Difference between revisions of "Muscle Regeneration"

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|backcolour =CDE472
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|linkpage =Musculoskeletal System - Pathology
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|linktext =Musculoskeletal System
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|maplink = Musculoskeletal System (Content Map) - Pathology
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|pagetype =Pathology
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|sublink1=Muscles - Pathology
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|subtext1=MUSCLES
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<br>
 
===Response to injury===
 
===Response to injury===
  
 
*Limited array of ways in which to respond to injury
 
*Limited array of ways in which to respond to injury
**[[:Category:Muscles - Degenerative Pathology|Degeneration]]
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**[[Muscles - degenerative#Degeneration|Degeneration]]
**[[Muscle Necrosis|Necrosis]]
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**[[Muscles - degenerative#Necrosis|Necrosis]]
**Regeneration
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**[[Muscles - normal#Regeneration|Regeneration]]
**[[Muscle Atrophy|Atrophy]]
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**[[Muscles - degenerative#Atrophy|Atrophy]]
**[[Muscle Hypertrophy|Hypertrophy]]
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**[[Muscles - hyperplastic and neoplastic#Hypertrophy|Hypertrophy]]
  
 
*Large number of factors indicing the changes above, e.g.:
 
*Large number of factors indicing the changes above, e.g.:
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**Nutritional deficiencies
 
**Nutritional deficiencies
 
**Ichaemia
 
**Ichaemia
**[[:Category:Muscles - Developmental Pathology|Hereditary diseases]]
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**[[Muscles Developmental - Pathology|Hereditary diseases]]
  
  
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**If these conditions are not met (e.g. severe thermal damage) '''fibrosis''' will occur
 
**If these conditions are not met (e.g. severe thermal damage) '''fibrosis''' will occur
 
*Stages:
 
*Stages:
#Nuclei in [[Muscle Necrosis|necrotic segement]] disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or [[Muscle Calcification|mineralise]]
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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]]
 
#Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
 
#Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
 
#Satellite cells move to centre
 
#Satellite cells move to centre
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*Regeneration by '''budding'''
 
*Regeneration by '''budding'''
 
**When conditions are not optimal, disrupted sacrolemma
 
**When conditions are not optimal, disrupted sacrolemma
**E.g. injection of irritating substance, trauma, [[Muscle Ischaemia|infarction]]
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**E.g. injection of irritating substance, trauma, [[Muscles - degenerative#Ischaemia|infarction]]
 
**Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
 
**Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
 
*Monophasic lesions - all at same phase above
 
*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]]
  
[[Category:Muscles - Pathology]]
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 +
 
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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 20:08, 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