Extracorporeal Shockwave Therapy

“After shockwave therapy, we see structural deterioration in tissue… [his] tendon looked worse than when he had his tear.” -Seth O’Neill

Seth O’Neill delivered an outstanding presentation at this year’s Tendon Summit, covering topics such as the debated relationship between tendon structure and pain, the tendon’s capacity for long‑term adaptation, the role of contraction type in management, the emerging evidence linking calf pathology to ACL injury risk, and several other clinically relevant aspects of tendinopathy.

A consequential theme in his talk was the importance of accurately identifying the specific pathological subgroup rather than treating all Achilles tendinopathies as a single, homogeneous entity. Seth argues that many underwhelming clinical trials likely stem from poor subgroup delineation, with different pathological phenotypes responding in markedly different ways to the same treatment approach.

One case study he highlighted involved an athlete with an intra‑tendon tear who experienced significant structural deterioration following Extracorporeal Shockwave Therapy (ESWT).

Longitudinal UTC scans revealed the athlete’s combined Echo Type III and IV percentages (representing disorganized to amorphous matrix structure)  increased from just over a combined 20% of the tendon to almost 40% immediately after ESWT treatment.

Seth’s lecture covered far more than we can address here, but this case provides a useful opportunity to zoom in on ESWT and examine what current evidence suggests about its clinical utility in Achilles tendinopathy.

The Tendinopathy Microenvironment: Why Mechanisms Matter

Healthy tendons maintain low vascularity through either reduced expression of pro‑angiogenic factors or active production of anti‑angiogenic signals. In contrast, tendinopathic tendons demonstrate hypervascularization, altered perfusion responses to exercise, and increased blood flow that correlates with pain [1]. Tendinopathy develops within a complex biological environment shaped by mechanical stress, inflammation, and vascular changes. Although many in performance and rehabilitation focus primarily on mechanical loading, it is important to recognize that these three drivers influence one another and create a self‑reinforcing cycle that disrupts normal tendon homeostasis [2].

This broader context matters when evaluating any proposed intervention, including ESWT, because many of the mechanisms attributed to shockwave therapy are positioned as ways to influence these same mechanical, inflammatory, and vascular processes [3-6].

ESWT delivers high-amplitude acoustic pulses with the intention of eliciting mechanobiological responses [4]. These pulses can be delivered as focused or radial energy, where focused shockwaves target deeper structures, while radial shockwaves generate lower amplitude pressure waves that mainly affect superficial tissues (Korkakais). In tendon tissue, the sound waves are claimed to impose physical strain on tenocytes and the surrounding extracellular matrix, converting mechanical stimuli into biochemical signals [4].

Across recent reviews, ESWT is described as influencing a broad range of biological processes:

• “improve tissue healing and alter pain responses through central or peripheral mechanisms.” [3]

• “promotes angiogenesis, (facilitates) the formation of new capillaries, alters nociceptive signaling, and potentially reverses degenerative changes.” [4]

• “stimulates vascular regeneration, angiogenesis, and increased blood flow, all contributing to tissue healing and inflammation reduction…to address pain and facilitate tissue repair.” [5]

• ”stimulate tissue healing through multiple mechanisms, including neovascularization, enhanced blood supply, increased growth factor expression, anti-inflammatory effects, and stimulation of collagen synthesis.” [7]

These wide‑reaching claims would make ESWT appear to be an undisputed positive.

But one claim should raise a red flag for anyone looking closely.

A recurring theme in ESWT literature is the notion that increased vascularity is beneficial for tendon healing.  Angiogenesis may support oxygenation and the subsequent nutrient delivery which is required for positive adaptations to occur. However, this rationale warrants careful scrutiny as hypervascularization is a hallmark of tendinopathy.

The broader literature on tendon vascularization is conflicted regarding angiogenesis. Some authors support the stimulation of angiogenesis as beneficial while others suggest that inhibiting vessel formation (or even actively promoting vessel regression) may also contribute to improved outcomes [1]. A controlled balance appears important, as excessive angiogenesis can promote fibrosis, disorganized collagen deposition, adhesion formation, and impaired mechanical strength [1]. 

The detailed mechanisms of action are extensive but not without controversy. Obtaining in‑vivo human data remains difficult, and many of the proposed mechanisms are inferred from animal studies or in‑vitro models [1-6]. While this is an area we plan to explore in depth in the Tendon Summit Insider, it is beyond the scope of the current Debrief. Instead, we will sidestep the mechanistic debate for now and take a closer look at outcomes. We do not want to spend an exorbitant amount of time discussing a theoretical fire if we do not see any smoke.

Reconciling the Reviews

Of the four reviews cited above: they appear to be providing starkly different interpretations of the literature. Understanding why requires looking closely at what each review actually evaluated and how their methodological choices shaped their conclusions.

