Osteoarthritis: What It Is, Why It Occurs, and How It Is Treated

Osteoarthritis is the most common joint disease in the world. According to the World Health Organization, it affects more than 500 million people globally, and in Spain it is the leading cause of chronic musculoskeletal pain in people over the age of 50. Despite this, many misunderstandings persist about its nature, its progression and what can actually be done to manage it.

It is not simply "age-related wear and tear". It is not inevitable or identical in all joints. It is not treated the same in the knee as it is in the hand or hip. And pain, which is the most visible symptom, does not always correlate with radiological severity - there are people with severe osteoarthritis on imaging who have little pain, and people with mild osteoarthritis who have significant functional limitation.

This guide explains what osteoarthritis is, how it occurs, how it differs from other joint diseases, what types exist depending on the joint affected, and what treatment options are scientifically supported to reduce pain and maintain joint function.

What is osteoarthritis: more than "wear and tear"?

Osteoarthritis (also called osteoarthritis in Anglo-Saxon literature) is a degenerative joint disease that affects the hyaline cartilage - the tissue that lines the bony surfaces inside the joint - and all the structures that make up the joint: the subchondral bone, synovial membrane, ligaments and periarticular tendons.

For decades it was considered a purely mechanical disease: cartilage wears out through use and does not regenerate. The current understanding is more complex. Osteoarthritis involves an imbalance between the processes of cartilage synthesis and degradation, mediated by mechanical, inflammatory, metabolic and genetic factors. Articular cartilage, although it has no blood vessels or nerve endings of its own, is in constant communication with the synovial fluid and responds to mechanical and biochemical signals from the joint environment.

When the balance is disrupted - by mechanical overload, chronic low-intensity inflammation, structural nutrient deficits or genetic factors - chondrocytes (the cartilage cells) begin to produce more degradative enzymes than matrix molecules. The progressive result is the loss of cartilage thickness and elasticity, the appearance of osteophytes (bony projections at the joint edges), inflammation of the synovial membrane and, in advanced stages, bone-on-bone contact.

Osteoarthritis vs. arthritis: a distinction that matters

The terms are often used interchangeably in everyday language, but they describe different processes with different causes, evolution and treatment.

Osteoarthritis is degenerative and slowly progressive. It is mainly caused by an imbalance between the regenerative capacity of cartilage and the factors that degrade it. Inflammation is present, but it is secondary to the structural damage, not its primary cause. It mainly affects load-bearing joints (knees, hips, lumbar spine) and hands.

Arthritis is a broader term for joint inflammation as a primary phenomenon. It includes autoimmune diseases such as rheumatoid arthritis - where the immune system attacks the synovial membrane - and psoriatic arthritis, reactive arthritis or ankylosing spondylitis. In these conditions, inflammation is the cause, not the consequence, and treatment is fundamentally different: it includes disease-modifying drugs (DMARDs) and biologics that have no indication in osteoarthritis.

Distinguishing them correctly is not a semantic detail - it is the starting point of proper management.

Causes and risk factors: why osteoarthritis occurs

Osteoarthritis has no single cause. It is a multifactorial disease where several factors converge to break the balance of articular cartilage.

Age. The regenerative capacity of chondrocytes decreases progressively. From the age of 50, the risk increases significantly, although osteoarthritis is not an inevitable consequence of aging - it is a process that age facilitates but requires other cofactors to develop.

Overweight and obesity. They increase the mechanical load on weight-bearing joints (knees, hips, spine). But the relationship is not only mechanical: adipose tissue produces adipokines - proinflammatory cytokines - which have a direct effect on articular cartilage. This is why osteoarthritis of the hands is also more prevalent in obese people, even if the hands do not bear any body load.

Genetic factors. There is a documented hereditary predisposition, especially in hand and hip osteoarthritis. Twin studies suggest that the heritability of knee osteoarthritis is approximately 40-65%.

Previous joint injuries. Injuries to ligaments, menisci or cartilage that are not adequately treated or that leave mechanical sequelae significantly increase the risk of osteoarthritis in that joint. Post-traumatic osteoarthritis can develop in young joints that otherwise would not be at risk.

