WOUND HEALING

Wound: Disruption of cellular and anatomic continuity of a tissue.
Erosion: Focal loss of epidermis that does not penetrate the dermis and heals without scarring.
Ulcer: Focal loss of both epidermis and dermis that heals with scarring.

Type I Wounds:
- Superficial loss involving the epidermis and superficial dermis.
- Heal by epithelialization with negligible granulation and no contraction.
Type II Wounds:
- Extend deep into dermis, involving full thickness of the dermis and into subcutaneous tissue.
- Type II A: Wounds without significant tissue loss.
- Type II B: Wounds with substantial loss that heal by granulation, contraction, and epidermization.

Immediate Response:
- Release of inflammatory mediators from damaged cells, platelets, tissue macrophages, and mast cells.
- Arteriole dilatation increases blood flow into the wound area.
Growth Factors Involved:
- Vascular endothelial growth factor (VEGF) causes hyperpermeability leading to fluid influx and inflammatory cell migration.

Neutrophils:
- Initial inflammatory cells that engulf bacteria via phagocytosis, release tissue-damaging substances, and contribute to inflammation.
- Release cytokines and growth factors.
Key Cytokines for Wound Repair:
- Tumor necrosis factor α (TNF-α)
- Interleukin 1 (IL-1)
- Various chemokines (e.g., CCL2, CXCL10)
Platelets:
- Aggregate at the wound site; release thromboxanes, prostaglandins, glycoproteins, and growth factors that help in wound closure and cell migration.

Recruitment:
- Monocytes become macrophages, producing cytokines in response to inflammation.
TGF-β Function:
- Acts as both pro-inflammatory and anti-inflammatory cytokine.
Granulation Tissue Formation:
- Macrophages produce extracellular matrix components aiding in the scaffold for new tissue formation.

Attraction by Chemokines:
- Participate in the progression to fibrosis and produce growth factors influencing wound healing.

Begins approximately 24 hours after wounding with keratinocyte migration from wound edges and hair follicles.
Keratinocytes flatten and elongate, lose attachments, and migrate over the provisional matrix composed of fibrin and fibronectin.
Over several days, they increase in number and begin to proliferate, with peak activity around day 1-2 post-wounding.

Keratinocytes express matrix metalloproteinases (MMPs) to degrade barriers that hinder migration.
FGF-1, EGF, and PDGF are important growth factors aiding in the re-epithelialization.

Formation of New Blood Vessels:
- Stimulation begins during the inflammatory phase, with increased permeability of existing capillaries facilitating endothelial cell migration and capillary formation.
Granulation Tissue Appearance:
- Characterized by a red granular appearance from capillary loops and a rich ECM that supports further healing.

Fibroblast Recruitment:
- Fibroblasts deposit extracellular matrix components, transitioning from type III to mature type I collagen.
Myofibroblasts:
- Intermediate between fibroblasts and smooth muscle cells, contribute to wound contraction and can lead to abnormal scarring.

Intrinsic Factors:
- Size of the wound, blood supply, age, health, nutritional status.
Extrinsic Factors:
- Drugs taken by the patient, presence of infections, and underlying diseases affecting healing processes.

Characterized by long-lasting inflammation, impaired cell migration, and microbial colonization affecting healing efficiency.

Condition complicating wound healing due to underlying pathology, increased susceptibility to infection, and impaired growth factor signaling.

Abnormal fibrous responses that vary in characteristics, with keloids often extending beyond original injury sites.

Involves structural changes in the dermis, with observable differences in collagen organization and skin texture compared to normal tissue.