periodontal immunology Flashcards by Charlotte Watkins

what is gingivitis?

inflammation localised to gingival tissues
acute inflammation
normal physiological response to infection or injury

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what is periodontitis?

inflammation of gingival tissues and supporting periodontal structures
chronic inflammation
pathological inflammatory response associated with tissue destruction

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describe healthy gingiva

stippled

pink

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describe gingiva with gingivitis?

red

swollen

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describe gingiva with periodontitis?

significant plaque accumulation

inflammation

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what is the trigger for (gingival) inflammation?

plaque bacteria

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what does supragingival mean?

above gum line

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what immune components are in saliva?

antimicrobial proteins
peptides
antibodies
S-IgA
lysozyme
peroxidase
lactoferrin
mucins
agglutinins
cystatins
histatins

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what is gingival crevicular fluid?

subgingival defence- array of microbial factors prevent access to underlying tissues

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what antimicrobial components are in gingival crevicular fluid?

AMPs
cytokines
chemokines
lactoferrin
IgG

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how does the gingival eptithelium protect?

physical barrier

functional barrier- activation of TLR

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what antimicrobial components are in oral mucosa?

AMPs
cytokines
chemokines

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why is poor oral hygiene the predominant aetiological factor in periodontitis?

leads to accumulation of plaque bacteria which lead to pro-longed and sustained activation of inflammtaory pathways in gingival tissues

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what other factors contribute to periodontitis?

type of bacteria present in plaque

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what is the ecology of the oral biofilm?

early colonisers gram+ , aerobic, commensal species
colonise, modify environment creating new attachment sites for late colonisers
late colonisers gram- , anaerobic

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describe periodontal pathogens

present in low numbers at healthy sites
increased numbers in diseased sites
can be absent from diseased sites

what is polymicrobial dysbiosis?

community of micro-organisms that work together to actively disrupt the normal homeostatic balance in the oral cavity for their own benefit

how do some bacteria gain a competitive advantage?

some succumb to inflammation

accessory and periodontal pathogens eg P gingivalis persist adapting to inflammatory environment

what are 4 virulence factors of P gingivalis?

asaccharolytic
gingipains
atypical LPS
inflammophilic

what does asaccharolytic mean?

nutrients from breakdown of proteins and peptides

- no carbs meaning inflammatory environment gives access to nutrients

what are gingipains?

proteases with broad-specificity

-degrade host proteins

what is atypical LPS?

TLR4 antagonist

what does inflammophilic mean?

inflammatory environment favours expression of virulence

only expresses full range under inflammatory conditions
dormant in health

what are the main aetiology factors of periodontits?

accumulated plaque bacteria
presence of periodontal pathogens
polymicrobial dysbiosis
susceptible host

what are the clinical signs of periodontitis?

increased pocket depth -attachment loss alveolar bone destruction

what does increased TLR stimulation cause?

increased production of pro-inflammatory mediators triggers acute inflammatory response -redness, swelling, bleeding -increased vasodilation, cell migration

what are the main cell type in initial gingivitis?

neutrophils

what do neutrophils do?

recruit monocytes, which are activated and differentiates into macrophages lymphocytes recruited to fine-tune the immune response

what do osteoblasts do?

synthesise and secrete bone tissue (osteoid) | bone formation

what do osteoclasts do?

resorb bone | derived from monocyte/macrophage

what are bone formation and resorption regulated by in health?

RANKL/ RANK/ OPG triad

what is the role of adaptive immunity in periodontal destruction?

T and B lymphocytes present in early lesion aggregate rich in CD4 T & B cells evident unable to regulate dysbiotic biofilm B cell/plasma cells predominate advanced lesions IgG fails to regulate protective prevents systemic infection destructive inflammation induced alveolar bone loss

what is the role of neutrophils in periodontal tissue destruction?

excessive infiltration associated with chronic inflammation microbial subversion degradative enzymes -major source matrix metalloproteinases inflammatory cytokines and O2 radicals contribute to hypoxic environment CT destruction manifests clincally as loss of attachment

how does inflammation lead to bone loss?

activated B + T cells in perio lesion secrete RANKL RANKL binds RANK to induce osteoclast differentiation OPG binds to RANKL preventing RANKL binding RANK inhibiting osteoclast differentiation low OPG, high RANKL many monocytes recruited differentiate into osteoclasts

what are the 7 cellular and molecular events linking bacterial induced inflammation w/ pathologic tissue destruction

1. bacterial products bind TLRs on epithelium, stimulating secretion of cytokines, chemokines and AMPs (inflammation) 2. vasodilation and selective recruitments of leukocytes - mainly neutrophils 3. bacterial products further activate neutrophils, more pro-inflammatory mediators released- loop 4. activated lymphocytes express RANKL - RANKL/OPG balance disrupted 5. RANKL binds RANK on osteoclast precursors. activates osteoclastogenesis leading to alveolar bone resorption 6. pro-inflammatory cytokines contribute to bone resorption by inhibiting bone formation 7. elevated and dysregulated MMP activation contributes to CT tissue destruction