What is Osteoarthritis
A plain-English explanation of what actually happens inside a joint when osteoarthritis develops — the biology, the pain, the risk factors, and why understanding it helps you make better decisions about your care.
Osteoarthritis is the most common joint disease in the world.1 In the United Kingdom, approximately one in ten adults have clinically diagnosed osteoarthritis — around 8.75 million people sought treatment for it in 2013 alone, and prevalence has continued to rise since.2,3 And yet, despite how common it is, osteoarthritis remains one of the most misunderstood conditions in medicine.
Most patients arrive in clinic believing it is simply “wear and tear” — an inevitable consequence of getting older that nothing meaningful can be done about. That is not quite right, and understanding what osteoarthritis actually is will help you engage more meaningfully with your treatment options, whether surgical or non-surgical.
What is happening inside the joint?
A healthy joint is a remarkable piece of biological engineering. The ends of the bones are coated in a smooth, white tissue called articular cartilage, which acts as both a shock absorber and a near-frictionless gliding surface. In a normal hip or knee, the friction coefficient of this cartilage — the measure of how much resistance there is to movement — is lower than ice sliding on ice.4
In osteoarthritis, this cartilage gradually breaks down. It becomes softer, then fibrillated — a term that describes the fraying, like worn rope — and then progressively thinner, until in advanced disease it is gone entirely. This leaves bone pressing directly against bone, which is what patients and surgeons mean when they describe a joint as “bone on bone.”1
This process does not happen overnight, and it does not happen in isolation.
It is not just about cartilage
One of the most important shifts in our understanding of osteoarthritis over the past two decades is the recognition that it is a whole-joint disease — not simply cartilage wear, but a complex, interrelated failure of every tissue that makes up the joint.5 As the cartilage breaks down, several other simultaneous changes occur:
- Subchondral bone changes — the bone immediately beneath the cartilage becomes thicker and denser (a process called sclerosis), and may develop small fluid-filled cavities called subchondral cysts.5
- Osteophyte formation — the body attempts to stabilise the failing joint by growing bony spurs around the edges, called osteophytes. These are visible on X-ray and are one of the features surgeons look for when assessing severity.
- Synovial inflammation — the synovium, the thin membrane that lines the joint and produces lubricating fluid, can become inflamed and thickened in osteoarthritis. This inflammation contributes significantly to pain and swelling.6
- Muscle wasting — pain, reduced movement, and the body’s protective instincts lead to progressive weakening of the muscles around the joint. This in turn increases the mechanical load on the already damaged cartilage, creating a cycle that can accelerate deterioration.
Understanding that osteoarthritis involves all of these tissues — not just cartilage — has important implications for how it is treated. Exercise and muscle strengthening, for example, are not merely about pain relief; they directly address the muscle wasting component of the disease and reduce the load transmitted through the joint.
Why does it cause pain?
This is a question that surprises many patients: articular cartilage itself has no nerve supply. The cartilage loss, therefore, is not directly painful. The pain of osteoarthritis arises from the surrounding structures that do have rich nerve endings — the subchondral bone, the joint capsule, the synovium, the ligaments, and the periosteum (the membrane covering the outer surface of bone).7
This explains a phenomenon that puzzles patients and sometimes their doctors: the severity of pain does not always correspond to the severity of X-ray changes. It is entirely possible to have severely reduced joint space on an X-ray with relatively manageable pain, or to be severely disabled by pain with X-ray findings that look only moderately abnormal.8 The X-ray shows the cartilage loss; it does not show the complex neurological, inflammatory, and psychological factors that determine how much that cartilage loss hurts.
This discordance has an important practical implication: X-ray findings alone should never be the sole reason to proceed to surgery. The decision to operate is based on your symptoms, function, and quality of life — not on what the pictures show.9
Who develops osteoarthritis — and why?
Osteoarthritis becomes more prevalent with increasing age, but age alone does not cause it. The major risk factors are well established in the scientific literature:1,3
- Age — prevalence rises sharply after the age of 45, and the condition is significantly more common after 60.
- Body weight — obesity is the single strongest modifiable risk factor. Excess weight increases the mechanical load across weight-bearing joints, and adipose (fat) tissue also produces inflammatory mediators that may directly damage cartilage.1
- Previous joint injury — a history of fracture into a joint, meniscal tear, anterior cruciate ligament injury, or significant joint trauma substantially increases the lifetime risk of osteoarthritis in that joint, sometimes by several decades.
- Genetics — there is a clear hereditary component, particularly for hand and knee osteoarthritis. If a parent or sibling has osteoarthritis, your risk is meaningfully increased.10
- Joint shape — conditions such as hip dysplasia (where the socket is shallow or maloriented) or femoroacetabular impingement (abnormal contact between the ball and socket) predispose certain individuals to early cartilage damage and osteoarthritis, sometimes in their thirties or forties.
