Can Arthritis Be Reversed? An Honest Look at the Evidence
"Reverse your arthritis" is one of the most common promises in health marketing, and one of the most misleading. The honest answer depends on which arthritis you have and what you mean by "reversed". In osteoarthritis, worn cartilage does not meaningfully regrow, but pain and function can improve a great deal. In rheumatoid arthritis, remission is a real, measurable outcome, and a minority of people stay well even off medication. Gout comes closest to a cure: keep uric acid low enough for long enough and the crystals that cause it dissolve. This page sets out what the evidence supports, where it is still emerging, and how to recognize claims that go beyond it.
Key takeaways
- "Reversal" means three different things: fewer symptoms, repaired joint structure, or disease remission. Each type of arthritis allows a different mix. Strong
- Osteoarthritis: adult cartilage has very limited repair capacity, but exercise and weight loss can substantially reduce pain and improve function. Strong
- Regrowing cartilage with PRP or stem cell injections is not supported by rigorous trials; drugs such as sprifermin and knee joint distraction show small structural gains and remain investigational or specialist options. Contested Emerging
- Rheumatoid arthritis: remission is a defined, achievable goal with early treat-to-target therapy; sustained drug-free remission happens in a minority (about 15% in one long-term cohort). Strong
- Gout: keeping serum urate below 6 mg/dL dissolves urate crystals and shrinks tophi over months to years, but crystals can return if treatment stops. Strong
- Be wary of anyone promising to "cure" or "regrow" joints, especially if they sell the product or suggest stopping prescribed medicine. Strong
What "reversal" could mean
When people ask whether arthritis can be reversed, they usually mean one of three things. Keeping them separate is the single most useful step in judging any claim.
| Meaning | What it looks like | How it is measured |
|---|---|---|
| Symptom reversal | Less pain and stiffness, better walking, climbing stairs and sleep | Validated pain and function scores (for example WOMAC or KOOS) |
| Structural reversal | Lost cartilage regrows, erosions heal, crystal deposits disappear | X-ray joint space, MRI cartilage thickness, ultrasound or dual-energy CT, joint-fluid analysis |
| Disease remission | The underlying disease process is switched off, with or without ongoing treatment | Defined criteria, such as DAS28 or Boolean remission in RA, or serum urate below target in gout |
Symptoms and structure are only loosely linked. A systematic review of population studies found that among people with x-ray evidence of knee osteoarthritis, the share who actually had knee pain ranged from 15% to 81%, and many people with knee pain had normal x-rays.3 That cuts both ways: you can feel much better without your x-ray changing, and an x-ray "improving" does not guarantee you will feel better. Strong
At a glance: OA vs. RA vs. gout
| Type | Symptoms | Structure | Remission or cure |
|---|---|---|---|
| Osteoarthritis | Often improve substantially with exercise and weight loss Strong | Cartilage regrowth not shown in a clinically meaningful way Contested | No defined remission; joint replacement for end-stage disease |
| Rheumatoid arthritis | Can largely resolve with effective treatment Strong | Treatment aims to stop new damage; established erosions generally do not fully repair | Remission is a defined target; drug-free remission in a minority Strong |
| Gout | Flares stop once crystals are cleared Strong | Crystals dissolve and tophi shrink; bone erosions may persist Strong | Crystal-free state achievable, but usually requires ongoing urate control Strong |
Not sure which type you have? The RA vs. OA comparison walks through the differences in symptoms, tests and treatment.
Osteoarthritis: why cartilage rarely regrows Strong
Osteoarthritis is a disease of the whole joint — cartilage, bone, synovium, ligaments and muscle — but the loss of smooth articular cartilage is its hallmark. Cartilage has no blood supply, no nerves, and relatively few cells, which limits how well it can heal. Leading reviews describe prevention and disease modification as goals of active research rather than established treatments.1
Mechanism: a near-permanent collagen scaffold
Using the carbon-14 "bomb-pulse" method, researchers dated the collagen in knee cartilage from 23 people born between 1935 and 1997. Virtually no collagen was replaced after skeletal maturity, and neither osteoarthritis nor tissue damage changed that. The authors concluded that the collagen matrix of adult articular cartilage is essentially a permanent structure.2 The cells can still make some new matrix components, but rebuilding the collagen framework itself is something the adult joint barely does.
