Ferry Senjaya
Definition
Wound healing is the response to acute or chronic injury, a process by which a damaged tissue is restored, as closely as possible, to its normal state
fibrin deposition Platelets release PDGF & TGF-, attracting inflammatory cells
vascular permeability increases, aiding infiltration of inflammatory cells into the wound Neutrophils peak at 24 hours debridement Monocytes macrophages (peak within 2-3 days) Macrophages produce PDGF & TGF-, attracting fibroblast collagen production
Proliferative Phase
Begin around day 3, as fibroblast arrive ; lasts through
week 3 Fibroblast : attracted & activated by PDGF & TGF- Collagen synthesis (mainly type III), angiogenesis, & epithelialization occur Total collagen content increases for 3 weeks, until collagen production & breaksown become equal remodelling phase begins
Remodelling Phase
Increased collagen production & breakdown continue for
6 months to 1 year Type I collagen replaces type III until it reaches 4:1 ratio of type I to type III Wound strength increases as collagen reorganizes along lines of tension & is cross-linked Vascularity decreases Fibroblast & myofibroblasts cause wound contraction
Mechanical Properties
Wounds have little strength during the first 2-3 weeks
(inflammatory & proliferative phase) By the third week, the wound begin to gain strength rapidly as remodelling occurs Wound have 50% of their final strength at 6 weeks, & most of their final strength a few weeks later Strength may continue to slowly increase until 6 to 12 months fron the time of injury Max strength is about 75% of normal tissue
contraction, epithelialization occurs A single layer of cells advances from the wound edges (& adnexal structures in partial thickness wounds), then stratifies If epithelialization is prolonged as in healing by secondary intention or in the deep partial-thickness wound or burn, the inflammatory phase lasts longer, resulting in increased collagen production & contraction
periosteum, & surrounding tissue become osteoblasts Osteoconduction : osteoblasts enter the fracture site A callus then forms, containing fibroblasts, osteoblasts, & other cells Chondroblasts produce ground substance, fibroblasts produce collagen, osteoblasts produce hydroxyapatite
occur At first the callus consists of poorly organized woven bone, which is remodeled by osteoclasts & osteoblasts into lamellar bone The more rigidly fixed & well reduced the fracture is, the less prominent the callus formation & endochondral ossification are ; healing mainly occur by apposition Once remodeling is finished, the healed bone structure is the same as normal bone, with no remaining scar
The inflammatory phase is minimal Epitenon cells move to the site of injury, producing collagen, acting like fibroblasts Intrinsic healing is increased by tendon motion
Inflammatory, proliferative, & remodelling phases occur After hemostasis, inflammatory cells infiltrate the wound Fibroblasts are attracted & produce collage, which is eventually remodelled Adhesions forms between the site of injury & surrounding tissues, & acts as pathway for cell migration & revascularization Adhesions, & therefore extrinsic healing, are increased by immobilization
macrophages & Schwann cells (Wallerian degeneration) The proximal axons each produce one or more myelinated regenerating fibers with growth cones at the distal end of each fiber (regenerating units) The regenerating units grows distally, directed by chemical factors
regeneration All hepatic cells, are involved in recreating normal heopatic histology without scar formation Scarring (cirrhosis) occurs with chronic or severe damage
Wound Closure
Primary closure 2. Delayed primary closure 3. Secondary closure
1.
Primary Closure
Wound closed surgically soon after creation
Secondary Closure
Wound closes over time by contraction
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