Difference between revisions of "Muscle Regeneration"

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===Response to injury===
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*Limited array of ways in which to respond to injury
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**[[Muscles - degenerative#Degeneration|Degeneration]]
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**[[Muscles - degenerative#Necrosis|Necrosis]]
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**[[Muscles - normal#Regeneration|Regeneration]]
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**[[Muscles - degenerative#Atrophy|Atrophy]]
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**[[Muscles - hyperplastic and neoplastic#Hypertrophy|Hypertrophy]]
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*Large number of factors indicing the changes above, e.g.:
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**Trauma
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**Toxins
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**Infectious agents
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**Nutritional deficiencies
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**Ichaemia
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**[[Muscles - developmental|Hereditary diseases]]
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*Specific diagnosis is often not possible based on morphological or histological features alone
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*Additional tests, clinical information and history are often required
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===Regeneration===
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[[Image:Muscle regeneration.jpg|right|thumb|100px|<small><center>Muscle regeneration (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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*Skeletal muscle myofibres have substantial regenerative ability
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*Success depends on:
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**An intact '''sarcolemmal tube''' - to act as a support and guide
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**Availability of '''satellite cells''' - to act as progenitor cells for new sarcoplasm production
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**Macrophages to clear up cell debris
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**If these conditions are not met (e.g. severe thermal damage) '''fibrosis''' will occur
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*Stages:
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#Nuclei in [[Muscles - degenerative#Necrosis|necrotic segement]] disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or [[Muscles - degenerative#Calcification|mineralise]]
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#Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
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#Satellite cells move to centre
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#Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina
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#Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing
 +
#Growing and differentiating fibre, striations appear - formation of sarcomeres
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#Nuclei move to peripheral position (2-3 weeks after initial injury)
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*Regeneration by '''budding'''
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**When conditions are not optimal, disrupted sacrolemma
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**E.g. injection of irritating substance, trauma, [[Muscles - degenerative#Ischaemia|infarction]]
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**Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
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*Monophasic lesions - all at same phase above
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===Rigor Mortis===
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*Muscles remain biochemically active after the death of an animal
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*Following a period of relaxation, contraction and stiffening occurs
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*Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke
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*Onset faster in ATP deprived animals (starvation, hunting, tetanus...)
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*May be absent in cachetic animals
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*Disappears due to autolysis or putrefaction
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*See [[General Pathology - Post-Mortem Change#Rigor Mortis|general pathology]]
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**Damage occured at one time, e.g. trauma or one toxin exposure
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*Multiphasic lesions - different stages as described above
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**Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin

Revision as of 20:06, 18 August 2008

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()Map MUSCULOSKELETAL SYSTEM (Map)
MUSCLES



Response to injury

  • Large number of factors indicing the changes above, e.g.:


  • Specific diagnosis is often not possible based on morphological or histological features alone
  • Additional tests, clinical information and history are often required

Regeneration

Muscle regeneration (Image sourced from Bristol Biomed Image Archive with permission)
  • Skeletal muscle myofibres have substantial regenerative ability
  • Success depends on:
    • An intact sarcolemmal tube - to act as a support and guide
    • Availability of satellite cells - to act as progenitor cells for new sarcoplasm production
    • Macrophages to clear up cell debris
    • If these conditions are not met (e.g. severe thermal damage) fibrosis will occur
  • Stages:
  1. Nuclei in necrotic segement disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or mineralise
  2. Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
  3. Satellite cells move to centre
  4. Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina
  5. Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing
  6. Growing and differentiating fibre, striations appear - formation of sarcomeres
  7. Nuclei move to peripheral position (2-3 weeks after initial injury)
  • Regeneration by budding
    • When conditions are not optimal, disrupted sacrolemma
    • E.g. injection of irritating substance, trauma, infarction
    • Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
  • Monophasic lesions - all at same phase above

Rigor Mortis

  • Muscles remain biochemically active after the death of an animal
  • Following a period of relaxation, contraction and stiffening occurs
  • Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke
  • Onset faster in ATP deprived animals (starvation, hunting, tetanus...)
  • May be absent in cachetic animals
  • Disappears due to autolysis or putrefaction
  • See general pathology


    • Damage occured at one time, e.g. trauma or one toxin exposure
  • Multiphasic lesions - different stages as described above
    • Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin
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