Periodontal Immunology Flashcards
What are the characteristics of gingivitis?
inflammation localised to gingival
acute inflammation
normal physiological response to infection or injury
What are the characteristics of periodontitis?
inflammation of gingival tissues and supporting periodontal structures
chronic inflammation
pathological inflammatory response associated with tissue destruction
What immune factors are found in gingival crevicular fluid?
- AMPs
- Cytokines
- Chemokines
- Lactoferrin
- IgG
- Neutrophils
What immune factors are found in oral mucosa?
AMPs
Cytokines
Chemokines
What immune proteins are found in saliva?
- S-IgA
- Lysozyme
- Peroxidase
- Lactoferrin
- Mucins
- Agglutinins
- Cystatins
- Histatins
Where will neutrophils lyse in normal health?
gingival sulcus
What are the early colonisers typically?
commensal aerobic (generally gram positive) species
What are the 3 keystone pathogens implicated in periodontitis?
Porphyromonas gingivalis
Tannerella forsythia
Treponema denticola.
gram negative anerobes
What is the term coined to describe pathological oral environment?
polymicrobial dysbiosis
Disruption of commensal microbial communities in susceptible hosts.
What are the late colonisers typically?
gram negative anaerobes
What bacterial species reduces as inflammation increases?
commensal species that are incompatible with inflammation
What are the virulence factors of P.gingivalis that evade immunity?
- Asaccharolytic (breakdown of proteins for nutrients)
- Gingipains (proteases with broad-specificity)
- Atypical LPS (tlr4 antagonist that blocks signalling)
- Inflammophilic
- Drives dysbiosis in susceptible hosts
Is P.gingivalis early or late coloniser?
late gram negative anaerobic coloniser
What is the aetiology of periodontitis associated with?
- accumulated plaque bacteria
- presence of periodontal pathogens
- polymicrobial dysbiosis
What are hallmark signs of periodontitis?
attachment loss
increased pocket depth
bone loss
What immune factors increase in gingivitis?
increased TLR stimulation
increased production of pro-inflammatory mediators
What cell type is predominant in gingivitis?
neutrophils
What immune under reaction disease can contribute to PD disease?
leukocyte adhesion deficiency - patients have neutrophils however they are found in blood and cannot migrate into tissues
(immune under reaction)
What is an excessive neutrophil infiltration associated with?
chronic inflammation -
source of matrix metalloproteinases
release inflammatory mediators
create hypoxic environment
What is the role of adaptive immunity in periodontal destruction?
CD4, T and B cells present in early lesions, unable to regulate dysbiotic biofilm, contribute to inflammation and bone loss through RANKL production but also limit infection to site and prevent it becoming systemic
Why is there no bone loss in health?
in health bone formation and bone resorption are coupled regulated by rankl/rank/opg triad
How does inflammation lead to bone loss?
activated T/B cells in periodontal lesion secrete RANKL (unbalancing)
RANKL binds RANK to induce osteoclast differentiation
What does OPG do?
OPG prevents RANKL binding RANK
OPG inhibits osteoclast differentiation
What are the molecular events that link bacterial induced inflammation with pathologic tissue destruction
- Bacterial products bind TLRs, stimulating cytokine, chemokine, and AMP production.
- Vasodilation and leukocyte recruitment (neutrophils, monocytes, lymphocytes).
- Activated neutrophils release pro-inflammatory mediators, amplifying inflammation.
- Activated lymphocytes express RANKL, disrupting RANKL/OPG balance.
- RANKL binds RANK on osteoclast precursors, inducing osteoclastogenesis and bone resorption.
- Pro-inflammatory cytokines (IL-1, IL-6, IL-17, TNF-α) inhibit bone formation.
- Dysregulated MMP activation contributes to connective tissue destruction.
What are osteoclast precursors?
monocytes
What are the pro-inflammatory cytokines that contribute to bone resorption?
IL-1, IL-6, IL-17. TNF-alpha
