 Introduction In the previous two blogs, we discussed pulsed electromagnetic field therapy (December 17, 2025) and acupuncture (November 15, 2025) as potential treatments for osteoarthritis (OA), and we cited two comparative studies reporting that extracorporeal shock wave therapy (ESWT) was more effective than both modalities (1,2). However, the small sample sizes of these trials, together with conclusions based solely on meta-analyses, make such claims potentially tenuous. Nevertheless, it remains valuable to examine ESWT in greater detail—specifically, to review the clinical evidence supporting its effectiveness and to discuss its proposed mechanisms of action. We also review the range of ESWT devices currently available on the market for both medical professionals and consumers. Two types of shock waves In ESWT, a focused shock wave is a high-pressure, nonlinear acoustic pulse characterized by an extremely rapid rise time (<10 ns), a high positive peak pressure (10–100 MPa), short pulse duration (~1–10 µs), a subsequent tensile (negative-pressure) phase, and a broad frequency spectrum ranging from kilohertz to megahertz. In most focused ESWT devices used in medical practice, shock waves are generated using one of three physical principles: electrohydraulic (spark-gap), electromagnetic, or piezoelectric mechanisms (3). By contrast, some devices produce so-called radial shock waves, which are generated by the impact of a ballistic projectile and result in radially dispersing pressure waves with maximal pressure at the applicator surface rather than at depth. From a physical standpoint, these waves are closer to pressure pulses than to true shock waves, and radial devices are therefore not generally considered genuine shock wave generators. The practical implications of this distinction will be discussed further below when device characteristics are examined. ESWT device characteristics Five parameters are commonly used to characterize an ESWT device: 1. Energy Flux Density (EFD) is the most important parameter. It represents the amount of energy delivered per unit area per pulse, measured in mJ/mm2. Devices are typically classified as low-, medium-, or high-energy, as shown below. EFD (mJ/mm²) Classification < 0.08 Low energy 0.08–0.28 Medium energy > 0.28 High energy 2. Peak pressure includes both the positive (P⁺) and negative (P⁻) pressure components. P⁺ reflects the compressive force and is important for mechanotransduction, whereas P⁻ produces cavitation and plays a key role in biological signaling as well as in assessing potential tissue risk. Typical P⁺ values for focused ESWT devices range from 20 to 100 MPa, whereas radial devices operate at much lower pressures, typically 1–10 MPa. That said, peak pressure alone can be misleading because it does not account for pulse duration or focal size. 3. Pulse rise time and duration also influence biological effects. In most ESWT systems, rise times are less than 10 ns and pulse durations range from 1 to 10 μs. Shorter pulses tend to deliver high instantaneous mechanical stress, minimize thermal effects, and preferentially activate mechanical signaling pathways. 4. Pulse repetition frequency for most devices ranges from 1 to 8 Hz. In clinical practice, the total number of pulses per session vary from 500 to 3000, depending on the indication. While pulse repetition frequency does not alter the EFD, it directly affect overall treatment duration. 5. Focal volume and penetration depth represent a major distinction between focused and radial ESWT. In focused ESWT, energy is concentrated within an ellipsoid focal zone located at depths of approximately 10-60 mm. In contrast, radial ESWT delivers its highest energy at the skin surface, with rapid attenuation such that penetration rarely exceeds 1–2 cm. Focused ESWT is therefore often preferred for osteoarthritis—particularly knee osteoarthritis—where therapeutic targets may include deeper periarticular tissues, entheses, and subchondral bone. Comparing ESWT devices When comparing ESWT devices, the most important features to consider are the type of shock wave (focused vs. radial), the EFD at the focal point (mJ/mm²), and the focal depth and volume. Equally important are pulse reproducibility and whether device parameters are measured and reported in accordance with IEC standards. Clinical studies using ESWT, should at a minimum, specify the EFD and the total pulse count delivered during treatment. Numerous educational videos are available online explaining the differences