1. What is arthrosis and how it develops
Arthrosis (osteoarthritis, OA) is a chronic degenerative joint disease driven by progressive breakdown of articular cartilage with subsequent involvement of the subchondral bone, synovium, ligaments and muscles. The term "arthritis" (Greek arthron + -itis "inflammation") is technically inaccurate for arthrosis — the main pathogenetic axis is mechanical wear, although a secondary inflammatory component is present at all stages.
Pathogenesis develops as a cascade:
- Microdamage stage — imbalance between synthesis and degradation of type II collagen and matrix proteoglycans. Chondrocytes shift to a catabolic phenotype.
- Fibrillation stage — the superficial cartilage layer "frays" and loses smoothness. Microcracks appear.
- Subchondral bone exposure — cartilage is destroyed, bone rubs on bone. Reactive osteophytes and bone cysts form.
- Deformity stage — the joint loses congruence; varus or valgus deformity develops. Pain becomes constant.
According to WHO (Global Burden of Disease 2023), 528 million people worldwide have arthrosis, making it the leading cause of chronic pain and disability in people over 50.
2. Arthrosis vs arthritis — the key difference
The most common clinical mistake is confusing these diagnoses. They differ fundamentally in mechanism, treatment and prognosis.
| Feature | Arthrosis | Arthritis |
|---|---|---|
| Nature | Mechanical wear | Immune-inflammatory or metabolic process |
| Pain pattern | On loading, eases at rest | At rest, at night, in the morning |
| Morning stiffness | 5–30 minutes | >60 minutes |
| Localisation | Large weight-bearing joints | Small symmetric joints |
| ESR, CRP | Normal | Elevated |
| RF, ACPA | Negative | Often positive (RA) |
| Treatment | Exercise, NSAIDs, regenerative medicine, joint replacement | Disease-modifying therapy (methotrexate, biologics) |
See: arthrosis: overview and arthritis (systemic).
3. Kellgren–Lawrence stages
The Kellgren–Lawrence radiographic classification (1957) is the global standard for assessing arthrosis severity and is used in all clinical guidelines (OARSI, AAOS, NICE).
- Stage 0 — normal. No radiographic signs.
- Stage I (doubtful) — possible small osteophytes, doubtful joint space narrowing. Clinically: episodic load-related pain. The ideal moment for regenerative methods.
- Stage II (minimal) — clear osteophytes, possible joint space narrowing. Regular load-related pain, 10–20 min of morning stiffness. Best target for regenerative treatment — Effect on cartilage tissue.
- Stage III (moderate) — multiple osteophytes, marked narrowing, subchondral sclerosis, possible cysts. Pain almost constant.
- Stage IV (severe) — large osteophytes, gross deformity, bone-on-bone. Constant pain, including at rest. Joint replacement is the method of choice. Regenerative treatment can reduce pain temporarily but does not solve the problem.
4. Arthrosis by joint
4.1 Gonarthrosis (knee arthrosis)
The most frequent location — 250 million patients worldwide. Women over 50 are affected more often. Key risk factors: BMI >25, varus/valgus deformity, prior meniscus tear, repeated injuries. See: gonarthrosis.
4.2 Coxarthrosis (hip arthrosis)
The most "disabling" arthrosis — quickly limits mobility. Pain is more often felt in the groin, sometimes referred to the knee (a diagnostic pitfall). Particularly difficult for regenerative methods because of the joint depth — ultrasound navigation is critical. See:coxarthrosis.
4.3 Shoulder arthrosis (omarthrosis)
Less common because the shoulder is non-weight-bearing, but painful. Often linked to long-standing rotator cuff tendinopathy. Compensatory scapular movement may mask the symptoms.
4.4 Rhizarthrosis (basal thumb arthrosis)
Affects the thumb base, typical for women over 50 and pianists/massage therapists. Impairs grip, opening jars, turning keys. See: rhizarthrosis.
4.5 Ankle arthrosis
More often post-traumatic (after malleolar fractures, ligament tears). Common in athletes and dancers. See: ankle arthrosis.
4.6 Spondyloarthrosis (facet joint arthrosis)
Arthrosis of the spinal facet joints — a frequent cause of chronic back pain in older adults. See: facet syndrome.
5. Diagnostics
Standard algorithm:
- Clinical examination. History, range of motion, tenderness, crepitus, deformity. Functional tests (McMurray, Patrick, Trendelenburg).
- X-ray in 2 views — basis for K-L classification. Should be performed weight-bearing for load-bearing joints.
- Ultrasound — assessment of synovitis, effusion, osteophytes, tendon and ligament status. Cheaper and more accessible than MRI for screening.
- MRI 1.5 T or 3 T — gold standard for cartilage, meniscus, bone marrow oedema, cysts. Mandatory for suspected osteonecrosis or for planning regenerative therapy.
- Blood tests — to differentiate from arthritis: ESR, CRP, CBC, RF, ACPA, uric acid.
- Joint aspiration (with significant effusion) — synovial fluid analysis with cell count and crystals.
For MRI interpretation see our guide "How to read an MRI".
6. Risk factors and prevention
Non-modifiable: age (a sharp rise after 50), sex (women 2× more often), genetics (FRZB, GDF5), congenital traits (hip dysplasia, flat feet).
Modifiable:
- Excess weight — every kilo adds 4 kg of load on the knee while walking. A 5 kg weight loss reduces the risk of symptomatic gonarthrosis by 50%.
- Sedentary lifestyle — synovial fluid is produced by movement. "Rusting" is a real mechanism.
- Unbalanced sport — high-impact (professional asphalt running, weightlifting, martial arts) accelerates progression.
- Injuries — ACL rupture increases arthrosis risk 5–7×. Post-injury rehabilitation is critical.