Work or sports overload. Repetitive physical work with sustained joint loading (construction, agriculture, some impact sports) is associated with increased risk of osteoarthritis in specifically overloaded joints.

Deficiency of structural micronutrients. Articular cartilage depends on the availability of structural proteins - mainly type II collagen - and extracellular matrix glycosaminoglycans. The synthesis and maintenance of these structures require specific cofactors: vitamin C, silicon, zinc, manganese and amino acids such as glucosamine. A chronic deficit of these nutrients does not directly cause osteoarthritis, but it can compromise the regenerative capacity of cartilage when overloaded . Learn more about joint health in this complete guide

Types of osteoarthritis according to the affected joint

Osteoarthritis can affect any synovial joint, but has a predilection for specific joints. Symptoms, functional limitation and treatment options vary by location.

Knee osteoarthritis (gonarthrosis)

This is the most prevalent form and has the greatest impact on quality of life. The knee is a high-load, high-range-of-motion joint - a combination that makes it particularly vulnerable. Symptoms include pain with activity (especially going up and down stairs, getting out of a chair or walking on uneven surfaces), morning stiffness for less than 30 minutes, crepitus with joint movement and, in advanced stages, varus (bowlegged) or valgus (X-knee) deformity.

Adapted physical exercise is one of the pillars of non-pharmacological treatment with the most evidence: it strengthens the periarticular musculature, reduces the load on the cartilage and improves proprioception. Low-impact activities such as swimming, static cycling or pool work have a particularly favorable profile. You could continue reading about Knee osteoarthritis: exercises and use of the bicycle for more information on this subject.

Hand osteoarthritis (rhizarthrosis and interphalangeal osteoarthritis)

This is the most common form in women, especially after menopause. Heberden's nodes (in the distal interphalangeal joints) and Bouchard's nodes (in the proximal joints) are its most characteristic manifestation. Rhizarthrosis - osteoarthritis of the trapeziometacarpal joint of the thumb - causes pain at the base of the thumb and functional limitation for activities requiring grasping (opening jars, turning keys, writing).

In contrast to knee osteoarthritis, mechanical loading is less important in hand osteoarthritis, and systemic hormonal and inflammatory factors are more relevant. Local treatment (orthoses, thermotherapy, strengthening exercises of the intrinsic musculature of the hand) plays a more central role.

Osteoarthritis of the hip (coxarthrosis)

This is the second most frequent location and the one that most frequently leads to joint replacement surgery. The typical pain is located in the groin, radiating to the thigh or knee, and is aggravated by prolonged walking and on initiation of movement after rest. Limitation of hip internal rotation is often the first clinical sign.

Arthrosis of the spine (spondylosis)

Degeneration of the intervertebral discs and facet joints is almost universal with age. It does not always produce symptoms: many people have significant degenerative changes on imaging without associated pain. When it does produce symptoms, chronic low back or neck pain and stiffness are the main symptoms. The appearance of osteophytes may compress nerve structures and produce radiculopathy.

Symptoms of osteoarthritis: how to recognize it

The cardinal symptom is joint pain with specific characteristics that distinguish it from other types of joint pain:

It is a mechanical rhythm pain , increases with activity and is relieved with rest. In advanced stages, pain may appear at rest and even at night. It is insidious in onset: it usually appears gradually, without a clear triggering episode. Morning stiffness is short - less than 30 minutes - unlike rheumatoid arthritis, where morning stiffness can last for hours. Crepitus on joint movement (the characteristic "crackle") is common. In active phases there may be joint effusion with increased volume.

Pain intensity does not correlate linearly with radiological damage - this is one of the most clinically relevant phenomena in osteoarthritis. A patient with radiological grade 4 (the maximum) osteoarthritis may have manageable pain, and another with grade 2 may be very functionally limited. Central factors (central nervous system sensitization, psychological state, sleep quality) greatly modulate pain perception in chronic osteoarthritis.

