Management of Ankle Osteochondral Lesions

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Original Editor - Ewa Jaraczewska based on the course by Helene Simpson Top Contributors - Ewa Jaraczewska, Jess Bell, Lucinda hampton, Kim Jackson and Jorge Rodríguez Palomino

Definitions[edit | edit source]

Cartilage is a connective tissue characterised by three components: polysaccharides ( a cellular component composed of ground substance), fibrous proteins, and interstitial fluid with water as a main component.[1] Cartilage gets its nutrition via diffusion from surrounding tissues as it has no direct blood supply, lymphatics and nerves.[1] There are three types of cartilaginous tissues, each with different composition and function: hyaline, fibrocartilage and elastic cartilage.

  • Hyaline cartilage: is a connective tissue located at the ends of bones. Its primary cells are chondrocytes. Their role is to maintain the cartilage extracellular matrix (ECM), which is responsible for biological and mechanical function of the cartilage. Hyaline cartilage ECM contains:[2]
    • Collagen type II (10-20%)
    • Proteoglycan (1-10%)
    • Water (65-85%)
  • Fibrocartilage is a "transitional tissue between hyaline cartilage and dense regular connective tissue such as tendons and ligaments."[1] It contains:
    • High levels of type I collagen
    • Type II collagen
    • Small component of ground substance [1]
  • Elastic cartilage: is a flexible connective tissue cartilage with ability to withstand repeated bending.[1] Elastic cartilage components are:[1]
    • Type II collagen
    • Elastic fibres
    • Large chondrocytes

Subchondral bone is located below the hyaline cartilage and cement line and is responsible for providing mechanical and nutritional support for cartilage. Its mechanical properties include shock absorption. [3] The subchondral bone contains vessels that have a direct contact with hyaline cartilage layer. 50% of cartilage nutrients are distributed via perfussion of the subchondral bone vessels.[4]

Osteochondral lesions (OCL) are defects affecting the structure of the cartilaginous surface and underlying subchondral bone. When lesion's healing phase begins and tissue is formed, the fibrocartilage is often the new tissue, which has mechanical disadvantage to the hyaline. In some cases, hyaline cartilage forms during the repair process, but the mechanism of hyaline vs fibrocartilage formation is unknown.[1]

Healing of OCL[edit | edit source]

Osteochondral lesions have poor healing capacity. [5] The study completed in animals[6] demonstrates the following stages of healing in the OCL:[5]

Week 1-2: Initial fibrin repair, damaged site begins to fill with blood clot and fibrous tissue, mesenchymal cell recruitment is initiated

Week 4-8: Cartilage formation starts adjacent to the damaged cartilage

Weeks 8 -12: Bone formation begins through endochondral ossification

Week 18: New bone formation continues

Week 26: Completion of the healing process

OCL Aetiology[edit | edit source]

The aetiology of the osteochondral lesion can be:

  • traumatic (80% of cases)[7]
  • joint malalignments[8]
  • ligament laxity (38% of patients)[7]
  • instability (39% of patients)[7]
  • genetic predisposition[8]
  • endocrine factors[7][8]
  • avascular necrosis[8]
  • metabolic factors[7]

There are three types of trauma leading to development of OCL: compaction, shearing or avulsion.

Osteochondral Lesion of the Ankle[edit | edit source]

According to Ferkel et al,[9] a high percentage of patients with lateral ankle instability developed intra-articular pathology. In the ankle joint, the osteochondral lesion can be found in the talar. The osteochondral lesion of the talar cartilage (OCT) and subchondral bone can cause a partial or complete detachment of the fragment. There are six categories of the lesion:

  • chondral (cartilage only)
  • chondral-subchondral (cartilage and bone)
  • subchondral (intact overlying cartilage)
  • cystic

In addition to the above categories of the lesion, OCT can be stable or unstable, non-displaced or displaced.

