Wound Healing

Wound Healing - Stitching Stories

Restoration of tissue architecture & function post-injury.

• Healing Types:
  • Regeneration: Complete tissue restitution; original structure restored.
  • Repair: Patching with connective tissue; scar formation.

⭐ Wound strength reaches ~70-80% of normal skin by 3 months, mainly due to Type I collagen deposition and remodeling.

Wound Healing - Repair Relay

• 1. Hemostasis & Inflammation (0-3 days)
  • Cells: Platelets (clot), Neutrophils (PMNs; debris removal ~24-48h), Macrophages (phagocytosis, growth factors).
  • Events: Vasoconstriction, platelet plug, coagulation, inflammation.
• 2. Proliferation (3 days - 3 weeks)
  • Cells: Fibroblasts (Collagen Type III), Endothelial cells (angiogenesis), Keratinocytes (epithelialization).
  • Events: Granulation tissue, neovascularization, re-epithelialization, wound contraction (myofibroblasts).
• 3. Maturation & Remodeling (3 weeks - 2 years)
  • Cells: Fibroblasts.
  • Events: Collagen Type III → Type I, ↑ cross-linking & tensile strength, scar maturation, vascular regression.

⭐ Wound tensile strength reaches ~70-80% of normal skin by 3 months. The critical switch from Type III to Type I collagen occurs during remodeling.

Wound Healing - Cellular Crew

• Key Cells & Timeline:

  • Platelets (Seconds-Hours): Hemostasis, release growth factors (PDGF, TGF-β).
  • Neutrophils (24-48 hrs): Phagocytosis, debris removal.
  • Macrophages (48-96 hrs → weeks):
    • M1: Pro-inflammatory, phagocytosis.
    • M2: Anti-inflammatory, repair, angiogenesis (VEGF), fibroblast activation (TGF-β, PDGF).
  • Lymphocytes (Week 1 onwards): Immune modulation.
  • Fibroblasts/Myofibroblasts (Day 3 → weeks): Collagen (Type III then I) synthesis, wound contraction.
  • Endothelial Cells (Day 3 → weeks): Angiogenesis (VEGF, FGF).
  • Keratinocytes (Day 1 → weeks): Re-epithelialization (EGF, KGF).

• Key Growth Factors:

  • PDGF: Platelets, MΦ; chemotaxis, proliferation (fibroblasts, smooth muscle).
  • FGF (FGF-2): MΦ, fibroblasts; angiogenesis, fibroblast proliferation, ECM deposition.
  • TGF-β: Platelets, MΦ, fibroblasts; ↑collagen synthesis, ↓MMP activity, fibrosis.
  • VEGF: MΦ, endothelial cells; angiogenesis, ↑vascular permeability.
  • EGF/KGF: Platelets, MΦ, keratinocytes; keratinocyte migration, proliferation.

• ECM Dynamics:

  • Components: Collagen (Type III → Type I), Elastin, Proteoglycans, Fibronectin.
  • Remodeling: Matrix Metalloproteinases (MMPs) degrade ECM; Tissue Inhibitors of Metalloproteinases (TIMPs) regulate MMPs.

⭐ Type III collagen is predominant in early granulation tissue (first few days), later replaced by stronger Type I collagen (by week 2-3). Ratio of Type I to Type III collagen increases as the wound matures. 📌 Three comes before One in Tissue repair (Type III then Type I).

Wound Healing - Boosters & Blockers

• Systemic Factors:
  • Boosters: Good nutrition (Protein, Vit C, Zinc, Copper).
  • Blockers: Advanced age, Diabetes (DM), Glucocorticoids, Chemotherapy, Poor perfusion (PVD, shock), Anemia, Immunosuppression, Smoking.
• Local Factors:
  • Boosters: Good blood supply, clean wound, appropriate closure.
  • Blockers: Infection (most common delay), Mechanical stress (movement, tension), Foreign bodies, Ischemia, Necrosis, Large size/poor location, Radiation.

⭐ Infection is the single most common and important cause of delayed wound healing.

Wound Healing - Repair Mishaps

• Deficient Scar Formation:
  • Dehiscence: Wound rupture, often post-surgery.
  • Ulceration: Inadequate vascularization during healing.
• Excessive Scar Formation:

  • Hypertrophic Scar: ↑ Type I collagen; confined to original wound boundaries.

  • Keloid: ↑ Type I & III collagen; grows beyond original boundaries; genetic link.

    ⭐ Keloids are particularly common in individuals of African descent and frequently recur after excision.

• Exuberant Granulation (Proud Flesh): Excessive granulation tissue; protrudes, blocking re-epithelialization.
• Contractures: Exaggerated wound contraction leading to deformities (e.g., palms, soles, post-burns).

High‑Yield Points - ⚡ Biggest Takeaways

• Primary intention: Clean edges, minimal scar. Secondary: Large defect, granulation, myofibroblast contraction, marked scar.
• Healing: Inflammation (PMNs, Mφ), Proliferation (Type III collagen, granulation), Maturation (Type I collagen, ↑strength).
• Keloids grow beyond wound margins; Hypertrophic scars stay confined. Both = excess collagen.
• Infection is the #1 cause of impaired healing.
• Vitamin C (collagen synthesis) & Zinc vital for repair.
• Tensile strength: ~70-80% original strength by 3 months; never 100%.