and clinical roles of focused and radial ESWT. Two accessible examples that provide a useful overview of both techniques—and how they may complement one another—include: Clinical Proofs that ESWT is effective in the treatment of knee osteoarthritis Multiple randomized controlled trials and meta-analyses (4–8) consistently show that ESWT reduces pain and improves function in patients with knee osteoarthritis when compared with sham treatment or other conservative interventions. In many studies, these benefits persist for weeks to several months. Several trials also demonstrate a dose–response relationship, with medium-energy protocols producing superior clinical outcomes compared with low-energy treatments (9–11). In addition, focused ESWT—which is capable of reaching deeper structures such as subchondral bone—may provide better joint-related outcomes than radial devices (12). A simplified summary of reported EFD ranges and associated biological effects is shown below:
Importantly, the beneficial effects of ESWT may extend even to patients with advanced disease. A recent study by CP, K. et al. (13) reported clinical improvements in patients with Kellgren–Lawrence (K–L) grade 4 osteoarthritis. Similarly, a randomized clinical trial by Choi, I.J. et al. (14) demonstrated reductions in suprapatellar effusion and improvements in inflammatory symptoms following ESWT, providing in vivo support for its anti-inflammatory effects. Evidence for true disease-modifying effects—such as structural preservation of articular cartilage—remains mixed and incomplete. Preclinical studies and mechanistic human data suggest that ESWT can stimulate subchondral bone remodeling and activate anabolic signaling pathways in chondrocytes, which are biologically plausible disease-modifying mechanisms. However, robust long-term randomized controlled trials incorporating quantitative MRI endpoints or histological evidence of slowed cartilage loss are still scarce. Notably, at least one randomized controlled trial (15) reported potential adverse effects on cartilage under a specific low-dose protocol, highlighting that not all ESWT treatment regimens are necessarily structurally protective. In summary, the evidence supporting symptomatic relief from ESWT in knee osteoarthritis is strong, whereas convincing proof of durable cartilage preservation in humans will require more standardized, long-term imaging-based clinical trials. Comparing ESWT with other therapies for osteoarthritis A systematic review and meta-analysis by Chen, L. et al. (16) compared ESWT with a wide range of treatment modalities across different forms of osteoarthritis. The analysis focused specifically on pain reduction and functional improvement. The overall findings are summarized in the table below.
“+” indicates results favoring ESWT over the comparator; “–” indicates comparable or superior results for the comparator; “?” indicates insufficient or inconsistent evidence. HA: hyaluronic acid; PRP: Platelet Rich Plasma These findings can be contrasted with the results reported by Cao, S. et al. (2), who restricted their analysis to non-pharmacological interventions for knee osteoarthritis—a study discussed previously in the November 15, 2025 blog on acupuncture for knee OA. Selected results from that analysis are reproduced below for comparison. Efficacy rankings based on the Visual Analog Scale (VAS) pain scores: shock wave therapy > needle-knife (acupotomy) > laser therapy > acupuncture > ultrasound > exercise > transcutaneous electrical nerve stimulation Efficacy rankings based on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) subscales:
The two datasets overlap in their comparison of ESWT with ultrasound and acupotomy (needle-knife). For ultrasound, the findings are consistent: ESWT outperformed ultrasound in both analyses. In contrast, the results for acupotomy diverge. Cao, S. et al. reported that ESWT was superior for both pain reduction and functional improvement, whereas Chen, L. et al. found acupotomy to perform as well as—or better than—ESWT in these same outcomes. These discrepancies highlight the need for well-designed, head-to-head randomized controlled trials directly comparing treatment modalities. Meta-analyses based on small, heterogeneous trials with variable protocols and controls have inherent limitations and should be interpreted with appropriate caution. ESWT Mechanism of Action Clinical studies indicate that ESWT typically employs low- to medium-energy flux densities to elicit beneficial