This is why claims that a supplement, diet or injection "regrows cartilage" deserve particular scrutiny. It does not mean OA inevitably worsens: many people's symptoms stay stable for years, and some improve. It means the most reliable gains come from changing how the joint is loaded and how the person functions, not from rebuilding tissue.
Osteoarthritis: symptoms can improve a lot Strong
If "reversal" means feeling and moving better, the evidence in osteoarthritis is encouraging. The 2019 American College of Rheumatology/Arthritis Foundation guideline makes strong recommendations for exercise, weight loss in people with knee or hip OA who have overweight or obesity, self-management programs and tai chi.7
- Weight loss plus exercise (the IDEA trial). In this 18-month randomized trial of 454 older adults with overweight or obesity and painful knee OA, the diet-plus-exercise group lost an average of 10.6 kg (11.4% of body weight). They ended with less pain and better function than both the diet-only and exercise-only groups, along with lower levels of the inflammatory marker IL-6. Knee compressive forces were lower in the diet group than with exercise alone.4 Strong
- Exercise. A Cochrane review of 54 trials found high-quality evidence that land-based exercise reduced knee pain by about 12 points on a 0–100 scale immediately after treatment, an effect the authors described as comparable with NSAIDs, with benefits persisting at a smaller size for two to six months.5 Strong
- Exercise does not "wear out" cartilage. A systematic review of randomized trials found that knee-loading exercise did not appear harmful to cartilage in people with or at risk of knee OA, though the evidence quality was low.6 Emerging
Osteoarthritis: PRP, stem cells & regeneration Contested Emerging
Regenerative injections are widely marketed, often at considerable out-of-pocket cost. Here is how they have fared in rigorous, controlled trials.
| Approach | Best evidence | Evidence |
|---|---|---|
| Platelet-rich plasma (PRP) | RESTORE trial, 288 people with mild-to-moderate knee OA: three PRP injections were no better than saline placebo for pain or for MRI cartilage volume at 12 months, and 29 of 31 secondary outcomes showed no difference.8 The ACR/AF guideline strongly recommends against PRP for knee and hip OA.7 | Contested |
| "Stem cell" / cell-based injections | Phase 3 trial, 480 people: bone-marrow concentrate, fat-derived stromal vascular fraction and umbilical-cord mesenchymal cells were no better than a corticosteroid injection for pain at 12 months, and no group showed a significant change in MRI osteoarthritis scores.9 The ACR/AF guideline strongly recommends against stem cell injections for knee and hip OA.7 | Contested |
| Sprifermin (experimental growth-factor drug) | FORWARD trial, 549 people: the higher dose increased cartilage thickness by about 0.05 mm versus placebo over two years — statistically significant but of uncertain clinical importance, with no difference in WOMAC symptom scores.10 Not an approved treatment. | Emerging |
| Knee joint distraction | Small studies show symptom improvement and increased joint space; see below.1112 | Emerging |
| Supplements (glucosamine, collagen, etc.) | Not shown to rebuild cartilage; effects on symptoms are small and inconsistent. See glucosamine and collagen. | Contested |
Researchers have not given up on regeneration: products differ, some people report benefit, and better-targeted therapies may emerge. But at present, no injection has been shown in high-quality trials to rebuild cartilage in a way that people can feel. If you are considering one, ask what trial evidence supports that specific product, what it costs, and whether it is regulated for this use. The osteoarthritis page covers evidence-based medicines and injections.
Knee joint distraction Emerging
Knee joint distraction is a surgical, joint-preserving procedure in which an external frame holds the two sides of the knee slightly apart for about six weeks, unloading the cartilage. It is aimed mainly at younger people with severe knee OA who hope to delay a knee replacement.
- A 2021 systematic review pooled 11 papers covering just 127 patients in 7 cohorts (including 2 randomized trials). It found improvements in pain, function and imaging measures of cartilage that lasted up to at least nine years, but stressed that the evidence is still limited.11
- In a randomized trial of 60 people aged 65 or younger with end-stage knee OA, distraction was not inferior to total knee replacement at one year on most patient outcomes, and mean joint space width increased by 1.2 mm. However, 60% of distraction patients developed pin-track infections.12
This is one of the few interventions with measurable structural gains in OA, which is why it attracts interest. It is also intensive, available at few centers, and backed by small numbers of patients, so it is best viewed as an emerging specialist option rather than a general route to "reversing" arthritis.
