Godlick 16.txt

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Author:
emm64
ID:
120431
Filename:
Godlick 16.txt
Updated:
2011-12-03 14:22:25
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F2 Tissue Repair
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Description:
F2 Tissue Repair
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  1. Injury Pathway Summary
  2. Wound Factors
    • type of injury- limited vs substantial; this dictates how repair process works
    • location- ex oral epithelium (can regenerate), vs brain/cardiac muscles (cannot regenerate) > different responses
    • health status of individual- certain wounds will heal slower if their health is compromised (ex HIV, diabetes, many other diseases)
  3. Regeneration
    • Healing of a tissue with its own cells
    • i.e., renewal of cells (and architecture when possible) by a precursor cell population
    • Goals:
    • Preservation of tissue architecture and function
    • - Parenchyma and stroma
  4. Fibrous repair
    • When regeneration cannot occur or fails to fully repair the wound
    • Processes:
    • Formation of highly vascularized “granulation” tissue
    • Deposition of type 1 collagen
    • Goals:
    • Preservation of gross tissue architecture
    • Preservation of as much of the normal tissue function as possible
    • Sequester (wall-off) area of injury
  5. Repair Players:
    • Cells and their secreted products
    • Fibroblasts
    • Macrophages
    • Others (epithelium, smooth muscle, etc.)
    • Extracellular matrix
    • Fibers (e.g., collagen)
    • Basement membrane
    • Ground substance
    • Clotting factors
    • Blood vessels
  6. Small defined wounds
    • scab-fibrin clotted blood
    • actute inflammation-neutrophils accumulate
    • Proliferation
    • -Regional basal cells proliferate
    • Migration
    • -Basal cells migrate from edges of wound
    • -Migrating cells lay down basement membrane
    • -Basement membrane and extracellular matrix provide scaffolding for ordered regeneration of epithelium
    • Fibroblasts migrate to wound
    • -Produce ECM
    • -Type III collagen (temporary)
    • --Granulation tissue
  7. ECM Repair Role
    • Cells interact with extracellular matrix(via integrins)n
    • e.g., Integrin receptors on cells
    • Signals important for proliferation, differentiation, migration critical for healing
  8. Granulation Tissue
    • Temporary Scaffolding for healing
    • -Lots of Fibroblasts and macrophages
    • -Type III collagen
    • -Neovascularization / Angiogenesis-Lots of new blood vessels
    • -Excess extracellular fluid
    • --Edema
    • --From leaky blood vessels
    • Ultimately replaced By regenerated tissue OR scar tissue
  9. Scar Tissue
    • Type I Collagen
    • less vascular
    • some fibroblasts and macrophages
  10. Angiogenesis
    Endothelial Progenitor Cells-EPC
  11. Macrophages in Healing
    • Replace PMNs
    • Eat dead celwls
    • Clear debris
    • Release cytokines
    • -Attract more fibroblasts for repair
    • -Angiogenesis
  12. Macrophage Healing Essentials
    • 1) for removal of tissue & debris, know the terms phagocytosis, collagenase (to remove Type III collagen), elastase
    • 2) antimicrobial activity- via ROS (reactive oxygen species),
    • 3) calling in fibroblasts and directing regeneration- PDGF (platelet derived growth factor) and TGF-beta,
    • 4) angiogenesis- VEGF (vascular endothelial growth factor),
    • 5) remodeling of ECM- TGF-beta and PDGF, collagenase
  13. Epithelial Role in Healing
    Regeneration
  14. Fibroblast Role in Healing
    • Replace Granulation Tissue
    • Type I collagen
    • Other ECM components
  15. Goal of Large or Repeat wound healing
    • fibroproliferative response
    • patch the tissue rather than restore
  16. Fibroproliferative Process
    • Inflammatory Response
    • Removal of dead and damaged Tissue
    • Proliferation & migration of connective tissue cells
    • Proliferation of parenchymal cells if possible
    • Angiogenesis and formation of granulation tissue
    • Synthesis of ECM (including collagen)
    • Tissue remodeling
    • Wound contraction
    • Increased wound strength over time
  17. Wound Contraction
    Fibroblasts gradually have a slight change in phenotype to express more actin Myofibroblasts
  18. Myofibroblasts
    Fibroblasts that have phenotype to express more actin to contract large wounds
  19. Fibrosis
    • scar formation, via deposition of collagen by fibroblasts, with a goal of preserving as much as possible the tissue architecture
    • guided by macrophages and to some extent, T-lymphocytes
    • remember growth factor PDGF (recruit fibroblasts, to make more collagen),
    • Results from increased collagen synthesis and decreased collagen degradation
  20. granulomatis formation-
    • type of chronic inflammation
    • purpose of granuloma is to wall off infectious agent, that cannot be destroyed, but body doesn’t want to spread to other areas
    • central area with no blue dots (area of fibrosis), sequestering microorganisms, surrounded by lymphocytes and macrophages that are ready to prevent spread of the trapped organism
    • -upper left: large macrophages can fuse together, again to prevent spread of pathogens

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