What Is Gonarthrosis? Symptoms, Causes, and Treatment

Gonarthrosis is the medical term for osteoarthritis of the knee, the most common form of joint disease worldwide. It involves a gradual breakdown of the cartilage that cushions the ends of the thighbone and shinbone, along with changes in the bone, synovial lining, and surrounding tissues. About 250 million people globally are affected, and while the condition cannot be reversed, a range of treatments can meaningfully reduce pain and improve function at every stage.

More Than Worn-Out Cartilage

The old textbook picture of gonarthrosis as simple “wear and tear” on cartilage has been replaced by something more complex. Research now shows that the disease affects every tissue in the knee joint equally, not just the cartilage surface.¹ The synovial membrane that lines the joint capsule becomes inflamed, and that inflammation has been tied to both worsening structural damage and increasing pain over time. Several recognized risk factors for knee osteoarthritis, including aging, obesity, joint trauma, and repetitive mechanical loading, appear to drive the disease in part by disrupting the biology of that synovial lining.²

At a tissue level, what is going on is a communication breakdown. Cells throughout the joint, including cartilage cells, synovial cells, and bone cells, send and receive chemical signals called cytokines. In a healthy joint those signals keep a balance between building tissue up and breaking it down. In gonarthrosis, chronic low-grade inflammation tips that balance toward destruction.¹ At the same time, abnormal bone remodeling creates tiny cracks and new blood vessels at the boundary between cartilage and bone, letting inflammatory molecules cross between the two tissues more freely than they should.³ Understanding that gonarthrosis is a whole-joint disease, not a cartilage-only problem, matters because it explains why pain and disability don’t always line up neatly with what an X-ray shows.

Symptoms and the Puzzle of Pain

The hallmark symptom is pain around or behind the kneecap that gets worse with activity, especially climbing stairs, squatting, or walking on uneven ground. Early on, the pain often appears after prolonged use and fades with rest. As the disease progresses, you may notice stiffness first thing in the morning or after sitting for a while, typically lasting under half an hour. Swelling around the joint comes and goes and is usually worse after activity. In later stages, people often describe a feeling of instability or the knee “giving way,” along with a gritty or crunching sensation during movement.

One genuinely puzzling feature of gonarthrosis is the gap between what imaging shows and how much pain a person feels. A systematic review of the literature found that among people with knee pain, only about 15 to 76 percent showed structural osteoarthritis on X-ray, and among people whose X-rays did show osteoarthritis, only 15 to 81 percent actually reported pain.⁴ In other words, some people with severely damaged cartilage walk around comfortably, while others with mild structural changes are in significant pain.

A key part of the explanation involves how the nervous system processes pain signals. Research has identified a phenomenon called pain sensitization, where nerve pathways in and around the knee (peripheral sensitization) and in the brain and spinal cord (central sensitization) become amplified over time. A systematic review and meta-analysis confirmed that sensitization is present in people with knee osteoarthritis and appears linked to how severe their symptoms are.⁵ Essentially, the longer the knee has been sending pain signals, the more efficiently the brain learns to process them, and pain can persist even when the structural damage hasn’t worsened. This is one reason that treatments targeting the nervous system, like certain antidepressants or physical therapy approaches focused on graded exposure, can sometimes help knee pain even though they do nothing to cartilage directly.⁶

Who Gets It and Why

Age is the single biggest risk factor, but gonarthrosis is not an inevitable consequence of getting older. Globally, women account for about 60 percent of all osteoarthritis cases, and the gap widens after age 40.⁷ Several factors contribute to that disparity. Differences in joint anatomy and alignment, lower muscle strength around the knee, hormonal shifts (particularly after menopause), and higher rates of obesity all play a role. Women also tend to present for treatment at more advanced stages and report greater pain and functional limitation than men at the same level of structural damage.⁸

Body weight deserves its own mention because its influence is both mechanical and metabolic. Every extra kilogram of body weight translates to roughly four extra kilograms of force on the knee with each step.⁹ But excess body fat also produces hormones called adipokines, such as leptin, which have been linked to cartilage damage, synovial inflammation, and joint swelling independent of body weight itself.¹⁰ That metabolic dimension helps explain why hand osteoarthritis is also more common in people who are overweight, even though the hands don’t bear body weight.

