The effect of focused extracorporeal shock wave therapy on collagen matrix and gene expression in normal tendons and ligaments

Summary

Reasons for performing study: Extracorporeal shock wave therapy (ESWT) is frequently used in equine practice, but little is known about its biological action.

Objectives: To study the effects of ESWT on matrix structure and gene expression levels in normal, physiologically loaded tendinous structures in ponies.

Methods: Six Shetland ponies, free of lameness and with ultrasonographically normal flexor and extensor tendons and suspensory ligaments (SL), were used. ESWT was applied at the origin of the suspensory ligament and the mid-metacarpal region of the superficial digital flexor tendon (SDFT) 6 weeks prior to sample taking, and at the mid-metacarpal region (ET) and the insertion on the extensor process of the distal phalanx (EP) of the common digital extensor tendon 3 h prior to tendon sampling. In all animals one forelimb was treated and the other limb was used as control. After euthanasia, tendon tissue was harvested for real-time PCR to determine gene expression levels and additional samples were taken for histological evaluation and biochemical analyses

Results: Histologically a disorganisation of the normal collagen structure was observed 3 h after ESWT, remnants of which were still visible after 6 weeks. While degraded collagen levels showed an increase at 3 h post treatment (P = 0.012) they were reduced at 6 weeks post ESWT (P = 0.039). Gene expression for both COL1 (P = 0.004) and MMP14 (P = 0.020) was upregulated at 6 weeks after treatment.

Conclusions: Exposure of normal tendinous tissue to ESWT is not uneventful; it leads to a disorganisation of matrix structure and changes in degraded collagen levels. The upregulation of COL1 expression 6 weeks after ESWT may be indicative for repair.

Potential relevance: The observed disorganisation of the collagen network warrants caution when using ESWT. Exposing noninjured tissue to ESWT should be avoided and it may be advisable to restrict exercise in recently treated patients. However, the induced tissue disorganisation might also be a trigger for repair in chronic tendinopathies.