Discussion

Ever since the first application of extracorporeal shock waves damage to the kidney, liver, and lung has been described. With regard to the musculoskeletal system, chondroid metaplasia of muscle as well as influences on bony healing have been reported (Haupt 1997). In a review article, Rompe et al. (1997) list animal studies propagating positive effects on osteo-genesis (Ekkernkamp et al. 1992, Graff 1989, Haupt et al. 1992, Johannes et al. 1994) and compare them to reports on negative influences (Augat et al. 1995, Forriol et al. 1994, Graff et al. 1988, Perren 1993, Seemann et al.

1992, Yeaman et al. 1989), focusing on osteo-cyte damage, dysplasia of the growth plates, delay of fracture healing, and a decrease in mechanical stability. With regard to experimental and clinical studies, the author concludes that to date there is no clear evidence of osteo-genetic effects of high-energy shock waves.

To our knowledge, no comparable in vivo examinations have been published on tendons. In a recent lecture Maier et al. (2001) reported in vitro experiments with calcified turkey tendons. While energy flux densities of 0.5mJ/mm2 did not lead to decreased tensile strength after 1500 shock wave impulses, energy flux densities of 0.9 and 1.2mJ/mm2 significantly reduced tensile strength of the tendon. Schmitz (2001) reported about cellular and molecular investigations after SWA to the noninjured distal rabbit femur. Focussing on the quadriceps tendon lying in the shock wave field, he confirmed the data reported by Rompe et al. (1998a) for the Achilles tendon. Beginning at an energy flux density of 0.5 mJ/ mm2 there were signs of matrix alterations within the tendon, and edemaotus swelling of the paratenon.

Nevertheless, there is vast experience concerning tendon reaction after mechanical injuries with regenerating processes starting from the surrounding soft tissues (extrinsic healing) but also from the tendon itself (intrinsic healing). Among sheathless tendons the rabbit Achilles tendon has been investigated most intensively (Hefti and Stoll 1995). The alterations described range from necrosis, granulocyte invasion, thickening of the para-tenon, capillary proliferation, proliferation of extracellular matrix with chondroid metaplasia, and finally replacement of granulation tissue by scar tissue. A restitutio ad integrum cannot be expected (Gelberman et al. 1991, Kvist et al. 1987, Mohr 1987, Postacchini et al. 1987).

The present study demonstrated an animal model to reveal the chronological reaction of rabbit Achilles tendon and paratenon upon the administration of extracorporeal shock waves. Ultrasound, as a widely available tool for the assessment of tendopathies, did not reveal any direct injury to the rabbit Achilles tendon. On the other hand, there was a dose-dependent increase in the A-P tendon diameter and evidence of fluid accumulation in the adjacent soft tissues. As far as muscular and bony structures could be evaluated no damage was observed. Depending on the intensity of the shock waves histopathological changes associ ated with blunt trauma were observed, i.e., degenerative alterations of tendon, inflammatory cells, increased numbers of capillaries, as well as edema and fibrosis in the paratenon. Although the extent of histopathological changes varied among the experimental animals within each treatment group, there was a marked increase in alterations exhibited both in tendon and paratenon with growing shock wave intensity. Similar observations have been published for various soft-tissue organs after high-energy SWA. However, it must be made clear that the results of the animal model cannot be directly extrapolated to humans and that the energy levels in rabbits are not directly comparable to energies used in humans. Nevertheless, when correlating our sonographical and histopathological data with the postraumatic findings in the literature we conclude that up to an energy flux density of 0.28mJ/mm2 there is no evidence of marked damage to tendon and adjacent tissues. All changes observed were reversible within 4 weeks. At an energy flux density of 0.60 mJ/ mm2 there was marked damage to the tendon and paratenon with an increase of tendon diameter, fibrinoid necrosis, and inflammatory and reparative peritendinous reactions. These changes had not completely disappeared after 4 weeks, and decrease of tensile strength might be anticipated, resulting in partial or complete tears of the tendon.

Clinically, in ultrasound or in magnetic resonance image (MRI) examinations, we did not find any signs of traumatic tendon alterations after extracorporeal SWA in over 300 patients now followed for at least 2 years, with the maximum energy flux density applied being 0.28 mJ/mm2. For fear of ruptures in already damaged tendons, we do not recommend high-energy shock waves for the treatment of tendon pathologies in humans until further studies have been performed.

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