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A Novel Pathomechanical Concept Explains the Fatty Muscular Changes Following Tendon Tear

Authors: DC Meyer et al.

References: Presented at AAOS 2004

Abstract
Fatty muscle infiltration following tendon tear is not primarily degenerative but a physiological consequence of the muscle fiber rearrangement.

Tendon degeneration and tears are frequent causes of painful disability in man. They are associated with musculotendinous retraction, atrophy and infiltration of the muscle with fat. After few weeks, these changes become irreversible and represent the main cause for persistent disability despite successful tendon healing. These changes are currently considered to represent a non–specified degenerative process involving the muscle fibers.

We studied the muscular changes caused by unilateral tendon release, myotendinous retraction and delayed repair in the infraspinatus muscle of eight sheep using computertomography, MRI, histology and electronmicroscopy.

At sacrifice (75weeks after tendon release) the muscle had retracted by 2.6cm (13 percent, P<0.0001), the pennation angle had increased from 22 ± 2.5degrees to 50 ± 11degrees (P<0.0001) and the mean muscle fiber length had shortened from 32 ± 3mm to 16 ± 5mm (50 percent, P<0.0001). In electron and light microscopy, we found essentially normal muscle fibers with an unaltered fiber diameter and myofibrillar structure, while interstitial fat and fibrous tissue had increased from 3.7 percent to 46 percent (P<0.0001) of the muscle volume. Geometric modeling showed that the increase of the pennation angle separates the muscle fiber bundles like limbs of a parallelogram.

We hypothesize that the fat tissue serves to fill opportunistically the mechanically created spaces between muscle fibers and is not primarily the consequence of a degenerative process. These gaps may quantitatively be predicted with this model. Therefore, to reverse muscle changes caused by tendon retraction we will have to restore pennation angle and muscle fiber length.

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