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(connecting two media, each with a different density; e.g. oil/water) and pass through homogenous elastic tissue without damage to the majority of the area is medically important. Unfocused extracorporeal shockwaves radially spread with an energy flow density per pulse smaller than 0.1 mJ/mm2 2,3


, which decrease


the power by one third for every centimeter that penetrates into the tissue.


Biological effects of HERST The stimulating effect of defocused e x tr acor pore al-gener at ed shockwaves on biological processes within the tissues reached has increasingly become the centre of interest over the last few years. The biological mechanism of action after a shockwave is still unknown to a large extent. Biological reactions of liberation of different agents (measured


by


immunohistochemistry) such as vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (ENOS), and proliferating cell nuclear antigen (PCNA) have been reported4,5


.


On the subcellular level, the damages are the increase of permeability of the cell membrane6 lesions of the cytoskeleton7


, , and


changes to the mitochondria, endoplasmatic reticulum, and nuclear membrane of the cell that may lead to apoptosis8


. Shockwaves


are also effective as a means of increasing local blood circulation and metabolism, as well as having a high antibacterial effect.


Pathophysiology of cellulite Nobody can deny that the term ‘cellulitis’ has been misused, because


Figure 2 Shockwave therapy from Zimmer


MedizinSysteme (ZWave®) prime-journal.com | June 2012 ❚ 57


Figure 1 Treatment of the left thigh with shockwave therapy (ZWave®)


in medicine the suffix ‘itis’ refers to an inflammation or infection. Therefore, ‘cellulitis’ might refer to any inflammation of the cells involved. In cellulite, there is no inflammation or infection, but perhaps an alteration of interstitial tissues. There was a time when cellulite was thought to be a mere increase of fat in subcutaneous tissues associated with an altered


lymphatic and venous flow, and lymphatic stasis. Furthermore, there was a deeply rooted notion that cellulite was closely related to the specific stasis subsequent to hypotonia or venous and lymphatic disease. It was therefore assumed that a previous varicose disease should exist for cellulite to appear. In fact, this is infrequently true. Most often, the interstitial


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