Optimized Modeled Myofascial Release Enhances Wound Healing in 3-Dimensional Bioengineered Tendons: Key Roles for Fibroblast Proliferation and Collagen Remodeling.

Autor: Zein-Hammoud M; Department of Basic Medical Sciences, University of Arizona, College of Medicine, Phoenix, Arizona., Standley PR; Department of Basic Medical Sciences, University of Arizona, College of Medicine, Phoenix, Arizona. Electronic address: standley@email.arizona.edu.
Jazyk: angličtina
Zdroj: Journal of manipulative and physiological therapeutics [J Manipulative Physiol Ther] 2019 Oct; Vol. 42 (8), pp. 551-564. Date of Electronic Publication: 2019 Nov 23.
DOI: 10.1016/j.jmpt.2019.01.001
Abstrakt: Objective: The purpose of this study was to evaluate the mechanisms of action of optimized myofascial release (MFR) on wound healing using a 3-dimensional human tissue construct.
Methods: Bioengineered tendons were cultured on a deformable matrix, wounded using a steel cutting tip, then strained in an acyclic manner with a modeled MFR paradigm at 103% magnitude for 5 minutes. Imaging and measurements of the width and wound size were performed daily, and the average tissue width of the entire bioengineered tendon was measured, and wound size and major and minor axes of the elliptical wound were additionally measured. Assessments of actin and collagen were performed by immunofluorescence, and Gomori's trichrome staining and fibroblast nuclei deposition was quantified using the CellProfiler analysis software.
Results: Optimized modeled MFR treatment significantly reduced the wound size and increased both collagen density and cell deposition at the wound site. All measures of wound healing improvements required the presence of proliferating fibroblasts.
Conclusion: Myofascial release-induced cell deposition and collagen density at wound sites required actively proliferating fibroblasts. If clinically translatable, our results support a mechanism by which MFR improves patient wound healing.
(Copyright © 2019. Published by Elsevier Inc.)
Databáze: MEDLINE
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