Difference between revisions of "Muscle Regeneration"
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| + | {{review}} | ||
| + | |||
| + | {{toplink | ||
| + | |backcolour =CDE472 | ||
| + | |linkpage =Musculoskeletal System - Pathology | ||
| + | |linktext =Musculoskeletal System | ||
| + | |maplink = Musculoskeletal System (Content Map) - Pathology | ||
| + | |pagetype =Pathology | ||
| + | |sublink1=Muscles - Pathology | ||
| + | |subtext1=MUSCLES | ||
| + | }} | ||
| + | <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 | ||
| − | **[[ | + | **[[Muscles Degenerative - Pathology#Degeneration|Degeneration]] |
| − | **[[ | + | **[[Muscles Degenerative - Pathology#Necrosis|Necrosis]] |
| − | **Regeneration | + | **[[Muscle Regeneration - Anatomy & Physiology|Regeneration]] |
| − | **[[ | + | **[[Muscles Degenerative - Pathology#Atrophy|Atrophy]] |
| − | **[[ | + | **[[Muscles Hyperplastic and Neoplastic - Pathology#Hypertrophy|Hypertrophy]] |
*Large number of factors indicing the changes above, e.g.: | *Large number of factors indicing the changes above, e.g.: | ||
| Line 14: | Line 26: | ||
**Nutritional deficiencies | **Nutritional deficiencies | ||
**Ichaemia | **Ichaemia | ||
| − | **[[ | + | **[[Muscles Developmental - Pathology|Hereditary diseases]] |
| Line 31: | Line 43: | ||
**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 [[ | + | #Nuclei in [[Muscles Degenerative - Pathology#Necrosis|necrotic segement]] disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or [[Muscles Degenerative - Pathology#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 | ||
| Line 40: | Line 52: | ||
*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, [[ | + | **E.g. injection of irritating substance, trauma, [[Muscles Degenerative - Pathology#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 | ||
| + | |||
| + | ===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 [[Post-Mortem Change - Pathology#Rigor Mortis|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 | ||
Revision as of 20:59, 13 August 2009
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Response to injury
- Limited array of ways in which to respond to injury
- 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
- 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:
- Nuclei in necrotic segement disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or mineralise
- 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
- Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina
- 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
- 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