Osteoarthritis

Osteoarthritis (OA) is the most common form of arthritis and a leading cause of pain and disability worldwide. It is a progressive joint disease characterised by cartilage degradation, subchondral bone remodelling, osteophyte formation, synovial inflammation, and loss of joint function. In Australia, approximately 2.2 million people are affected, with the knee and hip being the most commonly involved joints. OA prevalence increases steeply with age, affecting over 30% of adults over 65 years.

OA is not simply "wear and tear" — it is a complex, multifactorial condition involving mechanical, metabolic, and inflammatory processes. Risk factors include age, female sex, obesity (the most modifiable risk factor), prior joint injury, occupational loading, and genetic predisposition. The knee, hip, hand (distal and proximal interphalangeal joints, first carpometacarpal joint), and spine are most commonly affected. Generalised OA involves multiple joint groups simultaneously.

This guideline outlines the Australian primary care approach to diagnosis, assessment, and management of OA, with emphasis on exercise, weight management, self-management education, and appropriate use of pharmacotherapy. Joint replacement remains the definitive treatment for end-stage OA unresponsive to conservative management.

OA was historically conceived as a purely degenerative process, but is now understood to involve active biological processes across all joint tissues. The primary pathological changes occur in articular cartilage, subchondral bone, synovium, and periarticular soft tissues.

Cartilage degradation results from an imbalance between anabolic and catabolic processes in chondrocytes. Pro-inflammatory cytokines (IL-1β, TNF-α) stimulate matrix metalloproteinases (MMPs) that degrade collagen and proteoglycan. Progressive cartilage loss leads to subchondral bone exposure and altered joint biomechanics.

Subchondral bone changes include sclerosis, cyst formation, and osteophyte development. Osteophytes form at joint margins as a reparative response to biomechanical stress. Bone marrow lesions (visible on MRI) correlate with pain severity and predict disease progression.

Synovial inflammation (low-grade synovitis) is present in most symptomatic OA joints. Synovial macrophages produce inflammatory mediators that amplify cartilage destruction and sensitise periarticular nociceptors. Central sensitisation contributes to pain in many OA patients, particularly those with widespread pain or significant psychological comorbidity.

OA typically presents with insidious onset of joint pain, stiffness, and functional limitation. The pattern of joint involvement and clinical features vary by joint site.

Clinical diagnosis of OA in patients >45 years with typical joint pain, no inflammatory morning stiffness (<30 minutes), and no features of inflammatory arthritis can be made clinically — imaging is not required to initiate management. NICE criteria for knee OA: age ≥45, activity-related knee pain, morning stiffness <30 minutes.

OA is primarily a clinical diagnosis. Investigations are indicated when the diagnosis is uncertain, to exclude other causes, or to guide management decisions including surgical planning.

Severity assessment in OA guides management intensity and surgical referral timing. Both symptom severity and functional impact should be assessed. Radiographic severity (Kellgren-Lawrence grading) correlates poorly with symptoms.

Validated tools: WOMAC (Western Ontario and McMaster Universities Osteoarthritis Index) for knee/hip OA; AUSCAN for hand OA; KOOS (Knee injury and Osteoarthritis Outcome Score). These tools track response to treatment and guide surgical referral timing.

OA management is multimodal and should be individualised. Exercise and weight management are the cornerstones of treatment and have the strongest evidence. Pharmacotherapy provides symptom relief but does not modify disease progression. Surgery (joint replacement) is reserved for severe, refractory disease.

• Exercise therapy: The most effective intervention for OA pain and function. Both aerobic exercise (walking, cycling, swimming) and strengthening (quadriceps strengthening for knee OA; hip abductor strengthening for hip OA) are effective. Exercise reduces pain, improves function, and reduces surgical need. Prescribe specific exercise programmes via physiotherapy.
• Weight management: Every kilogram of body weight lost reduces knee joint load by 4 kg. Weight loss of 5–10% body weight significantly reduces knee OA pain and may delay joint replacement. Refer to dietitian and/or structured weight management programme. Consider pharmacotherapy for obesity (orlistat, GLP-1 agonists).
• Self-management education: OA-specific education programmes (such as Arthritis Australia’s Jointlyapp or MOVE programme) improve self-efficacy, pain, and function. Provide written resources and direct patients to evidence-based programmes.
• Assistive devices: Walking aids (cane, frame) reduce joint load and improve function. Knee bracing (valgus unloader brace for medial compartment knee OA). Footwear modification. Hand splints for first CMCJ OA.
• Joint replacement: Total knee or hip replacement is highly effective for severe OA. Refer when conservative management has failed after a minimum of 3–6 months of adequate treatment and quality of life is significantly impaired.

