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Arthritis: latest treatments and the role of the nurse

Susan M Oliver
Independent Nurse Specialist Rheumatology
Nurse Adviser for the National Rheumatoid Arthritis Society
Member of Standards of Arthritis Relief (SOAR)

It is widely believed that arthritis is "a disease of the elderly" and that there is nothing that can be done.(1) This view poorly serves those trying to cope with the pain and loss of function, and often results in those affected failing to seek medical advice. Healthcare professionals should ensure that these views are dispelled - there is always something that can be done.
Arthritis affects the joints and the joint lining or capsule (and surrounding tissues), although there are different characteristics related to the different forms of arthritis. There are over 200 types of arthritis, and osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common forms.(2) The value of being able to differentiate between OA and RA (and other forms of inflammatory arthritis) is an important one as treatment and management differ. A simple template can support practitioners in assessing patients for OA and RA.(3)
Table 1 briefly describes some of the most common forms of arthritis, and Figure 1 shows the joints most commonly affected in OA and RA.



In OA, the cartilage covering the bones gradually breaks down and as a result causes pain and swelling. New bone formations (osteophytes - bony spurs) can occur on the joint, causing an additional stressor to the integrity of the joint capsule (see Figure 2). OA is a degenerative disease and is sometimes described as "primary" (idiopathic) or "secondary" OA. There are predisposing factors to primary OA, such as ageing or obesity. Secondary OA can develop as a result of anatomical derangement or ­previous trauma (eg, an old rugby injury).


From time to time OA can "flare" as a result of exacerbations, causing a secondary inflammatory response and leading to increased pain, swelling and tenderness. Individuals should receive appropriate analgesia and other therapeutic and nontherapeutic options as outlined in Table 2. If there is a flare, individuals should be reassessed and may need a step-up in their analgesia and additional support, depending upon their presenting problems.


Current and new treatments in OA
Although there is now a greater understanding of the disease process and the changes that occur to bone causing OA, and although research is continually looking for new treatments, so far no new therapies have been found that have structure-modifying abilities in humans.(11)

Nonpharmacological treatments
Nonpharmacological options are increasingly recognised as having an important role in enhancing self-management strategies and reducing symptoms of OA.(12) Nonpharmacological options include:

  • Education about the disease, pacing, pain ­management and treatment options.
  • Exercise.
  • Weight loss.
  • Adaptive devices and aids (eg, arch supports and appropriate footwear, use of splints, walking aids, chair raisers) (see Table 2).

Wherever possible a multidisciplinary team should provide this support in combination with pharmacological treatment (when indicated) to improve outcomes.(13)
Nursing interventions (eg, education, medication reviews and pain management advice) have proved their value by being effective in reducing chronic nonsteroidal anti- inflammatory drug (NSAID) use, improving pain control and reducing polypharmacy.(14,15)

Pharmacological treatments
For most individuals, current pharmacological options for OA support the initial use of simple analgesia (eg, paracetamol). If this fails to provide effective pain relief, compound analgesics should be considered. For short periods of time, individuals experiencing a flare of OA may also require an NSAID. The development of cyclo-oxygenase (COX)-II selective inhibitors has been an important additional pharmacological option for those at high risk of gastrointestinal adverse events.(16)
Corticosteroid intra-articular injections, particularly for troublesome joints (eg, the knee), can be effective in relieving symptoms.(17) Early research evaluating the benefits of intra-articular hyaluronan therapies have shown some potentially promising results in reducing NSAID consumption.(10) There remains a lack of high-quality research evidence to adequately support the benefit of many complementary therapies, although glucosamine (1,500mg/per day) has demonstrated mild-to-moderate benefits in pain relief for some individuals.(8)

Inflammatory joint diseases
The three most common forms of inflammatory joint diseases are:

  • RA - can be seronegative or seropositive RA.
  • Ankylosing spondylitis (AS).
  • Psoriatic arthritis (PsA).

Inflammatory joint diseases encompass a group of musculoskeletal diseases that develop as a result of a faulty immune response that causes an immune attack against the body's own tissues (autoimmunity). In RA the tissues targeted by the autoimmune response are the synovial tissues (see Figure 3).


There are differences between the different types of inflammatory arthritis. These differences can be described in terms of:

  • The target tissues of the autoimmune response.
  • Unique diagnostic criteria (eg, joints classically affected and specific symptoms).
  • Predisposing factors for susceptibility to the ­disease (genetic links such as a positive HLA B27 for those with AS).
  • Differences in age of onset and male:female ratio.

Current and new treatments in RA
Table 3 identifies the therapies available for RA, AS and PsA.


Nonpharmacological treatments
See advice for OA.

