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unions in dogs [ 32 ]. Wang et al demonstrated that shock wave therapy enhanced callus
formation and induced cortical bone formation in acute fractures in dogs and the effect of
shockwave therapy appeared to be time
- dependent [ 33 ]. Forriol et al, however, reached an
alternative conclusion and thought that shockwave treatment might delay bone healing
[
34 ]. The conflicting results are due different types of animals and different shockwave
dosages used. Wang et al had demonstrated that high - energy shockwave therapy produces
a significantly higher bone mass including BMD (bone mineral density), callus size, ash
and calcium contents, and better bone strength than the control group after fractures of the
femurs in rabbits. The effects of low
- energy shockwave therapy were less prevailing with
comparable results as compared to the control. Therefore, the effect of shockwave therapy
on bone mass and bone strength appeared to be dose
- and time - dependent [ 35 ]. Many
other studies also investigated the effect of shockwave therapy on bone healing in
animals. The important findings included superoxide mediates shockwave induction of
ERK
- dependent osteogenic transcription factor (CBFA - 1) and mesenchymal cells
differentiation toward osteoprogenitors [ 36 ]. Extracorporeal shockwave promotes bone
marrow stromal cell growth and differentiation toward osteo - progenitors associated with
TGF - β1 and VEGF induction [ 37 ]. Physical shockwave mediates membrane
hyperpolarization and Ras activation for osteogenesis in human bone marrow stromal
cells [
38 ], Shockwave promotes bone regeneration by the recruitment of mesenchymal
stem cells and expressions of TGF - β1 and VEGF [ 39 ].
Shockwave therapy for insertional tendinopathy
Many studies investigated the effect of shockwave therapy on insertional tendinopathies.
Rompe et al demonstrated dose
- related effects of shockwave on rabbit tendo Achilles, and
suggested that energy flux density of more than 0.28 mJ/mm
2
should not be used
clinically in the treatment of tendon disorders [ 40 ]. In their study, a statistically significant
increase of capillary formation was noted with higher energy shock wave (0.60 mJ/mm
2
),
which also caused more tissue reaction and potential damage to the tendon tissue. Wang et
al had demonstrated that shockwaves enhance neovascularization with formation of new
capillary and muscularized vessels at the tendon
- bone junction of the Achilles tendons in
dogs [ 41 ]. In another study in rabbit model, Wang et al further demonstrated that
shockwave therapy induces the ingrowth of neo - vessels (neovascularization) including
capillary and muscularized vessels than the control at the tendon - bone junction.
Shockwave therapy releases angiogenetic growth and proliferating factors including e
NOS, VEGF, and PCNA [ 42 ]. The e NOS and VEGF began to rise in as early as one
week and remained high for 8 weeks, then declined to baseline in 12 weeks; whereas the
increase of PCNA and neo
- vessels began in 1 weeks and persisted for 12 weeks and
longer. Therefore, the mechanism of shockwave therapy may have involved the
improvement in agniogenetic growth factors, which in turn induce neovascularization and
improve blood supply at the tendon
- bone junction of the Achilles tendon in rabbits.
Chronic tendinopathy is an overuse syndrome manifested with pain and tenderness due to
mucoid and chondroid degeneration and formation of plump tenocytes and increased
fibroblastic and myofibroblastic cells and absent inflammatory cells [
43 ]. Some studies
reported that chronic painful tendinopathy exhibited increased occurrence of sprouting
nonvascular sensory, substance P
- positive nerve fibers and decreased occurrence of
vascular sympathetic nerve fibers, and suggested that the altered sensory - sympathetic
innervation may play a role in the pathogenesis of tendinopathy [44].