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Lacosamide, a prescription medicine approved for epilepsy, showed potential to limit osteoarthritis-related cartilage damage and pain in laboratory studies and mice. The 2026 findings do not show that it reverses osteoarthritis in people: the drug has not been established as an osteoarthritis treatment, and the reported experiments were preclinical.
What did the 2026 study find?
The study, “Collagen II hydrogel-mediated sustained delivery of lacosamide attenuates cartilage degeneration and pain in osteoarthritis,” tested lacosamide in primary human osteoarthritis (OA) chondrocytes, cartilage explants and mice with surgically induced OA. It reports that lacosamide reduced inflammatory cartilage breakdown and increased markers associated with cartilage-building activity. In mice, treatment was associated with less cartilage degeneration and less pain. The PubMed record identifies the paper as published in Bioactive Materials in 2026.
These results have different levels of relevance. Human chondrocytes are cartilage cells studied outside the body; they are not patients receiving treatment. Cartilage explants are also laboratory samples. The animal findings are encouraging research results, but they cannot establish that the same benefits occur in people or that existing joint damage can be repaired clinically.
How might lacosamide affect cartilage?
The researchers focused on Nav1.7, a sodium channel associated with pain signaling. Earlier work described by Yale in 2024 found Nav1.7 in cartilage-producing cells and reported reduced joint damage in two mouse OA models when the channel was genetically deleted in those cells. Yale also described cartilage protection in mice using Nav1.7-blocking medicines, including carbamazepine. That work supplies biological context; it does not establish a human OA treatment.
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In the 2026 study, lacosamide increased secretion of HSP70 and midkine, which the authors link to anabolic and anti-catabolic responses. The abstract also reports that, in the tested human OA cell assays, lacosamide was more potent at lower concentrations than carbamazepine or oxcarbazepine at suppressing IL-1β-induced catabolism and promoting anabolism. These are laboratory comparisons, not evidence that lacosamide is more effective or safer for patients.
What did the mouse treatment comparisons show?
The study reports benefits after both systemic and intra-articular lacosamide administration in its mouse OA model. Intra-articular treatment—delivery into the joint—provided superior cartilage protection and pain relief at one-tenth the dose used for systemic administration in that model. This figure is an animal-study comparison, not a human dose or a recommendation for joint injections.
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The researchers also tested a thermoresponsive hydrogel based on collagen II as a way to deliver lacosamide locally and sustain its release. They report that the material prolonged drug retention in the joint and improved therapeutic durability in the model. It is an experimental delivery strategy, not an available consumer treatment.
Does this mean lacosamide can reverse arthritis in people?
No. The study supports describing lacosamide as a potential OA research candidate, not as a proven treatment that reverses human joint damage. The reported work does not demonstrate clinical benefit in people, establish an appropriate human dose, or show that patients should take lacosamide or receive it by injection for OA. A prescription epilepsy drug should not be started, stopped or repurposed for joint pain without a clinician’s direction.
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The headline’s “may help reverse” wording signals a possibility being investigated. The experiments suggest effects on cartilage breakdown and building-related markers, but that is not the same as showing that established damage is reversed in a person. The cited sources do not establish the availability or status of human OA trials.
Independent reader supportYour contribution helps us test, update, and keep practical guides available for everyone.What can people with osteoarthritis do now?
Osteoarthritis has no cure, but established care focuses on managing symptoms and maintaining function. The NIH overview lists options including physical activity, weight management, oral and topical pain relievers, anti-inflammatory medicines, corticosteroid injections for temporary relief, and surgery when appropriate. Which options fit depends on the person’s symptoms, health and goals, so treatment decisions belong with a healthcare professional.
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Supplements such as glucosamine and chondroitin are not proven substitutes for care. The National Center for Complementary and Integrative Health says evidence for knee OA is inconsistent and effects on joint structure remain uncertain.
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