biological responses in osteoarthritis without causing tissue damage. How this mechanical energy interacts with cells and biomolecules—and which molecular pathways translate these interactions into therapeutic effects—is therefore of considerable interest. A clearer understanding of these mechanisms can inform more rational ESWT protocol design tailored to specific patient populations. ESWT delivers very high peak stresses with an extremely rapid rise time to cellular structures, particularly cell membranes. The resulting steep spatial pressure gradients, together with cavitation effects, activate mechanotransduction pathways, many of which have been identified over the past two decades. Most mechanistic studies to date have been conducted in animal models or in isolated cells and tissues derived from cartilage and subchondral bone. Dose effect, angiogenesis, cartilage/subchondral bone remodeling A clear dose-dependent effect of ESWT was demonstrated by Wang, C.-J. et al. (17) using a surgically induced knee osteoarthritis (KOA) rat model. In this study, an optimal dose of 800 pulses delivered at an energy flux density of 0.22 mJ/mm², administered once or twice weekly, was sufficient to inhibit deterioration of both articular cartilage and subchondral bone in periarticular regions. These effects were assessed using X-ray imaging, histomorphological analysis, and immunohistochemistry. Articular cartilage integrity was evaluated by immunostaining for collagen type II and matrix metalloproteinase-13 (MMP-13), whereas subchondral bone remodeling and angiogenesis were assessed through immunostaining of von Willebrand factor (vWF), vascular endothelial growth factor (VEGF), bone morphogenetic protein-2 (BMP-2), and osteocalcin. The main biological effects observed in response to ESWT can be summarized as follows:
Effect on bone homeostasis Direct effects of ESWT on bone homeostasis—specifically on osteoblast and osteoclast differentiation—have been reported by Li, B. et al. (18) and Chen, B. et al. (19). Using cultured rabbit bone marrow–derived stem cells, these authors demonstrated that ESWT promotes differentiation toward osteoblasts, as shown by classical histochemical staining and mRNA profiling of osteogenesis-related markers, including alkaline phosphatase (ALP), osteocalcin (OCN), osteoprotegerin (OPG), and runt-related transcription factor 2 (Runx2). In vivo, using a rabbit model of osteoporosis, ESWT increased trabecular bone volume, number, and thickness, while reducing trabecular separation in the femur when compared with untreated controls. To examine effects on osteoclastogenesis, immortalized mouse macrophage RAW264.7 cells induced with receptor activator of nuclear factor κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) were used as a model system. In this context, ESWT inhibited differentiation into osteoclasts, as determined by histochemical staining and reduced mRNA expression of two key osteoclast markers, cathepsin K and dendritic cell–specific transmembrane protein (DC-STAMP). ESWT also suppressed cell proliferation and reduced expression of NFATc1 as well as p65, a subunit of the NF-κB transcriptional complex, indicating that inhibition of NF-κB signaling underlies the anti-osteoclastogenic effect. Consistent with these findings, ESWT increased trabecular bone volume, number, and thickness and decreased trabecular separation in mouse femora. The principal cellular effects of ESWT on bone homeostasis can be summarized as follows:
Zhao, Z. et al. (20) identified an additional molecular pathway mediating the effects of ESWT in subchondral bone–derived stem cells. Using primary human stem cells isolated from patients with knee osteoarthritis, the authors showed that ESWT increased colony-forming capacity in a dose-dependent manner. This effect was driven by enhanced proliferation without measurable changes in apoptosis. Although no significant effect on osteogenic differentiation was observed, ESWT strongly suppressed adipogenic differentiation and modestly enhanced chondrogenic differentiation. Expression of cartilage-related markers, including collagen type II and proteoglycans, was consistently higher than in untreated controls. Notably, these phenotypic changes were associated with increased expression of the mechanosensitive co-transcriptional regulators YAP and TAZ and their translocation into the nucleus. YAP/TAZ signaling is well recognized for its role in mechanotransduction, organ size regulation, tissue regeneration, wound healing, and stem cell maintenance. These effects may be summarized schematically as:
