Scar formation, wound healing, and C-reactive protein
THE CONTEXT
Repair by scarring replaces injured tissue with connective tissue when regeneration cannot occur. The passage also describes factors affecting wound healing and the significance of C-reactive protein in inflammation.
Indications and sequence of scar formation
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Repair occurs by connective tissue replacement and scar formation when injured tissue cannot proliferate or when its structural framework is damaged and cannot support regeneration.
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The main steps are clot formation, inflammation, angiogenesis with granulation tissue formation, fibroblast migration and proliferation, collagen synthesis, and connective tissue remodeling.
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Macrophages orchestrate repair by eliminating offending agents and producing cytokines and growth factors that stimulate proliferation of the cells involved in repair.
Regulation of matrix deposition
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TGF-b is a potent fibrogenic agent.
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Extracellular matrix deposition depends on the balance between fibrogenic agents, matrix metalloproteinases that digest the matrix, and tissue inhibitors of matrix metalloproteinases.
Clinical aspects of wound healing
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Cutaneous wounds heal by primary union, also called healing by first intention, or secondary union, also called healing by secondary intention.
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Secondary healing involves more extensive scarring and wound contraction.
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Infection and diabetes can alter wound healing. The type, volume, and location of the injury also influence healing.
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Excessive collagen production can cause skin keloids.
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Persistent stimulation of collagen synthesis in chronic inflammatory diseases causes tissue fibrosis, often with extensive tissue loss and functional impairment.
C-reactive protein
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C-reactive protein (CRP)* is an acute-phase reactant that acts as an opsonin. During acute inflammation, IL-6 stimulates hepatocytes to produce CRP.
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CRP is a sensitive but nonspecific marker of inflammation. It increases in acute illnesses and inflammatory conditions, including bacterial infection and myocardial infarction.
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Higher baseline plasma CRP levels are associated with increased risk of chronic heart disease and stroke, possibly through the inflammatory response associated with atherosclerosis.