- Sex — osteoarthritis is more common in women than men, and the gap widens significantly after the menopause, suggesting that oestrogen may play a protective role in cartilage metabolism.1
- Occupation and repetitive loading — certain occupations involving heavy lifting, prolonged standing, or repetitive joint stress are associated with higher rates of knee osteoarthritis in particular.
How is osteoarthritis diagnosed?
The current NICE guideline (NG226, 2022) is clear on this point: osteoarthritis is a clinical diagnosis.9 This means it is diagnosed based on your symptoms and examination findings, not on imaging alone. The classic diagnostic criteria are:
- Age 45 or over
- Activity-related joint pain
- Morning stiffness lasting no more than 30 minutes
If these three criteria are met and there are no atypical features suggesting an alternative diagnosis — such as inflammatory arthritis, gout, or malignancy — X-rays and blood tests are not routinely required to make the diagnosis and begin treatment.
That said, X-rays remain valuable for assessing severity, planning surgery, and ruling out other causes of joint pain. The Kellgren-Lawrence grading system (grades 0 to 4) is the most widely used radiographic classification, based on features including joint space narrowing, osteophyte formation, subchondral sclerosis, and cyst formation.11
Can osteoarthritis be reversed?
Currently, no treatment has been proven to restore lost cartilage or reverse the structural changes of established osteoarthritis in the clinical setting — though this remains an active and promising area of research. However, the goals of management are clear and achievable: reduce pain, improve function, maintain quality of life, and delay or avoid the need for surgery where possible.
Weight loss, targeted exercise, appropriate analgesia, and activity modification can make a very significant difference to symptoms and function, even in the presence of substantial structural disease. The NICE guideline identifies exercise and weight management (where appropriate) as the two most important first-line treatments — not medication, and not surgery.9
Understanding what osteoarthritis is — and what it is not — is the foundation for making informed decisions about your care. The articles that follow in this guide will take you through each stage of the journey, from living well with osteoarthritis to understanding what surgery involves, how to assess the risks, and what recovery looks like.
- Osteoarthritis is a whole-joint disease — cartilage, bone, synovium, and muscle are all involved, not just cartilage.
- Cartilage has no nerve supply, so pain comes from surrounding structures. This is why X-ray severity and pain severity do not always match.
- The single strongest modifiable risk factor is body weight — even modest weight loss can meaningfully reduce joint load and symptoms.
- Osteoarthritis is a clinical diagnosis — your symptoms and examination findings matter more than your X-ray appearances alone.
- Exercise and weight management are the two most important first-line treatments according to NICE — not medication, and not surgery.
- No treatment currently reverses osteoarthritis, but symptoms and function can be very significantly improved with the right management.
Pathophysiology
The primary initiating event in osteoarthritis pathogenesis remains debated, but current evidence points to a failure of the chondrocyte — the cartilage cell — to maintain matrix homeostasis in the face of mechanical or biochemical stress. Catabolic cytokines, particularly interleukin-1 beta (IL-1β) and tumour necrosis factor alpha (TNF-α), upregulate matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzymes, which degrade the two principal components of the cartilage matrix: collagen type II and aggrecan.
Simultaneously, subchondral bone undergoes complex remodelling. Increased osteoclast activity initially leads to bone loss, followed by excessive osteoblast activity producing sclerotic, mechanically inferior bone. TGF-β plays a context-dependent and complex role in this process. The synovium contributes via macrophage-driven release of additional catabolic mediators, creating a self-amplifying inflammatory loop within the joint.
Radiographic Grading
The Kellgren-Lawrence (KL) classification remains the most widely used radiographic grading system (grades 0–4), though it has well-recognised limitations in predicting symptom severity. Grade 0 indicates no features; grade 4 indicates severe joint space narrowing with large osteophytes, subchondral sclerosis, and deformity. The OARSI (Osteoarthritis Research Society International) atlas provides a more granular semi-quantitative assessment.
MRI-based assessment using validated scoring systems such as MOAKS (MRI Osteoarthritis Knee Score) or WORMS (Whole-Organ Magnetic Resonance Imaging Score) allows simultaneous evaluation of cartilage morphology, bone marrow lesions, meniscal integrity, synovitis, and effusion — providing a more complete picture of disease burden than plain radiographs alone.
