n62861 janet86017 kimmyincali 550 Users are discussing this topic

PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Osteoarthritis written for patients

Osteoarthritis (OA) is a clinical syndrome of joint pain accompanied by varying degrees of functional limitation and reduced quality of life. It is the most common form of arthritis, and one of the leading causes of pain and disability worldwide. The most commonly affected peripheral joints are the knees, hips and small joints of the hands.[1] 

OA is characterised by localised loss of cartilage, remodelling of adjacent bone and associated inflammation. A variety of traumas may trigger the need for a joint to repair itself. OA includes a slow but efficient repair process that often compensates for the initial trauma, resulting in a structurally altered but symptom-free joint. However, in some people, because of either overwhelming trauma or compromised repair, symptomatic OA eventually presents. There is a great deal of variation in clinical presentation and outcome seen between different people, and also at different joints in the same person.[1] 

  • OA is one of the most common chronic diseases, with an estimated overall prevalence in the general adult population of 11% for hip OA and 24% for knee OA, respectively.
  • OA is age-related, with manifestations often not occurring until middle age.

NEW - log your activity

  • Notes
    Add notes to any clinical page and create a reflective diary
  • Track
    Automatically track and log every page you have viewed
  • Print
    Print and export a summary to use in your appraisal
Click to find out more »

Risk factors[3] 

  • Genetic factors:
    • Heritability estimates for hand, knee, and hip OA are about 40-60%.
    • The responsible genes are largely unknown.
  • Constitutional factors:
    • Ageing.
    • Female sex.
    • Obesity.
    • High bone density - risk factor for development of OA.
    • Low bone density - risk factor for progression of knee and hip OA.
  • Local, largely biomechanical, risk factors:
    • Joint injury.
    • Occupational and recreational stresses on joints.
    • Reduced muscle strength.
    • Joint laxity.
    • Joint malalignment.

A diagnosis of OA can be made clinically without investigations if a person:[1] 

  • Is aged 45 years or over; and
  • Has activity-related joint pain; and
  • Has either no morning joint-related stiffness or morning stiffness that lasts no longer than 30 minutes.


  • Joint pain that is exacerbated by exercise and relieved by rest. Rest and night pain can occur in advanced disease. Knee pain due to OA is usually bilateral and felt in and around the knee. Hip pain due to OA is felt in the groin and anterior or lateral thigh. Hip OA pain can also be referred to the knee and, in males, to the testicle on the affected side.
  • Joint stiffness in the morning or after rest.
  • Reduced function and participation restriction.


  • Reduced range of joint movement.
  • Pain on movement of the joint or at extremes of joint movement.
  • Joint swelling/synovitis (warmth, effusion, synovial thickening).
  • Periarticular tenderness.
  • Crepitus.
  • Absence of systemic features such as fever, and rash.
  • Bony swelling and deformity due to osteophytes - in the fingers this presents as swelling at the distal interphalangeal joints (Heberden's nodes) or swelling at the proximal interphalangeal joints (Bouchard's nodes).

    Herberden's nodes

  • Joint instability.
  • Muscle weakness/wasting around the affected joint.
  • Clinical examination: diagnosis is usually based on clinical examination.
  • Plain X-rays: when disease is advanced it can be seen on plain X-rays. The diagnostic features that can be seen on X-ray are shown below:
  • Body weight and body mass index: should be recorded.
  • MRI: may be useful to distinguish other causes of joint pain.
  • Blood tests: are normal in OA. Consider checking baseline FBC, creatinine and LFTs before starting a patient on non-steroidal anti-inflammatory drugs (NSAIDs).
  • Joint aspiration: may be considered for swollen joints to exclude other causes such as septic arthritis and gout. See the separate article on Joint Injection and Aspiration
  • Doctors and patients can use Decision Aids together to help choose the best course of action to take.
  • Compare the options  