Rheumatoid arthritis: remission is real Strong
Rheumatoid arthritis (RA) is an autoimmune disease, and its story is very different from OA's. Modern treatment can switch the inflammation off, and doctors have formal definitions for when that has happened. International treat-to-target recommendations set remission as the primary goal (with low disease activity as an alternative, especially in long-standing disease), checking disease activity every one to three months while it is active and adjusting treatment until the target is reached.15
| Definition | Threshold | Notes |
|---|---|---|
| DAS28 remission | Disease Activity Score (28 joints) below 2.6 | Widely used in clinics; corresponds to the older ARA remission criteria16. Less stringent: some swollen joints can remain. |
| ACR/EULAR Boolean remission (2011) | Tender joints, swollen joints, CRP (mg/dL) and patient global assessment (0–10) all ≤ 1 | Stringent definition developed for trials17 |
| Boolean 2.0 (2022 revision) | As above, but patient global assessment ≤ 2 | Endorsed by ACR and EULAR; better agreement with index-based criteria18 |
| SDAI remission | Simplified Disease Activity Index ≤ 3.3 | Index-based alternative to Boolean17 |
Timing matters. In data from four randomized trials, 20.6% of people with early RA met Boolean 2.0 remission six months after starting treatment, compared with 6.0% of people with established RA.18 (These are trial figures, using strict criteria; rates of low disease activity are higher.) This is part of why rheumatologists talk about a "window of opportunity" early in the disease. Treatment aims to stop new joint damage; erosions that have already formed generally do not fully repair, which is another reason early diagnosis matters.
Drug-free remission in RA Strong (it happens) Emerging (who can taper)
A smaller group of people go further: their RA stays quiet after all disease-modifying drugs are stopped. In the Leiden Early Arthritis Clinic, 155 of 1,007 people with RA diagnosed between 1993 and 2011 (about 15%) achieved sustained DMARD-free remission. People treated with early methotrexate and disease-activity-steered therapy were several times more likely to reach it than those treated in the 1990s, and at remission their physical function was at the level of the general population.20 The authors concluded that RA chronicity "can be influenced".
Gout: the closest thing to a cure Strong
Gout is caused by monosodium urate crystals that form when blood uric acid stays too high. Unlike worn cartilage, those crystals can dissolve — if urate is kept low enough for long enough. The 2020 ACR guideline recommends a treat-to-target goal of serum urate below 6 mg/dL for people on urate-lowering therapy.22 (See urate thresholds.)
- Crystals disappear. In 18 people with proven gout whose urate was brought down to normal, crystals vanished from the joint fluid of every joint followed. It took between 3 and 33 months, and longer in people who had had gout longer.23
- Tophi shrink. In 63 people with tophaceous gout, the lower the average urate during treatment, the faster the tophi shrank.24
- The target is reachable. In a UK randomized trial of 517 people, nurse-led care with patient education and treat-to-target urate-lowering therapy got 95% of patients below 6 mg/dL at two years, versus 30% with usual care, and all secondary outcomes, including flares and tophi, favored the nurse-led group.25
What lifestyle can and can't do
What lifestyle can do
- Substantially reduce OA pain and improve function through exercise and, where relevant, weight loss45
- Lower knee joint loading and inflammatory markers such as IL-64
- Modestly lower uric acid in gout (diet, weight loss, less beer and sugary drinks)22
- Support overall health and the effectiveness of medical treatment in RA
Lifestyle is not a consolation prize: in knee OA it is the core treatment, and in RA and gout it works alongside medication. A Cochrane review of dietary interventions in RA found that some diets, such as a Mediterranean-style diet, may reduce pain, but the trials were small and at moderate to high risk of bias.21 Emerging See the anti-inflammatory diet, exercise and movement, supplements and complementary approaches for RA.
Red flags for "cure" marketing Strong
Researchers who reviewed online marketing found widespread direct-to-consumer promotion of unapproved stem cell interventions by U.S. businesses, and called for stronger regulatory oversight.13 The FDA has warned consumers that many marketed "regenerative medicine" products — including stem cells, fat-derived stromal vascular fraction and "ortho-biologics" — are unapproved, and that it has received reports of blindness, tumor formation and infections linked to them.14 Be cautious if a product or clinic:
- promises to "cure," "reverse" or "regrow" arthritis or cartilage;
- relies on testimonials and before-and-after stories rather than published randomized trials;
- claims to treat many unrelated conditions with the same product;
- asks for large cash payments up front for a treatment insurers and guidelines do not support;
- suggests you stop or reduce prescribed medication — especially disease-modifying drugs for RA or urate-lowering drugs for gout;
- calls itself "FDA registered" or cites a trial registration as though that means the product is approved or proven;
- discourages you from discussing it with your own doctor.
