Section 1: Epidemiology and aetiology
The American College of Rheumatology defines the osteoarthritic disorders (OAD) as a heterogeneous group of conditions that lead to joint symptoms and signs that are associated with defective integrity of articular cartilage with related changes in the underlying bone at the joint margins.1
OADs are classified according to site, whether an obvious causative factor can be identified (primary or secondary), and as generalised (GOA) - affecting three or more joint sites - or localised OA, which may only affect a single joint such as a hip or knee.
Radiographic features can also be used to classify OA:
- Joint space narrowing
- Osteophyte formation
- Subchondral sclerosis
- Cyst formation
- Abnormalities of bone contour.
These features are combined within a variety of scales of OA severity. The most widely used is the Kellgren-Lawrence grading system.2 Grading on a 0-4 scale occurs in comparison with a handbook of index X-rays.
Post-mortem studies have shown OA changes are present in most people as they age.
More severe OA results in radiological change.
In a Dutch study of 6,585 people in a single village, hand and foot OA were of increasing prevalence from age 40, with 75 per cent of women in their seventh decade having severe OA changes in the distal interphalangeal (DIP) joints.3
Knee OA is more common than hip OA and both occur more frequently in women than men. OA appears to be equally spread across ethnic and geographical populations, although knee OA appears more prevalent in African-American women than in Caucasian controls.
The development of OA can be considered to be a combination of genetic predisposition and the product of a number of cumulative risk factors.
Polyarticular GOA has a strong hereditary component. Nodal GOA occurs in family groups with a stronger expression in females in an autosomal dominant fashion.4
The genetic influence on OA appears polygenic and may involve genes of collagen structure or alterations in bone and cartilage metabolism.
Specific risk factors for OA are well known.
Obesity remains the most important factor in promoting premature OA in women, especially after the menopause, and represents a potentially modifiable risk. Hormone mediation is important, as the changes of widespread nodal OA often start around the menopause.
There is an association between the abnormally flexible soft tissues in hypermobile patients and premature OA. OA occurs with greater frequency in diabetes (diffuse spinal OA), ochronosis, hyperuricaemia and even hypertension.
Injury of the knee or hip predisposes to OA, especially after injury of the meniscus or cruciate ligaments or fracture.
Repetitive actions of a single joint such as use of the thumb in factory work and knees in plumbers may lead to high levels of OA-related disability in specific working populations.
Childhood joint diseases that lead to abnormally shaped joints and loading patterns (such as after slipped femoral capital epiphyseal disease) lead to premature OA, and sports activities that involve repetitive trauma and joint injury are associated with knee OA.
Section 2: Diagnosis
The majority of OA remains asymptomatic and is only encountered on incidental X-ray. The most important clinical feature of OA is usually pain, often related to joint usage.
Pain varies with time and activity and can be cyclical over a 24-hour period.
Stiffness is often reported by patients with OA. After rest it becomes difficult to re-start movement with any fluidity until joints 'warm up'. Patients with OA have a sense of joint instability, especially in the knee and hip.
Swelling associated with OA can either be bony (osteophytes) in the fingers or can be soft tissue (synovial swelling and joint effusions). Patients with OA may experience flares of joint inflammation that appear to mimic the flares seen in inflammatory conditions such as rheumatoid arthritis (RA).
In some cases, joint effusions may be particularly prominent, especially in shoulders and knees. This form of OA can be cool to the touch and associated with the finding of crystals of calcium pyrophosphate or hydroxyapatite in the joint fluid.
Clinical subsets of OA
- Premature hip OA in adults - men aged 20-40 who develop isolated hip OA for no apparent reason.
- Premature OA in a single joint after trauma - most commonly post-meniscectomy knee.
- Knee/hand OA in obese perimenopausal women - often non-progressive and causes few problems once Heberden's/Bouchard's nodes form.
- Inflammatory erosive OA - often in the hands and sometimes difficult to distinguish from RA (the clue is often in the presence of osteophytic nodes and the involvement of DIP joints, which are untouched by RA).
- Rapidly progressive OA - usually rapidly progressing OA hip that quickly leads to hip joint destruction.
- Diffuse idiopathic skeletal hyperostosis (DISH) - also known as Forestier's disease, involves OA and prominent hyperostotic change and large osteophytes in the spine. It affects predominantly men and increases in severity with age and body weight.
Blood tests are unhelpful in diagnosing or managing OA. Plain X-rays still represent the best way of imaging joints for either diagnosis or management.
There is a clear discrepancy between the pain and functional difficulties in OA and the extent of radiographic change. Caution is needed in equating X-ray change with the presence of pain.
It is important to consider that weight-bearing radiography is most appropriate for weight-bearing joints such as the knees to reflect true joint space loss.
OA, especially in the knee, can be associated with the radiographic appearance of chondrocalcinosis suggesting crystal deposition over a prolonged period. Whether the crystals arise from the OA or are part of the active process of joint damage is debatable.
MRI can give an idea of involvement of peri-articular soft tissues such as ligaments and tendons and also be used to assess the thickness of articular cartilage.
Arthroscopy can determine the degree of OA involvement prior to surgery, or may be used as a treatment to clear debris from the joint.
Section 3: Management
A sequential approach to OA treatment is outlined in the box, with the focus on education and self-management before the application of other interventions is considered.
Simple analgesics remain the mainstay of most guidelines on OA therapy. The main drawback to these approaches tends to be the demand made by patients for stronger therapies when they are unable to develop a self-management approach.
