Introduction / Definition

Hip osteoarthritis (OA) is a progressive, chronic condition characterised by the breakdown of articular hyaline cartilage, fibrocartilaginous remodeling, subchondral bone sclerosis, cyst formation, and marginal osteophytosis. Historically classified simply as 'primary' (idiopathic) or 'secondary', contemporary understanding recognises that the majority of cases historically deemed idiopathic are secondary to subtle morphological abnormalities, notably femoroacetabular impingement (FAI) and developmental dysplasia of the hip (DDH).

Epidemiology

• Prevalence: Affects approximately 5–10% of adults over the age of 45 in developed nations, with lifetime risk estimated at 25%.
• Demographics: Incidence increases steeply after 50 years of age. Male and female distribution is broadly equal overall, although superolateral subluxation and dysplasia patterns predominate in females, whereas primary concentric and cam-associated OA predominate in males.
• Risk Factors:
  • Systemic: Advanced age, genetic predisposition, female sex (post-menopausal), and elevated body mass index (BMI).
  • Mechanical: Repetitive high-impact loading, prior intra-articular fractures (e.g. acetabular or femoral head fractures), Legg-Calvé-Perthes disease, slipped capital femoral epiphysis (SCFE), DDH, and cam/pincer FAI morphology.

Relevant Anatomy & Biomechanics

• Articular Geometry: The hip is a congruous ball-and-socket synovial joint. The acetabulum is deepened by the fibrocartilaginous acetabular labrum, which enhances fluid-film lubrication and stability.
• Biomechanics (Pauwels Principles):
  • Joint reactive force (R) during single-leg stance equals 2.5–3 times body weight, determined by the lever arm ratio between body weight (W) and abductor muscular force (A).
  • Using a walking stick in the contralateral hand creates an opposing moment arm, decreasing required abductor force and cutting joint reaction forces by up to 50%.
• Pathoanatomy: Loss of type II collagen and proteoglycan content reduces cartilage water-binding capacity. Chondrocyte cloning and apoptosis follow, yielding fissuring, eburnation, subchondral microfractures, synovial hypertrophy, and capsular contracture, classically leading to a fixed flexion, external rotation, and adduction deformity.

Classification

Kellgren-Lawrence Radiographic Grading System

• Grade 0: Normal radiograph; no features of OA.
• Grade 1: Doubtful joint space narrowing (JSN) and possible osteophytic lipping.
• Grade 2: Definite osteophytes and possible JSN on anteroposterior views.
• Grade 3: Moderate multiple osteophytes, definite JSN, some sclerosis, and possible deformity of bone contour.
• Grade 4: Large osteophytes, marked JSN, severe sclerosis, and definite bony contour deformity.

Tönnis Classification (Specific to Dysplasia/Hip OA)

• Grade 0: No signs of OA.
• Grade 1: Mild increased sclerosis of head and acetabulum, slight joint space narrowing, slight marginal osteophytes.
• Grade 2: Moderate joint space narrowing, small subchondral cysts, loss of femoral head sphericity.
• Grade 3: Severe joint space narrowing or obliteration, large cysts, severe head deformity, necrosis.

Morphological / Migration Subtypes

• Superolateral: Most common; frequent in dysplasia; early loss of superior joint space with lateral femoral migration.
• Medial (Concentric): More common in inflammatory arthritides and primary OA; medial cartilage loss; may lead to protrusio acetabuli (Kohler's line breach).
• Inferior: Less common; associated with inferior osteophytes ('weeping' osteophytes).

Clinical Presentation & Examination

History

• Insidious onset of groin and anterior thigh pain, often radiating to the knee (via the obturator and femoral nerves).
• Pain on initial weight-bearing (start-up pain) easing with gentle movement, but worsening toward the end of the day; nocturnal rest pain signifies advanced disease.
• Functional limitations: Inability to put on shoes and socks, difficulty cutting toenails, and reduced walking tolerance.

Physical Examination

• Gait: Antalgic gait (shortened stance phase on affected side) or Trendelenburg gait (abductor insufficiency dropping contralateral hemipelvis).
• Inspection: Fixed deformities—typically flexion, external rotation, and adduction.
• Palpation: Groin tenderness over the femoral triangle; absence of localized trochanteric tenderness (differentiating from greater trochanteric pain syndrome).
• Range of Motion: Earliest and most sensitive clinical sign is restriction and pain on internal rotation in 90° flexion. Loss of extension (positive Thomas test) confirms fixed flexion deformity.
• Special Tests: FABER test (Patrick's test) localises groin pain; FADIR test provokes anterior impingement.
• Leg Length Assessment: Apparent limb length discrepancy secondary to pelvic tilt or true discrepancy from articular cartilage collapse and proximal femoral migration.

Investigations

Plain Radiography

• Standard series: Weight-bearing anteroposterior (AP) pelvis, dedicated AP hip, and lateral projection (Dunn 45°/90° or cross-table lateral).
• Hallmark Features:
  1. Joint space narrowing (focal or uniform)
  2. Subchondral sclerosis (eburnation)
  3. Osteophyte formation (acetabular and femoral)
  4. Subchondral cysts (geodes)
• Key Measurements:
  • Lateral Centre-Edge Angle of Wiberg (LCEA): <20° indicates dysplasia; >40° indicates pincer morphology (normal 25°--39°).
  • Tönnis acetabular roof angle: >10° indicates dysplastic instability.
  • Alpha angle (Dunn view): >55° denotes cam morphology.

Advanced Imaging

• MRI / MR Arthrography: Not routinely required for established OA. Indicated in early chondral damage, labral pathology, or suspected avascular necrosis (AVN) with normal plain radiographs.
• CT Scanning: Helpful for complex acetabular/femoral bone loss, severe protrusion, dysplastic retroversion, or 3D robotic arthroplasty templating.
• Diagnostic Intra-articular Injections: Fluoroscopic or ultrasound-guided local anaesthetic injection helps differentiate intra-articular hip pathology from lumbar spine radiculopathy or sacroiliac pathology.