When to see a doctor Strong
Book an appointment if you:
- have joint swelling, morning stiffness lasting more than about 30 minutes, or pain in several small joints of the hands or feet for more than a few weeks — early RA treatment gives the best chance of remission;
- have had a suspected gout attack, visible lumps (tophi), or two or more flares a year;
- have OA that limits walking, sleep or work despite exercise and weight management;
- are thinking about an injection or procedure marketed as regenerative;
- are in remission and want to discuss whether reducing medication is reasonable.
Frequently asked questions
Can osteoarthritis be reversed?
Not in the sense of regrowing lost cartilage: no treatment has been shown to rebuild worn cartilage in a way that clearly improves how people feel. But OA symptoms are not fixed. Exercise and, for people with overweight, weight loss reliably reduce pain and improve function, sometimes substantially. In the IDEA trial, adults with knee OA who lost about 11% of their body weight through diet plus exercise had less pain and better function than those who did either alone. This is educational information, not medical advice.
Can cartilage grow back?
Adult articular cartilage has very limited repair capacity. A radiocarbon-dating study found that the collagen framework of knee cartilage is essentially not replaced after skeletal maturity, with or without osteoarthritis. Experimental approaches such as the drug sprifermin and knee joint distraction have produced small measurable increases in cartilage thickness or joint space, but these remain investigational or specialist options. Platelet-rich plasma and stem cell injections have not been shown to rebuild cartilage in rigorous trials.
Can rheumatoid arthritis go into remission or be cured?
Remission is a real, measurable goal in rheumatoid arthritis, defined by validated criteria such as a DAS28 score below 2.6 or the ACR/EULAR Boolean definition. Early treatment with disease-modifying drugs adjusted to reach a target gives the best chance. A minority of people, about 15% in one long-running Dutch early-arthritis cohort, reach sustained remission without any disease-modifying drugs. For most people remission depends on continuing treatment, and stopping medication often leads to a flare, so any tapering should only be done with a rheumatologist.
Can gout be cured?
Gout is often described as the most treatable form of arthritis. When serum urate is kept below about 6 mg/dL, usually with urate-lowering medication, urate crystals dissolve over months to years, flares stop and tophi shrink. In one study crystals disappeared from joint fluid in all 18 joints followed, taking 3 to 33 months. The catch is that urate rises again if treatment stops, so crystals can re-form. Never stop urate-lowering therapy without speaking to your doctor.
Can diet or supplements reverse arthritis?
No diet or supplement has been shown to reverse joint damage. Weight loss through diet clearly helps knee osteoarthritis symptoms and lowers urate in gout, and an anti-inflammatory eating pattern supports overall health, but dietary trials in rheumatoid arthritis are small and their effects uncertain. Supplements should be discussed with a doctor or pharmacist, especially if you take other medicines.
Are stem cell injections for knee arthritis worth it?
Current evidence does not support them. In a randomized trial of 480 people with knee osteoarthritis, three types of cell injection were no better than a corticosteroid injection for pain at 12 months, and none changed MRI scores of joint structure. The 2019 American College of Rheumatology/Arthritis Foundation guideline strongly recommends against stem cell injections for knee and hip osteoarthritis, and the FDA has warned consumers about unapproved regenerative medicine products.
