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

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.

Modeled Osteopathic Manipulative Treatments: A Review of Their in Vitro Effects on Fibroblast Tissue Preparations.

A key osteopathic tenet involves the body's ability to self-heal. Osteopathic manipulative treatment (OMT) has been evolved to improve this healing capacity. The authors' in vitro work has focused on modeling 2 common OMT modalities: myofascial release (MFR) and counterstrain. Their studies have evaluated the effects of these modalities on wound healing, cytokine secretion, and muscle repair. The key components of the host response to mechanical forces are fibroblasts, which are the main fascial cells that respond to different types of strain by secreting anti-inflammatory chemicals and growth factors, thus improving wound healing and muscle repair processes. The purpose of this review is to discuss the cellular and molecular mechanisms by which MFR and other OMT modalities work, in particular, the role of strained fibroblasts in inflammation, wound healing, and muscle repair and regeneration. Changing MFR parameters, such as magnitude, duration, direction, and frequency of strain, might uniquely affect the physiologic response of fibroblasts, muscle contraction, and wound healing. If such results are clinically translatable, the mechanisms underlying the clinical outcomes of OMT modalities will be better understood, and these treatments will be more widely accepted as evidence-based, first-line therapies.

Duration and magnitude of myofascial release in 3-dimensional bioengineered tendons: effects on wound healing.

CONTEXT: Myofascial release (MFR) is one of the most commonly used manual manipulative treatments for patients with soft tissue injury. However, a paucity of basic science evidence has been published to support any particular mechanism that may contribute to reported clinical efficacies of MFR. OBJECTIVE: To investigate the effects of duration and magnitude of MFR strain on wound healing in bioengineered tendons (BETs) in vitro. METHODS: The BETs were cultured on a deformable matrix and then wounded with a steel cutting tip. Using vacuum pressure, they were then strained with a modeled MFR paradigm. The duration of MFR dose consisted of a slow-loading strain that stretched the BETs 6% beyond their resting length, held them for 0, 1, 2, 3, 4, or 5 minutes, and then slowly released them back to baseline. To assess the effects of MFR magnitude, the BETs were stretched to 0%, 3%, 6%, 9%, or 12% beyond resting length, held for 90 seconds, and then released back to baseline. Repeated measures of BET width and the wound's area, shape, and major and minor axes were quantified using microscopy over a 48-hour period. RESULTS: An 11% and 12% reduction in BET width were observed in groups with a 9% (0.961 mm; P<.01) and 12% (0.952 mm; P<.05) strain, respectively. Reduction of the minor axis of the wound was unrelated to changes in BET width. In the 3% strain group, a statistically significant decrease (-40%; P<.05) in wound size was observed at 24 hours compared with 48 hours in the nonstrain, 6% strain, and 9% strain groups. Longer duration of MFR resulted in rapid decreases in wound size, which were observed as early as 3 hours after strain. CONCLUSION: Wound healing is highly dependent on the duration and magnitude of MFR strain, with a lower magnitude and longer duration leading to the most improvement. The rapid change in wound area observed 3 hours after strain suggests that this phenomenon is likely a result of the modification of the existing matrix protein architecture. These data suggest that MFR's effect on the extracellular matrix can potentially promote wound healing.