone loss
osteoclasts are similar to macrophages
