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OA Hip

Must KnowHipthinKbox SBA

Clinical image

Severe hip osteoarthritis (Tönnis grade 3)

Severe hip osteoarthritis (Tönnis grade 3). Source: Wikimedia Commons — Mikael Häggström, M.D.; CC0 1.0. Image binary is embedded locally in this package; original source and licence are retained.

Key points

  • 10% primary
  • 90% secondary
    • AVN
    • DDH
    • Perthes
    • SUFE
    • Protrusio
    • Trauma

Management

  • History: pain and functional limits
  • Cl exams
  • Investigate
  • Assuming all conservative measures are tried and have been unsuccessful, I would offer her cemented THA

Which THA

  • I will use a force closed taper slip cemented femoral stem of ODEP 10A rating
  • Should have straight forward instrumentation
  • Introducer should allow even pressurisation
  • I will use a direct lateral approach

Hardinge

  • Assuming that patient is adequately consented, relevant notes and X-rays are obtained, leg marked and prepared and WHO time out done
  • Lateral position
  • Landmark: ASIS, GT, Line of femur
  • Incision: Longitudinal mid lateral 5 cm proximal and 10 cm distal to tip of GT
  • IN plane: none
  • 3cm above GT is Superior gluteal nerve
  • Structures at risk: SGN, FNV, transverse br of circumflex femoral a

Posterior approach

  • Double risk of sciatic nerve injury
  • Similar time
  • Less visible acetabulum
  • Increased risk of cup anti version
  • More dislocations
  • Less Trendelenberg gait and better haris hip score

Posterior

  • Assuming that patient is adequately consented, X-rays and notes are obtained, leg marked and prepped and WHO timeout done,
  • my position of patient is: Lateral
  • Landmark: GT
  • Incision: with hip flexed 90 degree, a straight incision hand breadth below iliac crest on to the GT down to SOF.
  • IN plane: none
  • Superficial: split G Max
  • Deep: Divide SER close to femur, except QF (Br of LSFA)
  • Sciatic n: deep to piriformis and superficial to SER
  • Risk: Sciatic n, Br of Inf Gluteal vessels

OA

  • OA is a complex degenerative disorder of the entire synovial joint characterized by
  • progressive loss of articular cartilage and
  • subchondral bone remodelling.

Pathology

  • Initial change is the damage to Tangential zone
    • Disorganisation of collagen network
    • Loss of proteoglycan
    • Swelling
  • Hypertrophic repair process starts
  • Repair fails: leads to fibrillations parallel to surface
  • Balance between anabolic and catabolic process is shifted in favour of catabolism

Key points

Pathology-Cartilage Catabolism

  • Cartilage break down products are released in to synovial fluid causing inflammation and Macrophage activation
  • Breakdown products
    • Chondroitin so4
    • keratan so4
    • PG fragments

Macrophage

  • PMN activation: Synovitis
  • Release
    • Cytokines
    • Proteinases
    • Oxygen free radicals

Cartilage changes

  • increased
    • water content
    • chondrocyte activity and proliferation
    • IL1
    • MMP
    • Cathepsin B and D
  • Decreased
    • Collagen content
    • PG quality and size
    • Keratan SO4
    • Youngs modulus

MMP

  • Molecule responsible for cartilage degradation
  • Secreted by synoviocytes and chondrocytes
  • Activated by IL1
  • Include
    • Stromelysins
    • gelatinise
    • collagenase

Histology

  • Loss of chondrocytes
  • Replication and Breakdown of tidemark
  • Eburnation (Ivory like appearance) of subchondral bone

Aging vs OA

Written/reviewed by Kishore Puthezhath

Professor of Orthopaedics and Consultant Paediatric Orthopaedic Surgeon

FRCS (Tr & Orth) revision resource

Reviewed: September 2026