24th February 2025

Osteoarthritis (OA)

Overview of OA

OA is a common chronic degenerative condition of the joint cartilage, affecting millions of patients across the UK, resulting in a significant economic impact due to lost working days. The pathogenesis is thought to be a dynamic process of cartilage loss, synovial inflammation and bone remodelling, mediated by matrix metalloproteinases. OA is characterised by pain and, as the disease progresses, deformity and loss of function. It typically affects the large, weight-bearing joints such as the knees, hips and spine.

Risk factors for OA include: female gender, advancing age, family history, obesity, previous trauma and vitamin D deficiency. Secondary OA can occur due to endocrine (acromegaly), metabolic (haemochromatosis, hyperparathyroidism), inflammatory (crystal arthropathy) and neuropathic (diabetes mellitus) conditions.

Signs and symptoms of OA

The most common symptom is pain, which typically improves with rest and worsens with activity, but OA sufferers also complain of stiffness, joint instability and reduced range of movement. In advanced cases deformity occurs, including the classical findings of Bouchard’s nodes (at the proximal interphalangeal joints) and Heberden’s nodes (at the distal interphalangeal joints) in generalised nodal OA (see Figure 1). In lower limb OA, compensation in gait due to antalgia can result in muscle wasting and, consequently, weakness, contributing to the risk of falls.

Image source: Wikimedia Commons (2006). Heberden-Arthrose, Licensed under a Creative Commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Heberden-Arthrose.JPG (Accessed: 17 January 2024).

Investigation of OA

The mainstay of diagnosis in OA is a comprehensive clinical assessment, where the history and examination findings are correlated, augmented by radiological studies. Of note, the radiological findings of X-rays correlate poorly with the described severity of symptoms and, indeed, the function of the joint in terms of daily living activities. The typical X-ray findings are: loss of joint space, subchondral sclerosis, subchondral cysts and osteophyte formation (see Figure 2).

Image source: Wikimedia Commons (2012). Osteoarthritis left knee, Licensed under a Creative Commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Osteoarthritis_left_knee.jpg (Accessed: 17 January 2024).

Laboratory investigations are rarely required, and if they are, it is to exclude other causes, such as crystal arthropathy (where joint aspiration for microscopy may be indicated) or RA (where inflammatory markers will be raised and auto-antibodies likely detected).

Management of OA

The effective management of OA requires a coordinated, holistic, multidisciplinary approach, aiming to minimise symptoms and maximise function. Unless there is a secondary cause, there are no pharmacological therapies that can halt or reverse the disease process. The impact of OA cannot be overstated in terms of poor quality of life and mental health, namely the deleterious effect on the ability to work, enjoy leisure activities, self-care and sleep. Important aspects of care include:

• Functional assessment by both physiotherapists and occupational therapists for joint supports, walking aids and adaptations to the home environment. Exercises can be taught to optimise joint function and reverse muscle wasting, helping with mobility and, importantly, overall cardiovascular health.
• Weight loss should be encouraged, particularly if central, weight-bearing joints are primarily affected, as ongoing mechanical stress will cause progressive joint damage.
• Analgesia should be titrated in a stepwise manner, taking into account the distribution of joints affected, patient comorbidities and potential drug reactions, as comorbidity is common. The management of patient expectations regarding pain relief is an important consideration of chronic pain management.
  • Step 1: Regular Paracetamol 1 g, four times a day, with a topical NSAID gel such as diclofenac (particularly for hand and knee disease).
  • Step 2: Switch topical for oral NSAIDs such as ibuprofen, if not contraindicated (either relatively due to age or absolutely due to cardiovascular, gastrointestinal or renal disease). The risk may be reduced by co-administering a proton pump inhibitor. Alternatively, for disease predominantly affecting a specific joint, intra-articular corticosteroid injections may be beneficial (up to 3-4 injections per year). There is no evidence for oral or injected viscosupplements.
  • Step 3: In refractory cases or where previous therapies are contraindicated, weak opiates such as codeine may be used, with or without neuropathic agents such as gabapentin or pregabalin.
  • Step 4: NICE does not recommend strong opiates such as morphine for refractory pain, otherwise difficult to manage; therefore, the next step is referral to Orthopaedics for the consideration of a joint replacement, especially if there is a significantly reduced quality of life.

References

• Clunie, G, Wilkinson N, Nikiphorou E, Jadon D. Oxford Handbook of Rheumatology. Fourth Edition. Oxford: Oxford University Press; 2018
• Badlissi F. Osteoarthritis [Internet]. BMJ Best Practice. BMJ Publishing Group; 2023 [Cited 2023 August 17]. Available from: https://bestpractice.bmj.com/topics/en-gb/192