Classification System for OCT[edit | edit source]

  • Berndt and Harty[10] classification system for radiographic staging of osteochondral lesions of the talus. It applies to traumatic and non-traumatic aetiology of the lesion:[11]
    • Stage I: with the foot in inverted position, the lateral border is compressed against the face of the fibula, the collateral ligament remains intact.
    • Stage II: with progressive foot inversion, lateral ligament is ruptured and the avulsion of the chip begins
    • Stage III: the chip is fully detached but remains in place
    • Stage IV: detached chip is displaced following inversion
  • Loomer et al[12] added a stage V to Berndt and Harty classification system:[11]
    • Stage I -IV as above
    • Stage V: presence of a subchondral cyst.
  • Ferkel and Sgaglione [13] developed a classification system based on computed tomography (CT)
    • Stage I: Cystic lesion with dome of talus (intact roof)
    • Stage IIa:Cystic lesion with communication to talar dome surface
    • Stage IIb: Open articular surface lesion with overlying undisplaced fragment
    • Stage III: Undisplaced lesion with lucency
    • Stage IV: Displaced fragment[14]
  • Hepple et al[15] developed a classification system based on magnetic resonance imaging (MRI). [14]
MRI classification of OCL. Adapted from AA, Sesin C, Rosselli M. Osteochondral defects of the talus with a focus on platelet-rich plasma as a potential treatment option: a review. BMJ Open Sport Exerc Med. 2018 Feb 1;4(1):e000318.

Clinical Presentation[edit | edit source]

Patient with OCL will report deep ankle pain associated with weight-bearing, limitations in range of motion, impaired function, stiffness, feeling of catching, and locking. In addition patient may experience tenderness and swelling around medial and lateral ankle. [7]Examination often reveals subtalar and talonavicular joints range of motion restrictions, impaired ligamentous ankle stability and hindfoot malalignment. [11] [7]

Diagnostic Procedures[edit | edit source]

  • AP and lateral X-ray completed in weight-bearing position[7]
  • MRI captures the integrity of soft tissue and subchondral cancellous bone[16]
  • CT allows a better resolution of bony pathologies, but offers less information on articular cartilage wear and soft tissues[7]
  • SPECT CT enables information received from both MRI and CT . It should be used with caution due to the amount of radiation the patient is exposed to by having this procedure[7]
  • Ankle arthroscopy allows for a direct visualisation of the entire joint[7]

Outcome Measures[edit | edit source]

Comprehensive Rehabilitation[edit | edit source]

General principles in rehabilitation management[edit | edit source]

There is a lack of high quality evidence for a specific treatment protocol in the management of the ankle osteochondral lesion. [17]When establishing goals, planning the treatment and choosing the interventions, the clinician must consider the biological phases of healing. In general, rehabilitation program should:

  • Be comprehensive and include multi-modal functional training
  • Include minimum of six weeks of supervised rehabilitation training
  • Address postural control, balance and proprioception retraining
  • Incorporate entire kinetic chain to improve overall strength
  • Include activities to maintain range of movement
  • Include measures to protect the ankle joint by making the patient wear a lace-up brace

Special Concerns[edit | edit source]

In the management of the osteochondral lesions the following rehabilitation considerations must apply:[17]

  1. Avoid shear forces
  2. Avoid comprehensive forces
  3. Recovery is slow
  4. Monitor pain
  5. Prevent development of the compensatory movements

Shear forces[edit | edit source]

Shear forces are often the underlying cause for OCL in chronic ankle instability.

Shear forces are to be avoided for over 3 months [17]

Compressive forces[edit | edit source]

Fibrocartilage is not as strong as hyaline cartilage.

Full weight bearing should be delayed for as long as six weeks, based on certain clinical factors[17]

Slow Recovery[edit | edit source]

Repair of cartilage takes time.