Prasanth reports ESWT provided reductions in pain (VAS), improved functional scores (VISA-A, RM, AOFAS), and “structural recovery.” Majidi echoed these sentiments, stating: “The overall findings of the meta-analysis demonstrated a significant reduction in pain with the use of ESWT” [4,5]. Taken at face value, these reviews suggest ESWT may offer meaningful clinical benefit. 

But Korakakis challenges these results, claiming the conclusions are limited by various shortcomings.

One of the main contentions is that there was insufficient weighing of SWT’s comparative effects against sham controls. Without adequate sham comparison, it becomes difficult to determine whether observed improvements reflect a true treatment effect rather than merely placebo responses.

Ni’s paper directly addresses this concern, by excluding any trials which did not include a sham arm within their study. When doing so, the results showed no significant differences between ESWT and sham groups in pain or patient reported outcomes [7].

They also performed extensive subgroup analyses to explore whether specific clinical profiles might respond differently. A small signal emerged for patients with symptoms of less than 12 months, but Ni emphasized that this “benefit is transient and not robust,” arising only from exploratory subgroup analyses.

A second main argument raised by Korakakis concerns the lack of sufficient differentiation between tendinopathy types in prior reviews. This includes both the pooling of different tendons and the failure to distinguish midportion from insertional Achilles tendinopathy. 

When re-examining Prasanth and Majidi through this lens, these limitations become apparent. Prasanth’s work only included 1 study pertaining to Achilles tendinopathy (which did not measure any structural qualities) and Majidi’s paper only included 2 (one of which was the same study included within the Prasanth review).

Given these parameters, it is unsurprising that Korakasis’ review found no significant differences in disability outcomes or pain scores between intervention and control groups.

Their conclusion does not mince words:

“We cannot recommend the use of SWT for either insertional Achilles tendinopathy or midportion Achilles tendinopathy.” [3]

Nail in the Coffin?

It would be easy to write off the use of ESWT at this point.

Caution is urged. Doing so may be premature and intellectually dishonest.

None of the above reviews touched on the primary concern Seth brought forth in his case study: impact on the physical structure. While structure is very likely to impact broader categories of pain and reported function, these measures are not synonymous (echoes back to our previous discussion of effectiveness vs efficacy). So even though these reviews indicate little global impact in the areas investigated, the picture may be incomplete.

“Averages lie. Averages are useless”

Seth bombastically made this statement within his lecture to draw attention to how many (in his opinion) misinterpret literature discussing the link between tendon structure and outcomes. The same point could be made regarding ESWT. When grouping results, important within‑subject adaptations may be obscured.

A case report by Hsu illustrates this possibility. In contrast to the deterioration observed in Seth’s athlete, Hsu documented observable improvement in hypoechoic lesions following ESWT [8].  This single case does not overturn the broader evidence, but it does reinforce the need to examine structural responses more closely.

As noted previously, Seth argued that tendinopathies cannot be treated as a singular, homogenous group. Specific treatment approaches are warranted to match the exact pathology in front of us. It is possible that distinguishing features exist that render shockwave therapy beneficial for certain presentations and could explain the divergent structural responses observed across cases.

Although there are no systematic reviews that focus primarily on structural changes in response to ESWT, a few clinical trials provide preliminary insight.

In healthy adults, Leong reported transient alterations in Achilles tendon structure following radial ESWT. Echo type I decreased and echo type II increased three hours after the first session, yet both returned to baseline before week two, with no further structural changes detected across later sessions. These findings suggest that ESWT produces a brief, reversible alteration in tendon organization in healthy tissue rather than a cumulative structural effect [9]. 

In individuals diagnosed with Achilles tendinopathy, Gatz found no significant structural alterations over time when assessed with UTC, power Doppler, or B‑mode ultrasound. Only shear wave elastography detected increased compliance in the ESWT point‑focused group. This indicates that while ESWT may influence certain mechanical properties, these changes do not appear to translate into detectable improvements in tendon structure across imaging modalities [10]. 

Taken together, these findings show relative insignificance in structural outcomes. So while individual responses may vary in ways group‑level analyses cannot fully capture, we have failed to tease out any differentiating factors. 

Conclusion:

Across reviews, clinical trials, and case reports, ESWT presents a complicated and often contradictory picture. Group‑level analyses consistently show limited impact on pain, disability, or functional outcomes when compared with sham controls, and Achilles‑specific evidence remains sparse. Yet individual cases, including those highlighted by Seth and Hsu, demonstrate that structural responses can diverge meaningfully within single tendons even when averaged results suggest little overall effect.