Diagnosis: when to consult and what to expect

The diagnosis of osteoarthritis is fundamentally clinical: the history of pain, its rhythm and its characteristics, together with the physical examination of the joint, are sufficient for diagnosis in most cases. Imaging tests (simple X-ray as a first line; MRI if there are diagnostic doubts or other pathologies are suspected) confirm and stage the structural damage, but are not indispensable for initiating treatment.

Consultation with the physician is recommended when:

Joint pain interferes with daily activities for more than two weeks. Joint swelling, warmth or redness appears (which may indicate an active inflammatory component or a different pathology). There is fever associated with joint pain (a warning sign for septic arthritis). The pain is very intense, of sudden onset or of inflammatory rhythm (worse at rest, better with movement).

Blood tests are normal in primary osteoarthritis - the differential diagnosis with inflammatory arthritis is based on the fact that in the latter inflammatory markers (CRP, ESR) are usually elevated and autoantibodies (rheumatoid factor, anti-CCP) may appear.

Treatment of osteoarthritis: what works and what is the evidence?

There is no treatment that reverses the damage already done to articular cartilage. The goal of treatment is to reduce pain, maintain joint function and slow progression. International clinical guidelines (EULAR, ACR, OARSI) are consistent in pointing out that non-pharmacological treatment has as much or more evidence than pharmacological treatment, and should be the basis of management.

Non-pharmacological treatment (first line)

Adapted physical exercise. This is the intervention with the most evidence in knee and hip osteoarthritis. Exercise reduces pain, improves function and quality of life, and has effects on synovial inflammation comparable to those of NSAIDs in some studies. The type of exercise should be adapted to the affected joint and the patient's level of fitness: muscle strengthening, low-impact aerobic exercise, proprioception and flexibility exercises.

Weight control. In knee and hip osteoarthritis, weight loss reduces joint mechanical load and inflammatory mediators derived from adipose tissue. It is estimated that each kilogram of weight lost reduces the load on the knee by approximately 4 kg during walking.

Education and self-management. Therapeutic education programs that teach patients to understand their disease, modify activities and manage pain have been shown to reduce perceived disability and improve adherence to treatment.

Physical therapy. Manual therapy, supervised exercises and pain modulation techniques (TENS, thermotherapy, hydrotherapy) have evidence of short- to medium-term benefit in osteoarthritis of the knee and hip.

Pharmacological treatment

Paracetamol. It was the first-line analgesic in the classic guidelines, but its efficacy in osteoarthritis has been questioned in the most recent meta-analyses. Its safety profile remains favorable at the correct doses.

Topical and oral NSAIDs. NSAIDs have greater analgesic efficacy than paracetamol in osteoarthritis. The topical formulation (diclofenac gel) has comparable efficacy to the oral formulation with less systemic risk, and is preferred in older people or those with gastrointestinal or cardiovascular comorbidities. Oral NSAIDs should be used at the lowest effective dose and for the shortest possible time.

Chondroprotectors: glucosamine and chondroitin sulfate. They are indicated in osteoarthritis of the knee in the European guidelines (EULAR), although the evidence is heterogeneous. Some trials show benefit in pain and function; others find no difference with placebo. The quality of the product (crystalline form of glucosamine, purity of chondroitin) affects the results and may explain part of the heterogeneity.

Intra-articular infiltrations. Intra-articular corticosteroids have short-term (weeks) analgesic efficacy. Intra-articular hyaluronic acid has more debated evidence, with some studies showing medium-term functional benefit in knee osteoarthritis.

Nutrition and micronutrients in the management of osteoarthritis

Articular cartilage, although avascular, depends on nutrient diffusion from synovial fluid to maintain its metabolic function. The availability of certain micronutrients has implications for the synthesis and maintenance of the cartilage extracellular matrix.

Silicon participates in the synthesis of type II collagen (the main collagen of cartilage) and in the formation of the proteoglycans of the extracellular matrix. Bioavailable orthosilicic acid is the form that the body can use for these processes; insoluble forms such as silicon dioxide are not absorbed. The tissue concentration of silicon decreases with age, which coincides temporally with the increased prevalence of osteoarthritis.Silicon for the joints, in my opinion, is of vital importance.

