Knee

Osteoarthritis of the knee

Video

Western Health Orthopaedic Registrar presentation – Management of Osteoarthritis of the Knee in the Active Patient by Dr Darren Webb

Western Health Orthopaedic Registrar presentation – Knee Osteoarthritis by Dr Pandelis Dimitriou

Aetiology

mechanical derangement

  • raised contact pressures in articular cartilage
  • → fragmentation of the collagen fibre network
  • → progressive loss of cartilage
  • → exposure of subchondral bone.
  • Eg
    • Osteoarthritis due to fracture malunion, genu varum, post medial meniscectomy

As the cartilage becomes less capable of taking load, the subjacent bone becomes more dense in response to loading. reduced compliance of the subchondral bone further contributes to the loss of articular cartilage. Osteophytes form in an attempt to ↑ the weight bearing area. Adult mature chondrocytes do not appear to be able to undergo mitosisChondrocyte clustering is probably due to loss of matrix between previously separated cells rather than from cell division Thus true healing of an articular cartilage defect cannot occurHowever, healing by scar formation can occur ie healing by fibrocartilage derived from underlying cancellous bone. For this to occur need to have connection between joint & underlying cancellous bone e.g. by drilling. For this fibrocartilage to persist & effectively line the joint surface – need to remove the primary mechanical cause for the initial cartilage destruction e.g. by osteotomy

Evidence for Surgical repair of articular cartilage of the knee

Reviewed by

Dr Andrew Mattin
MBBS | Accredited Orthopaedic Registrar

Background

  • Chondral injury is a challenging , common problem.
  • Cartilage has a limited capacity to heal.
  • Chondral lesions are believed to progress and cause OA
  • There is limited evidence that any intervention alters the natural history.
  • Advances in surgical technique attempt to better manage this problem.

Pathology

  • Partial thickness lesions have limited capacity to heal.
  • Healing can occur if subchondral bone is envolved.
  • Articular cartilage lacks direct blood supply.
  • Nutrients delivered by interstitial fluid.
  • Diffusion of fluid requires intact matrix.
  • Fibrin clot formation in osteochondral injury, vascular in growth and marrow cell migration allow formation of fibrocartilage. (Type 1 cartilage)
  • This lacks longevity as it has no matrix microstructure.
  • Well contained, isolated defects < 2 cm2  may be asymptomatic and non degenerative
  • Poor correlation between progression to radiological  OA and symptoms.

Classification

Outerbridge Classification

  • Grade 0: normal cartilage
  • Grade I: cartilage with softening and swelling
  • Grade II: a partial-thickness defect with fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter
  • Grade III: fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm
  • Grade IV, exposed subchondral bone.

Surgical candidates

  • Full thickness lesions, Outerbridge III, IV.
  • Size > 2 cm2
  • Age < 40 yo.
  • Approximately 5% of patients undergoing knee arthroscopy fit this criteria.

Treatment

  • Microfacture.
  • Osteochondral autograft transfer OAT.
  • Autologous chondrocyte implantation ACI.
  • Microfacture
    • First line treatment option for full thickness cartilage defects.
    • Low morbidity, easy technique.
    • Debrided to stable edges, zone of calcified cartilage is removed. Bleeding and fibrin formation.
    • Undifferentiated mesenchymal cells in clot mature to form fibrocartilage repair, type II collagen.
    • Improvement at 2 years but inconclusive beyond that.
  • Osteochondral Autograft Transplantation
    • OATS. Mosaicplasty.
    • Harvest viable intact cartilage and bone plugs from a  less valuable site.
    • Gaps fill with fibrocartilage.
    • Large fragments 10mm or smaller plugs can be used.
    • Good results in 92% femoral condyle lesions at 10 years. (Hangody, Fules 831 pt.JBJS 2003.)
  • Autologous Chondrocyte Implantation
    • Harvesting of chondrocytes 200-300mg, taken to lab, enzymatic removal of extracellular matrix, culture expansion of chondrocytes.
    • Periosteal patch used to cover the cells to cast as structural scaffold.
    • Fibrocartilage superficial layer.
    • Good results at 7.4 years in 51 of 61 patients, level III retrospective cohort comparison. Compared to debridement alone. (Peterson 2002.)
  • Autologous chondral implantation v’s Osteochondral autograft transplantation
    • Bentley et al. JBJS 2003.
    • Level I prospective randomisation clinical trial, ACI or mosaicplasty. 58/ 42.
    • Average lesion 4.66cm2.
    • Symptoms 7 years preop, followed 19 months post op.
    • 53% medial femoral condyle, 25% patella, 18% lateral femoral condyle, 3% trochlear.
    • No significant difference in outcome Cincinnati knee rating scale (walk, stairs, squat, run, jump, pivot.) and Stanmore functional rating system scores (Pain 1-4).
  • Autologous Chondrocyte implantation v’s Microfracture
    • Knutsen et al. JBJS 2004. Level 1 randomised control study.
    • 80 patients randomised without OA or instability.
    • 12, 24 month follow up.
    • No significant difference based on Tegner score (level of activity 0-10), Lysholm score (Limp, aids, pain, swelling, locking, instability, squatting).
    • Arthroscopy in 76% at 2 years did not show any difference using ICRS (International cartilage repair society) grading system.
    • Younger, more active patients had better outcomes in both groups.
  • Osteochondral autograft transplantation v’s microfacture.
    • Gudas et al. Arthroscopy 2005.
    • 57 athletes, mean 24.3 years.
    • No prior surgery.
    • Modified hospital for special surgery (HSS) (pain, ROM, stability, walking, aids,stairs),
    • ICRS scores (pt questionnaire, Surgeon evaluation),
    • Radiological, MRI and clinical assessment up to 36 months.
    • Arthroscopy at 1 year with histology taken. Both groups showed significant clinical improvement at average of 37 months.
    • OAT’s had significantly better results than microfracture 1,2,3 years with modified HSS evaluation.
    • 93% OAT’s returned to sport at 6/12.
    • 52% microfracture.

Conclusion

  • No clear benefit between ACI and OAT or ACI and microfracture.
  • ACI results in structurally better cartilage than microfracture however there has been no clinical benefit
  • demonstrated.
  • Microfracture should still be the first line treatment due to less patient morbidity associated with one stage procedure.
  • OAT may be the best treatment for younger athletes.

References

  • JBJS. The Evidence for Surgical repair of articular cartilage of the knee.