Pharmacotherapy in OA provides symptom relief to facilitate exercise and daily function. No pharmacological agent has proven disease-modifying efficacy. Treatment should be the lowest effective dose for the shortest necessary duration.

OA flares present as acute worsening of pain and swelling, often triggered by overactivity, weather changes, or concurrent illness. Acute flare management focuses on short-term pain relief while maintaining function.

• Confirm the flare is OA-related. Exclude septic arthritis (fever, hot swollen joint, systemic unwell) and crystal arthritis (acute onset, severe pain, hyperuricaemia). Aspirate and send for MC&S and microscopy if diagnostic uncertainty.
• Short-term analgesia escalation: increase paracetamol to regular dosing; add or increase topical NSAID; short course oral NSAID (5–7 days) if not contraindicated; intra-articular corticosteroid if significant effusion.
• Ice or heat application to affected joint for symptomatic relief.
• Relative rest from provocative activities for 48–72 hours; resume gentle exercise as tolerated.
• Review exercise programme with physiotherapist to identify and address triggering factors.
• Review weight management plan — flares are often associated with weight gain.
• Assess if surgical referral is now indicated given the frequency and severity of flares impacting quality of life.

Ongoing monitoring of OA focuses on pain, function, weight, exercise adherence, and medication safety. Regular review motivates patients and allows timely escalation when needed.

Modified management considerations for specific population groups with osteoarthritis.

Aboriginal and Torres Strait Islander peoples experience higher rates of musculoskeletal conditions including osteoarthritis, often at a younger age due to higher rates of obesity, diabetes, and occupational and recreational joint injuries. Access to specialist services and joint replacement surgery is inequitable.

Stewardship in OA focuses on avoiding opioid prescribing, limiting long-term NSAID use, and ensuring pharmacotherapy supports rather than replaces exercise and self-management.

• Avoid chronic opioid prescribing: No evidence for long-term efficacy in OA. High risk of dependence, opioid-induced hyperalgesia, falls, and cognitive impairment. If already prescribed, initiate structured tapering plan. Short-term use (weeks) while awaiting surgery may be acceptable in exceptional cases.
• NSAIDs: Use lowest effective dose for shortest duration. Reassess need at every prescription. Monitor renal function, blood pressure, and GI symptoms. Prefer topical over oral NSAIDs in elderly and those with cardiovascular or renal risk. Add PPI for GI protection when oral NSAIDs used >2 weeks.
• Avoid ineffective treatments: Glucosamine and chondroitin: not recommended (no proven efficacy in high-quality trials). Arthroscopic knee washout and debridement: no benefit over sham surgery for knee OA. Intra-articular hyaluronic acid: not recommended (RACGP guidelines); remove from management plans if previously prescribed.
• Duloxetine: PBS Authority required for chronic musculoskeletal pain. Document indication. Reassess at 3 months. Taper to discontinue — do not stop abruptly (discontinuation syndrome).
• Ensure exercise is prescribed: Exercise is the most effective intervention and should be prescribed as specifically as a medication. Refer to physiotherapy for exercise programme prescription.

OA is a chronic, progressive condition. The prognosis varies widely — many patients maintain good function with appropriate management for years, while others progress to severe disability requiring joint replacement. Early, proactive management significantly influences outcomes.

• RACGP — Guideline for the management of knee and hip osteoarthritis (3rd edition); 2018
• Osteoarthritis Research Society International (OARSI) — Guidelines for the non-surgical management of knee, hip, and polyarticular OA; 2019
• NICE — Osteoarthritis: care and management (CG177); 2022
• Hunter DJ, Bierma-Zeinstra S — Osteoarthritis; Lancet 2019
• Kolasinski SL et al. — 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee; Arthritis Care Res 2020
• Toupin-April K et al. — Self-management programs for osteoarthritis; Cochrane Database Syst Rev 2015
• Therapeutic Guidelines: Rheumatology — Osteoarthritis; available via eTG complete
• Arthritis Australia — osteoarthritis.org.au patient resources and MOVE programme