Osteoarthritis: Contemporary management strategies

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Reference: June 2026 | Issue 6 | Vol 12 | Page 8

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Osteoarthritis (OA) is a chronic, degenerative joint disorder characterised by pain, stiffness, and progressive functional impairment. It is the most prevalent form of arthritis worldwide, affecting more than 500 million individuals, and represents a leading cause of chronic pain, disability, and reduced productivity.¹

Despite the substantial global burden of OA, effective disease-modifying therapies remain limited. Most currently available treatments primarily address symptoms, such as pain and functional limitations, rather than altering the underlying joint degeneration.² These limitations highlight the need for innovative strategies towards prevention, early intervention and disease modification.

The prevalence of OA is rising steadily, driven primarily by ageing populations, increasing obesity rates, and rising physical inactivity.³ Key modifiable risk factors, including obesity, joint injury, and occupational hazards, present opportunities for primary prevention.^4,5 Early identification of high-risk individuals and targeted interventions may reduce disease incidence or slow progression.⁵

Current evidence-based guidelines emphasise symptom management through non-pharmacological strategies, including structured exercise therapy, weight management, and patient education.^2,3 Despite robust recommendations, adherence to these strategies remains low, highlighting the need for more effective implementation and patient engagement strategies.^2,3

Management of OA is multimodal and stepwise, incorporating non-pharmacological, pharmacological and, when appropriate, surgical interventions. Non-pharmacological interventions form the foundation of treatment, with pharmacological therapies providing additional symptomatic relief. Surgical interventions are reserved for advanced disease refractory to conservative measures.^2,3

Non-pharmacological management

Non-pharmacological strategies are recommended as first-line therapy by major international guidelines, including those from the National Institute for Health and Care Excellence (NICE) and the American College of Rheumatology (ACR).^2,3 Core elements include structured patient education, lifestyle modification, exercise therapy, and weight management.

Structured education improves self-efficacy, encourages adherence to exercise, and enhances coping strategies, thereby improving clinical outcomes. Evidence from systematic reviews, including Cochrane analyses, demonstrates that programmes incorporating OA-specific information and behavioural interventions yield small, but statistically significant improvements in pain and function.¹ Education is most effective when embedded within long-term management and combined with exercise and lifestyle interventions.

Despite robust evidence supporting non-pharmacological management, implementation remains suboptimal. Barriers to implementation include limited access to services such as multidisciplinary care from physiotherapists and dieticians.^2,3 Insufficient reimbursement and patient misconceptions regarding efficacy contribute to the underutilisation of these interventions. Patient-related factors such as low motivation and expectation for pharmacological and/or surgical intervention contribute to the challenge.²

There are several well-established community- and primary care-based programmes for OA in Ireland. These initiatives such as GLA:D^® Ireland and Arthritis Ireland programmes are modelled on a community-delivered, physiotherapist-led programme.^7,8 The GLA:D^® programme is a scalable model to deliver first-line OA care.⁷ Observational registry data indicates that the GLA:D^® programme demonstrates clinically meaningful improvements in pain and function for OA patients.⁷

These community initiatives represent earlier access to conservative management, integration of education and exercise, and a reduced reliance on the acute hospital setting.^7,8 This model has demonstrated consistent effectiveness across international healthcare settings.^7,8

Exercise therapy

Exercise therapy remains the cornerstone of OA management. High-quality evidence from randomised controlled trials and systematic reviews demonstrates that both aerobic and resistance exercise significantly reduce pain and improve physical function in patients with knee and hip OA.¹ Exercise targets peri-articular muscle strengthening, joint flexibility, and aerobic capacity enhancement, all of which are essential for improving joint stability and reducing symptom burden.¹

Adherence to exercise regimens, however, remains a major challenge. Estimates suggest that up to 87 per cent of patients with knee OA do not meet recommended exercise levels, increasing the risk of sedentary-associated morbidity and further functional decline.⁹ Structured educational interventions have been shown to improve adherence and coping strategies, leading to clinically meaningful improvements in both pain and function.¹

Although no single exercise modality has demonstrated superiority, recommendations typically include a minimum of 12 supervised sessions over three months, with at least two sessions per week.¹ Programmes should be individualised based on patient capability, comorbidities, and preferences to maximise engagement and benefit.

