Wound healing: Special sites

Wound healing in tissues

The regenerative potential depends on whether tissue cells are:

• Labile: continuously dividing (e.g. skin, GI epithelium, bone marrow). These tissues heal well.
• Stable: quiescent but can proliferate if stimulated (e.g. liver, kidney tubules, fibroblasts, endothelium). These tissues have limited regeneration.
• Permanent: non-dividing (e.g. neurons, cardiac myocytes). These tissues heal by scarring only.

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Brain

• Neurons are permanent (non-dividing) cells and cannot regenerate once lost.
• Injury results in liquefactive necrosis.
• Repair is by astrocytic gliosis (proliferation of astrocytes forming a glial scar).
• Functional recovery is limited as neuronal connections are not restored.

Myocardium

• Cardiac myocytes are permanent cells with no true regeneration.
• After infarction, cardiac myocytes undergo coagulative necrosis.
• This triggers acute inflammation, followed by formation of granulation tissue and eventual replacement of the original myocardium with dense fibrous scar tissue.
• Scar restores structure but lacks contractile function (increases risk of chronic heart failure.

Peripheral Nerves

• Axons can regenerate if the cell body remains intact.
• Distal segment undergoes Wallerian degeneration (axon & myelin breakdown, macrophage clearance).
• Schwann cells proliferate, forming guiding tubes (Bands of Büngner).
• Axonal regrowth occurs at ~1–3 mm/day.
• Functional recovery depends on distance and alignment.

Tendon

• Healing occurs mainly by fibroblast activity producing type III collagen initially, later remodelled into type I collagen.
• Scar tissue forms, which has less elasticity and strength than native tendon.
• Intrinsic healing (from tenocytes) and extrinsic healing (from surrounding tissue and blood supply) both contribute.
• Adhesion formation can impair gliding function, especially in hand tendons.

Summary table of necrosis types