Extracorporeal shock wave therapy in inflammatory diseases: molecular mechanism that triggers anti-inflammatory action.

Abstract: Shock waves (SW), defined as a sequence of single sonic pulses characterised by high peak pressure (100MPa), a fast rise in pressure (< 10 ns) and a short lifecycle (10 s), are conveyed by an appropriate generator to a specifictarget area at an energy density ranging from 0.03 to 0.11 mJ/mm2. Extracorporeal SW (ESW) therapy was first used onpatients in 1980 to break up kidney stones. During the last ten years, this technique has been successfully employed in orthopaedicdiseases such as pseudoarthosis, tendinitis, calcarea of the shoulder, epicondylitis, plantar fasciitis and severalinflammatory tendon diseases. In particular, treatment of the tendon and muscle tissues was found to induce a long-timetissue regeneration effect in addition to having a more immediate anthalgic and anti-inflammatory outcome. In keepingwith this, an increase in neoangiogenesis in the tendons of dogs was observed after 4-8 weeks of ESW treatment. Furthermore,clinical observations indicate an immediate increase in blood flow around the treated area. Nevertheless, thebiochemical mechanisms underlying these effects have yet to be fully elucidated.In the present review, we briefly detail the physical properties of ESW and clinical cases treated with this therapy. Wethen go on to describe the possible molecular mechanism that triggers the anti-inflammatory action of ESW, focusing onthe possibility that ESW may modulate endogenous nitric oxide (NO) production either under normal or inflammatoryconditions. Data on the rapid enhancement of endothelial NO synthase (eNOS) activity in ESW-treated cells suggest thatincreased NO levels and the subsequent suppression of NF-B activation may account, at least in part, for the clinicallybeneficial action on tissue inflammation.