Although associated with frequent adverse effects, the increasing realisation that OA represents an inflammatory condition leads to the logical conclusion that NSAIDs may be effective in OA pain relief. There is now some trial evidence that topical NSAIDs can bring about symptom relief.
Some patients find topical capsaicin to be effective.
Where NSAIDs are not tolerated or are ineffective, patients with widespread pain and inflammation in OA can respond well to courses of low-dosage prednisolone (5mg daily) if not contraindicated. There is little evidence to support this approach but it is often used with good effect in clinical practice.
Intra-articular steroid injections may prove especially useful in knees and the bases of thumbs when symptomatic and associated with joint swelling.
Their use in inflammatory hip OA is more controversial and should be weighed up with care in order not to risk further joint progression.
There are now a variety of agents that mimic the physical properties of articular cartilage in viscosity and physical strength used for knee OA.
The use of intra-articular hyaluronic acid injections remains uncertain and clinical trial evidence exists for short-term symptomatic benefit. They are associated with a risk of a flare up of inflammatory symptoms.
Supplements are in widespread use in OA for symptom relief, although often not accompanied by any study evidence for efficacy. The short-term efficacy of both glucosamine compounds and rose hip extract are supported by well-conducted studies.
Physiotherapy has a role in OA both in symptom relief when treating local joints and in educating patients towards exercise programmes, muscle strengthening and weight loss.
Pain management, both with cognitive behavioural support and complex analgesics such as amitriptyline may be effective in helping to control chronic pain in OA.
Other physical therapies such as chiropractic, osteopathy and massage techniques can contribute to the relief of OA symptoms.
Of the many surgical techniques offered for OA, joint replacement, joint resurfacing and joint fusion are evidence-based and in widespread use to treat patients with end-stage OA.
Other techniques, such as arthroscopic joint lavage and joint manipulation under anaesthetic, are still widely used but are not evidence-based.
Chondro-protection and cartilage re-growth
The gold standard therapy for OA would involve stimulation and re-growth of damaged cartilage leading to an arrest of the progressive disease process.
While one study supports a role for glucosamine hydrochloride in disease control, showing slowing of joint space narrowing in a group of patients with OA knee taking glucosamine, the search for an effective chondro-protective agent continues.
|A sequential approach to OA management|
|Education||To give an understanding of the condition and appreciate variables that can be modified - written information and verbal education.|
|Empowerment||To de-medicalise OA and move towards self-management.|
|To determine which factors to concentrate on and to set objectives - ie weight loss/exercise.|
|Symptom relief||Analgesics, injections, physiotherapy, supplements, rubifacients. Alternative/complementary therapies.|
|Minimise handicap||Rehabilitation techniques - muscle strengthening, use of aids and maintenance of activity. Footwear adaptation, orthotics.|
|Limit progression||Weight loss, use of muscle strengthening,|
continuation of exercise, modification of activities.
|Cognitive factors||Understand and be positive about the ability to|
manage symptoms and consequences without major life
Section 4: Monitoring and assessment
The monitoring of the outcome of OA intervention has become complex, using a variety of outcome measures.
There has been a need to try to unify outcome measures across organisations to enable researchers and clinicians to recognise standard methods of outcome assessment.
Organisations such as the Osteoarthritis Research Society have devised standardised approaches to outcome measurement in clinical trials (response criteria).5
Pain may be measured in various ways but usually utilises visual analogue scales or simple patient-based questionnaires (McGill pain questionnaire) given over time.
In addition, to fully appreciate the impact of OA on the individual it is necessary to use validated scales of impairment and function (Health Assessment Questionnaire, HAQ or Arthritis Impact Measurement Scales, AIMS) and handicap or quality of life (SF-36).
There are also process measures of OA progression. These include biochemical markers of disease activity such as matrix turnover, matrix synthesis and inflammation that do not find widespread clinical use and remain research tools.
None of the available markers can at present supplant the evidence of progressive joint space loss given by regular radiographs, which remain the standard in clinical practice.
Before any decision is made to introduce new or interventional treatments for OA, or to consider surgery, it is important to take account of both the patient's and the clinician's perspective on the nature and impact of OA on that individual.
1. Altman R, Asch E, Bloch D et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum 1986; 29: 1,039-49.
2. Kellgren J H, Lawrence J S. Radiological assessment of osteo-arthrosis. Ann Rheum Dis 1957; 16: 494-501.
3. Van Saase J L, Van Romunde L K, Cats A, Vandenbroucke J P, Valekburg H A. Epidemiology of OA: Zoertermeer survey. Comparison of radiological OA in a Dutch population with that of 10 other populations. Ann Rheum Dis 1989; 48: 271-80.
4. Stecher R M. Heberden's nodes: heredity in hypertrophic arthritis of the finger joints. Am J Med Sci 1941; 210: 801-9.
5. Zhang W, Moskowitz R W, Nuki G et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage 2008; 16: 137-62.
- www.patient.co.uk/showdoc/40001173 - patient friendly site for information on OA
- www.arc.org.uk - OA patient leaflet to download from arc site
- www.oarsi.org - OARSI site for full access subscription required
- www.rheumatology.org - ACR guidelines on the medical management of OA
- www.rcplondon.ac.uk - Royal College of Physicians London guidelines on OA management
- www.nice.org.uk/Guidance/CG59 - NICE guidelines on OA
For an archive of all GP clinical reviews visit www.healthcarerepublic.com/clinical/GP