Pharmacological treatments
Treatment for RA should include the appropriate management of pain, including simple or compound analgesia, and may also require the use of NSAIDs or COX-II inhibitors.(16) Many of the principles of self-management outlined in OA can also be used to ­support individuals with RA.
It is sometimes necessary to prescribe oral cortico-steroids (steroids), although the regular use of steroids remains controversial. Steroids can be administered when there is an exacerbation of the disease or while waiting for new therapies to become effective in controlling the disease. In recent years, the preferred method of administration for flares is by either an intravenous infusion of methylprednisolone or an intramuscular injection of Depo- Medrone (Pharmacia). Intra-articular injections of steroids may be preferred if inflammation (synovitis) is present in only one or two joints (although septic arthritis must always be excluded).

New ways of using old therapies for treating RA
The last few years have been an exciting and inspiring time for those caring for individuals with RA as treatments have had significant positive impact on controlling the disease and improving the individual's ability to cope with their disease. The need to identify and treat individuals with RA promptly is supported by a strong body of research evidence.(18) Research evidence has identified the need for aggressive and prompt treatment for those with RA to prevent the long-term consequences of irreparable damage to joints (and the resulting surgery for joint replacements). There is also a substantial body of evidence that identifies the risk to RA patients from potential serious cardiovascular disease.(19,20) This evidence has resulted in traditional therapies known as disease-modifying drugs (DMARDs) being used earlier in the disease process and often in combination therapy to control the disease (see Table 3).

New treatments for RA
Research has identified the key cell interactions implicated in amplifying the normal immune response to inflammation and the cellular interactions that occur as a result of the autoimmune responses in RA. Two pivotal cytokines (chemical messenger proteins) responsible for activating an immune response are tumour necrosis factor a (TNFa) and interleukin-1 receptor agonist (IL-1ra). The release of these two cytokines results in other proinflammatory cytokines being activated; this is often referred to as an inflammatory cascade. Using monoclonal antibody technology, biologically engineered therapies have been developed to target TNFa and IL-1ra. These therapies (often termed biologics) disarm these two key cytokines responsible for the inflammatory cascade by preventing them locking into their appropriate cytokine receptors, which enable their chemical message to be activated.
Research evidence and experience so far appears to show greater benefits of treatment than traditional DMARD therapies. Benefits include reduction in tender and swollen joints, pain and fatigue and global health improvements. Evidence also appears to support biologic therapies having a significant effect on reducing joint damage that occurs as a result of the disease process in RA. For a more detailed paper on biologic therapies, see references 21 and 22.
Individuals who are eligible for treatment with biologic therapies have active disease that is resistant to traditional DMARDs. Guidelines have been published by NICE on the prescribing of etanercept and infliximab for those with RA and etanercept for young people who have juvenile idiopathic arthritis (JIA).(23,24)
New therapies continue to be trialled, and current studies include B-cell depletion treatments (rituximab - used at present in non-Hodgkin's lymphoma) and therapies that block the early recognition of antigens by blocking cell-to-cell communication between antigen-presenting cells and T-cells.
Before starting treatment and regularly during treatment, individuals should be assessed and reviewed to reduce any risks related to treatment with new therapies (see Table 4). If there are clinical signs that suggest any infection (including symptoms suggestive of tuberculosis), deterioration or changes in cardiac or neurological function, or changes in the blood picture (eg, decrease in blood cell types and/or platelets), the patient should be referred for an urgent medical review. If an infection is suspected, patients should not receive their next biologic treatment until they have been thoroughly assessed. If an infection is present, this should be treated before recommencing biologic therapy. This has particular relevance because of the biologic therapies' unique and highly effective method of blocking the normal immune response. There are potentially life-threatening risks to patients who fail to recognise infections and get them treated promptly.(25) Effective communication between all practitioners caring for those receiving biologic therapies reduces the potential risks of treatment.(26)


"Standards of Care for Arthritis" have just been launched by the Arthritis and Musculoskeletal Alliance (ARMA). These standards will provide an essential framework for identifying quality indicators in the care of those with arthritis. In addition, recent initiatives have recognised the significant role that nurses have in the field of chronic disease areas such as arthritis. Although, in general, individuals with RA (and other inflammatory forms of arthritis) have more complex disease than those with OA, there are many common and important areas of care that all nurses should be able to provide to those coping with arthritis. These include advice on pain management, education and support on learning to cope with their disease, and pharmacological and nonpharmacological treatments, reducing risks and enhancing concordance related to medications and blood monitoring.
"Standards of Care for Arthritis" was launched by the Arthritis and Musculoskeletal Alliance (ARMA) in October this year, and provides primary care teams with a useful document to ensure an essential ­framework for identifying quality indicators in the care of those with arthritis.