Physical therapy and adjuncts

Physical therapy interventions, including manual therapy, stretching, and joint mobilisation may provide modest incremental benefits beyond exercise alone.² Evidence indicates that combining manual therapy with exercise results in greater functional improvement compared with exercise alone, supporting physiotherapy as an adjunct rather than a standalone intervention.² Accordingly, physiotherapy is most appropriately utilised as an adjunct to exercise rather than as an independent treatment modality.²

Assistive devices, such as braces, insoles, and walking aids, may further enhance mobility and reduce pain. In particular, knee valgus braces have demonstrated modest efficacy in alleviating symptoms in medial compartment knee OA.³ These interventions should be tailored to individual patient characteristics, including disease severity, joint alignment, and activity level.³

Weight loss

Obesity is a significant, modifiable risk factor for OA, especially in weight-bearing joints such as the knees.⁴ Excess weight increases joint loading and contributes to inflammation through adipokine-mediated pathways.⁴ Increased body habitus increases mechanical stress on articular cartilage and subchondral bone.⁴ In addition to the biomechanical effects, adipose tissue secretes pro-inflammatory cytokines and adipokines, leading to systemic and local joint inflammation  in OA patients.^4,5

Weight reduction has been shown to significantly improve pain, physical function, and even joint structure. Clinical guidelines recommend a minimum weight loss of 5 per cent, with greater reductions yielding enhanced benefits.⁴ Greater weight loss confers proportional benefits, including potential slowing of radiographic disease progression and cartilage loss.^4,5 These outcomes underscore the importance of weight management in guideline-recommended first-line therapy.^4,5

Sustained weight loss offers long-term advantages, slowing functional decline and augmenting the effects of structured exercise programmes.^4,5 Combined dietary and exercise interventions in overweight and obese individuals consistently produce clinically meaningful improvements in pain and mobility. Additional strategies, such as activity pacing and sleep optimisation, further improve disease management.^4,5

Despite these benefits, long-term adherence to lifestyle modifications remains a significant challenge for many patients, necessitating structured multidisciplinary support and ongoing follow-up. Psychological, environmental and behavioural factors can hinder many patients.^4,5

Emerging therapies

GLP-1 receptor agonists:
Glucagon-like peptide-1 (GLP-1) receptor agonists, commonly used for obesity and type 2 diabetes, have emerged as a promising therapeutic option in OA.^6,7

GLP-1 receptor agonists may be beneficial in OA patients through multiple complementary mechanisms.^6,7 Sustained weight loss reduces mechanical loading on weight-bearing joints. Their potential utility extends beyond promoting weight loss, since GLP-1 receptor agonists have exhibited anti-inflammatory and chondro-protective properties in pre-clinical studies.

GLP-1 agents demonstrate anti-inflammatory properties such as reduced production of pro-inflammatory cytokines, including IL-1β and TNF-α, alongside inhibition of NF-κB signalling pathways.^6,7 Chondro-protective benefits include inhibition of matrix metalloproteinase activity, decreased chondrocyte apoptosis, and increased matrix synthesis.^6,7

Recent clinical evidence, including the Semaglutide Treatment Effect in People with Obesity (STEP) trials, demonstrated that semaglutide significantly improved pain, physical function, and weight loss in patients with knee OA and obesity.⁵ In addition to randomised trial data, observational studies suggest these agents may reduce cartilage loss and the need for surgical intervention.⁸ While promising, further randomised trials are needed to confirm long-term efficacy, disease-modifying potential, and cost-effectiveness.⁸

Clinically these agents may also confer metabolic modulation benefits via improved insulin resistance and improved lipid profile, reducing cartilage degeneration. The integration of GLP-1 agonists into the management of OA demonstrates a shift towards targeting metabolic drivers of disease.^5,8 These agents may be particularly beneficial in patients with metabolic syndrome and inflammatory OA phenotypes, or for patients wishing to delay surgical intervention.^5,8

Pharmacological management

When non-pharmacological measures fail to control symptoms adequately, pharmacological therapy may be introduced in a patient-centred, stepwise approach.^2,6 The choice of therapeutic agent should be based on efficacy, safety profile and patient comorbidities.^2,6

Analgesics:
Oral non-steroidal anti-inflammatory drugs (NSAIDs) provide the most consistent and clinically meaningful pain relief, with multiple network meta-analyses reporting moderate improvements in pain and function compared to placebo.⁶ Both traditional non-selective NSAIDs and selective cyclooxygenase-2 (COX-2) inhibitors demonstrate comparable efficacy.⁶ Selective COX-2 inhibitors provide comparable efficacy, with an improved gastrointestinal safety profile, making them preferable in patients with a higher risk of an adverse gastrointestinal event.⁶

Despite the efficacy of NSAIDS, use is limited by gastrointestinal, cardiovascular, and renal adverse effects, particularly with long-term therapy.⁶ The guidelines recommend prescribing the lowest clinically effective dose and monitoring closely.

Historically paracetamol was prescribed as a first-line analgesic in OA patients, but systematic reviews and meta-analyses report effect sizes close to placebo.⁶ As paracetamol demonstrates minimal benefit, it is no longer emphasised in current guidelines.⁶ Paracetamol can be prescribed in patient groups where NSAID therapy is unsuitable, however, patients should be advised regarding the lack of efficacy.⁶

Opioids are generally discouraged due to limited efficacy and the high risk of dependence, sedation, and risk of falls in the elderly population.⁶ Evidence has demonstrated that opioids provide only minimal improvements in pain and a significant risk of harm. Opioids should only be prescribed after other therapeutic agents have been trialled and and should be prescribed at the lowest effective dose.⁶

Duloxetine, a serotonin-norepinephrine reuptake inhibitor (SNRI), may offer moderate pain relief, particularly in OA patients with central sensitisation or comorbid mood disorders such as anxiety and depression.⁶ Several clinical trials have demonstrated moderate improvements in pain and function.

