title: Reduced muscle fiber force production and disrupted myofibril architecture in patients with chronic rotator cuff tears.
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.
authors.affiliation: 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.
authors.forename: Christopher L
authors.initials: CL
authors.lastname: Mendias
authors.affiliation: Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Stuart M
authors.initials: SM
authors.lastname: Roche
authors.affiliation: Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Julie A
authors.initials: JA
authors.lastname: Harning
authors.affiliation: Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Max E
authors.initials: ME
authors.lastname: Davis
authors.affiliation: 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.
authors.forename: Evan B
authors.initials: EB
authors.lastname: Lynch
authors.affiliation: Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Elizabeth R
authors.initials: ER
authors.lastname: Sibilsky Enselman
authors.affiliation: Department of Radiology, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Jon A
authors.initials: JA
authors.lastname: Jacobson
authors.affiliation: 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.
authors.forename: Dennis R
authors.initials: DR
authors.lastname: Claflin
authors.affiliation: School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.
authors.forename: Sarah
authors.initials: S
authors.lastname: Calve
authors.affiliation: Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
authors.forename: Asheesh
authors.initials: A
authors.lastname: Bedi
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D000368:Aged; D005109:Extracellular Matrix / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D006801:Humans; D008264:Macrophages / Q000473:pathology; D008297:Male; D046529:Microscopy, Electron, Transmission; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000473:pathology / Q000502:physiology / Q000648:ultrastructure; D009133:Muscular Atrophy / Q000473:pathology / Q000503:physiopathology; D009210:Myofibrils / Q000473:pathology / Q000648:ultrastructure*; D017006:Rotator Cuff / Q000473:pathology*; D000070636:Rotator Cuff Injuries; D012518:Sarcomeres / Q000473:pathology / Q000648:ultrastructure; D013708:Tendon Injuries / Q000473:pathology*
keywords: Rotator cuff; fatty degeneration; macrophages; myosteatosis; permeabilized muscle fibers; sarcomeres