Lucan · Conditions

Hip osteoarthritis

Australian guidance: RACGP Guideline for Knee and Hip Osteoarthritis

1. Definition and epidemiology

Hip osteoarthritis (OA) is the most common form of arthritis and a leading cause of disability worldwide, characterised by pathological changes across the whole joint complex including cartilage, subchondral bone, synovium, and periarticular structures such as ligament, tendon, and muscle. It is more common in women than men, and its prevalence increases significantly with age; the condition is exceedingly rare in people younger than 30 years. In Australia, OA affects an estimated 2.2 million people as of 2015, and the number is projected to rise to approximately 3.1 million by 2030 as the population ages and obesity rates increase. Importantly, radiographic changes of OA do not always correlate with symptoms, and radiographic findings alone are not an indication for management.

2. Pathophysiology

Hip OA results from dynamic and complex interactions across the whole joint, involving inflammatory, mechanical, molecular, and metabolic changes that tip the balance between tissue injury and repair toward net degeneration, as described in Robbins Ch 26 and elaborated in eTG Rheumatology. The traditional "wear and tear" model is now superseded by recognition that local and systemic inflammation play a key secondary role. Damaged articular cartilage releases proteoglycan fragments and collagen breakdown products into the joint space, triggering synoviocyte release of interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF-alpha). These cytokines upregulate matrix metalloproteinases and aggrecanases, accelerating chondrocyte apoptosis and extracellular matrix degradation. As cartilage loses its compressive resilience, increased mechanical stress is transmitted to the subchondral bone, resulting in sclerosis, cyst formation, and microfracture. Osteophytes form at joint margins via periosteal osteoblast proliferation. Pain in OA does not arise from cartilage itself, which is aneural; rather it originates from synovitis, subchondral bone oedema (visible on MRI as bone marrow oedema lesions), osteophyte-related periosteum disruption, capsular distension from effusion, and muscle spasm. In chronic disease, central sensitisation can amplify pain perception independently of structural severity, which explains why pain severity correlates poorly with radiographic grade.

3. Clinical presentation and diagnostic criteria

Hip OA is diagnosed clinically; laboratory and imaging investigations are rarely required for diagnosis. The cardinal symptom is activity-related pain localised to the anterior groin or lateral hip, often referred to the anterior thigh or knee, that is worse with weight-bearing and relieved by rest. In early disease, pain has an insidious onset; as disease advances, rest pain and nocturnal pain may develop. Morning or post-inactivity stiffness is typically brief, lasting less than 30 minutes, distinguishing OA from inflammatory arthritides in which stiffness is prolonged. On examination, the most sensitive early sign is restricted and painful internal rotation of the hip; log-roll test is often positive. Antalgic gait and Trendelenburg sign may be present. Bony swelling at the joint margins is a later finding. Alerting features requiring urgent reassessment include systemic symptoms (fever, weight loss), nocturnal pain unrelated to movement, rapid progression, or a history of malignancy, which may indicate septic arthritis, osteonecrosis, insufficiency fracture, or metastatic disease.

4. Investigations and AU-specific cutoffs

Hip OA is primarily a clinical diagnosis; imaging and blood tests are not required in patients with a typical presentation.

Plain radiograph (AP pelvis and lateral hip): Indicated when the presentation is atypical or to stratify severity before referral for joint replacement. Classic findings are asymmetric joint space narrowing (superolateral pattern predominant at the hip), subchondral sclerosis, subchondral cysts, and osteophytes. Radiographic severity (Kellgren-Lawrence grade) correlates poorly with symptoms; a substantial proportion of people with radiographic OA are asymptomatic.

Blood tests: Not required for diagnosis of typical OA; inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) are usually normal or only mildly elevated. Bloods are ordered selectively to exclude rheumatoid arthritis (rheumatoid factor [RF], anti-CCP antibody), crystal arthropathy (serum urate), or infection (full blood count [FBC]).

Synovial fluid analysis: If an effusion is present, aspiration may be performed to exclude gout, calcium pyrophosphate deposition, or septic arthritis. OA synovial fluid is non-inflammatory with a white cell count typically below 1,000 x 10^6/L.

MRI: Reserved for exclusion of alternative diagnoses such as osteonecrosis, labral tear, or stress fracture when clinical features are atypical. Hip injections require radiological guidance; this is distinct from knee injections where landmark guidance is adequate.

5. Management

Management follows a stepped, biopsychosocial, chronic disease model with non-pharmacological strategies as the foundation and pharmacological treatment as an adjunct, per both the RACGP guideline and eTG Rheumatology. There is no cure or proven disease-modifying therapy; management goals are to optimise pain control, maintain physical function, and maximise quality of life.

Education and self-management: All patients should receive explanation of the condition using positive, non-catastrophic language. Avoid terms such as "bone-on-bone" or "degenerative" in early disease. Patient education improves adherence and can reduce pain and improve function. A "bad day" management plan should be provided at diagnosis.

Land-based exercise (strong recommendation, RACGP): Individualised progressive land-based exercise should be offered to all patients with hip OA regardless of age, radiographic severity, or pain level. For hip OA, combining aerobic exercise with progressive lower limb muscle strengthening and balance training is generally recommended. The specific exercise modality (walking, resistance training, Tai Chi, stationary cycling, Hatha yoga) is a conditional neutral recommendation for hip OA, as no single form has been shown to be superior. Referral to a physiotherapist or exercise physiologist to initiate a supervised programme may improve adherence.

