Arthritis and Pain Management: Pain in Specific Conditions

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30 minutes

Pain and rheumatoid arthritis (RA)

The pain of arthritis is most often multifocal. In one sample of patients with arthritis, more than 90% reported at least moderate pain over the previous month [1]. One-half to two-thirds of patients with RA rank pain as their most important symptom [2] and pain is strongly related to functional impairment and the development of disability [1], [3].

Arthritis pain can occur as a result of local or systemic inflammation or as the result of a degenerative process. Rheumatoid arthritis results in severe inflammation in multiple joints and other organ systems where any connective tissue may be involved, along with the reticular framework that connects and supports the organ. It is important that patients thought to have RA are referred early to a rheumatologist [4]. Permanent structural damage occurs early in the course of the active process and early intervention with disease modifying drugs slows the progression of structural joint damage and improves long-term outcomes as well as overall quality of life [4]. The importance of early referral can be seen in the following:

  • Patients with RA have been shown to have an improved long term outcome when treated by a rheumatologist
  • A delay of more than 12 weeks in treatment results in a missed opportunity to improve long-term outcome.

Rheumatoid factor positivity, a raised acute phase response, and erosions on X-ray are associated with poor outcome but absence at presentation should not preclude diagnosis or referral. NICE has produced early referral guidelines including an algorithm for newly diagnosed RA. Early referral is advised by the NICE guidelines in the event of clinical suspicion of RA, supported by the presence of any of the following apply:

  • The small joints of the hands or feet are affected.
  • More than one joint is affected.
  • There has been a delay of 3 months or longer between onset of symptoms and seeking medical advice.

The American Rheumatism Association has identified clinical features associated with persistent synovitis and a poor prognosis. These include-

  • The number of joints affected (the more joints the worse the prognosis).
  • The presence of both swelling and tenderness in affected joints.
  • A positive MCP squeeze test.
  • The involvement of PIP’s and MCP’s and symmetry of the joints affected.

Inflammation may result from infection, crystal deposition, antigen-antibody complex deposition and/or trauma. In the joint, there are many changes, which may stimulate nociceptors in the joint capsule or the surrounding tissue, which results in pain. These are vascular engorgement of the synovial membrane, interstitial oedema and tissue infiltration by plasma cells, lymphocytes and macrophages.

Clinically, the relationship between pain and inflammation is unclear and the response to pain varies greatly with the disease progression and the individual. Whatever the relationship, it is usually the pain that motivates people to seek help.

You may like to read the relevant chapters in Melzack & Wall [5].

For the Clinical Guidelines on the management of Rheumatoid Arthritis please consult

Pain in Osteoarthritis (OA)

OA is a localised degenerative response from wear and tear on the joint, which primarily affects weight-bearing joints. Inflammation and degeneration are separate but related processes and the latter can result from inflammation. Degeneration seems to be accelerated in patients with arthritis or rheumatological disease where, initially, there is a breakdown of joint cartilage followed by bony destruction. The bony destruction is characterised by bony spurs along the marginal aspect of the joint.

OA can be defined as a spectrum of disorders of synovial joints, characterised by focal areas of destruction of the articular cartilage, accompanied by sclerosis of the underlying bone and marginal hypertrophy of both soft and hard tissue. Considered to be an almost inevitable consequence of ageing, OA affects nearly 10% of the population past the age of 60 years [6].

The pain generating structures include raised intraosseous pressure, inflammation and stress on the capsule and periarticular tissues, as well as the pain of bone rubbing on bone.

The inflammatory synovitis in OA is not as marked as in RA; however, it is present both clinically and pathologically, and probably explains the flares of worsening symptoms described by some patients. The quality and intensity of pain in OA varies, and it shows no specific features to differentiate it from other causes of articular pain. In OA, it appears that there are changes in the proteoglycans and collagen fibres of cartilage which are now traceable and which may explain the aetiology and sequence of ultimate degenerative joint changes [7]. There are also superimposed external forces upon cartilage that contribute to degeneration, such as genetic factors, trauma and mechanical stress.