Knee alignment matters, too. If your legs naturally bow inward or outward, that concentrates force on one side of the joint. Bowlegged (varus) alignment roughly doubled the risk of developing knee osteoarthritis in one large study, and the effect was especially pronounced in people who were also overweight.¹¹ A systematic review confirmed strong evidence that malalignment in either direction is an independent risk factor for the disease getting worse once it’s established.¹²

Previous injury is another well-documented trigger. Anterior cruciate ligament (ACL) tears are a major culprit: roughly half of people with an ACL injury develop symptomatic osteoarthritis within 10 to 15 years, regardless of whether the ligament was surgically reconstructed.¹³ Meniscus tears, tibial plateau fractures, and even repeated minor sprains all raise the long-term odds. The term “post-traumatic osteoarthritis” covers these cases, and preventing or quickly stabilizing knee injuries is one of the few genuinely disease-modifying strategies we have right now.¹⁴

Diagnosis Beyond the X-Ray

Most of the time, gonarthrosis is diagnosed clinically. Your doctor listens to your symptoms, examines the knee for swelling, tenderness, reduced range of motion, and crepitus (that grinding sensation), and combines that with your age and history. Plain X-rays remain the standard imaging tool. They reveal joint space narrowing, bone spurs, and sclerosis (hardening) of the bone beneath the cartilage. Severity is commonly graded on the Kellgren-Lawrence scale, from 0 (normal) to 4 (severe).

MRI is not routinely needed for diagnosis but can be valuable in ambiguous cases or when surgery is being planned. MRI picks up cartilage damage, meniscal tears, bone marrow lesions, and synovial inflammation that X-rays miss entirely. Studies comparing MRI-based grading to the Kellgren-Lawrence X-ray scale have shown very high correlation between the two, which suggests that when MRI is used, it generally confirms what plain films show while adding detail about soft-tissue structures.¹⁵ Blood tests are not part of the standard workup for gonarthrosis. They are mainly used to rule out other conditions, such as rheumatoid arthritis or gout, when the presentation isn’t straightforward.

Non-Surgical Treatment

Treatment guidelines from every major rheumatology society put exercise and weight management first, ahead of any medication. This is not a polite suggestion. The evidence is genuinely strong.

Exercise and Strengthening

Quadriceps weakness is one of the most consistent findings in people with knee osteoarthritis, and strengthening those muscles directly reduces pain and improves daily function. Randomized trials show that even a simple five-week program of isometric (static-hold) quadriceps exercises produces measurable improvements in strength, pain, and function compared to no exercise.¹⁶ Another trial looking at quadriceps-strengthening exercises found significant reductions in pain intensity and improvements in several quality-of-life domains, including vitality, physical function, and general health perception.¹⁷ Low-impact aerobic activity like swimming, cycling, or walking on flat ground is also recommended. The key is consistency over intensity.

Weight Loss

Because each kilogram of body weight creates roughly four kilograms of force on the knee per step, even modest weight loss can make a meaningful difference.⁹ Multiply that by thousands of steps a day and the cumulative reduction in joint stress is substantial. The benefits go beyond mechanics. In obese patients who achieved major weight loss, researchers documented reduced joint inflammation, lower levels of inflammatory blood markers, and a shift in cartilage biomarkers suggesting less degradation and more repair.¹⁸ Regardless of the method used, reducing body fat appears to address both the mechanical and inflammatory drivers of the disease.¹⁹

Pain Medication

When exercise and weight loss aren’t enough on their own, anti-inflammatory painkillers (NSAIDs) are the most commonly used medication. A practical finding that many people aren’t aware of: topical NSAIDs, the creams and gels you rub directly onto the knee, work about as well as oral NSAIDs for pain relief and stiffness in knee osteoarthritis.²⁰ The safety advantage of the topical route is considerable. A network meta-analysis combining clinical trial data with real-world evidence found that topical NSAIDs carried roughly half the risk of gastrointestinal bleeding compared to oral NSAIDs, along with lower risks of cardiovascular events and even all-cause mortality.²¹ The trade-off is that topical versions can cause local skin reactions. Oral NSAIDs cause more gut problems.²² For someone with knee osteoarthritis who doesn’t also have widespread pain elsewhere, starting with a topical gel before moving to pills is a reasonable strategy.

Injections

Corticosteroid injections into the knee have been used for decades to provide short-term pain relief, particularly during flare-ups. They work, but the effect fades after weeks to months, and repeated injections may accelerate cartilage loss in some people. Hyaluronic acid (HA) injections aim to restore some of the lubricating properties of joint fluid, but when compared head-to-head with steroids and placebo in a network meta-analysis, no meaningful difference was detected among the three.²³

Platelet-rich plasma (PRP) injections have shown more promise. That same meta-analysis found that PRP produced the best overall outcomes at three, six, and twelve months compared to steroids, hyaluronic acid, and placebo.²³ A separate systematic review and network meta-analysis confirmed PRP and the combination of PRP plus HA as the most effective options for improving function and reducing pain over a year of follow-up, without raising the rate of side effects above placebo.²⁴ A prospective study found that combining PRP and HA gave significantly better pain relief at six months than either injection alone, especially in moderate knee osteoarthritis.²⁵ Despite this growing evidence, PRP is not yet covered by most insurance plans and preparation methods vary widely between clinics, which makes it harder to compare results across studies.