Finally, it is worth noting the apparent discrepancy between the findings of Li, B. et al. (18), who observed ESWT-induced osteogenic differentiation in healthy rabbit bone marrow stem cells, and those of Zhao, Z. et al. (20), who did not detect osteogenic differentiation in subchondral bone stem cells derived from patients with knee osteoarthritis. Differences in species, tissue origin, and disease state may plausibly account for this divergence and underscore the complexity of translating mechanistic findings across experimental models. Apoptosis and autophagy The effects of ESWT on apoptosis and autophagy have been demonstrated in a cellular model of osteoarthritis using primary rat chondrocytes stimulated with interleukin-1β (IL-1β) (21). This model was validated by showing that IL-1β downregulated collagen type II expression, a hallmark of cartilage degeneration, and that ESWT was able to reverse this effect. The authors further demonstrated that ESWT inhibited IL-1β–induced apoptosis, as assessed by Annexin V–FITC/propidium iodide flow cytometry. In contrast, autophagy was enhanced, as evidenced by changes in both mRNA and protein expression of key autophagy markers, including Beclin-1, Atg5, LC3B, and p62. This dual effect—suppression of apoptosis alongside activation of autophagy—is consistent with the overall protective role of ESWT in cartilage degeneration. The anti-apoptotic effect of ESWT also aligns with earlier findings reported by Zhao, Z. et al. (22), who observed reduced nitric oxide (NO) levels in the knee joint and synovial fluid following ESWT in a rabbit model of knee osteoarthritis. Given the established pro-apoptotic role of NO in chondrocytes, this observation provides additional mechanistic support. The key molecular effects can be summarized as follows:
Reactive oxygen species (ROS) signaling Building on earlier reports of increased intracellular reactive oxygen species (ROS) following ESWT, Shen, P.-C. et al. (23) used primary porcine chondrocytes to characterize this response in greater detail. They demonstrated a dose-dependent but transient increase in ROS levels, peaking at approximately 10 minutes after treatment and returning to baseline within one hour. The authors identified xanthine oxidase as the primary source of ROS generation. Importantly, this transient ROS burst was followed by increased extracellular matrix (ECM) synthesis, without adverse effects on cell viability or proliferation. Enhanced ECM production was accompanied by increased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and ERK1/2, as well as nuclear translocation of nuclear factor erythroid 2–related factor 2 (Nrf2), a key transcription factor regulating cellular antioxidant and detoxification pathways. These findings suggest that a brief, well-controlled ROS signal acts as a beneficial second messenger rather than a source of oxidative damage in the context of ESWT. The principal signaling events can be summarized as follows:
1a,25-Dihydroxy vitamin D3 rapid signaling pathway Using a surgically induced rat model of knee osteoarthritis combined with a proteomic approach, Hsu, S.-L. et al. (24) showed that ESWT treatment (800 impulses delivered at 0.18 mJ/mm² and 4 Hz) optimally induced expression of protein disulfide isomerase–associated 3 (Pdia-3) within two weeks of treatment. Pdia-3 has been implicated as a membrane-associated co-receptor for 1α,25-dihydroxyvitamin D₃ (1α,25(OH)₂D₃, calcitriol), which, together with the classical nuclear vitamin D receptor, mediates rapid, non-genomic signaling. This rapid signaling pathway is known to activate voltage-gated Ca²⁺ channels, increase intracellular Ca²⁺ flux, and trigger several downstream kinase cascades (25). Activation of the 1α,25-dihydroxyvitamin D₃ rapid signaling pathway in ESWT-treated articular cartilage and subchondral bone was supported by increased expression of four downstream effectors—ERK1, osteoprotegerin (OPG), alkaline phosphatase (ALP), and matrix metalloproteinase-13 (MMP-13)—all of which are associated with bone remodeling and formation. The proposed signaling cascade can be summarized as follows:
Vitamin D–related signaling is increasingly recognized as relevant in osteoarthritis because of its central role in regulating calcium homeostasis, bone turnover, and chondrocyte function. Articular cartilage and subchondral bone both express components of the vitamin D signaling machinery, and disturbances in this pathway have been associated with altered bone remodeling, cartilage degradation, and OA progression. Beyond its classical genomic actions, rapid, non-genomic vitamin D signaling influences mechanosensitive pathways, intracellular calcium flux, and kinase activation—processes that are highly responsive to mechanical stimuli. The ability of ESWT to engage this rapid signaling axis therefore provides a plausible mechanistic link between mechanical energy delivery and coordinated biological responses in cartilage and subchondral bone, particularly in the mechanically driven environment of osteoarthritis. Wnt5a/Ca2+ signaling pathway Evidence for activation of the Wnt5a/Ca²⁺ signaling pathway by ESWT was reported by Yu, L. et al. (26) using both an in vivo chemically induced rat model of knee osteoarthritis and in vitro experiments with bone marrow–derived mesenchymal stem cells (BMMSCs) isolated from rat femur and tibia. Immunostaining of subchondral bone plates from KOA rats treated with radial ESWT (1 bar, 6 Hz, 800 pulses) revealed higher Wnt5a expression compared with both sham-treated KOA rats and normal controls. This increased expression correlated with improved histological morphology, reflected by lower Mankin scores, relative to sham-treated animals. In vitro, BMMSCs exposed to ESWT exhibited a time-dependent increase in Wnt5a expression. Levels peaked approximately 30 minutes after treatment and gradually declined with longer exposure times of up to 3 hours. Quantitative RT-PCR indicated that optimal Wnt5a induction occurred at 0.6 bar with a 30-minute exposure. ESWT also induced expression of several downstream components of the Wnt5a/Ca²⁺ pathway, including calcium/calmodulin-dependent protein kinase II (CaMKII), phospholipase C (PLC), and protein kinase C (PKC), with variable temporal patterns over a 3-hour time course. The proposed signaling sequence may be summarized as:
The authors attributed the observed improvements in cartilage and subchondral bone morphology following ESWT to activation of the Wnt5a/Ca²⁺ signaling pathway. However, such a conclusion should be interpreted with caution. Wnt5a is a pleiotropic signaling molecule involved in a wide range of biological processes, including embryonic development, inflammation, and cancer. Notably, Wnt5a has also been implicated in osteoarthritis pathogenesis, where it may promote cartilage degradation and inflammation by activating catabolic pathways, increasing matrix-degrading enzymes such as MMPs, and disrupting joint homeostasis (27,28). Taken together, these findings suggest that while ESWT can modulate Wnt5a/Ca²⁺ signaling, the net biological outcome is likely to be highly context-dependent, influenced by dose, timing, tissue state, and disease severity. Mechanistic Summary Taken together, the available mechanistic evidence suggests that ESWT acts as a pleiotropic biomechanical stimulus that engages multiple, interconnected signaling pathways in cartilage and subchondral bone. At low to medium energy flux densities, ESWT delivers rapid, high-peak mechanical stress that activates mechanotransduction at the cell membrane, leading to downstream modulation of inflammation, apoptosis, autophagy, and tissue remodeling. ESWT promotes angiogenesis and subchondral bone remodeling, enhances osteoblast differentiation while suppressing osteoclastogenesis, and shifts stem cell fate away from adipogenesis toward chondrogenesis. Transient increases in reactive oxygen species function as second messengers that activate MAPK and Nrf2-dependent antioxidant pathways, supporting extracellular matrix synthesis without compromising cell viability. ESWT also engages rapid, non-genomic vitamin D signaling through Pdia-3, linking mechanical stimulation to calcium flux and bone-forming cascades. Finally, modulation of non-canonical Wnt5a/Ca²⁺ signaling highlights the context-dependent nature of ESWT responses, emphasizing the importance of dose, timing, and disease state. Collectively, these mechanisms provide a biologically plausible framework for the clinical benefits of ESWT in knee osteoarthritis while underscoring the need for carefully optimized treatment protocols. Common commercially available ESWT devices Commercially available ESWT systems can be broadly divided into two categories: clinical-grade devices intended for use by medical professionals and devices marketed directly to consumers for general wellness applications. Clinical ESWT Devices (Professional Use) Clinical ESWT devices are designed to deliver