Management

Non-Operative Management

Recommended for all patients prior to surgical consideration:

• Lifestyle & Physiotherapy: Low-impact aerobic exercise, structured core/abductor strengthening, and weight reduction (reducing joint contact forces).
• Walking Aids: Contralateral walking stick or crutch.
• Pharmacotherapy: Per NICE and AAOS guidelines, oral NSAIDs (with proton pump inhibitor cover) are first-line pharmacological agents. Paracetamol demonstrates limited clinical efficacy. Weak opioids may be used short-term only for acute flares.
• Intra-Articular Injections: Image-guided corticosteroid injections provide short-term symptom relief (2–12 weeks). Viscosupplementation (hyaluronic acid) and platelet-rich plasma (PRP) are not recommended in national guidelines due to lack of cost-effective, reproducible benefit.

Operative Management

Joint Preservation

Reserved for pre-arthritic or early OA (Tönnis 0–1) in young, active patients:

• Hip Arthroscopy / Surgical Dislocation: Labral debridement/repair and femoral osteochondroplasty for isolated FAI.
• Periacetabular Osteotomy (Ganz PAO): For symptomatic acetabular dysplasia before irreversible cartilage loss.

Total Hip Arthroplasty (THA)

The gold-standard definitive intervention for end-stage hip OA with debilitating pain and functional deficit resistant to non-operative treatment.

• Surgical Approaches:
  • Posterior (Moore / Southern): Splits gluteus maximus, releases short external rotators (piriformis, obturator internus, gemelli). Excellent acetabular/femoral exposure; sciatic nerve at risk; requires capsule and conjoined tendon repair to minimise dislocation risk.
  • Direct Lateral (Hardinge): Enters interval through anterior split in gluteus medius and vastus lateralis. Lower dislocation rate, but risk of superior gluteal nerve branch injury and persistent postoperative Trendelenburg lurch.
  • Direct Anterior (Hueter): Enters internervous (femoral and superior gluteal nerves) and intermuscular (tensor fasciae latae and sartorius) plane. Low dislocation rate; leaves posterior structures intact. Associated with learning curve, potential lateral femoral cutaneous nerve (LFCN) neuropraxia, and early femoral stem complications.
• Fixation Strategies:
  • Cemented: Polymethylmethacrylate (PMMA) fixation utilizing modern 3rd-generation cementing techniques (pulsatile lavage, vacuum mixing, retrograde cement gun introduction with canal plug, pressurisation). Superior survival and reduced periprosthetic fracture risk in osteoporotic bone and elderly patients (>70 years).
  • Uncemented: Rely on initial press-fit stability and subsequent bone ingrowth/ongrowth (hydroxyapatite, porous titanium surfaces). Widely favoured in younger active patients with favourable bone quality (Dorr Type A/B).
  • Hybrid: Uncemented cup with cemented femoral stem, popularised in UK registry data to balance acetabular biological fixation with low femoral loosening and periprosthetic fracture rates.
• Bearing Surfaces:
  • Ceramic-on-Highly Crosslinked Polyethylene (CoP) and Metal-on-Highly Crosslinked Polyethylene (MoP): Predominant modern bearing couples demonstrating outstanding low-wear long-term results.
  • Ceramic-on-Ceramic (CoC): Lowest wear rate, optimal for young patients, but carries risk of squeaking and catastrophic (though rare) brittle fracture.

Complications

Post-Arthroplasty Complications

• Prosthetic Joint Infection (PJI): 0.5–1.0% incidence. Risk increased by diabetes, smoking, obesity, and immunosuppression. Managed via DAIR (debridement, antibiotics, and implant retention) or single/two-stage revision based on chronicity and organism.
• Dislocation: 1–3%. Influenced by surgical approach, implant orientation (Lewinnek safe zone: 40° ± 10° inclination, 15° ± 10° anteversion), abductor tension, and spinopelvic hypermobility/stiffness.
• Periprosthetic Fractures: Classified by Vancouver criteria for femoral fractures. Higher risk with uncemented collarless tapered wedge stems in elderly osteopenic patients.
• Venous Thromboembolism (VTE): Deep vein thrombosis (DVT) and pulmonary embolism (PE). Mitigated via mechanical prophylaxis, tranexamic acid, and chemical anticoagulation per NICE NG89 guidelines.
• Aseptic Loosening and Osteolysis: Mediated by macrophage activation and pro-inflammatory cytokines in response to particulate bearing wear debris.
• Nerve Injury: Sciatic nerve (peroneal division most vulnerable) or femoral nerve. Risk heightened in limb lengthening >2 cm or severe dysplasia.

Exam Pearls

• Biomechanics: Contralateral stick reduces joint reactive forces across the affected hip by roughly 50% by eliminating required abductor counter-torque.
• Physical Exam: Loss of internal rotation in flexion is consistently the earliest clinical sign of hip osteoarthritis.
• Diagnostic Injection: A fluoroscopically guided intra-articular bupivacaine injection achieving >80% temporary pain relief distinguishes intrinsic intra-articular hip pathology from referred lumbar spine pain.
• Fixation Trends: Registry data (e.g. NJR, AOANJRR) consistently show that cemented femoral stems in patients over 70 years of age have significantly lower periprosthetic fracture rates and revision rates compared to uncemented stems.
• Spinopelvic Mechanics: Patients with stiff lumbo-sacral spines fail to tilt the pelvis posteriorly when sitting; this causes functional anterior acetabular impingement and raises posterior dislocation risk post-THA.