When Surgery Becomes the Conversation

Surgery is generally reserved for people who have exhausted conservative measures and still have significant pain and disability. The options depend on how much of the knee is affected and how old and active you are.

If the damage is mainly in one compartment of the knee (usually the inner side), two options compete. High tibial osteotomy (HTO) involves cutting the shinbone and realigning it to shift weight away from the damaged compartment. Unicompartmental knee arthroplasty (UKA, sometimes called a partial knee replacement) resurfaces just the damaged compartment with metal and plastic components. A meta-analysis comparing the two found that HTO had a higher complication rate and fewer patients achieved excellent or good functional outcomes, but offered a greater range of motion.²⁶ Another meta-analysis supported those findings on complications, noting that the older closing-wedge type of HTO had a significantly higher rate of eventual conversion to total knee replacement compared to UKA, while the newer opening-wedge technique had a lower revision rate that was not statistically different from UKA.²⁷ For younger, active patients, HTO preserves the natural joint and buys time before a future replacement becomes necessary. One study concluded that HTO is a reasonable alternative to UKA even when cartilage damage is severe, especially in relatively young patients.²⁸

Total knee arthroplasty (TKA) replaces the entire joint surface and is the standard procedure for advanced gonarthrosis affecting more than one compartment. Long-term data from a ten-year prospective study of TKA for gonarthrosis reported excellent or good outcomes in 86 percent of patients, with a crude prosthetic survival rate of 98 percent. Around 62 percent of patients could walk more than 500 meters, and the median range of motion reached 104 degrees.²⁹ Modern implants and techniques have improved on those numbers, but residual pain after TKA still occurs in a minority of people. Some of that persistent pain is thought to be related to the central sensitization discussed earlier: if the nervous system has been amplified for years before surgery, removing the structural source of pain doesn’t always reset the pain processing back to normal.³⁰

The Search for Disease-Modifying Drugs

Every treatment discussed so far manages symptoms. None of them has been proven to halt or reverse the structural damage of gonarthrosis. That gap has fueled an enormous research effort into disease-modifying osteoarthritis drugs (DMOADs). Dozens of candidates are in various stages of development, targeting different parts of the disease process: anti-inflammatory agents aimed at specific cytokines, enzyme inhibitors that block cartilage-degrading proteins, growth factors designed to stimulate cartilage repair, and even gene therapies using small RNA molecules to silence destructive pathways.³¹

A few have made headlines. Tanezumab, an antibody that blocks a nerve growth factor, reduced hip and knee pain effectively, but it came with serious safety problems including accelerated joint destruction and more joint replacements, particularly when combined with oral NSAIDs. Other candidates like lorecivivint (a Wnt pathway inhibitor) have shown encouraging early safety and efficacy profiles.³¹ As of mid-2023, however, no DMOAD has been approved for clinical use, and several that once looked promising have failed in later-stage trials. The barrier is not just finding drugs that slow cartilage loss on MRI; it is proving that slowing structural damage translates into less pain and better function for patients, which turns out to be surprisingly hard given the pain-structure disconnect at the heart of this disease.³²

Cardiovascular Risk and the Value of Staying Active

A less obvious consequence of gonarthrosis is its link to cardiovascular disease. A large cohort study found that people with knee osteoarthritis had a roughly 26 percent higher risk of cardiovascular disease, a 20 percent higher risk of heart attack, and a 29 percent higher risk of stroke compared to people without the condition.³³ The likely explanation is that chronic knee pain discourages physical activity, and prolonged inactivity raises cardiovascular risk. Osteoarthritis is also a leading cause of chronic pain broadly, and chronic pain is independently associated with higher rates of depression.³⁴

The encouraging finding from that same cardiovascular study is that exercise appeared to blunt the risk. People with knee osteoarthritis who exercised at least once a week did not show a statistically significant increase in cardiovascular disease risk, while those who were inactive did.³³ This finding reinforces that staying physically active with gonarthrosis is not just about knee health. It feeds into overall longevity and mental well-being in ways that joint replacement alone cannot address.

An Evolutionary Footnote

One of the more intriguing angles on why knee osteoarthritis is so common comes from evolutionary biology. Humans are the only living primates that walk fully upright, and that transition demanded a dramatically redesigned knee. A 2020 study profiled the genetic switches that control cartilage cell activity in human knees and found that during our evolutionary adaptation to bipedalism, natural selection reshaped the regulatory DNA near genes responsible for cartilage development. Some of those same reshaped regions overlap with genetic variants known to raise osteoarthritis risk today.³⁵ In a sense, the gene sequences that helped our ancestors walk and run efficiently on two legs may also be the sequences that leave us vulnerable to joint disease later in life. It is a humbling reminder that gonarthrosis is not simply a failure of modern lifestyle, though weight and inactivity make it worse. Some susceptibility is baked into the biology of being human.

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