precisely controlled energy flux densities (EFDs) and pulse frequencies. These systems are capable of generating substantial mechanical forces that can modulate tissue physiology, including effects on subchondral bone remodeling, angiogenesis, and chondrocyte mechanotransduction. As such, their safe and effective use requires appropriate training in dosimetry, anatomical targeting, and patient selection. Improper self-application—particularly without imaging guidance or professional assessment—may result in subtherapeutic treatment or, in some cases, tissue injury. For this reason, focused ESWT devices operating at medium to high EFDs are typically restricted to clinical settings. It is also important to note that there are currently no FDA-approved focused ESWT devices intended for direct consumer or self-use, especially at the energy levels required to reach deep joint tissues such as the knee. Focused shockwave systems are generally regulated as prescription-only medical devices due to safety considerations and the need for clinical oversight. Many are used off-label for osteoarthritis based on clinician judgment and emerging evidence rather than explicit FDA indications. Examples of focused and radial ESWT devices commonly found in outpatient physical therapy, sports medicine, and rehabilitation clinics are listed below. Device parameters—such as pressure or EFD, pulse frequency, and applicator size—are adjustable and tailored to the clinical indication and patient tolerance. Focused type: OrthoGold 100 (MTS) Endopuls FSWT (Enraf-Nonius) PiezoWave2® (Richard Wolf) DolorClast® Focused Shock Waves (EMS Electro Medical System SA) Emfocus (GZ MTS Electronics Co., Ltd.): Electromagnetic focused ESWT Radial type: Endopuls 811 (Enraf-Nonius) DolorClast® Radial Shock Waves (EMS Electro Medical System SA) Softshock 2.0 (Medray Laser & Technology): Radial ESWT device. Z Wave® Q (Zimmer MedizinSystems): Radial ESWT device. Klinogicare Shockwave Storm Radial (Klinogicare) PHS Radial Shockwave, PHS6B (PHSDME) AWT Radial Shockwave Therapy (Hedone/clinics) INWAVE Radial Shockwave (INWAVE Medical) MTS SWT9 Radial ESWT System (GZ MTS Electronics Co., Ltd.) Modus ESWT® Radial Shockwave (Refizo) An example of a modular mixed-use type Duolith® SD1 Ultra (Storz Medical): A modular system for both focused and radial ESWT with optional Ultrasound diagnostics. Consumer-Targeted “Shockwave” Devices A separate category includes devices marketed directly to consumers for general wellness, pain relief, or soft-tissue massage. While some of these products advertise “shockwave” technology and adjustable energy output, they are not FDA-cleared for specific medical indications such as osteoarthritis or tendinopathy. Reported energy outputs are typically not standardized to clinical EFD measurements, are rarely independently verified, and lack validation in peer-reviewed clinical trials. These devices generally deliver lower, more variable energy levels rather than those of true therapeutic shock waves. Consequently, they should not be considered equivalent to clinical ESWT systems and should be used with caution. Examples of consumer-market devices include: Shape Tactics Radial Shockwave Therapy Device (Cavitation Machines) PSP20 Extracorporeal Shock Wave Therapy Machine (Pervita Medical) Q60A Extracorporeal Shock Wave Therapy (Sheyera) MODOY ESWT02 (MODOY) Finding a provider of shock wave therapy Primary care doctors, orthopedic surgeons, and physical therapists can offer reliable information or references. Additional resources and platforms include: Shockwave Provider Directories Several private or industry-associated directories list clinics or providers offering shockwave treatments:
These directories are not exclusively physical therapists, but they include PTs alongside other clinicians. Vendor-Specific “Find a Provider” Tools Some shockwave device manufacturers maintain provider locators through their own channels. For example, SoftWave Clinics site lets patients locate clinics (including physical therapy clinics) that use its technology. These are useful if you know the brand of devices being used in your area. Local Clinic Search and Therapy Networks You can also use generalized health provider search services (not specialty directories) to find ESWT-offering PT practices. For example, JustHealthy.com and similar “find a provider near me” services list nearby clinics offering shockwave therapy based on city or zip code. References
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