In assessment, using the tools already described, the classic symptom is pain on use of the affected joint. Pain is generally insidious in onset, localised and not associated with any systemic disturbance [8]. Pain in the early stages is relieved with rest, but later the pain occurs at rest and at night, thus becoming a significant problem [9]. Vague discriminators may be that the pain of OA is associated with exercise (compared with rest with RA) and, although there may be early morning stiffness and gelling (stiffening of the joint with inactivity) they are often much less marked. X-rays and symptoms in OA correlate poorly. The pain and subsequent limitations in mobility are usually chronic and necessitate physical, psychological and social adjustments for the sufferer.

OA is found all over the world. There are racial variations in disease expression, e.g. OA of the hand is common in Caucasian women and OA of the knee is rare in the Chinese. Rarely patients may show a familial variant of premature OA. OA can affect the peripheral and the spine joints. In the hands, the joints are affected. In order of diminishing likelihood are CMC joint of the thumb, DIP, PIP, MCP and wrist joints. Hip OA behaves as a separate disease entity, being more common in men, occurring in younger patients and showing less correlation with changes in other joints. Hip OA can cause referred pain to the knee, leading to diagnostic confusion. Spinal OA or spondylosis is a radiological diagnosis where there is loss of disc height, bony sclerosis and osteophytes. It is universal as age advances. It gives rise to a stiff painful spine.

It is important to maintain good mobility and muscle tone unless nerve root compression occurs, which does so rarely. Spondylosis is degenerative and therefore entirely different from spondylitis which is inflammatory. In view of its universality, findings of spondylosis on X-ray are often diagnostically irrelevant to the presenting back pain. Indeed back symptoms and radiological signs correlate even more poorly than for peripheral joint OA.

For clinical guidelines on the care and management of osteoarthritis in adults please consult

Other Rheumatalogical Conditions

It is impossible to cover all of the rheumatological conditions that could be seen within a health care setting. The following are classes and examples of conditions and if you are specifically interested in any one of them, take this opportunity to evaluate pain management in regards to this condition or class. It may be useful to consider how the following classes and conditions differ or are similar to the management of any chronic painful condition and to the management of OA and RA. Classes include:

  • Systemic connective tissue disease, e.g. Sytemic lupus erythematosus; Sjögren's syndrome,
  • Vasculitides and related disorders, e.g. large vessel vasculitis, Wegener's granulomatosis
  • Seronegative spondyloarthropathies, e.g. ankylosing spondylitis, psoriatic arthritis
  • Arthritis associated with infectious agents, e.g. Lyme disease, AIDS-associated rheumatic syndromes, Whipple's disease
  • Rheumatic disorders associated with metabolic, endocrine and haematological disease e.g. gout, sickle cell disease
  • Bone and cartilage disorders e.g. Paget's Disease of the bone, osteoporosis
  • Hereditary, congenital and inborn errors of metabolism associated with rheumatic syndromes e.g. bone and joint dysplasias, osteogenesis imperfecta.
  • Nonarticular and regional musculoskeletal disorders e.g. fibromyalgia, entrapment neuropathies
  • Neoplasms and tumour like lesions.


  1. McKenna, F., Wright, V., 1985. Pain and rheumatoid arthritis.. Ann Rheum Dis, Ann Rheum Dis 44, 805.
  2. Wall, P.D., R, M., 2006. Textbook of Pain., 5th ed. Churchill Livinstone, Edinburgh.
  3. Cailliet, R., 1991. Neck and arm pain, 3rd.rd ed. F.A. Davis, Philadelphia.
  4. Hamerman, D., 1989. The biology of osteoarthritis.. N Engl J Med, N Engl J Med 320, 1322-30.
  5. Moskowitz, R.W., 1981. Management of osteoarthritis.. Bull Rheum Dis, Bull Rheum Dis 31, 31-5.
  6. Wolfe, F., 1984. Arthritis and musculoskeletal pain.. Nurs Clin North Am, Nurs Clin North Am 19, 565-74.
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