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Tissue - Proliferating potential of cell types
Labile cells - Continuously dividing cells. e.g. epidermis, epithelial cells, bone marrow cells
Stable cells
- Quiescent cells
- Undergoes division occasionally
- Liver, kidney pancreas, fibroblasts, endothelial cells
Permanent cells
- Non–dividing cells
- Neurons, muscle cells (cardiac, skeletal)
Hence, healing occurs by
- Healing by regeneration
- Healing by substitution
Depending on the proliferation potential of the cellsas described above.
Wound healing
Wound healing is not a separate process and occurs along with the inflammatory reaction. It is a complex but orderly phenomenon involving a number of processes.
Namely,
- Acute inflammatory reaction following initial injury
- Parenchymatous cellular regeneration
- Migration and production of parenchymatous and connective tissue cell
- Extracellular matrix, protein synthesis
- Remodelling of connective tissue
Healing by primary union or first intention
- This type of healing occurs in clean surgical approximated incision ie. limited bleeding and tissue destruction.
- The sequence of events occurring in primary union is given below
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0 hour
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Clot filling the incised area
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3-24 hour
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Neutrophilic infiltration
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48 hour
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Basal cell proliferation and epithelial closure takes place by 24-48 hours
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72 hours
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Macrophages replace neutrophils. Granulation tissue begins to appear. Collagen is arranged vertically
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120 hours
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Incised space is filled with granulation tissue. Neovascularisation is maximal. Collagen fibre begin to appear and epithelial proliferation is maximal
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2 weeks
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Proliferation of fibroblast with continuous collagen accumulation producing a scar. Type III collagen is deposited early in scar tissue and is replaced by adult type I collagen which accounts for wound strength. Newly formed blood vessels disappear.
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8 week
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Scar tissue consists of granulation tissue which is devoid of inflammation covering intact epidermis.
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Healing by second intention
- The wound involved shows extensive loss of cells and tissue. e.g. infarction, ulceration, abscesses, surface wound with large defects. The wound is filled with tissue debris, a few erythrocytes and bacteria. Abundant granulation tissue (soft, pink, granular appearance of wound surfaces) grows in from the margin to fill the defect but at the same time the wound contracts i.e., the defect is marked by depression and decrease from its original size. Microscopically granulation tissue consists of new capillaries, fibroblasts, collagen and proteoglycan rich ground substance. Initially granulation tissue is soft and spongy due to leaky blood vessels.
Injury – open wound – excess loss of tissue – infected – necrosis – inflammation
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Blood clot
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24 hours – neutrophils infiltrate to destroy irritant
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48-72 hours – macrophages and lymphocytes infiltrate
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Removal of necrotic and cellular debris by liquefaction by macrophages
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Red granules from underneath (granulation tissue) represent proliferating capillaries. Fibroblast also proliferate to fill the gap
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There is a definite order.
Base - capillaries grow vertically and project towards the surface. Fibroblast grows perpendicular to capillary and parallel to surface – pulling pressure of the wound
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Surface – fibroblasts are arranged parallel to capillaries exerting tension towards wound surface for easy closure. This arrangement differentiates granulation tissue from fibrosarcoma which lacks orderly arrangement
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The surface is closed by the epithelium proliferating from the margin
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The tissue is devoid of sweat gland, sebaceous gland, hair and hair follicles and pigment. So, the scar appears dry and unpigmented white and puckered as it becomes avascular and shrinkage of collagen
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Septic wound - Healing by substitution
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Exuberant granulation or proud flesh
- Sometimes the granulation continues to grow in abnormally large amount due to irritant, movement or trauma which prevents healing. This condition is called proud flesh or excess granulation tissue.
Keloid
- Keloid is another condition. Reason for its development is not known. The connective tissue below the epithelial covering continues to proliferate. This condition may recur after the removal. This is found in horses and black people having some genetic or familial predisposition.
Systemic and local factors influencing wound healing
Systemic factors
- Nutritional
- Vitamins – vitamin C is required for collagen synthesis
- Proteins deficiency – starvation
- Sulphur containing amino acids (methionine and cystine) are important and required for intermediate forms of collagen
- Zinc – as metalloenzyme, it is essential for remodelling of extracellular matrix
- Metabolic factors
- Diabetes mellitus – delays healing
- Hyperadrenocortism
- Circulatory stasis or adequacy of blood supply
- Inadequate blood supply – delays healing
- Hormones – concurrent glucocorticoid therapy hinders inflammatory and reparatory process
Local factors
- Infection can delay healing
- Mechanical – movements directly affect wound healing
- Foreign bodies impede healing
- Size, location and type of wound
- Cold inhibits wound healing
Others
- Old age-Healing is slower than young ones.
- Chemotherapeutic agents
- Radiation
- Immunodeficiency
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