Weight management (strong recommendation, RACGP): For overweight patients (body mass index [BMI] of 25 kg/m2 or above) or those with obesity (BMI of 30 kg/m2 or above), a minimum weight loss target of 5 to 7.5% body weight is recommended. Combining weight loss with exercise produces greater symptomatic benefit than either alone.

Adjunctive physical treatments: Aquatic exercise or hydrotherapy, a short course of massage therapy, and manual therapy (stretching, soft tissue, and joint mobilisation) may be offered as conditional recommendations to support engagement with active management. Heat therapy (hot packs) may be used as a self-management adjunct. Assistive walking devices (cane used in the contralateral hand) may improve pain and stability.

Intra-articular corticosteroid injection (conditional recommendation): May provide short-term pain relief. Hip injections require radiological guidance. Injection may be repeated at three-monthly intervals if needed, with caution regarding repeated use. If joint replacement is being planned, avoid injection within six months of surgery to reduce infection risk.

Surgical referral: Refer to an orthopaedic surgeon for total hip replacement (THR) when severe persisting functional impairment or pain persists despite maximal nonsurgical management. Timely referral is important; the proportion of patients with hip OA who ultimately require surgery is higher than for knee OA. Weight loss before surgery is recommended given that obesity increases perioperative complications and is associated with higher revision rates.

6. Pharmacology and AU PBS notes

Oral NSAIDs including COX-2 inhibitors (conditional recommendation, RACGP; preferred over paracetamol per eTG): Agents including ibuprofen immediate-release 200 to 400 mg three or four times daily, naproxen 250 to 500 mg twice daily, celecoxib 100 to 200 mg daily, etoricoxib 30 to 60 mg daily, or meloxicam 7.5 to 15 mg daily may be offered at the lowest effective dose for the shortest time necessary. Oral NSAIDs are preferred over paracetamol for OA but carry greater potential for harm, particularly in older people and those with gastrointestinal, renal, or cardiovascular risk factors. Co-prescription of a proton pump inhibitor (PPI) is recommended for patients with elevated gastrointestinal risk. No Pharmaceutical Benefits Scheme (PBS) streamlined authority code is specific to OA for NSAIDs; they are dispensed as standard Schedule 4 items. Diclofenac carries the highest cardiovascular risk among non-selective NSAIDs and should be avoided in patients with established cardiovascular disease.

Paracetamol (conditional neutral, RACGP): A trial of paracetamol immediate-release 1 g orally every four to six hours as necessary (maximum 4 g daily) or modified-release 1.33 g every eight hours is reasonable when NSAIDs are contraindicated or not tolerated. Reduce dose in patients who are malnourished, frail, or have decompensated cirrhosis due to risk of hepatotoxicity from relative glutathione depletion. Discontinue if no benefit is demonstrated on trial.

Topical NSAIDs: Diclofenac 1% gel up to four times daily, diclofenac 2% gel once or twice daily, ibuprofen 5% gel up to four times daily, or piroxicam 0.5% gel up to four times daily may be considered as adjuncts with minimal systemic absorption and a favourable safety profile. RACGP takes a conditional neutral position on topical NSAIDs for hip OA; eTG supports a short-term trial. Topical capsaicin is not recommended for hip OA.

Duloxetine (conditional recommendation, RACGP; conditional, eTG): Duloxetine 30 mg orally daily for one week, increased to 60 mg daily (maximum 120 mg daily), may be considered for patients with widespread pain or coexisting depression, or when pain persists despite implementing all standard strategies. Note that the Therapeutic Goods Administration (TGA) has not approved duloxetine specifically for OA; it is used as an investigational agent for this indication.

Strongly not recommended (RACGP): Oral and transdermal opioids, viscosupplementation (hyaluronic acid) injections for hip OA, doxycycline, strontium ranelate, IL-1 inhibitors, stem cell therapy, platelet-rich plasma (PRP) injections, glucosamine and chondroitin, vitamin D supplements, and acupuncture should not be offered.

7. Complications and monitoring

Disease progression: Hip OA follows an unpredictable course; it may progress slowly, stabilise, or occasionally improve. Acute flares of pain and swelling can occur and should be anticipated in the "bad day" management plan. Disease progression does not always correlate with symptoms. Approximately 30% of patients with knee OA and a higher proportion with hip OA ultimately require joint replacement surgery.

NSAID-related harm: Regular users require monitoring of renal function, blood pressure, and cardiovascular risk. Annual review of NSAID necessity is recommended. A trial of dose reduction or cessation should be attempted when symptoms stabilise.

Central sensitisation: In patients with chronic hip OA pain, central sensitisation independent of radiographic severity may develop and may require specific pharmacological management (duloxetine, low-dose tricyclics, or gabapentinoids in consultation with a pain specialist or rheumatologist).

Falls risk: Hip OA impairs proprioception, muscle strength, and gait, substantially increasing falls risk in older patients. Systematic falls risk assessment including medication review (avoiding sedatives, opioids), balance training, and home hazard review forms part of holistic OA management.

Comorbidity management: The majority of patients with OA have at least one comorbid condition. OA is associated with higher rates of hypertension, type 2 diabetes, depression, and obesity compared with age-matched peers. Optimising management of comorbidities should be explicitly addressed in every OA management plan.

Post-surgical monitoring: After total hip replacement, deep vein thrombosis (DVT) and pulmonary embolism (PE) prophylaxis, mobilisation, and physiotherapy-guided rehabilitation are standard. Prosthetic joint infection is a rare but serious complication; patients should be counselled to report early warning signs (fever, wound discharge, increasing joint pain).

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.