Extracorporeal softwave therapy (ESWT) is widely used in clinical practice. In addition to its original use in kidney stone disintegration, shock waves are now used for the treatment of a variety of regenerative indications. Mechanotransduction stimulates the body’s biological healing processes at the cellular level. In areas of wound healing, orthopaedics or erectile dysfunction, very good, well-founded treatment successes are achieved.
The molecular mechanism of action is based on the activation of cellular signaling molecules which stimulate the blood circulation (vascularisation) of the affected tissue. 1–7 Shock waves induce the proliferation and migration of cells, have anti-apoptotic, anti-inflammatory as well as analgesic effects. 1,2,8–20
Benefits of SoftWave Therapy in neuronal regeneration:
Studies have shown that ESWT has a positive effect on the expression of important growth factors such as BNDF (brain-derived neurotrophic factor), BMP (bone morphogenetic protein) and TGF-β (transforming growth factor), FGF-2 (fibroblast growth factor), IGF-1 (insulin growth factor) and PCNA (proliferating cell nuclear antigen). 21–26 In particular, the proangiogenic factor VEGF (the vascular endothelial growth factor) and its associated receptor VEGF-R2 are upregulated. 27–29 Studies indicate that VEGF exerts a neuroprotective effect and prevents secondary damage to neural tissue after spinal cord injury. 29,30 These studies showed that VEGF stimulates endothelial and neural cells, acts neurotropically and neuroprotectively, and promotes neural cell division. Blocking of the VEGF signalling pathway led to cell death and after spinal cord injury, expression of VEGF decreased, which was associated with a worsening of the pathological condition. 29 Increased expression of VEGF and an improvement in tissue vascularization by ESWT therefore represent a promising treatment approach.
Recent research results in the rat model show that ESWT stimulates VEGF expression and angiogenesis after spinal cord injury and leads to an improved restoration of motor and sensory function.29,31–33 In particular, it has been shown that the use of low-energy shock waves does not lead to nerve tissue damage. 29
SoftWave Therapy stimulates the expression of VEGF, reduces secondary damage to injured nerve tissue and improves the restoration of motor function. Therefore, it would be desirable to use this innovative therapeutic strategy in everyday clinical practice to accompany the treatment of spinal cord injuries.
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- Mittermayr, R. et al. Extracorporeal Shock Wave Therapy (ESWT) Minimizes Ischemic Tissue Necrosis Irrespective of Application Time and Promotes Tissue Revascularization by Stimulating Angiogenesis. Ann. Surg. 253, 1024–1032 (2011).
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- Kisch, T. et al. Repetitive shock wave therapy improves muscular microcirculation. J. Surg. Res. 201, 440–445 (2016).
- Ellah, M. A. et al. Changes of renal blood flow after ESWL: Assessment by ASL MR imaging, contrast enhanced MR imaging, and renal resistive index. Eur. J. Radiol. 76, 124–128 (2010).
- Vardi, Y., Appel, B., Jacob, G., Massarwi, O. & Gruenwald, I. Can low-intensity extracorporeal shockwave therapy improve erectile function? A 6-month follow-up pilot study in patients with organic erectile dysfunction. Eur. Urol. 58, 243–248 (2010).
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- Cho, Y. S. et al. Effect of extracorporeal shock wave therapy on scar pain in burn patients: A prospective, randomized, single-blind, placebo-controlled study. Medicine (Baltimore). 95, e4575 (2016).
- Cai, Z. et al. Effects of Shock Waves on Expression of IL-6, IL-8, MCP-1, and TNF-alpha Expression by Human Periodontal Ligament Fibroblasts: An In Vitro Study. Med. Sci. Monit. 22, 914–921 (2016).
- Zhao, Z. et al. Extracorporeal shock-wave therapy reduces progression of knee osteoarthritis in rabbits by reducing nitric oxide level and chondrocyte apoptosis. Arch. Orthop. Trauma Surg. 132, 1547–1553 (2012).
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- Weihs, A. M. et al. Shock wave treatment enhances cell proliferation and improves wound healing by ATP release-coupled extracellular signal-regulated kinase (ERK) activation. J. Biol. Chem. 289, 27090–104 (2014).
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