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  2. Symmons D, Bankhead C. Healthcare needs assessment for musculoskeletal diseases. London: Arthritis Research Campaign; 1994.
  3. Standards of Arthritis Relief. Osteoarthritis and rheumatoid arthritis: standards of arthritis relief template. London:?SOAR; 2003.
  4. Ryan S, Oliver S. Rheumatoid arthritis. Nursing Standard 2002;16(20):45-52.
  5. Cornell T. Ankylosing spondylitis: an overview. Prof Nurse 2004;8:431-2.
  6. Hill J. Rheumatology nursing: a creative approach. London: Churchill Livingstone; 1998.
  7. Brandt KD. Non-surgical treatment of osteoarthritis: a half century of advances. Ann Rheum Dis 2004;63:117-22.
  8. Moore A, Edwards J, Barden J, McQuay H. Bandolier's little book of pain. Oxford:?OUP; 2003.
  9. Klippel JH, Dieppe PA. Practical rheumatology. London: Mosby; 1995.
  10. Doherty M, Lanyon P, Hosie G. Osteoarthritis of the knee and hip. Rheumatic diseases in practice. London: Arthritis Research Campaign; 2001.
  11. Brandt KD. Non-surgical treatment of osteoarthritis: a half century of "advances". Ann Rheum Dis 2004;63:117-22.
  12. Jordan KM, Arden NK, Doherty M, et al. Eular recommendations 2003:?an evidence based approach to the management of knee osteoarthritis; report of a task force on the standing committee for international clinical studies including therapeutic trials. Ann Rheum Dis 2003;62:1145-55.
  13. Oliver S. Multidisciplinary disease management in rheumatology. Prof Nurse 2003;19(3):137-41.
  14. Jones AC, Coulson L, Muir K, et al. A nurse delivered advice intervention can reduce chronic non-steroidal ­anti-inflammatory drug use in general practice: a randomised controlled trial. Rheumatology 2002;41:14-21.
  15. Glasgow ACA, Glasgow JA. Development of a nurse-led chronic pain clinic in UK primary care.Int J Clin Pract 2002;56:21-5.
  16. NICE. Guidance on the use of cyclo-oxygenase (COX II) selective inhibitors, celecoxib, rofecoxib, meloxican and etodolac for osteoarthritis and ­rheumatoid arthritis. London:?NICE; 2001.
  17. Arroll B, Goodyear-Smith F. Corticosteroid infections for osteoarthritis of the knee:?meta-­analysis. BMJ 2004;328:869-70.
  18. Grigor C, Capell H, Stirling A, et al. Effect of a treatment strategy of tight control for rheumatoid arthritis (TICORA study):a single blind randomised control study. Lancet 2004;364:263-9.
  19. Pincus T, Callahan LF. The side effects of rheumatoid arthritis:joint destruction, disability and early ­mortality. Br J Rheumatol 1993;37 Suppl 1:28.
  20. Singh G, Mithal A, Mendelsohn A, et al. Acute myocardial infarctions in rheumatoid arthritis and diabetes: a tale of two diseases and a call for action. Presented at Eular, Berlin; 2004.
  21. Oliver S. The immune system and new therapies for inflammatory joint disease. Musculoskeletal Care 2003;1:44-57.
  22. Oliver S. The immune system and new treatments. In: Oliver S, editor. Chronic disease nursing: a rheumatology example. Bedfordshire: Whurr; 2004.p. 123-48.
  23. NICE. Guidance on the use of ­etanercept and infliximab for the ­treatment of rheumatoid arthritis. Technology Appraisal 36. London: NICE; 2002.
  24. NICE. Etanercept for juvenile ­idiopathic arthritis. London:?NICE; 2002.
  25. Molloy E, Ramakrishnan S, Murphy E, Barry B. Morbidity and mortality in rheumatoid patients during treatment with adalimumab and infliximab. Rheumatology 2004;43:522-3.
  26. Edwards J. An exploration of patients' experiences of anti-TNFa ­therapy. Musculoskeletal Care 2004;2:40-50.

Arthritis Research Campaign Professionally endorsed website. Patient ­information can be downloaded
National Rheumatoid Arthritis Society (NRAS)
W:www.­ Patient ­organisation providing ­appropriate support for those with inflammatory arthritis. Also have a volunteer network programme for patients
Arthritis Care
Excellent support for those with osteoarthritis
National Association for Ankylosing Spondylitis
Psoriatic Alliance all patients with psoriasis and psoriatic arthritis. Runs patient conferences and provides ­information leaflets
Royal College of Nursing    
For members and nonmembers. Access to the Rheumatology Forum newsletter, guidance ­documents and information on educational events     
Patient advice and nurse resource page - features general ­information, educational events/courses and additional resources Primary Care Rheumatology Society
Excellent resources, ­including small modules on joint examinations, etc
British Society for Rheumatology
Access to some guideline ­documents ­without full membership
Soar Group template    
For free template T:0207 313 6377