Holistic approach to assessment and management

  • The effect of OA on a person's function, quality of life, occupation, mood, relationships and leisure activities should be assessed. Consider:
    • Current thoughts and beliefs - their concerns, expectations, knowledge about OA.
    • Their support network - ascertain whether there is a carer and, if so, how the main supporter is coping (their ideas, concerns and expectations).
    • Current mood (screen for depression) - determine whether there is any other stress.
    • Pain assessment - ask what the patient has tried, including any drugs used (dose, side-effects, timing). Ask whether there are other treatable sources of pain (eg, periarticular pain, trigger finger, ganglion or bursitis). Enquire whether a chronic pain syndrome has developed.
    • Promote function and reduce adverse effects on activities and sleep; referral to physiotherapy and/or occupational therapy may be indicated.
    • Consider any comorbidities that may affect choice of treatment or fitness for surgery. Ask whether the patient is prone to falls - and whether this can be minimised.
  • An annual review should be considered for any person with one or more of the following:[1] 
    • Troublesome joint pain
    • More than one joint with symptoms
    • More than one comorbidity
    • Taking regular medication for OA

Core treatments

These should be offered to everyone with OA:[1] 

  • Education, advice and access to information: both oral and written information should be provided.
  • Exercise: should be encouraged in all people with OA, regardless of their age, comorbidity, pain or disability. This should include exercise for general aerobic fitness and local muscle strengthening. As well as helping weight loss, exercise itself will help to build muscle strength and endurance and can lead to reduced pain and improved joint function. Physiotherapy may be useful.
  • Weight loss advice: if the patient is overweight/obese. This will reduce the load on their joints and help to improve pain.
  • The use of local heat or cold (thermotherapy) should be considered as an adjunct to core treatments.
  • Aids and devices:
    • Advice on appropriate footwear (including shock-absorbing properties) as part of core treatments for people with lower limb OA.
    • Biomechanical joint pain or instability: should be considered for assessment for bracing/joint supports/insoles as an adjunct to their core treatments.
    • Assistive devices (eg, walking sticks and tap turners) should be considered as adjuncts to core treatments for people with OA who have specific problems with activities of daily living.

Drug treatments[1] 

  • Paracetamol and/or topical NSAIDs should be considered ahead of oral NSAIDs, cyclo-oxygenase 2 (COX-2) inhibitors or opioids.
  • If paracetamol or topical NSAIDs are insufficient for pain relief for people with OA then the addition of opioid analgesics should be considered. Risks and benefits should be considered, particularly in older people.
  • Topical treatments:
    • Consider topical NSAIDs for pain relief in addition to core treatments for people with knee or hand OA.
    • Topical capsaicin should be considered as an adjunct to core treatments for knee or hand OA.[4] 
    • Do not offer rubefacients for treating OA.
  • NSAIDs and highly selective COX-2 inhibitors:
    • Where paracetamol or topical NSAIDs are ineffective for pain relief for people with OA then substitution with an oral NSAID/COX-2 inhibitor should be considered.
    • Where paracetamol or topical NSAIDs provide insufficient pain relief for people with OA then the addition of an oral NSAID/COX-2 inhibitor to paracetamol should be considered.
    • Use oral NSAIDs/COX-2 inhibitors at the lowest effective dose for the shortest possible period of time.
    • When offering treatment with an oral NSAID/COX-2 inhibitor, the first choice should be either a standard NSAID or a COX-2 inhibitor (other than etoricoxib 60 mg). In either case, co-prescribe with a proton pump inhibitor (PPI).
    • All oral NSAIDs/COX-2 inhibitors have analgesic effects of a similar magnitude but vary in their potential gastrointestinal, liver and cardio-renal toxicity; therefore, when choosing the agent and dose, take into account individual patient risk factors, including age. Consideration should be given to appropriate assessment and/or ongoing monitoring of these risk factors.
    • If a person with OA needs to take low-dose aspirin, consider other analgesics before substituting or adding an NSAID or COX-2 inhibitor (with a PPI) if pain relief is ineffective or insufficient.
  • Compared with placebo, glucosamine, chondroitin, and their combination do not reduce joint pain or have an impact on narrowing of joint space.[5] Glucosamine is not recommended for the treatment of OA.[6]
  • Intra-articular injections:
    • Intra-articular corticosteroid injections should be considered as an adjunct to core treatments for the relief of moderate-to-severe pain in people with OA.
    • Do not offer intra-articular hyaluronan injections for the management of OA.
  • Topical herbal treatments: although topical capsaicin has been recommended as a treatment option, there is otherwise not a great deal of evidence from studies to show that herbal remedies are effective:[7]
    • Arnica gel probably improves symptoms as effectively as a gel containing an NSAID.
    • Comfrey extract gel probably improves pain.
    • There has been no strong evidence for capsicum extract gel.

