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Article Abstract

Background: Rotator cuff tears (RCTs) are a common shoulder pathology associated with degenerative muscle changes, including fatty accumulation (myosteatosis), muscle atrophy, and fibrosis. The purpose of this study was to utilize immunohistochemistry to analyze muscle changes associated with RCT and compare histologic features with magnetic resonance imaging results across all RCT types and sizes.

Methods: Rotator cuff muscle biopsies were obtained from 99 patients undergoing shoulder surgery. Twenty-nine patients without an RCT served as controls. Biopsy specimens were stained using LipidTOX to examine myosteatosis, while LAMININ and FIBRONECTIN immunohistochemistry staining were used to quantify myofiber cross-sectional area and fibrotic tissue abundance, respectively. Rotator cuff muscles were graded according to Goutallier classification.

Results: Myosteatosis was significantly higher in full-thickness tears compared with control no-tears (P = .0016) and partial-thickness tears (P = .0050). Massive full-thickness tears had significantly more myosteatosis than controls (P = .0019) and partial-thickness tears (P = .0037). Muscle biopsies from patients with a Goutallier classification of 2+ had significantly more myosteatosis than those with a Goutallier classification of 0 (P = .0001). Muscle biopsy specimens from full-thickness tears had significantly smaller myofiber cross-sectional areas when compared with partial-thickness tears (P < .0001) and controls (P < .0001). The extent of FIBRONECTIN abundance did not differ between groups.

Conclusion: With the largest known collection of human rotator cuff muscle specimens for histologic analysis, we found full-thickness tears develop significantly greater fatty accumulation and muscle atrophy. We do not find a correlation between FIBRONECTIN abundance and RCT type or size, indicating that further research is necessary to determine the extent of fibrosis correlation to RCT and poor outcomes following RCT repair surgery.

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http://dx.doi.org/10.1016/j.jse.2025.03.040DOI Listing

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