Take it easy with step 1 and step 2 and maintain partial weight bearing[17]

Monitor pain[edit | edit source]

Treatment must be individualised and patient's pain must be respected[17]

Compensatory movements[edit | edit source]

Faulty motor patterns must be corrected[17]

Ankle Osteochondral Lesions Treatment Strategies[17][edit | edit source]

Stage 1[edit | edit source]

  • Take it EASY
  • Move the talo-crural joints, but DO NOT compress or shear
  • Incorporate cardiovascular fitness
  • Maintain partial weight bearing

Examples of exercises:

Stage 2[edit | edit source]

  • This is a functional phase
  • It is considered a pre-participation phase
  • Focus on details
  • Progress from partial to full weight bearing and standing on two feet
  • Progress in load and complexity of the movement

Examples of exercises:

Stage 3[edit | edit source]

Resources[edit | edit source]

add appropriate resources here

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Armiento AR, Alini M, Stoddart MJ. Articular fibrocartilage - Why does hyaline cartilage fail to repair? Adv Drug Deliv Rev. 2019 Jun;146:289-305.
  2. ↑ Lakin BA, Snyder BD, Grinstaff MW. Assessing cartilage biomechanical properties: techniques for evaluating the functional performance of cartilage in health and disease. Annual review of biomedical engineering. 2017 Jun 21;19:27-55.
  3. ↑ Hu Y, Chen X, Wang S, Jing Y, Su J. Subchondral bone microenvironment in osteoarthritis and pain. Bone research. 2021 Mar 17;9(1):1-3.
  4. ↑ Imhof H, Sulzbacher I, Grampp S, Czerny C, Youssefzadeh S, Kainberger F. Subchondral bone and cartilage disease: a rediscovered functional unit. Investigative radiology. 2000 Oct 1;35(10):581-8.
  5. ↑ 5.0 5.1 Lydon H, Getgood A, Henson FMD. Healing of Osteochondral Defects via Endochondral Ossification in an Ovine Model. Cartilage. 2019 Jan;10(1):94-101.
  6. ↑ Shapiro F, Koide S, Glimcher MJ. Cell origin and differentiation in the repair of full-thickness defects of articular cartilage. J Bone Joint Surg Am. 1993 Apr;75(4):532-53.
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 Krause F, Anwander H. Osteochondral lesion of the talus: still a problem?. EFORT open reviews. 2022 Jun 1;7(6):337-43.
  8. ↑ 8.0 8.1 8.2 8.3 Mosca M, Grassi A, Caravelli S. Osteochondral Lesions of Ankle and Knee. Will Future Treatments Really Be Represented by Custom-Made Metal Implants?. Journal of Clinical Medicine. 2022 Jul 1;11(13):3817.
  9. ↑ Ferkel RD, Chams RN. Chronic lateral instability: arthroscopic findings and long-term results. Foot Ankle Int. 2007 Jan;28(1):24-31.
  10. ↑ BERNDT AL, HARTY M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am. 1959 Sep;41-A:988-1020.
  11. ↑ 11.0 11.1 11.2 Badekas T, Takvorian M, Souras N. Treatment principles for osteochondral lesions in foot and ankle. Int Orthop. 2013 Sep;37(9):1697-706.
  12. ↑ Loomer R, Fisher C, Lloyd-Smith R, Sisler J, Cooney T. Osteochondral lesions of the talus. Am J Sports Med. 1993 Jan-Feb;21(1):13-9.
  13. ↑ Ferkel RD, Sgaglione NA, DelPizzo W. Arthroscopic treatment of osteochondral lesions of the talus: long-term results. Orthop Trans. 1990;14:172–173.
  14. ↑ 14.0 14.1 Elghawy AA, Sesin C, Rosselli M. Osteochondral defects of the talus with a focus on platelet-rich plasma as a potential treatment option: a review. BMJ Open Sport Exerc Med. 2018 Feb 1;4(1):e000318.
  15. ↑ Hepple S, Winson IG, Glew D. Osteochondral lesions of the talus: a revised classification. Foot Ankle Int. 1999 Dec;20(12):789-93.
  16. ↑ Sophia Fox AJ, Bedi A, Rodeo SA. The basic science of articular cartilage: structure, composition, and function. Sports Health. 2009 Nov;1(6):461-8.
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 17.6 17.7 Simpson H. Osteochondral Lesions Course. Physioplus 2022
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