Osteoarthritis (OA) is a non-inflammatory, degenerative and chronic joint disease and is one of the most symptomatic diseases for the middle-aged and elderly population.¹  More prevalent in the female population, OA frequently affects the knees, hips, spine, hands and shoulders and is characterised by joint pain, stiffness and a limited range of movement. It is estimated that approximately 10% of people over 55 years can have OA affecting the knee joint. ²

OA was thought to be a normal consequence of ageing, leading to the term degenerative joint disease. However, now it is known that OA results from a complex interplay of multiple factors, including joint integrity, genetic predisposition, local inflammation, mechanical forces and cellular and biochemical processes.³

Pathophysiology

Healthy joints comprise two bones whose ends are covered in articular cartilage and lubricated with synovial fluid produced in the lining of the joint capsule. In the osteoarthritic joint, degeneration of the cartilage joint lining becomes thinner and is eventually lost, resulting in the roughened bones rubbing against each other. The cartilage becomes brittle, thin and over time can wear out completely. This subsequently leads to the cartilage not performing, causing the bone under the cartilage to thicken and spread out (known as osteophytes). Pain then occurs as the bones rub together. Due to thinner, less effective cartilage, inflammation occurs and the osteophytes grow outward and look knobbly in appearance. If the joint capsule thickens with increasing synovial fluid this may result in joint swelling, pain and stiffness, deformed shape around the joint. It also reduces the mobility of the joint. 

A joint is the site where any two or more bones articulate together; they are functional units of the musculoskeletal system and most skeletal muscle attaches to bones at the joint.⁴ Flexibility and movement of the skeleton are provided by joints. Supporting cartilage provides a smooth gliding surface that is lubricated by synovial fluid as the joint moves.

OA usually develops gradually over a number of years, the changes may be very mild for some patients and are hardly noticeable. The hips, knees, hands and the lower aspect of the spine are the most commonly affected areas; other affected areas are shoulders, elbows and feet. OA can occur in more than one joint at any given time and can cause pain, stiffness and restrict mobility.

Signs and symptoms

The severity of OA symptoms may vary between patients. The most common symptoms are pain, stiffness and disability. Pain is usually worse with increased use of the affected joint and relieved by rest. Pain is often described as dull, aching or throbbing and localised to the affected joint. Crepitations can be heard when the joint is moved sometimes. Angulation of the bone may be noted. Disability is noted, and for knee and hip OA, a reduction is noted in the amount of walking that can be achieved. Stair climbing can become difficult for the patient with knee OA.

Clinical features include:

• Crepitus
• Mild synovitis
• Reduced range of movements
• Pain on movement
• Gait abnormality
• Muscle atrophy.

Diagnosis

The diagnosis of OA is usually based on history and examination as there is no single test that can diagnose this disease. Therefore, a detailed history must be taken as well as a physical examination. X-ray of the affected joint is the most useful tool to confirm diagnosis. X-ray will show if there is joint space narrowing or if there are osteophytes present. X-rays are also indicated when joint replacement surgery is indicated. Other imaging techniques (MRI) may be useful. Other medical conditions, which may be present with an arthropathy, should be excluded before a diagnosis of OA is made. Blood tests include FBC, ESR, rheumatoid facto, profile and antiCCP to out rule other joint disease such as rheumatoid arthritis or infection. Synovial fluid analysis will differentiate OA from rheumatoid arthritis

Care and treatment plan

The principal aims of OA management are to reduce pain and stiffness as well as to maintain or improve joint mobility where possible. Patients with a diagnosis of OA need to understand their condition and the treatments available so that they can self manage their disease. The key to self management is the individual’s ability to manage the symptoms, treatment and lifestyle changes inherent to living with OA.⁵ The evidence from self management programmes indicate that they can increase patient self efficacy and management of their disease, and this leads to better symptom control. Education can be administered individually or in a group setting. Patients can often benefit from group programmes as they can develop coping skills in a supportive environment; patients learn from others who also have this condition. Patients who are experiencing pain due to OA often decrease their activity levels to protect their bodies from further pain. Periods of inactivity increase joint pain and stiffness, and will in turn cause muscle wasting and weakness.

