Etiology — what causes it

Multifactorial — age, prior hip injury or dysplasia, obesity, prior FAI morphology, genetics. The pathology involves cartilage loss, subchondral bone changes, capsular fibrosis, and synovitis.

Epidemiology — who gets it

Lifetime risk of symptomatic hip OA is around 25% (Murphy et al., Arthritis Rheum). More common in adults over 60. Lower female predominance than knee OA.

Clinical signs

Reduced hip range, especially internal rotation (often the first to go), positive FABER and FADIR, antalgic gait. Imaging — joint space narrowing, osteophytes, subchondral sclerosis.

Symptoms

Groin pain, sometimes referred to the buttock or anterior thigh. Worse with weight-bearing, walking, and stairs. Morning stiffness less than 30 minutes. Functional limitations on putting on shoes and socks are characteristic.

Best evidence for chiropractic treatment

Fransen et al. (Cochrane 2014) and OARSI 2019 support land-based exercise as a core first-line treatment. Manual therapy is a useful adjunct (Hoeksma et al., Arthritis Rheum). GLA:D Hip program produces meaningful improvements. Total hip replacement is reserved for advanced disease with significant functional limitation despite structured conservative care.

When to seek emergency care

Some symptoms need urgent medical attention — not a chiropractic visit. Call 911 or go to the nearest emergency department for: progressive limb weakness, loss of bowel or bladder control, saddle anesthesia (numbness in the groin/inner thighs), severe unrelenting pain unrelieved by position, signs of fracture after significant trauma, chest pain, stroke-like symptoms (face drooping, arm weakness, speech changes), or any rapidly worsening or unusual symptom.

Bottom line

Hip OA responds well to land-based exercise plus manual therapy. Surgery is for late-stage disease — capacity-building is first-line.