This tension reinforces a central theme from Seth’s lecture. Achilles tendinopathy is not a single condition. It is a collection of distinct pathological subgroups, each with its own structural profile, loading history, and biological behavior. When these presentations are pooled, meaningful differences may be diluted, and interventions that may influence specific phenotypes appear ineffective at the aggregate level.

The current evidence landscape suggests that ESWT is unlikely to provide broad or reliable benefit for Achilles tendinopathy as a whole. At the same time, dismissing the modality entirely may be premature.

Our responsibility is to guide clinical decisions with the strongest data currently supported by research while staying attentive to emerging patterns that may refine future practice.

We cannot anchor our beliefs in a position of ignorance. Assumed, but untested, parameters that might influence ESWT’s effectiveness cannot outweigh the evidence currently available. At the same time, we need to remain open to updating our understanding as more specific pathological features are identified and better‑designed studies clarify which tendons, under which conditions, respond in meaningful ways.

Next up, we review the lecture from Scot Morrison— a look at Management and Decision Making Frameworks and Models

Debrief written by: Jason Eure, PT, DPT, OCS, CSCS

Reference List

1) H Tempfer and A Traweger (2025) ‘Vascular dynamics in tendon health and pathology: exploring mechanisms and therapeutic opportunities’, European Cells and Materials, 53, pp. 65–81. Available at: https://doi.org/10.22203/ecm.v053a06.

2) Gehwolf R, Tempfer H, Cesur NP, Wagner A, Traweger A, Lehner C. Tendinopathy: The Interplay between Mechanical Stress, Inflammation, and Vascularity. Adv Sci (Weinh). 2025 Sep;12(36):e06440. doi: 10.1002/advs.202506440. Epub 2025 Aug 26. PMID: 40855996; PMCID: PMC12463082. 

3) Korakakis V, Kotsifaki R, Sotiralis Y, Malliaras P. Shockwave Therapy for Midportion and Insertional Achilles Tendinopathy: A Nail in the Coffin? A Systematic Review With Meta-Analysis. J Orthop Sports Phys Ther. 2026 May;56(5):282-299. doi: 10.2519/jospt.2026.13985. PMID: 42063301. 

4) K. Prasanth. et al. (2025) ‘Extracorporeal shockwave therapy for tendinopathies: a comprehensive literature review’, International Journal of Research in Medical Sciences, 13(8), pp. 3632–3637. Available at: https://doi.org/10.18203/2320-6012.ijrms20252447.

5) Majidi L, Khateri S, Nikbakht N, Moradi Y, Nikoo MR. The effect of extracorporeal shock-wave therapy on pain in patients with various tendinopathies: a systematic review and meta-analysis of randomized control trials. BMC Sports Sci Med Rehabil. 2024 Apr 24;16(1):93. doi: 10.1186/s13102-024-00884-8. PMID: 38659004; PMCID: PMC11041007.

6) Ulusoy İ, Yılmaz M, Tantekin MF, Güzel İ, Kıvrak A. There Is No Role for Extracorporeal Shock Wave Therapy in Chronic Insertional Achilles Tendinopathy: A Comparative Study with Conservative Treatment. J Am Podiatr Med Assoc. 2026 Apr 24;116(3):24. doi: 10.3390/japma116030024. PMID: 42200987. 

7) Ni T, Zhao Y, Pang L, Fu W. Extracorporeal shockwave therapy versus sham extracorporeal shockwave therapy for chronic Achilles tendinopathy: a meta-analysis of randomized controlled trials. PeerJ. 2026 Jan 6;14:e20506. doi: 10.7717/peerj.20506. PMID: 41522497; PMCID: PMC12786123. 

8)  Hsu YC, Wu WT, Chang KV, Han DS, Chou LW. Healing of Achilles tendon partial tear following focused shockwave: a case report and literature review. J Pain Res. 2017 May 19;10:1201-1206. doi: 10.2147/JPR.S132951. PMID: 28579818; PMCID: PMC5449124.

9)  Leong HT, Docking S, Girdwood M, Bonello C, Cook J, Rio E. Extracorporeal Shock Wave Therapy Immediately Affects Achilles Tendon Structure and Widespread Pressure Pain Thresholds in Healthy People: A Repeated-Measures Observational Study. Am J Phys Med Rehabil. 2019 Sep;98(9):806-810. doi: 10.1097/PHM.0000000000001203. PMID: 31021822.

10) Gatz M, Schweda S, Betsch M, Dirrichs T, de la Fuente M, Reinhardt N, Quack V. Line- and Point-Focused Extracorporeal Shock Wave Therapy for Achilles Tendinopathy: A Placebo-Controlled RCT Study. Sports Health. 2021 Sep-Oct;13(5):511-518. doi: 10.1177/1941738121991791. Epub 2021 Feb 13. PMID: 33586526; PMCID: PMC8404720.