Difference between revisions of "Muscle Regeneration"

Revision as of 17:18, 3 March 2011

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

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:

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

@@ Line 44: / Line 44: @@
 *Monophasic lesions - all at same phase above
-===Rigor Mortis===
+===[[Rigor Mortis]]===
-*Muscles remain biochemically active after the death of an animal
+[[Category:Muscles - Pathology]]
-*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
-[[Category:Musculoskeletal System - Pathology]]