The Pain Mechanism
Nociceptive input in OA arises from subchondral bone (via intraosseous hypertension and microfractures), the joint capsule, synovium, periosteum, and periarticular ligaments and muscles — none of which is cartilage. Central sensitisation — an amplification of pain signalling within the central nervous system — is increasingly recognised as a major contributor to chronic pain in OA, particularly in patients with disproportionate pain relative to structural findings. This has important implications for surgical outcome: central sensitisation is associated with poorer results after joint replacement.
All articles on this site are evidence-based and referenced to peer-reviewed literature, national guidelines, and registry data. References are in Vancouver format as used in medical journals.
1. Hunter DJ, Bierma-Zeinstra S. Osteoarthritis. Lancet. 2019;393(10182):1745–1759. SEMINAL REVIEW
doi:10.1016/S0140-6736(19)30417-9 · PMID: 31034380
2. Versus Arthritis. Musculoskeletal Calculator — Osteoarthritis Prevalence Estimates for England. Chesterfield: Versus Arthritis; 2013.
Available at: versusarthritis.org
3. Swain S, Sarmanova A, Mallen C, Kuo CF, Coupland C, Doherty M, Zhang W. Trends in incidence and prevalence of osteoarthritis in the United Kingdom: findings from the Clinical Practice Research Datalink (CPRD). Osteoarthritis Cartilage. 2020;28(6):792–801. UK EPIDEMIOLOGY
doi:10.1016/j.joca.2020.03.004 · PMID: 32224033
4. Greene GW, Banquy X, Lee DW, Lowrey DD, Yu J, Israelachvili JN. Adaptive mechanically controlled lubrication mechanism found in articular joints. Proc Natl Acad Sci USA. 2011;108(13):5255–5259. BASIC SCIENCE
doi:10.1073/pnas.1101002108 · PMID: 21402921
5. Loeser RF, Goldring SR, Scanzello CR, Goldring MB. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum. 2012;64(6):1697–1707. SEMINAL REVIEW
doi:10.1002/art.34453 · PMID: 22392533
6. Mathiessen A, Conaghan PG. Synovitis in osteoarthritis: current understanding with therapeutic implications. Arthritis Res Ther. 2017;19(1):18. REVIEW
doi:10.1186/s13075-017-1229-9 · PMID: 28148295
7. Kidd BL, Langford RM, Wodehouse T. Arthritis and pain. Current approaches in the treatment of arthritic pain. Arthritis Res Ther. 2007;9(3):214. REVIEW
doi:10.1186/ar2147 · PMID: 17659063
8. 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. SYSTEMATIC REVIEW
doi:10.1186/1471-2474-9-116 · PMID: 18764949
9. National Institute for Health and Care Excellence. Osteoarthritis in over 16s: diagnosis and management. NICE Guideline NG226. London: NICE; October 2022. NICE GUIDELINE
Available at: nice.org.uk/guidance/ng226
10. Valdes AM, Spector TD. Genetic epidemiology of hip and knee osteoarthritis. Nat Rev Rheumatol. 2011;7(1):23–32. REVIEW
doi:10.1038/nrrheum.2010.191 · PMID: 21079645
11. Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis. 1957;16(4):494–502. ORIGINAL ARTICLE
doi:10.1136/ard.16.4.494 · PMID: 13498604
12. GBD 2021 Osteoarthritis Collaborators. Global, regional, and national burden of osteoarthritis, 1990–2020 and projections to 2050: a systematic analysis for the Global Burden of Disease Study 2021. Lancet Rheumatol. 2023;5(9):e508–e522. GLOBAL BURDEN
doi:10.1016/S2665-9913(23)00163-7 · PMID: 37551507
- Osteoarthritis is a whole-joint disease — cartilage, bone, synovium, and muscle are all involved, not just cartilage.
- Cartilage has no nerve supply, so pain comes from surrounding structures. This is why X-ray severity and pain severity do not always match.
- The single strongest modifiable risk factor is body weight — even modest weight loss can meaningfully reduce joint load and symptoms.
- Osteoarthritis is a clinical diagnosis — your symptoms and examination findings matter more than your X-ray appearances alone.
- Exercise and weight management are the two most important first-line treatments according to NICE — not medication, and not surgery.
- No treatment currently reverses osteoarthritis, but symptoms and function can be very significantly improved with the right management.
Pathophysiology
The primary initiating event in osteoarthritis pathogenesis remains debated, but current evidence points to a failure of the chondrocyte — the cartilage cell — to maintain matrix homeostasis in the face of mechanical or biochemical stress. Catabolic cytokines, particularly interleukin-1 beta (IL-1β) and tumour necrosis factor alpha (TNF-α), upregulate matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzymes, which degrade the two principal components of the cartilage matrix: collagen type II and aggrecan.
