Biology Reference
In-Depth Information
Figure 3.1 Schematic drawing depicting the sites of action by shock waves in various
tissues (with the exception of peripheral nerves). The target cells of shock wave treat-
ment are embedded in the extracellular matrix, surrounded by various other cell types,
including resident and invading mononuclear and polymorphonuclear immune cells.
ESWT has been proved to induce the release of growth factors (e.g., FGF-2) from the
cells surrounding the target cells, to improve angiogenesis within the tissues, and to
reduce the secretion of inflammatory cytokines and the invasion of immune cells. On
the other hand, tissue-specific target cells are known to secrete factors such as
hypoxia-inducible factor-1 (HIF-1). Several of these processes are regulated via the acti-
vation of nitric oxide synthase (NOS); it should be noted that the extent to which these
processes are induced varies with the type of tissue (ECM, extracellular matrix; ERK,
extracellular signal-regulated kinase; FGF-2, fibroblast growth factor-2; VEGF-A, vascular
endothelial growth factor-A; SW, shock waves).
calcitonin gene-related peptide. However, a second application of the same
dose of shock waves had a cumulative effect on the treated nerves, leading to
delayed reinnervation (
Takahashi, Ohtori, Saisu, Moriya, &Wada, 2006
). It
appears, therefore, that shock wave-treated nerves develop a “memory
effect” after the first treatment, and ESWT repeated shortly after the first
treatment is not beneficial. It is expected that ESWT induces subtle changes
in the affected neurones whose axons have been treated.
Murata et al. (2006)
detected an increased expression of activating transcription factor 3 (ATF-3)
and growth-associated phosphoprotein 43 (GAP-43) in dorsal root ganglion
neurones of shock wave-treated rats, indicating that the molecular changes
after ESWT are not restricted to the treated axons: their cell bodies are also
