Tissue Repair and Skin Wound Healing

Factors Influencing Tissue Repair

• Host factors: Nutritional status, metabolic state (e.g., diabetes mellitus), circulatory status/vascular adequacy, and hormone levels (e.g., glucocorticoids) all impact healing.
• Site-specific factors: Well-vascularized tissues heal faster. Inflammation in areas like the peritoneal cavity can involve exudates that can either resolve or become organized tissue.
• Tissue type: Labile and stable tissues regenerate better than permanent tissues, which form only scars.
• Local factors delaying healing: Infections, ischemia, mechanical forces (e.g., movement, tension), and foreign bodies impair healing.

Healing of Skin Wounds

Healing by First Intention (Primary Union)

• Occurs with only epithelial layer injury.
• Primarily epithelial regeneration.
• Minimal cell death in clean surgical incisions.
• Steps:
  • Coagulation forms a clot to stop bleeding, provide a scaffold, and form a scab.
  • Neutrophils clear debris within 24 hours.
  • Epithelial cells migrate and proliferate along dermis.
  • Neutrophils are replaced by macrophages, granulation tissue forms, collagen appears.
  • Neovascularization peaks, fibroblasts produce ECM, epidermis regenerates.
  • Continued collagen accumulation, fewer inflammatory cells. Dermal appendages lost.
  • Scar forms (few inflammatory cells).

Healing by Second Intention (Secondary Union)

• Occurs with extensive tissue loss (large wounds, abscesses, etc.).
• Combination of regeneration and scarring.
• More intense inflammatory reaction, greater granulation tissue, increased ECM, large scar formation, myofibroblast contraction.
• Steps:
  • Intense inflammation due to large tissue defects.
  • Extensive granulation tissue forms.
  • Granulation tissue becomes a scar.
  • Epidermis regenerates, dermal appendages lost.
  • Wound contraction, large defects reduced to 5-10% original size.

Wound Strength

• One-week post-suture removal, strength is approximately 10% of unwounded skin.
  • Wound strength increases through collagen synthesis (first 2 months).
  • Strength reaches approximately 70-80% of normal by 3 months.

Fibrosis in Parenchymal Organs

• Abnormal collagen deposition in chronic (often inflammatory) diseases.
• Mechanisms similar to scar formation (largely due to TGF-β).
• Leads to organ dysfunction and failure (e.g., liver cirrhosis, pulmonary fibrosis, kidney disease, constrictive pericarditis).

Abnormalities in Tissue Repair

Deficient Scar Formation

• Inadequate granulation tissue or collagen deposition/remodeling.
• Leads to wound dehiscence or ulceration (frequent after abdominal surgery).

Excessive Repair

• Exuberant granulation tissue (proud flesh): Excessive granulation tissue, protrudes above skin surface, prevents re-epithelialization. Removal required.
• Hypertrophic scar: Excessive collagen accumulation, raised scar that often shrinks over time. Commonly after deep dermis injury.
• Keloid: Scar formation extending beyond original injury, no regression. Predisposition exists in some individuals (e.g., African descent).
• Desmoids (aggressive fibromatosis): Exuberant fibroblast and connective tissue proliferation. May recur.

Contractures

• Exaggerated wound contraction, causing deformity (claw hand, limited joint mobility). Common after burns.

Chronic Wound Defects

• Venous leg ulcers: Chronic venous hypertension (e.g., varicose veins), poor oxygen delivery.
• Arterial ulcers: Atherosclerosis, ischemia, commonly with diabetes.
• Pressure sores: Prolonged tissue compression, ischemia, in immobile patients.
• Diabetic ulcers: Small vessel disease causing ischemia, neuropathy, systemic metabolic issues, secondary infections.

This quiz explores the factors influencing tissue repair and the mechanisms of skin wound healing, including the distinction between healing by first intention and other types of healing. Understand the role of host and local factors, as well as tissue types, in the healing process. Test your knowledge on how these elements impact recovery.