Exercise and education

Exercise should be considered a core treatment for OA, irrespective of age, pain severity and disability, as it may reduce pain and improve disability. Patients with OA of the knee or hip can benefit from aerobic and strengthening exercises.⁶ Much of this evidence is seen from intensive physiotherapy programmes. Patients with OA should be taught appropriate exercises and followed up on. For lower limb OA, general fitness, walking and swimming can be a useful starting point, as the buoyancy of the water supports the joints. An exercise bicycle is recommended but this again will depend on the patient and the facilities available. Patients need to be reassured that the pain they experience when they exercise will not exacerbate their condition. For muscle strengthening, this depends on the joint involved. For hip and knee OA it is important to strengthen the quadriceps muscles – these exercises are easily performed on a chair or bed and should be performed twice or three times a day. OA of the hand exercises should be taught by a physiotherapist to improve strength.

Patients with hip or knee OA who are overweight will experience increased pressure on their joints that will lead to increased pain and possible deterioration of the joint. Evidence has shown that weight loss can reduce pain and increase function.⁷ The patient’s footwear should also be assessed: well-fitting and supportive footwear is ideal. Using soft insoles and wearing trainers will reduce the stress on knee joints. A walking stick or frame can also relieve some of the pressure on the joints. Sometimes, the use of a brace on the knee and thumb splints in OA of the thumb joint may be of benefit to reduce pain.

Pharmacological treatments

The safest oral medication is paracetamol and should be tried first as an initial therapy based on its cost, efficacy and toxicity profile. But, it should be used with caution in patients with excessive alcohol consumption and with active liver disease.⁸ Another pharmacological treatment used by patients, which is controversial, is complementary and alternative medicine (CAM). It has been estimated that up to 90% patients with OA use CAM treatments.⁹ The evidence for CAM treatment is poor and does not feature in the NICE guidelines. For example, Devil’s Claw, which some patients take for OA, has an anticoagulant or blood thinning effects and can therefore increase the risk of gastrointestinal bleeding if taken with an anti-inflammatory drug.¹⁰

The use of an additional anti-inflammatory gel that can be applied directly onto to the skin around the joint can be beneficial. This gel can reduce the systemic side effects from taking oral anti-inflammatory drugs. These gels may not be effective in hip OA as the joint lies too deep below the muscle.

Nutritional supplements with pharmaceutical properties, including glucosamine sulphate, are often used by patients with OA. A review of glucosamine sulphate concluded that it was as safe as placebo, the effect on pain was not significant and it may lead to only small improvements in function.¹¹

When further treatment is required this will include anti-inflammatory drugs such as Cox-2 inhibitors. Non-steroidal anti-inflammatory drugs (NSAIDs) may be more beneficial than paracetamol in both rest and activity pain but should only be used in the short-term for acute painful episodes as this class of drug has significant morbidity and mortality due to adverse effects on the gastrointestinal, renal and cardiovascular system. They should be taken with a proton pump inhibitor (PPI) to reduce gastric acid production, and hence, the risk of a stomach ulcer caused by the NSAID. There are many NSAID therapies such as ibuprofen, etoricoxib or Vimovo and a Cochrane review concluded that little evidence is available to differentiate between the efficacy of different NSAIDs.

The nurse should be aware of the medications used in OA and also of the potential side-effects and drug interactions such as Devil’s Claw and NSAID therapy. Knowledge of the patient’s medical history is also important. For example, a patient with a history of gastric ulceration should not be advised to take an NSAID therapy.

For some patients whose symptoms are not controlled by oral medication, an intra-articular injection maybe beneficial. Intra-articular injections are usually steroids and are usually reserved for acute flare up of OA. Viscosupplementation with hyaluronic acid preparations is thought to help restore the viscoelasticity of the synovial fluid and will therefore help pain and function. Injections may therefore offer relief for some patients whose pain is not controlled by other conservative measures, but one must not forget that they are not without their potential side effects. Any injection into a joint may potentially introduce infection (septic arthritis) and repeated steroid injections may lead to osteonecrosis of the joint.

