Tissue repair
Wound-disruption in the integrity of the skin, mucosal surfaces or organ tissue
Causes:
Disease process, accidental, intentional-surgical
4 phases of wound healing:
Haemostasis
Inflammation
Proliferation
Maturation
Wound repair is similar regardless of the
aetiology
Acute wounds- go through healing process quickly
Soft tissue and bone healing process time scale is different
Abnormal wound repair:
Increased mobility, morbidity and mortality
Poor cosmetic outcome
Health economic outcomes
Psychological sequelae for the patients
Soft tissue:
Classification of wound closure:
Primary intention-closing a wound rapidly- edges aligned
Secondary intention-extensive tissue loss- edges cannot be approximated
Delated primary healing-contaminated wound-therefore left open-wound closure
days after
Classification of wound contamination:
Clean- primary closure
Clean-contaminated- minimal spillage
Contaminated- gross spillage of GI tract
Dirty- purulent inflammation
Haemostasis : Bodies immediate response to prevent extreme loss of blood
Damaged arterial vessels rapidly constrict through the contraction of smooth muscle
through high cytoplasmic calcium levels
This leads to tissue hypoxia and acidosis
Production of vasoactive metabolites: NO
=vasodilation and relaxation of arterial vessels
Clot formation- coagulation cascade
, Intrinsic- endothelial damage-exposure of sub-endothelial tissues to blood=
activation of Hageman factor (factor 12)
Extrinsic- endothelial damage- exposure of tissue factor
Platelet activation- thrombin, thromboxane and ADP=platelets under morphological
changes=secrete alpha and sense granules
Histamine release-increases vasodilation and increased vascular permeability=
INFLAMMATION
Inflammation: Prevent infection now that the mechanical barrier is no longer intact
Initial:
Complement activation
Neutrophils:
Phagocytosis
NETS- netosis
Degranulation
Oxygen free radicals are produced as a by-product:
Bactericidal properties
Combine with chlorine=steralisation
Once finishes:
Apoptosis
Phagocytosed
Sloughed from the wound surface
Later:
Marcrophages: M1 and M2
Produce TGF-B and EGF=regulation of
inflammation, angiogenesis and formation of granulation tissue
lymphocytes: regulation of wound healing and adaptive responses
Tregs-supress IFN-Y production
Dendritic Epidermal T cells- regulation of keratinocytes by producing keratinocyte growth
factor and IGF-1
Inhibition of T cells=reduced collagen deposition and wound strength
Lipxins and production so arachidonic acid metabolism=anti-inflammatory= dampening of
the immune response= initiation of the next phase
Proliferation:
Simultaneous processes:
Angiogenesis
Formation of granulation tissue
Fibroblast migration
Wound-disruption in the integrity of the skin, mucosal surfaces or organ tissue
Causes:
Disease process, accidental, intentional-surgical
4 phases of wound healing:
Haemostasis
Inflammation
Proliferation
Maturation
Wound repair is similar regardless of the
aetiology
Acute wounds- go through healing process quickly
Soft tissue and bone healing process time scale is different
Abnormal wound repair:
Increased mobility, morbidity and mortality
Poor cosmetic outcome
Health economic outcomes
Psychological sequelae for the patients
Soft tissue:
Classification of wound closure:
Primary intention-closing a wound rapidly- edges aligned
Secondary intention-extensive tissue loss- edges cannot be approximated
Delated primary healing-contaminated wound-therefore left open-wound closure
days after
Classification of wound contamination:
Clean- primary closure
Clean-contaminated- minimal spillage
Contaminated- gross spillage of GI tract
Dirty- purulent inflammation
Haemostasis : Bodies immediate response to prevent extreme loss of blood
Damaged arterial vessels rapidly constrict through the contraction of smooth muscle
through high cytoplasmic calcium levels
This leads to tissue hypoxia and acidosis
Production of vasoactive metabolites: NO
=vasodilation and relaxation of arterial vessels
Clot formation- coagulation cascade
, Intrinsic- endothelial damage-exposure of sub-endothelial tissues to blood=
activation of Hageman factor (factor 12)
Extrinsic- endothelial damage- exposure of tissue factor
Platelet activation- thrombin, thromboxane and ADP=platelets under morphological
changes=secrete alpha and sense granules
Histamine release-increases vasodilation and increased vascular permeability=
INFLAMMATION
Inflammation: Prevent infection now that the mechanical barrier is no longer intact
Initial:
Complement activation
Neutrophils:
Phagocytosis
NETS- netosis
Degranulation
Oxygen free radicals are produced as a by-product:
Bactericidal properties
Combine with chlorine=steralisation
Once finishes:
Apoptosis
Phagocytosed
Sloughed from the wound surface
Later:
Marcrophages: M1 and M2
Produce TGF-B and EGF=regulation of
inflammation, angiogenesis and formation of granulation tissue
lymphocytes: regulation of wound healing and adaptive responses
Tregs-supress IFN-Y production
Dendritic Epidermal T cells- regulation of keratinocytes by producing keratinocyte growth
factor and IGF-1
Inhibition of T cells=reduced collagen deposition and wound strength
Lipxins and production so arachidonic acid metabolism=anti-inflammatory= dampening of
the immune response= initiation of the next phase
Proliferation:
Simultaneous processes:
Angiogenesis
Formation of granulation tissue
Fibroblast migration
