Musculoskeletal Conditions

• Rheumatoid Arthritis (RA)


  Autoimmune disorder where the body's immune system mistakenly attacks the synovium (lining of the joints), leading to inflammation
• Rheumatoid Arthritis (RA)


  • Chronic inflammation causes swelling, pain, stiffness, and eventually can damage cartilage and bone within the joint
  • Synovium becomes thickened and forms pannus, which invades and erodes the cartilage and bone
  • Can also affect other organs and systems in the body, leading to fatigue, fever, and weight loss
• Osteoarthritis (OA)


  Degenerative joint disease resulting from the breakdown of joint cartilage and underlying bone
• Osteoarthritis (OA)


  • Cartilage that cushions the ends of bones wears away, leading to pain, swelling, and stiffness in the joint
  • Bones may develop growths called osteophytes or bone spurs
  • Inflammation of the synovial membrane may occur, but it is secondary to the cartilage and bone changes and is not as prominent as in RA
• Risk factors for OA

  • Age
  • Joint injury or overuse
  • Obesity
  • Genetics
  • Joint misalignment
  • Metabolic factors
  • Other factors (hormonal changes, joint infections, repetitive joint movements)
• Causes of RA


  • Multifactorial: Genetic + Environmental factors (epigenetics)
  • Autoimmune
• Causes of RA


  • Genetic factors (higher rate of severe RA in first degree relatives)
  • Environmental factors (smoking linked to RA development, poorer response to treatment, and poorer prognosis)
  • Autoimmune
• Causes of OA


  • Age: Joint tissues become more susceptible to damage and repair mechanisms become less efficient
  • Joint injury or overuse: Previous joint injuries or repetitive stress on joints
  • Obesity: Excess body weight puts added stress on weight-bearing joints
  • Genetics: Tends to run in families
  • Joint misalignment: Structural abnormalities in the joints
  • Metabolic factors: Diseases like diabetes or hemochromatosis
• Treatment goals for RA

  • Autoimmune disorder: Treat the abnormal immune response
  • Genetic factors: Address the genetic predisposition
• Treatment goals for OA

  • Pain control
  • Improved function and decreased disability
  • Altering the disease process and its consequences
  • Patient education
• RA treatments


  • Drug treatments: DMARDs (csDMARDs + bDMARDs), corticosteroids, analgesics
  • Non-drug: Stop smoking, dietary changes, regular exercise
• RA drug treatments


  1. DMARD therapy: Start ASAP to induce clinical remission and prevent joint damage

  2. DMARD response should be apparent within 12 weeks

  3. Early DMARD use decreases rates of joint damage and makes the disease easier to control long-term

  4. bDMARDs used if remission not achieved or significant disease activity persists after csDMARDs

  5. Corticosteroids: Rapidly and effectively control severe inflammation, provide symptom relief and slow disease progression

  6. Analgesics: Assess pain severity and impact to guide management, improve function and reduce disability
• OA drug treatments


  • Paracetamol
  • NSAIDs (topical vs systemic)
  • Capsaicin
• OA paracetamol treatment


  1. Can be effective initial oral analgesic for mild to moderate knee or hip OA

  2. Patients who report no effect may be using inadequate doses (<2g/day)

  3. For persistent symptoms, consider regular dosing rather than prn

  4. Adherence to QID regimens often poor, SR-formulations may be useful

  5. If response inadequate, consider trial of NSAIDs instead of, or in combination with, paracetamol

  6. Do not continue if no benefit or treatment is harmful

  7. OA symptoms can fluctuate, if improved, consider stopping oral analgesia
• OA NSAID treatment


  1. Topical or systemic formulations

  2. Topical NSAIDs and capsaicin can be considered as an adjunct to other treatment strategies and as part of short-term self-management

  3. Topical NSAIDs often preferred to oral for early OA, especially if not widespread (less risk of systemic adverse effects)

  4. No single NSAID more effective than another, some patients respond better to one

  5. Maximal effect usually seen within two weeks

  6. Systemic NSAIDs may cause significant morbidity and mortality from GI, renal and CVS adverse effects, use carefully selected patients

  7. Minimise NSAID dose by using concurrent paracetamol, use at lowest effective dose for shortest possible time
• Topical or systemic formulations


  • Topical NSAIDs and capsaicin
  • Systemic NSAIDs
• Topical NSAIDs


  • Often preferred to oral for early OA, especially if not widespread
  • Less risk of systemic adverse effects than with oral NSAIDs
• No single NSAID more effective than another
• Maximal effect of NSAIDs are usually seen within two weeks
• Systemic NSAIDS


  May cause significant morbidity and mortality from GI, renal and CVS adverse effects
• Use of systemic NSAIDs


  In carefully selected patients reduces these risks
• Only consider using an oral NSAID first line for patients at low risk of harms from NSAID use
• Minimise NSAID dose


  • By using concurrent paracetamol
  • Intermittent NSAID (e.g. during acute exacerbations) has a lower risk of adverse effects
• Use NSAIDs at the lowest effective dose for the shortest possible time
• Capsaicin cream


  • Topical preparation derived from red chilli peppers
  • Depletes substance P (neurotransmitter for sensory nerves)- on exposure to capsaicin, neurons temporarily become insensitive to other stimulation
• Small but significant reduction in pain with capsaicin cream compared to placebo
• Capsaicin cream application


  Applied QID over the affected joint for >6 weeks
• Main adverse effect of capsaicin cream is a transient burning at the site of application, which decreases over time
• Opioids


  Very limited role in OA management – modest, if any, benefits and a significant risk of harms
• Only consider opioids if: severe persisting functional impairment due to pain, despite maximal conservative management; or patients awaiting surgery or in whom surgery is not possible
• Use of opioids


  • Prescribe on a short-term trial basis, as part of overall pain management strategy, with clear goals and regular review of treatment response and adverse effects
  • Before starting, have a plan for stopping ineffective therapy and discuss with patient
  • Prolonged use indicates the need for specialist assessment
• Quality of evidence for corticosteroids in OA is low
• Intra-articular corticosteroid injection


  • May provide symptom relief lasting from 4 to 12 weeks in patients with knee osteoarthritis
  • Useful to manage small numbers of acutely painful, swollen joints
  • Onset within a few hours; lasts several weeks
  • Repeat 3 monthly prn
• Adverse effects of intra-articular corticosteroid injections include transient increase in pain, risk of nerve damage and infection
• Emerging evidence suggests a possible small risk of joint deterioration and worsening symptoms over the long term with intraarticular corticosteroid injections
• Duloxetine


  • An antidepressant also used for chronic musculoskeletal pain
  • Reduces pain and improves physical function in knee OA
  • Exact mechanism of action not fully understood, thought to: modulate pain pathways in CNS, alleviate depression and anxiety associated with chronic conditions
• Duloxetine may have a similar efficacy to oral NSAIDs (but head-to-head comparisons are lacking)
• Duloxetine is an effective adjunct to oral NSAIDs
• Examples of CAM and other treatments

  • Viscosupplements (hyaluronan and hylan derivatives)
  • Glucosamine and chondroitin (care with warfarin, shellfish allergies)
  • Fish oil
  • Acupuncture
  • Electrotherapy with TENS
  • Thermotherapy
• No clear evidence base for efficacy of CAM and other treatments, typically not recommended by clinical guidelines but can still be widely used