Vitamin C is a cofactor in collagen synthesis - without adequate vitamin C, the hydroxylation of proline and lysine that stabilizes collagen chains cannot be completed. Vitamin D has receptors on chondrocytes and participates in the regulation of their metabolic activity; some epidemiological studies find an association between low vitamin D levels and increased radiological progression of osteoarthritis, although the interventional evidence is still inconsistent. Manganese and zinc are cofactors in enzymes involved in the synthesis of glycosaminoglycans.

No micronutrient has sufficient evidence to be considered a treatment for established osteoarthritis. Their role is more relevant in preventive strategies and metabolic support of cartilage than in the management of acute pain.

Surgery

Total arthroplasty (joint replacement) is the gold standard surgical treatment for advanced osteoarthritis with severe pain and functional limitation that does not respond to conservative treatment. The results in quality of life and function are excellent in the knee and hip. Knee arthroscopy is not indicated in osteoarthritis - clinical trials have not demonstrated superiority over conservative treatment.

What the current treatments can and cannot do

A realistic expectation is part of osteoarthritis management. No currently available treatment regenerates articular cartilage already lost. Effective treatments reduce pain, improve function, can slow progression, and make it possible to maintain an active life for years or decades before surgery is necessary - or avoided altogether if management is appropriate.

The progression of osteoarthritis is neither linear nor inevitable. There are people with grade 2-3 osteoarthritis of the knee who maintain excellent function for decades with active management (regular exercise, weight control, periodic physical therapy). The passive attitude - waiting until the pain becomes unbearable before taking action - is the one that produces the worst results.

Frequently asked questions about osteoarthritis

Is there a cure for osteoarthritis?

Not in the sense of reversing the structural damage already produced. However, "no cure" does not mean "no effective treatment". Pain can be controlled, function can be maintained and progression can be slowed with proper management. Joint replacement surgery, when indicated, produces excellent results in quality of life. The message that "osteoarthritis is untreatable" is clinically inaccurate and leads to neglectful attitudes that worsen functional prognosis.

Does cold make osteoarthritis worse?

Many people with osteoarthritis report increased joint pain and discomfort in cold weather or changes in atmospheric pressure. The physiological basis for this phenomenon is not fully elucidated - mechanisms related to changes in synovial fluid viscosity and sensitization of periarticular nociceptors have been proposed - but clinical experience consistently documents it. Cold does not accelerate structural damage, but it can modify the perception of pain and stiffness.

See what the Spanish Society of Rheumatology says about this:

Can you exercise with osteoarthritis?

Not only can it be done - it is one of the mainstays of treatment with the most evidence. Prolonged rest causes muscle atrophy, reduces joint support and worsens the functional prognosis. The type, intensity and frequency of exercise should be tailored to the affected joint, the stage of the disease and the patient's physical condition. Periods of acute pain may require a temporary reduction of the load, but not the abandonment of exercise.

What foods help or harm osteoarthritis?

There is no specific diet for osteoarthritis with strong evidence of structural modification. There is evidence that a pro-inflammatory diet (high in refined sugars, trans fats, ultra-processed) can amplify synovial inflammation and pain. A diet with an anti-inflammatory profile - rich in omega-3 fatty acids, vegetables, fruits, extra virgin olive oil and low in ultra-processed foods - has an indirect benefit on joint inflammation and weight control. Olive oil contains oleocanthal, a compound with anti-inflammatory properties whose mechanism has been compared to that of ibuprofen at the molecular level.

Does osteoarthritis only affect older people?

No. Although the prevalence increases significantly with age, osteoarthritis can affect young people with specific risk factors: previous joint injuries (post-traumatic osteoarthritis), obesity, genetic predisposition or work or sports overload. In high-performance athletes, post-traumatic knee osteoarthritis may appear from the age of 30-35 years if there were poorly resolved ligament or meniscus injuries.

We recommend this reading: EULAR - Recommendations for the management of knee and hip osteoarthritis (patient version).