Muscle Regeneration

()Map MUSCULOSKELETAL SYSTEM (Map) MUSCLES

Response to injury

• Limited array of ways in which to respond to injury
  • Degeneration
  • Necrosis
  • Regeneration
  • Atrophy
  • Hypertrophy

• Large number of factors indicing the changes above, e.g.:
  • Trauma
  • Toxins
  • Infectious agents
  • Nutritional deficiencies
  • Ichaemia
  • Hereditary diseases

• 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