Wound Healing Flashcards
inflammation
~48h after injury
hypoxic with fibrin clot
abundant bacteria + platelets
attraction/activation of infiltrating cells
neutrophils - matrix phagocytosis + free radicals
monocytes/macrophages - debridement/matrix turnover
new tissue formation
~2-10 days scab on surface new blood vessels predominate migration of epithelial cells granulation tissue formation re-epithelialisation
remodelling/migration
~1 year
disorganised collagen made by fibroblasts
wound contracted near surface
re-epithelialised wound raised
cell recruitment - youngest to oldest
platelets neutrophils macrophages fibroblasts lymphocytes
coagulation
death of some epithelial + dermal cells
damage to collagen fibres in tissue
small vessel rupture - inc vasodilation + permeability
blood released into wound + surrounding tissue
platelet deposition + aggregation
platelets de-granulate (cytokines + growth factors GF)
release PDGF, TGFb (both growth factors), fibronectin
formation of fibrin clot
macrophages in wound healing
remove wound debris cell recruitment + activation phagocytosis angiogenesis matrix synthesis regulation
keratinocytes in skin healing
migration/proliferation - integrins + adhesion molecules
ECM production
GF/cytokine production - VEGF (vascular endotheliar growth factor), TNFa, PDGF (platelet derived growth factor)
angiogenesis
release of proteases - dissolve non-viable tissue, penetrate fibrin barrier
migration/proliferation
single keratinocyte layer migrates under clot from wound edges across the wound to re-surface the area
during + migration, differentiation + stratification of neo-dermis occurs
fibrin clot
platelets + infl cells secrete re-epithelialisation factors
endothelial cell migration into wound
angiogenesis
starts as endothelial cell buds
move towards wound space
macrophages + keratinocytes provide angiogenic stimuli
initiated by production of GFs
new vessels start off leaky but integrity increases over time
fibrin clot degraded - proteases made by endothelial cells
fibroblasts
replicate in wound
dominant cell type at wound edge
synthesise + deposit ECM
myofibroblasts
fibroblasts differentiate into these
contractile function
effect wound closure
fibroblasts in connective tissue formation + remodelling
ECM production - serves as scaffold, tensile strength + resilience
GF production
angiogenesis
protease release
granulation tissue
established 3-5 days post-injury
fibroblasts, thin walled capillaries + loose ECM
connective tissue accumulates
eventual scar formation
exuberant granulation tissue (proud flesh) normal in the horse
scarring process
balance between ECM synthesis + degredation
inflammation is primary driver
prolonged scarring - fibrosis (permanent scar)
