Cells age. Some stop dividing but do not die. These senescent cells collect in bone, cartilage, tendon, and muscle, and researchers now want to know whether physical treatments can change them. In the past two years, studies have tested radial shockwave and EMTT (extracorporeal magnetotransduction therapy) against that question. This article covers what they found and where the evidence ends. Most of it comes from cells and animals. None of it shows that shockwave or EMTT reverses aging in people.
For the basics of senescence, fibrosis, and adhesion, start with cellular senescence, adhesion, and shockwave. This article goes wider, across tissues and across all three treatments we use.
What musculoskeletal senescence means
A senescent cell has stopped dividing but stays in the tissue. It releases inflammatory signals and enzymes called the senescence-associated secretory phenotype (SASP). In small numbers, for short periods, this is part of normal repair. When the cells build up with age and repeated injury, the SASP can disrupt the tissue around them.
"Musculoskeletal senescence" names that build-up in bone, cartilage, tendon, and muscle. It is a research concept, not a diagnosis. No routine clinical test exists, and we do not diagnose it.
Where senescent cells show up
Bone. A 2025 review by Falvino and colleagues in the International Journal of Molecular Sciences links senescent cells and the SASP to osteoporosis, osteoarthritis, and sarcopenia (age-related muscle loss). It also covers exercise as a way to modify senescence.
Joints. Chen and colleagues, in The American Journal of Sports Medicine (2025), found more senescence markers in bone-forming cells beneath the cartilage (subchondral bone) of arthritic knees, in human and rat tissue. The human sample was three patients.
Tendon. Stowe, Keller, and Connizzo, in Aging Cell (2024), studied mouse tendon tissue in the lab. Natural aging and induced senescence both cut new protein production while breakdown enzymes stayed active. The balance tipped toward degradation.
Muscle. The Falvino review lists senescence among the mechanisms behind sarcopenia. Most of that research is in cells and animals.
What happened when senescent cells were targeted with drugs
The best human test so far used drugs, not a physical treatment. Farr and colleagues, in Nature Medicine (2024), randomized 60 postmenopausal women to intermittent dasatinib plus quercetin (a senolytic combination meant to clear senescent cells) or control for 20 weeks.
The main result was negative. Bone resorption, the primary outcome, did not fall. A bone-formation marker rose at 2 and 4 weeks but matched control by week 20. In exploratory analyses, women with the highest senescent-cell burden did respond, including a 2.7% gain in wrist bone density at 20 weeks. The authors called for studies testing whether that burden predicts response.
Animals tell a similar story. In a 2023 Aging Cell study by Chin and colleagues, a senolytic drug helped aged mice with post-traumatic knee osteoarthritis less than it helped young ones. Age changes the response.
The lesson applies to shockwave and EMTT too. A convincing mechanism in the lab does not guarantee a result in the clinic.
Radial shockwave and senescence
Three recent studies tested radial shockwave on aging or senescent bone and joint cells. All three are preclinical.
Knee osteoarthritis (2025). In the Chen study, radial shockwave lowered senescence markers in the subchondral bone of arthritic rats and in bone-forming cells under inflammatory stress. Of three doses tested in rats, the lowest worked best. Shockwave matched treadmill exercise, and combining the two added nothing.
Osteoporotic bone and dose (2025). Luo and colleagues, in Regenerative Biomaterials, treated cells from osteoporotic bone at two intensities. At 3 bar, the cells built more bone and showed fewer signs of senescence. At 5 bar, they were overloaded and died. In rats with osteoporosis induced by removing the ovaries, 3 bar increased bone mass and lowered senescence-associated markers. More energy was not better.
Senile osteoporosis cells (2024). Wang and colleagues, in Bone, treated bone marrow stromal cells from people with age-related osteoporosis. Radial shockwave increased proliferation in a dose-dependent way and boosted bone- and blood-vessel-forming activity through a pressure-sensing channel called Piezo1. It also helped a senescence-accelerated mouse strain. The study did not measure senescence markers, so it shows an effect on aged bone cells, not removal of senescent ones.
Together, these studies suggest radial shockwave can influence aging bone cells in the lab and in animals, and that dose matters. They do not show the same in patients.
Focused shockwave: the evidence gap
We found no study that measured senescence after focused shockwave. Every senescence study above used a radial device. The question is open, not answered, and we claim no senescence effect for focused shockwave.
Its evidence is clinical. Randomized trials support it for plantar fasciitis and calcific rotator cuff tendinopathy, measured by pain and function, not senescence. Focused and radial shockwave are physically different, so results from one do not transfer to the other. Radial vs. focused shockwave explains why.
EMTT and senescence
EMTT uses a pulsed magnetic field, not a pressure wave. One study has looked directly at EMTT and a senescence marker, and it suggests EMTT may have a favorable effect on senescence-related activity in tendon cells. Mancini and colleagues published it in July 2025 in the International Journal of Molecular Sciences. We found no other EMTT study that measured senescence.
How it was done. The team grew tendon cells (tenocytes) from hamstring tendon taken from six men, aged 17 to 37, during ACL reconstruction. They treated the cells with a STORZ MAGNETOLITH device at rising doses:
- 40 mT, 1,000 impulses
- 80 mT, 1,000 impulses (the device's maximum field strength)
- 80 mT, 3,500 impulses, given once, twice, or three times in a row
Untreated cells served as controls.
