Reduced muscle fiber force production and disrupted myofibril architecture in patients with chronic rotator cuff tears

Christopher L Mendias; Stuart M Roche; Julie A Harning; Max E Davis; Evan B Lynch; Elizabeth R Sibilsky Enselman; Jon A Jacobson; Dennis R Claflin; Sarah Calve; Asheesh Bedi

doi:10.1016/j.jse.2014.06.037

Reduced muscle fiber force production and disrupted myofibril architecture in patients with chronic rotator cuff tears

J Shoulder Elbow Surg. 2015 Jan;24(1):111-9. doi: 10.1016/j.jse.2014.06.037. Epub 2014 Sep 3.

Affiliations

¹ Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA. Electronic address: cmendias@umich.edu.
² Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
³ Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA.
⁴ Department of Radiology, University of Michigan Medical School, Ann Arbor, MI, USA.
⁵ Department of Biomedical Engineering, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Surgery, Section of Plastic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
⁶ School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.

PMID: 25193488
DOI: 10.1016/j.jse.2014.06.037

Abstract

Background: A persistent atrophy of muscle fibers and an accumulation of fat, collectively referred to as fatty degeneration, commonly occur in patients with chronic rotator cuff tears. The etiology of fatty degeneration and function of the residual rotator cuff musculature have not been well characterized in humans. We hypothesized that muscles from patients with chronic rotator cuff tears have reduced muscle fiber force production, disordered myofibrils, and an accumulation of fat vacuoles.

Methods: The contractility of muscle fibers from biopsy specimens of supraspinatus muscles of 13 patients with chronic full-thickness posterosuperior rotator cuff tears was measured and compared with data from healthy vastus lateralis muscle fibers. Correlations between muscle fiber contractility, American Shoulder and Elbow Surgeons (ASES) scores, and tear size were analyzed. Histology and electron microscopy were also performed.

Results: Torn supraspinatus muscles had a 30% reduction in maximum isometric force production and a 29% reduction in normalized force compared with controls. Normalized supraspinatus fiber force positively correlated with ASES score and negatively correlated with tear size. Disordered sarcomeres were noted, along with an accumulation of lipid-laden macrophages in the extracellular matrix surrounding supraspinatus muscle fibers.

Conclusions: Patients with chronic supraspinatus tears have significant reductions in muscle fiber force production. Force production also correlates with ASES scores and tear size. The structural and functional muscle dysfunction of the residual muscle fibers is independent of the additional area taken up by fibrotic tissue. This work may help establish future therapies to restore muscle function after the repair of chronically torn rotator cuff muscles.

Keywords: Rotator cuff; fatty degeneration; macrophages; myosteatosis; permeabilized muscle fibers; sarcomeres.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adipose Tissue / pathology
Aged
Extracellular Matrix / pathology
Extracellular Matrix / ultrastructure
Female
Humans
Macrophages / pathology
Male
Microscopy, Electron, Transmission
Middle Aged
Muscle Contraction / physiology
Muscle Fibers, Skeletal / pathology
Muscle Fibers, Skeletal / physiology
Muscle Fibers, Skeletal / ultrastructure
Muscular Atrophy / pathology
Muscular Atrophy / physiopathology
Myofibrils / pathology
Myofibrils / ultrastructure*
Rotator Cuff / pathology*
Rotator Cuff Injuries
Sarcomeres / pathology
Sarcomeres / ultrastructure
Tendon Injuries / pathology*