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REPAIR
By
Shatha al sulh
• Replacement of damaged tissue by new healthy
one.
• Types:
• Regeneration: of the same type.
• By CT deposition:
– fibrosis: (scarring): all except CNS.
– Gliosis: in CNS.
What determines the type of
repair?
• By type of damaged cells as different cell
types have different capacity to divide.
Labile cells: Stable cells: Permenent cells:
•Contineously actively divide.
• have short G0
•Complete regeneration after
injury.
•E.g: surface epithelia & mm.
•G0 :physiological state of non
division of quiescent cells that
re-enter mitotic cell cycle when
needed.
•Limited capacity of division.
• remain in long G0 till need.
•Repair by regeneration or
fibrosis.
•E.g: parenchymal cells of
glandular organs,
mesenchymal cells as
fibroblats.
•No division in postnatal
life.
•Repair by CT deposition.
•E.g:nerve cells(gliosis),
cardiac ms. Cells
(fibrosis).
Factors affecting repair
I. Factors affecting efficiency & type of repair:
 Local factors:
– Type of damaged cells.
– Blood supply e.g ischaemia lead to defective repair.
– Persistent infection or FB.
– Extent of tissue damage.
 General factors:
– Age.
– Nutritional difficiencies e.g ptn, vit.C, D & zinc.
– Glucocorticoids & cytotoxic drugs.
– Endocrinal ds. E.g diabetes & cushing.
Factors affecting repair (cont.)
• II.Factors controlling the michanism of repair:
GF:
• Stimuli that control cell division.
• Mostly produced my macrophages.
• Include:
– EGF: mitogenic for epith. Cells & fibroblasts.
– PDGF:mitogenic for fibroblasts, neuroglia cells & smooth ms.
– FGF: fibroblast proliferation & form. Of new bl. Vs.
– TGFα: stimulatory (fibroblast proliferation ), inhibitory
(collagen degradation).
– TGFβ: stimulatory (fibrogenesis) inhibitory (growth inhibition
action).
– IL1 & TNF.
II.Factors controlling the michanism of
repair (cont.):
Cell to cell interaction (contact inhibition):
Normally: cells are in intimate contact prevent un-needed
division, due to inhibitory signals, receptors interaction &
chalones (growth inhibition factors as TGFβ which suppress
mitosis).
With tissue damage cell loss loss of contact inhibition
stimulate cells to divide till contact again ( at end of repair)
contact inhibition
Cell to matrix interaction:
Normally: with ECM ptns (fibronectin & laminin) with role in
cell migration, proliferation, differentiation & adhesion.
Abnormality in this interaction serious effects (as abnormal
repair).
II.Factors controlling the michanism of
repair (cont.):
Cell to cell interaction (contact inhibition):
Normally: cells are in intimate contact prevent un-needed
division, due to inhibitory signals, receptors interaction &
chalones (growth inhibition factors as TGFβ which suppress
mitosis).
With tissue damage cell loss loss of contact inhibition
stimulate cells to divide till contact again ( at end of repair)
contact inhibition
Cell to matrix interaction:
Normally: with ECM ptns (fibronectin & laminin) with role in
cell migration, proliferation, differentiation & adhesion.
Abnormality in this interaction serious effects (as abnormal
repair).

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4 1-repair

  • 2. • Replacement of damaged tissue by new healthy one. • Types: • Regeneration: of the same type. • By CT deposition: – fibrosis: (scarring): all except CNS. – Gliosis: in CNS.
  • 3. What determines the type of repair? • By type of damaged cells as different cell types have different capacity to divide. Labile cells: Stable cells: Permenent cells: •Contineously actively divide. • have short G0 •Complete regeneration after injury. •E.g: surface epithelia & mm. •G0 :physiological state of non division of quiescent cells that re-enter mitotic cell cycle when needed. •Limited capacity of division. • remain in long G0 till need. •Repair by regeneration or fibrosis. •E.g: parenchymal cells of glandular organs, mesenchymal cells as fibroblats. •No division in postnatal life. •Repair by CT deposition. •E.g:nerve cells(gliosis), cardiac ms. Cells (fibrosis).
  • 4. Factors affecting repair I. Factors affecting efficiency & type of repair:  Local factors: – Type of damaged cells. – Blood supply e.g ischaemia lead to defective repair. – Persistent infection or FB. – Extent of tissue damage.  General factors: – Age. – Nutritional difficiencies e.g ptn, vit.C, D & zinc. – Glucocorticoids & cytotoxic drugs. – Endocrinal ds. E.g diabetes & cushing.
  • 5. Factors affecting repair (cont.) • II.Factors controlling the michanism of repair: GF: • Stimuli that control cell division. • Mostly produced my macrophages. • Include: – EGF: mitogenic for epith. Cells & fibroblasts. – PDGF:mitogenic for fibroblasts, neuroglia cells & smooth ms. – FGF: fibroblast proliferation & form. Of new bl. Vs. – TGFα: stimulatory (fibroblast proliferation ), inhibitory (collagen degradation). – TGFβ: stimulatory (fibrogenesis) inhibitory (growth inhibition action). – IL1 & TNF.
  • 6. II.Factors controlling the michanism of repair (cont.): Cell to cell interaction (contact inhibition): Normally: cells are in intimate contact prevent un-needed division, due to inhibitory signals, receptors interaction & chalones (growth inhibition factors as TGFβ which suppress mitosis). With tissue damage cell loss loss of contact inhibition stimulate cells to divide till contact again ( at end of repair) contact inhibition Cell to matrix interaction: Normally: with ECM ptns (fibronectin & laminin) with role in cell migration, proliferation, differentiation & adhesion. Abnormality in this interaction serious effects (as abnormal repair).
  • 7. II.Factors controlling the michanism of repair (cont.): Cell to cell interaction (contact inhibition): Normally: cells are in intimate contact prevent un-needed division, due to inhibitory signals, receptors interaction & chalones (growth inhibition factors as TGFβ which suppress mitosis). With tissue damage cell loss loss of contact inhibition stimulate cells to divide till contact again ( at end of repair) contact inhibition Cell to matrix interaction: Normally: with ECM ptns (fibronectin & laminin) with role in cell migration, proliferation, differentiation & adhesion. Abnormality in this interaction serious effects (as abnormal repair).