mechanisms of periodontitis Flashcards
steps of periodontal destruction
- Build up of bacterial plaque
- Inflammation of the gingival margin
- Recession of the gingival margin
- Loss of periodontal attachment
- Apical migration of bacteria
- Resorption of supporting bone
- Loss of function of periodontal tissues
what factors are responsible for periodontal destruction?
bacterial colonisation - initiates disease
host immune response - soft and hard tissue damage
how do we know that bacteria are not the only factor causing periodontal destruction?
bacteria are similar in periodontitis and gingivitis
the bacterial colony can be quite distant from the site of damage
scale of damage is no associated with strains and quantity of bacteria
roles of neutrophils in periodontal destruction
neutrophils are recruited
try to control bacterial expansion by phagocytosis
release chemokines to recruit more immune cells for help
short lifespan - release damaging factors
What are pattern recognition receptors
examples and roles
- toll like receptors
- recognise Pathogen Associated Molecular Patterns (PAMPs)
- activate innate immune cells
- C-type lectin receptors
- NOD like receptors
- RIG like receptors
what are PAMPs
Pathogen-Associated Molecular Patterns
- bacterial LPS
- DNA/RNA
- peptides
activate innate cells
what occurs when the activated innate cell arrives in the lymphonode
- presents bacterial antigen to T cell
- provides 3 signals for naive T cell activation
- Th2 cells help B cells for further differentiation into antibody producing plasma cells
- B and T cells are released in blood and target infection sites
roles of plasma B cells
produce specific antibodies to neutralise bacterial toxins
Guide macrophage and neutrophil for bacterial phagocytosis
what does this show
many infiltrated immune cells
severe periodontal tissue damage
loss of junctional epithelial attachment
damaged gingival fibres
what happens during acute inflammation
short period of inflammation response
- bacteria eliminated effectively
- followed by rapid tissue repair and wound healing
what occurs during chronic inflammation
lasts longer than normal
- less effective controlling bacterial invasion
- less effective resolving inflammation
- no effective promoting tissue repair
which cytokines induce inflammation and what other consequences can they lead to ?
- IL-8:
- chemokine for cell recruitment (T cell and Neutrophils),
- but neutrophils produced ROS and RNS
- chemokine for cell recruitment (T cell and Neutrophils),
- IL-18: DC and Th1,
- but also induce endothelial cell apoptosis
- TNFa: Enhance macrophage activation,
- but Induce necrosis cell death
- IFNg, IL-1b, IL-12, 22, 23, 27…………………..
soft tissue damage
which cytokines suppress inflammation and how
- Produced by regulator T cells - T suppressing cells
- IL-10: Inhibiting Th1 activity
- IL-35: Suppressing Th17
- TGFb1: Suppressing Th1, Th17 and Th2
- Also promotes tissue repair
what harmful enzymes do macrophages and neutrophils produce and what are the consequences
- Matrix metalloproteinase (MMP)
- lysozyme
- elastase
- collagenase
- Myeloperoxidase (MPO)
destruction of dental lamina for junctional epithelial attachment
- kills host cells
- produce ROS and RNS
how does angiogenesis promoted by macrophages cause destruction?
- macrophages produce VEGF
- promotes angiogenesis
- blood vessels which build up in gingival tissue
- destroy gingival tissue
- cause chronic inflammation by recruiting more inflammatory cells
- destruction of PDL structure
