Wound Healing and Repair Processes

Study Notes

Repair is defined as the replacement of damaged tissue with a new healthy tissue.

Labile cells: These cells constantly divide and renew themselves. Examples include skin epithelium, mucosal lining of the gastrointestinal tract (GIT), and hematopoietic cells (blood cells).
Quiescent (Stable) cells: These cells divide only when necessary. Examples include liver cells, kidney cells, pancreas cells, smooth muscle cells, and fibroblasts.
Permanent cells: These cells do not divide and, when injured, typically heal by fibrous or glial tissue formation (only in the central nervous system (CNS)). Examples include nerve cells and skeletal/cardiac muscle cells.

Regeneration: New healthy cells of the same type replace damaged cells. This occurs via proliferation of adjacent, healthy cells. It happens with minor damage to labile and stable cells. Examples include mild liver injuries and bone fractures.
Fibrosis or gliosis: Damaged tissue is replaced with fibrous or glial tissue (in the CNS). This happens during the healing process of permanent cells, or in stable cells with significant damage. Examples include myocardial infarction (heals by fibrosis) and cerebral infarction (heals by gliosis).

Hemostasis: Immediately after injury, bleeding vessels form a clot to temporarily stop the bleeding. This involves vasoconstriction of blood vessels, aggregation, and adherence of platelets to damaged endothelium. The coagulation system also produces fibrin that forms a hemostatic plug over aggregated platelets
Inflammation: Polymorphs and macrophages mediate this process. Within 6-8 hours, polymorphonuclear leukocytes (PMNs) kill pathogens and break down dead tissue. Monocytes move into the wound and become macrophages, ingesting remaining debris.
Granulation tissue formation and re-epithelialization: Fibroblasts migrate into the wound. Angiogenesis (formation of new capillaries) occurs from the healthy blood vessels at the wound edge; new capillaries fill the wound defect. The newly formed capillaries and fibroblasts form granulation tissue. Re-epithelialization happens via healthy epidermal cells proliferating and migrating inwards from the wound edges.
Fibrous tissue formation and remodeling: Fibroblasts produce collagen fibers (types I and III). Excess collagen is gradually degraded (remodeled) by collagenase secreted by macrophages.
Wound contraction: Myofibroblasts (modified fibroblasts) resemble contractile smooth muscle cells. Their actions increase the wound's strength.

Primary union (first intention): Healing in clean, non-gaping wounds (stitched incisions). Leads to a small, thin, regular, and flat scar.
Secondary union (second intention): Extensive tissue loss in wounds that are large, infected, or contain abscesses or ulcers. Leads to a larger, thick, irregular, and elevated scar.

Local Factors:
- Type of damaged cells (labile, stable, or permanent)
- Severity of damage
- Presence of foreign bodies
- Presence of necrotic tissue
- Infection
- Irradiation
- Blood supply
General Factors:
- Patient's age
- Nutritional status
- Diseases (e.g., diabetes, malignancy, anemia)
- Medications (e.g., corticosteroids, chemotherapy)

Ulcers: Discontinuity of surface epithelium (skin or mucous membrane).
Sinus: Blind-ended track connecting an abscess cavity to the outside.
Fistula: Tract connecting two epithelial surfaces.
Weak atrophic scar: May lead to hernia.
Hypertrophied scar: Enlarged scar that doesn't extend beyond initial wound boundaries.
Keloid formation: Enlarged scar that extends beyond original wound boundaries and intrudes surrounding tissue.
Wound contracture: Exaggerated wound contraction can lead to functional impairments.