References
- Hunter DJ, Bierma-Zeinstra S. Osteoarthritis. Lancet. 2019;393(10182):1745–1759. PubMed 31034380
- Heinemeier KM, Schjerling P, Heinemeier J, et al. Radiocarbon dating reveals minimal collagen turnover in both healthy and osteoarthritic human cartilage. Sci Transl Med. 2016;8(346):346ra90. PubMed 27384346
- Bedson J, Croft PR. The discordance between clinical and radiographic knee osteoarthritis: a systematic search and summary of the literature. BMC Musculoskelet Disord. 2008;9:116. PubMed 18764949
- Messier SP, Mihalko SL, Legault C, et al. Effects of intensive diet and exercise on knee joint loads, inflammation, and clinical outcomes among overweight and obese adults with knee osteoarthritis: the IDEA randomized clinical trial. JAMA. 2013;310(12):1263–1273. PubMed 24065013
- Fransen M, McConnell S, Harmer AR, et al. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2015;1:CD004376. PubMed 25569281
- Bricca A, Juhl CB, Steultjens M, Wirth W, Roos EM. Impact of exercise on articular cartilage in people at risk of, or with established, knee osteoarthritis: a systematic review of randomised controlled trials. Br J Sports Med. 2019;53(15):940–947. PubMed 29934429
- Kolasinski SL, Neogi T, Hochberg MC, et al. 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee. Arthritis Care Res. 2020;72(2):149–162. PubMed 31908149
- Bennell KL, Paterson KL, Metcalf BR, et al. Effect of intra-articular platelet-rich plasma vs placebo injection on pain and medial tibial cartilage volume in patients with knee osteoarthritis: the RESTORE randomized clinical trial. JAMA. 2021;326(20):2021–2030. PubMed 34812863
- Mautner K, Gottschalk M, Boden SD, et al. Cell-based versus corticosteroid injections for knee pain in osteoarthritis: a randomized phase 3 trial. Nat Med. 2023;29(12):3120–3126. PubMed 37919438
- Hochberg MC, Guermazi A, Guehring H, et al. Effect of intra-articular sprifermin vs placebo on femorotibial joint cartilage thickness in patients with osteoarthritis: the FORWARD randomized clinical trial. JAMA. 2019;322(14):1360–1370. PubMed 31593273
- Jansen MP, Boymans TAEJ, Custers RJH, et al. Knee joint distraction as treatment for osteoarthritis results in clinical and structural benefit: a systematic review and meta-analysis of the limited number of studies and patients available. Cartilage. 2021;13(1 Suppl):1113S–1123S. PubMed 32698704
- van der Woude JA, Wiegant K, van Heerwaarden RJ, et al. Knee joint distraction compared with total knee arthroplasty: a randomised controlled trial. Bone Joint J. 2017;99-B(1):51–58. PubMed 28053257
- Turner L, Knoepfler P. Selling stem cells in the USA: assessing the direct-to-consumer industry. Cell Stem Cell. 2016;19(2):154–157. PubMed 27374789
- Important Patient and Consumer Information About Regenerative Medicine Therapies — U.S. Food and Drug Administration (FDA). fda.gov
- Smolen JS, Breedveld FC, Burmester GR, et al. Treating rheumatoid arthritis to target: 2014 update of the recommendations of an international task force. Ann Rheum Dis. 2016;75(1):3–15. PubMed 25969430
- Fransen J, Creemers MC, Van Riel PL. Remission in rheumatoid arthritis: agreement of the disease activity score (DAS28) with the ARA preliminary remission criteria. Rheumatology (Oxford). 2004;43(10):1252–1255. PubMed 15238643
- Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis. 2011;70(3):404–413. PubMed 21292833
- Studenic P, Aletaha D, de Wit M, et al. American College of Rheumatology/EULAR remission criteria for rheumatoid arthritis: 2022 revision. Ann Rheum Dis. 2023;82(1):74–80. PubMed 36280238
- Smolen JS, Edwards CJ, Konzett V, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biologic disease-modifying antirheumatic drugs: 2025 update. Ann Rheum Dis. 2026;85(6):991–1009. PubMed 41826212
- Ajeganova S, van Steenbergen HW, van Nies JA, et al. Disease-modifying antirheumatic drug-free sustained remission in rheumatoid arthritis: an increasingly achievable outcome with subsidence of disease symptoms. Ann Rheum Dis. 2016;75(5):867–873. PubMed 25972519
- Hagen KB, Byfuglien MG, Falzon L, Olsen SU, Smedslund G. Dietary interventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009;(1):CD006400. PubMed 19160281
- FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res. 2020;72(6):744–760. PubMed 32391934
- Pascual E, Sivera F. Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout. Ann Rheum Dis. 2007;66(8):1056–1058. PubMed 17223663
- Perez-Ruiz F, Calabozo M, Pijoan JI, Herrero-Beites AM, Ruibal A. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002;47(4):356–360. PubMed 12209479
- Doherty M, Jenkins W, Richardson H, et al. Efficacy and cost-effectiveness of nurse-led care involving education and engagement of patients and a treat-to-target urate-lowering strategy versus usual care for gout: a randomised controlled trial. Lancet. 2018;392(10156):1403–1412. PubMed 30343856