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TISSUE FORMATION (COMPROMISED TISSUE FORMATION, NORMAL …
TISSUE FORMATION
COMPROMISED
TISSUE FORMATION
REPEATED TISSUE INJURY
TRAUMA
TISSUE DISTRUCTION
PROLONGED
INFLAMMATION
MICRO-TRAUMA
CHRONIC LESION
PROLONGED
INFLAMMATION
IATROGENIA
SHEAR
FRICTION
PRESSURE
HYPOXIA
MICROISCHEMIA
CHRONIC LESION
ISCHAEMIA
NUTRIENT DEPRIVATION
TROPHIC LESION
HYPOXIA
LOWER IMMUNE
RESPONSE
INCREASED
BIOBURDEN
LOWER COLLAGEN
SYNTHESIS
IMPAIRED
EPITHELIZATION
INCREASED BIOBURDEN
BIOFILM MICROBES
INCREASED WBC RESPONSE
NEUTROPHILS
MACROPHAGES
MAST CELLS
INFLAMMATION
PLANKTONIC
MICROBES
INCREASED
INFLAMMATION
ELEVATED PROTEASES
M.M.P's
Neutrophil Elastase
LOW LEVEL OF
TISSUE INHIBITORS
M.M.P'S (TIMP's)
DESTRUCTION OF
GROWTH FACTORS AND CELLULAR RECEPTOR
;
PDGF
TGF-B
DEGRADATION OF
STRUCTURAL PROTEINS
Fibronectin
FURTHER DEGRADATION OF E.C.M.
INCREASED FIBRONECTIN DEGRADATION PRODUCTS
LOSS OF TYPE-2 TGH-B FIBROBLAST RECEPTORS REDUCTION IN LEVEL OF PDGF
DOWN-REGULATION OF KERATINS
UP-REGULATION OF B-6 INTEGRINS
CHRONIC WOUND
NORMAL
TISSUE FORMATION
IN HOMEOSTASIS
BIOMECHANICAL
INTERACTIONS
BIOCHEMICAL
INTERACTIONS
PHASES OF WOUND HEALING
Inflammation
Repair/Cell
Proliferation
Hemostasis/Vascular
Response
Vascular Breach
(Blood 2012 120:499-500)
Link Title
CCR2hi-Ly6Chi Monocyte (CCR2 receptor).
M1 Macrophage influx
CCR2-Guided Chemotaxis ?
Chemokines ?
VGEF-A from Monocyte Subset (TEM-like?)
Cell differentiation
2 more items...
Platelet Activation
Remodeling/Maturation
WOUND HEALING
GENE
WOUND MANAGEMENT
ALTERNATIVES
Wounds 2017;29(11 Suppl):S37–S42
http://www.woundsresearch.com/bohn
ACUTE INJURY
VASCULAR RESPONSE
PRO-ACTIVE WOUND MGMT
ADJUNCT THERAPY
ACCELERATED HEALING
INFLAMMATION
REPAIR - PROLIFERATION
REMODELING
NORMAL TISSUE FORMATION
CONTINUED
INFLAMMATION
EARLY AGGRESSIVE
WOUND MGM
T
