The connective tissue framework in skeletal muscle combines the contractile
myofibers into a functional unit, in which the contraction of myofibers is
transformed into movement via myotendinous junctions (MTJs) at their ends,
where myofibers attach to tendons/fascia. The cytoskeletal contractile myo
filament apparatus adheres through subsarcolemmal and transmembrane molecul
es to the surrounding extracellular matrix, with integrin and dystrophin as
sociated chains of molecules being the two main adhesion complexes. In shea
ring type of muscle injury both myofibers and the connective tissue framewo
rk are ruptured and thereby the functional tendon-muscle-tendon units are d
isrupted. The stumps of the ruptured myofibers are separated and at the sam
e time joined by a connective tissue scar, through which the ends of regene
rating myofibers try to pierce, but as the scar becomes more compact the en
ds attach to the scar by new mini-MTJs. During the early phase ruptured myo
fibers try to compensate for the lost MTJ attachment by reinforcing their i
ntegrin mediated lateral adhesion, which returns to normal low level after
formation of the mini-MTJs and at which time complementary increase of dyst
rophin and associated molecules on lateral sarcolemma takes place. The stum
ps appear to remain separated by and attached to the interposed scar for ma
ny months, possibly for ever, i.e. the original tendon-muscle-tendon units
may have become permanently divided into two consecutive units. Remarkably,
axon sprouts are able to penetrate through the interposed scar to form new
neuromuscular junctions on those abjunctional stumps which were denervated
by the rupture.