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Transtendinous Rotator Cuff Tear Repair with Bone Marrow Aspirate Concentrate Dermal Allograft Augmentation.

ABSTRACT: Rotator cuff tears involving the musculotendinous junction with a significant amount of tendon still attached to the footprint laterally represent a challenging scenario for shoulder arthroscopists. Because of these challenges, adjunctive techniques to bridge tissue gaps may be required, and biologic augmentation may be considered to improve the healing environment. The following technique presents a stepwise approach to accomplishing the dual goals of a stable anatomic repair and biologic augmentation of this difficult pattern of rotator cuff pathology.

SUBMITTER: Neff P

PROVIDER: S-EPMC8085041 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Myosteatosis is the pathological accumulation of lipid that occurs in conjunction with atrophy and fibrosis following skeletal muscle injury or disease. Little is known about the mechanisms by which lipid accumulates in myosteatosis, but many studies have demonstrated the degree of lipid infiltration negatively correlates with muscle function and regeneration. Our goal was to identify biochemical pathways that lead to muscle dysfunction and lipid accumulation in injured rotator cuff muscles, a model that demonstrates severe myosteatosis. Adult rats were subjected to a massive tear to the rotator cuff musculature. After a period of either 0 (healthy control), 10, 30, or 60 days, muscles were prepared for RNA sequencing, shotgun lipidomics, metabolomics, biochemical measures, electron microscopy, and muscle fiber contractility. Following rotator cuff injury, there was a decrease in muscle fiber specific force production that was lowest at 30d. There was a dramatic time dependent increase in triacylglyceride content. Interestingly, genes related to not only triacylglyceride synthesis, but also lipid oxidation were largely downregulated over time. Using bioinformatics techniques, we identified that biochemical pathways related to mitochondrial dysfunction and reactive oxygen species were considerably increased in muscles with myosteatosis. Long chain acyl-carnitines and L-carnitine, precursors to beta-oxidation, were depleted following rotator cuff tear. Electron micrographs showed injured muscles displayed large lipid droplets within mitochondria at early time points, and an accumulation of peripheral segment mitochondria at all time points. Several markers of oxidative stress were elevated following rotator cuff tear. The results from this study suggest that the accumulation of lipid in myosteatosis is not a result of canonical lipid synthesis, but occurs due to decreased lipid oxidation in mitochondria. A failure in lipid utilization by mitochondria would ultimately cause an accumulation of lipid even in the absence of increased synthesis. Further study will identify whether this process is required for the onset of myosteatosis.

Dataset Information

Transtendinous Rotator Cuff Tear Repair with Bone Marrow Aspirate Concentrate Dermal Allograft Augmentation.

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