While the safety profile shows that this agent is generally well tolerated, monitoring is advised for dry mouth, nausea and mood disturbance.⁶ Overall, current evidence supports a hierarchical, patient-centred approach to oral analgesia in OA, prioritising NSAIDs where appropriate, minimising opioid use, and considering alternative agents in selected patient populations.⁶

Topical analgesics:
The ACR and Osteoarthritis Research Society (OARSI) guidelines strongly endorse the use of topical NSAIDs as a first-line pharmacologic therapy. Topical NSAIDs are particularly recommended for knee arthritis, supported by strong quality evidence demonstrating significant improvement in pain and function and a more favourable safety profile than oral NSAIDs.⁶ Topical NSAIDS are particularly useful in elderly patients and those with cardiovascular or gastrointestinal risk factors.

Topical capsaicin is conditionally recommended by both ACR and OARSI guidelines. Capsaicin exerts its analgesic effect through desensitisation of nociceptive nerve fibres via depletion of substance P. Evidence demonstrates modest improvements in pain versus placebo. The magnitude of benefit is smaller than that observed with oral NSAIDs.⁶ Side effects, such as burning and irritation at the application site, may impact adherence. Capsaicin is best considered as an adjunctive agent in selected patient groups where other therapeutic options are limited or insufficient.⁶

Intra-articular therapies:
Intra-articular injections are used to provide targeted symptomatic relief when non-pharmacological interventions or oral analgesics are insufficient. Evidence shows that corticosteroid injections are effective for short-term pain reduction (typically lasting up to six weeks) by suppressing synovial inflammation.⁶ Corticosteroid injections are particularly effective during acute flares or if active synovitis is present.⁶ Evidence shows that repeated injections may accelerate cartilage loss, and clinical guidelines recommend limiting injections to three to four times per year per joint.⁷

Hyaluronic acid (HA) injections aim to restore synovial fluid viscoelasticity, improving lubrication and shock absorption. HA is a naturally occurring glycosaminoglycan critical for maintaining normal joint homeostasis. Evidence suggests HA injections deliver modest and variable improvements in pain and function, and that benefit is influenced by formulation and injection protocols.⁶

Platelet-rich plasma (PRP) injections, derived from autologous blood, provide concentrated growth factors that may promote tissue repair and modulate inflammation. Meta-analyses indicate PRP injections may produce longer-lasting relief compared with HA or placebo over six to 12 months.⁸ However, variability in preparation and administration protocols limits generalisability, highlighting the need for standardised, high-quality trials.⁸

Surgical management
Surgical intervention is typically reserved for patients with advanced OA who remain symptomatic despite optimised conservative therapy, and experience significant impairment in quality of life.⁹ Total joint arthroplasty (TJA) is the gold standard, demonstrating substantial, sustained improvements in pain and function.⁹

Uni-compartmental knee arthroplasty (UKA) offers faster recovery and early functional improvement, but has higher revision rates, underscoring the importance of careful patient selection.⁹ Arthroscopic procedures are no longer recommended for OA as evidence consistently shows no clinically meaningful benefit.¹⁰

High tibial osteotomy (HTO) is a joint-preserving option for younger patients with uni-compartmental OA and varus malalignment. Evidence from cohort studies and meta-analyses suggest HTO can delay the need for arthroplasty, though randomised trial data are limited and long-term outcomes vary.¹⁰ Surgical strategies should be individualised according to disease severity, age, activity level, and anatomical factors to optimise outcomes and longevity of the intervention.

Conclusion

OA is a highly prevalent and disabling condition with substantial individual and societal burden. Contemporary management emphasises a multimodal, stepwise approach, with non-pharmacological interventions forming the foundation. Despite strong evidence supporting these strategies, adherence remains suboptimal.

Exercise and weight management demonstrate the most consistent evidence for improving pain and function. Adjunctive interventions, including physical therapy, bracing, and patient education, further enhance outcomes. Interventions should be individualised, integrated into a comprehensive management plan, and maintained longitudinally to optimise short-term symptom relief and long-term functional outcomes. Addressing the gap between guideline recommendations and real-world practice will be critical to improving outcomes for OA patients.

Pharmacological therapies provide symptomatic relief, but are limited by adverse effects and a lack of disease-modifying properties. Emerging agents, particularly GLP-1 receptor agonists, represent promising avenues by targeting both metabolic and inflammatory pathways. Future efforts should focus on developing disease-modifying therapies and improving the long-term uptake of evidence-based interventions to optimise patient outcomes.^5,8