Simultaneously, subchondral bone undergoes complex remodelling. Increased osteoclast activity initially leads to bone loss, followed by excessive osteoblast activity producing sclerotic, mechanically inferior bone. TGF-β plays a context-dependent and complex role in this process. The synovium contributes via macrophage-driven release of additional catabolic mediators, creating a self-amplifying inflammatory loop within the joint.
Radiographic Grading
The Kellgren-Lawrence (KL) classification remains the most widely used radiographic grading system (grades 0–4), though it has well-recognised limitations in predicting symptom severity. Grade 0 indicates no features; grade 4 indicates severe joint space narrowing with large osteophytes, subchondral sclerosis, and deformity. The OARSI (Osteoarthritis Research Society International) atlas provides a more granular semi-quantitative assessment.
MRI-based assessment using validated scoring systems such as MOAKS (MRI Osteoarthritis Knee Score) or WORMS (Whole-Organ Magnetic Resonance Imaging Score) allows simultaneous evaluation of cartilage morphology, bone marrow lesions, meniscal integrity, synovitis, and effusion — providing a more complete picture of disease burden than plain radiographs alone.
The Pain Mechanism
Nociceptive input in OA arises from subchondral bone (via intraosseous hypertension and microfractures), the joint capsule, synovium, periosteum, and periarticular ligaments and muscles — none of which is cartilage. Central sensitisation — an amplification of pain signalling within the central nervous system — is increasingly recognised as a major contributor to chronic pain in OA, particularly in patients with disproportionate pain relative to structural findings. This has important implications for surgical outcome: central sensitisation is associated with poorer results after joint replacement.
All articles on this site are evidence-based and referenced to peer-reviewed literature, national guidelines, and registry data. References are in Vancouver format as used in medical journals.
1. Hunter DJ, Bierma-Zeinstra S. Osteoarthritis. Lancet. 2019;393(10182):1745–1759. SEMINAL REVIEW
doi:10.1016/S0140-6736(19)30417-9 · PMID: 31034380
2. Versus Arthritis. Musculoskeletal Calculator — Osteoarthritis Prevalence Estimates for England. Chesterfield: Versus Arthritis; 2013.
Available at: versusarthritis.org
3. Swain S, Sarmanova A, Mallen C, Kuo CF, Coupland C, Doherty M, Zhang W. Trends in incidence and prevalence of osteoarthritis in the United Kingdom: findings from the Clinical Practice Research Datalink (CPRD). Osteoarthritis Cartilage. 2020;28(6):792–801. UK EPIDEMIOLOGY
doi:10.1016/j.joca.2020.03.004 · PMID: 32224033
4. Greene GW, Banquy X, Lee DW, Lowrey DD, Yu J, Israelachvili JN. Adaptive mechanically controlled lubrication mechanism found in articular joints. Proc Natl Acad Sci USA. 2011;108(13):5255–5259. BASIC SCIENCE
doi:10.1073/pnas.1101002108 · PMID: 21402921
5. Loeser RF, Goldring SR, Scanzello CR, Goldring MB. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum. 2012;64(6):1697–1707. SEMINAL REVIEW
doi:10.1002/art.34453 · PMID: 22392533
6. Mathiessen A, Conaghan PG. Synovitis in osteoarthritis: current understanding with therapeutic implications. Arthritis Res Ther. 2017;19(1):18. REVIEW
doi:10.1186/s13075-017-1229-9 · PMID: 28148295
7. Kidd BL, Langford RM, Wodehouse T. Arthritis and pain. Current approaches in the treatment of arthritic pain. Arthritis Res Ther. 2007;9(3):214. REVIEW
doi:10.1186/ar2147 · PMID: 17659063
8. 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. SYSTEMATIC REVIEW
doi:10.1186/1471-2474-9-116 · PMID: 18764949
9. National Institute for Health and Care Excellence. Osteoarthritis in over 16s: diagnosis and management. NICE Guideline NG226. London: NICE; October 2022. NICE GUIDELINE
Available at: nice.org.uk/guidance/ng226
10. Valdes AM, Spector TD. Genetic epidemiology of hip and knee osteoarthritis. Nat Rev Rheumatol. 2011;7(1):23–32. REVIEW
doi:10.1038/nrrheum.2010.191 · PMID: 21079645
11. Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis. 1957;16(4):494–502. ORIGINAL ARTICLE
doi:10.1136/ard.16.4.494 · PMID: 13498604
12. GBD 2021 Osteoarthritis Collaborators. Global, regional, and national burden of osteoarthritis, 1990–2020 and projections to 2050: a systematic analysis for the Global Burden of Disease Study 2021. Lancet Rheumatol. 2023;5(9):e508–e522. GLOBAL BURDEN
doi:10.1016/S2665-9913(23)00163-7 · PMID: 37551507