Transcutaneous electrical nerve stimulation (TENS), where mild electrical impulses pass through the skin into the nerve fibres, has been shown to be effective in OA.

Surgical options

Patients with ongoing OA will reach a stage when their symptoms cannot be controlled by any of the above treatments and surgery may then be considered. For younger patients with knee and hip OA, osteotomy may be considered for the correction of malalignment, and in some cases arthroscopy – a washout of the joint that debrides any osteophytes – is performed. The surgical option for hip and knee OA is joint replacement. That is, the removal of bone ends and their replacement with a combination of metal and plastic components. These prostheses are long-lasting and studies have shown that after 10 years post surgery they still function well.¹²

OA causes pain, joint stiffness and function is reduced in the affected joint, but we now have treatments to manage the symptoms and improve the patient’s quality of life. Nurses play a pivotal role in the management of OA, which requires a combination of knowledge, understanding and expertise. Effective care outcomes can be achieved by ensuring there is good communication between the nurse and patient especially in this cohort of patients. Nurses need to work with both patient and families. 

Over the past decade we have seen a shift from secondary to primary care in patients with OA. This cohort of patients is now usually managed in the community. There is no cure for OA and a holistic review of each patient is necessary to decide a treatment plan in which the patient can live as full a life as possible. As education is the mainstay of treatment, nurse prescribers play a leading role in helping patients manage their disease by discussing the various alternatives and also directing them to the sources of support that are available.

References

1. Buckwalter JA, Saltzman CS, Brown T (2004) The impact of OA. Clinical Orthop Relat Res 427(suppl):S6-S16.
2. Jordan KM, Arden NK,Doherty M et al (2003) Eular recommendations 2003: an evidence-based approach to the management of knee OA:report of a task force of the standing Committee for International Clinical Studies Including Therapeutic  Trials (ESCISIT). Annals Rheumatology Dis 62;1145-55
3. Krasnokutsky S, Attur M, Palmer G, Samuels J, Abramson SB (2008) Current concepts in the pathogenesis of OA. OA cartilage 16(suppl 3); S1-3.
4. Kozier B, Erb G, Berman A, Snyder S, Lake R, Harvey S (2008) Fundamentals of Nursing Concepts, Process and Practice. Pearson, Harlow.
5. Barlow J (2001) How to use education  as an intervention in OA. Best Pract Res Clin Rheumatology 15(4):545-58
6. Roddy E, Zhang W, Doherty M et al (2005) Evidence-based recommendations for the role of exercise in the management  of OA of the hip or knee – The MOVE consensus Rheumatology 44(1):66-73.
7. Christensen R, Bartels EM, Astrup A, Bliddal H (2007) Effect of weight reduction in obese patients diagnosed with knee OA: a systematic review and meta-analysis. Ann Rheum Dis66(4)433-9.
8. National Collaborating Centre for Chronic Conditions (2008) OA: national clinical guidelines for care and management in adults. Royal College of Physicians, London.
9. Brien S, Prescott P, Bashir N, Lewith H, Lewith G (2008) Systematic review of the nutritional supplements dimethyl sulfoxide (DMSO) and methylsulfonylmethane (MSM) in the treatment of OA. OA Cartilage 16(11):1277-88
10. Lucas B (2005) Treatment options for patients with OA of the knee. Br J Nursing 14(18):976-81.
11. Towheed TE, Maxwell L, Anastassiades TP et al (2005) Glucosamine therapy for treating OA. The Cochrane Database of Systematic Reviews, Issue 2. Art. No: CD002946. DOI:10.1002/14651858.CD002946.pub2
12. Johnson GV-V, Worland RL, Keenan J, Norambuena N (2003) Patients demographics as a predictor of the ten year survival rate in primary total knee replacement . Br J Bone Joint Surg85(1):123-36