Collagen rich scar tissue: the necrotic myocardium is replaced by collagen-rich scar tissue weeks to months later
Formation of a fibrin clot to fill gap created by the wound (forms on the wounded skin as a barrier to invading microorganisms)
Type I (mature scare composed mostly of this)
Type III collagen in early matrix of granulation tissue
Type II in cartilage
Type IV in basement membranes
Myofibroblasts: responsible for wound contraction and deforming pathologic process called wound contracture; they express alpha-smooth muscle actin, desmin, and vimentin, and they respond to pharmacologic agents that cause smooth muscle to contract or relax
Vit C
Cells and proliferating capillaries (granulation tissue has these two major components, like the fibroblasts, myofibroblasts and macrophages)
Metalloproteinase (matrix MPs enable cells to migrate by degrading matrix proteins; members of this family include collagenase, stromelysin, and gelatinase)
Scar formation: infarct of kidney can heal by fibrosis; ECM framework destroyed
Maturation arrest of collagen assembly (keloid is exuberant scar tending to progress beyond site of initial injury and recurs after excision); keloids characterized by changes in ratio of type III to type I collagen
Foreign material (granulomatous inflammation is a subtype of chronic inflammation, which develops when acute inflammatory cells cannot digest the injurious agent)
Chronic viral hepatitis: hepatocytes form regenerative nodules that lack central veins and expand to obstruct blood vessels and bile flow.
Regeneration: superficial abrasions of skin heal by this process; cellular migration is predominant means by which wound surface is reepithelialized
Fibrosis: aberrant healing with collagen-rish scar tissue
Granulation tissue: repair of deep wonds
Primary and secondary intentions: healing in deeper wounds
Contact inhibition of epithelial growth and motility (need basal epithelial cells at wound margin to become activated and reestablish contact with other basal cells through extensive cell migration and mitosis)
Fibronectins (deposit at site of tissue injury; chemoattractant for variety of cells recruited to wound site over next several days);
cadherins and integrins not part of ECM, but are found at cell surface like selectins
Integrins
Apposition of edges (primary occurs with closely apposed edges and minimal tissue loss; secondary occurs in gouged wound when edges are far apart and there is substantial tissue loss)
3-5 days
neutrophils 12-24 hours after injury
mature scar tissue 2 weeks after injury
Phagocytosis
Type III (along with proteoglycans, glycoproteins, they make a temporary matrix)
Glial cells
Contracture
Neuroma: bulbous lesion consists of disorganized axons and proliferating Schwan cells and fibroblasts; the cut ends not in perfect alignment or are prevented from establishing continuity by inflammation
Postcapillary venule
Ulcer