Referral for consideration of joint surgery

  • Ensure that the person has been offered at least the core (non-surgical) treatment options before referral.
  • Base decisions on referral thresholds on discussions between patients, referring clinicians and surgeons, rather than using scoring tools for prioritisation.
  • Do not refer for arthroscopic lavage and debridement as part of treatment for OA, unless the person has knee OA with a clear history of mechanical locking (as opposed to morning joint stiffness, 'giving way' or X-ray evidence of loose bodies).
  • Consider referral for joint surgery for people with OA who experience joint symptoms (pain, stiffness and reduced function) that have a substantial impact on their quality of life and are refractory to non-surgical treatment.
  • Refer for consideration of joint surgery before there is prolonged and established functional limitation and severe pain.
  • Patient-specific factors (including age, sex, smoking, obesity and comorbidities) should not be barriers to referral for joint surgery.

These can include reduced mobility which can lead to problems with self-care and loss of employment.

  • Most people affected by OA do not become severely disabled.
  • Knee OA seems to have the worst prognosis with most cases deteriorating over a ten-year period. Hand OA has the best.
  • A recent study has shown that generalised OA is associated with the radiological progression of knee OA. Knee pain, baseline radiological severity, sex, quadriceps strength, knee injury and regular sport activities did not seem to be related to the progression of OA in the knee.[8]
  • Weight control.
  • Increasing physical activity.
  • Avoiding injury.
  • Improving education about OA including increased use of expert patient programmes.
  • Optimal management of symptoms by GPs to reduce the prevalence of disability due to OA.

Further reading & references

  1. Osteoarthritis: Care and management in adults; NICE Clinical Guideline (February 2014)
  2. EULAR recommendations for the non-pharmacological core management of hip and knee osteoarthritis; Annals of Rheumatic Disease (April 2013)
  3. Osteoarthritis; NICE CKS, April 2013
  4. Hochberg MC, Altman RD, April KT, et al; American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken). 2012 Apr;64(4):465-74.
  5. Wandel S, Juni P, Tendal B, et al; Effects of glucosamine, chondroitin, or placebo in patients with osteoarthritis BMJ. 2010 Sep 16;341:c4675. doi: 10.1136/bmj.c4675.
  6. British National Formulary
  7. Cameron M, Chrubasik S; Topical herbal therapies for treating osteoarthritis. Cochrane Database Syst Rev. 2013 May 31;5:CD010538. doi: 10.1002/14651858.CD010538.
  8. Belo JN, Berger MY, Reijman M, et al; Prognostic factors of progression of osteoarthritis of the knee: a systematic review of observational studies. Arthritis Rheum. 2007 Feb 15;57(1):13-26.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Michelle Wright
Current Version:
Peer Reviewer:
Dr John Cox
Document ID:
2547 (v25)
Last Checked:
Next Review:

Did you find this health information useful?

Yes No

Thank you for your feedback!

Subcribe to the Patient newsletter for healthcare and news updates.

We would love to hear your feedback!

Patient Access app - find out more Patient facebook page - Like our page