The senescence finding. p16 (the CDKN2A gene) is a standard marker of senescent cells. It was significantly lower than in untreated cells in every treated group. Repeated 80 mT treatment produced what the authors call a "senolytic-like" pattern: overall cell vitality fell, while the share of dividing (Ki67-positive) cells rose by about 7%, significant after the triple treatment. Their reading is that EMTT may pressure less responsive cells while the rest become more active.
The repair findings. Effects clustered at 80 mT. The 40 mT dose did little.
- Scleraxis, a marker of tendon-cell identity, rose in every treated group except the triple 80 mT treatment, where the rise was not significant.
- Collagen I and III rose after the single 1,000-impulse doses and after the double and triple 3,500-impulse treatments.
- MMP9, an enzyme that remodels matrix and helps cells move, rose only with the double and triple 80 mT treatments.
- After the triple 80 mT treatment, cells closed a scratched gap faster than untreated cells, with more stress fibers and reorganized adhesion points. These are signs of a cell ready to repair.
What it does not prove. The authors call the senolytic-like effect preliminary. They did not run the tests that would confirm senescent cells were cleared: senescence-associated β-galactosidase staining, SASP measurement, or single-cell analysis. The same pattern could reflect stress adaptation or other shifts in how cells regulate their cell cycle.
Two more cautions. The donors were young, so their cells likely carried little senescence to begin with. And the work was done in a dish. The study supports a dose-dependent effect of EMTT on human tendon cells and a drop in a key senescence marker. Whether EMTT reduces senescent cells in living tendon remains open.
EMTT's clinical evidence is separate and measures symptoms. A 2026 double-blind, sham-controlled trial by Hollander and colleagues found less pain with EMTT than sham at 12 weeks across patients with knee osteoarthritis, rotator cuff problems, and low back arthritis. It did not measure senescence. Why we sometimes pair EMTT with shockwave is covered in EMTT alone or with shockwave.
What this research does and does not show
- It is early. Nearly every study linking shockwave or EMTT to senescence used cells or animals. We found no human trial measuring senescence after either treatment.
- Dose matters. A moderate shockwave setting lowered senescence markers; a higher one killed cells. EMTT did little at its lower intensity.
- Exercise holds up. In arthritic rats, radial shockwave did no better than treadmill exercise. Exercise remains core care for aging joints, bone, and muscle.
- Drug results were mixed. The human senolytic trial missed its main outcome. Targeting senescence is a promising idea, not a proven treatment.
- No anti-aging claims. None of this shows that shockwave or EMTT reverses aging, regrows cartilage, or prevents osteoporosis.
How we use this in practice
This research helps explain how shockwave and EMTT may act on aging tissue. It does not change what we treat or how we decide. Decisions rest on the exam and on clinical evidence for the condition in front of us, such as tendon pain, plantar heel pain, or knee osteoarthritis. Exercise, strength work, and care from your physician, physical therapist, or surgeon remain central.
If stiffness or pain seems tied to getting older, start by finding out what is actually wrong. Musculoskeletal fibroaging covers how tissue changes with age. Or book a new patient exam.
Sources
- Chen L, Zhang Z, Ma X, et al. Radial extracorporeal shockwave therapy reduces subchondral osteoblast senescence in knee osteoarthritis. The American Journal of Sports Medicine. 2025;53(10):2352-2362. PMID 40673558. (link)
- Luo D, Chen Q, Xiao Z, et al. Shockwave-driven activation of endoplasmic reticulum stress in osteoblasts to enhance bone formation under osteoporotic conditions. Regenerative Biomaterials. 2025;12:rbaf069. PMID 40979831. (link)
- Wang B, Shao W, Zhao Y, et al. Radial extracorporeal shockwave promotes osteogenesis-angiogenesis coupling of bone marrow stromal cells from senile osteoporosis via activating the Piezo1/CaMKII/CREB axis. Bone. 2024;187:117196. PMID 39004161. (link)
- Mancini M, Vetrano M, Traversa A, Cauli C, Ceccarelli S, Malisan F, Vulpiani MC, Maffulli N, Marchese C, Visco V, Ranieri D. Electromagnetic transduction therapy (EMTT) enhances tenocyte regenerative potential: evidence for senolytic-like effects and matrix remodeling. International Journal of Molecular Sciences. 2025;26(15):7122. PMID 40806255. (link) (full text)
- Farr JN, Atkinson EJ, Achenbach SJ, et al. Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial. Nature Medicine. 2024;30(9):2605-2612. PMID 38956196. (link)
- Chin AF, Han J, Clement CC, et al. Senolytic treatment reduces oxidative protein stress in an aging male murine model of post-traumatic osteoarthritis. Aging Cell. 2023;22(11):e13979. PMID 37749958. (link)
- Stowe EJ, Keller MR, Connizzo BK. Cellular senescence impairs tendon extracellular matrix remodeling in response to mechanical unloading. Aging Cell. 2024;23(11):e14278. PMID 39039843. (link)
- Falvino A, Bonanni R, Tarantino U, et al. Which approach to choose to counteract musculoskeletal aging? A comprehensive review on the multiple effects of exercise. International Journal of Molecular Sciences. 2025;26(15):7573. PMID 40806700. (link)
- Hollander K, Burgkart R, von Eisenhart-Rothe R, Vester J, Gerdesmeyer L. Extracorporeal magnetotransduction therapy (EMTT) for management of musculoskeletal disorders: a double-blind, placebo-controlled, randomised trial. Journal of Back and Musculoskeletal Rehabilitation. 2026;39(3):885-895. PMID 41313312. (link)