- Vitamin D deficiency — increases OA risk by 25%. Target 25(OH)D >30 ng/ml.
7. Arthrosis treatment tree
The modern paradigm is a treatment pyramid moving from least invasive to most radical. Each step lasts a minimum of 6–12 months.
Step 1: Basic conservative care
Exercise (3×/week), weight management, orthoses, physiotherapy (magnet, laser, shockwave), paracetamol as needed. Effective in 60–70% of K-L I–II cases. See: physiotherapy vs regenerative.
Step 2: Symptomatic injection therapy
Short courses of NSAIDs, hyaluronic acid (3 injections at 1-week intervals). Corticosteroids — last resort, no more than 3×/year.
Step 3: Regenerative medicine
When steps 1–2 fail for 6–12 months. PRP, CGF, MFAT, BMAC under ultrasound navigation. Effectiveness 70–85% depending on stage. See: regenerative orthopedics.
Step 4: Surgery
Arthroscopy — only for concomitant mechanical blocks (meniscus tear with locking). Corrective osteotomy — for significant deformity with localised arthrosis. Joint replacement — for K-L IV.
8. The role of regenerative treatment
Regenerative treatment occupies a niche between conservative therapy and surgery. It is a biological method that restores joint tissues through injections of the patient's own growth factors and stem cells. Key advantages:
- Regeneration, not symptom masking. an effect on cartilage tissue (K-L I–II), reduced bone marrow oedema, restored synovial membrane.
- No corticosteroid side effects. Does not damage cartilage with repeated use; can be used as often as needed.
- WADA-compliant. Applicable to professional athletes with arthrosis.
- Compatible with other treatments. Boosts exercise; no conflict with disease-modifying therapy for RA.
- Delays joint replacement. By 5–10 years even at K-L III — critical for patients aged 50–60 who would otherwise need revision in their 70s.
Comparisons: Regenerative treatment vs joint replacement, PRP vs hyaluronic.
9. Lifestyle in arthrosis
Diet: Mediterranean (fish 2–3×/week, olive oil, vegetables, nuts) reduces inflammation. Vitamin D (target 25(OH)D 30–60 ng/ml), magnesium, omega-3. Limit red meat, refined sugar, trans fats.
Activity: at least 150 minutes of aerobic exercise per week (swimming, cycling, Nordic walking) plus 2 strength sessions (focus on muscles around the affected joint — quadriceps for gonarthrosis, glutes for coxarthrosis).
Weight: losing even 5–10% substantially reduces symptoms. Long-term goal: BMI <25.
Sleep and stress: chronic sleep loss and cortisol amplify pain perception. Sleep hygiene, mindfulness, psychotherapy if needed.
10. Frequently asked questions
Restoring cartilage to a fully healthy state is not yet possible with any method, including joint replacement (which replaces, not restores). However, progression can be stopped, pain significantly reduced and joint function restored.
Not necessarily. In 40% of patients with stage II arthrosis the disease stabilises for 10+ years with proper treatment and lifestyle. Key drivers of progression: excess weight (−1 kg = −4 kg load on the knee), sedentary lifestyle, untreated mechanical imbalances (flat feet, leg-length difference, spinal curvature), repeated corticosteroid injections.
Arthrosis is mechanical cartilage breakdown (wear). Arthritis is immune or metabolic inflammation. Arthrosis usually affects 1–2 large joints (knee, hip); arthritis affects several symmetric small joints. Morning stiffness in arthrosis lasts <30 min, in arthritis >60 min. Labs: in arthritis ESR, CRP, RF, ACPA are elevated — in arthrosis they are normal. Treatment differs fundamentally.
According to the Cochrane Review (2015) and OARSI guidelines, the effect is comparable to placebo. Some patients report subjective improvement (likely antioxidant effect). Not harmful, inexpensive, can be taken for 3–6 months as supportive therapy. They do not replace pathogenetic treatment.
Low-impact — strongly recommended: swimming, cycling on flat terrain, Nordic walking, elliptical, yoga, Pilates, water aerobics. High-impact — undesirable: running on asphalt, jumping, martial arts, tennis on hard courts. A sedentary lifestyle is contraindicated and accelerates progression.
Yes, temporarily. Hyaluronate improves joint "lubrication" and reduces pain for 6–12 months. But it does not trigger Effect on cartilage tissue. Effectiveness depends on stage: K-L II — good, K-L III — partial, K-L IV — almost no effect. Regenerative treatment can be combined with hyaluronate for synergy.
With repeated injections — yes. A JAMA systematic review (McAlindon, 2017) showed accelerated cartilage loss with triamcinolone every 3 months for 2 years. FDA: no more than 3 injections per year per joint. For long-term treatment regenerative methods are preferred — they treat the cause rather than mask the pain.
There are no absolute indications — it is always a shared decision. Typical candidate: K-L IV with axial deformity, severe pain at rest and at night, walking <500 m without rest, all conservative and regenerative methods exhausted. Up to that threshold other options should be tried, since replacement is irreversible.
Low-impact — yes, after 3–6 months: swimming, cycling, golf, walking, gentle yoga. High-impact (running, jumping, martial arts, advanced skiing) — not recommended: they accelerate prosthesis wear. Average prosthesis lifespan is 15–25 years; with high activity revision may be needed sooner.
Yes, the genetic component is 30–60% of risk (twin studies). FRZB, GDF5, LRP5 genes are associated with OA susceptibility. However "genes are not destiny" — lifestyle, weight, physical activity and early injury correction substantially reduce realisation of the genetic risk.
Clinic and method matching — free of charge
Describe your case and attach your MRI report. We will identify clinics that use the relevant methods and forward your request to them. No obligation; we reply within two working days.

