Ankle Osteoarthritis – A Review of the Current State of Knowledge

Osteoarthritis (OA) is the most common form of arthritis and is a major cause of morbidity and disability.¹ Approximately 15% of the world’s adult population is affected by joint pain and disability resulting from OA.² This makes OA a disease of very high socioeconomic impact for the individual patient, as well as for the whole of society. Ankle OA is much less frequent than OA of the hip and knee. However, due to its appearance in the younger age population, its impact on patients’ quality of life and work capacity is high.

The present paper provides a brief overview regarding the current knowledge on ankle OA with a primary focus on its stage-dependent treatment options.

Epidemiology and Pathomechanism
OA of the ankle affects 1–4% of the adult population.^3,4 There are several reported causes of ankle OA.⁵ These include primary, systemic (rheumatoid arthritis and other systemic diseases) and post-traumatic OA. Unlike hip and knee OA, which are mostly of primary origin,⁶ ankle OA is predominantly of post-traumatic origin.⁷ In a study of 406 ankles with end-stage OA, we found that the underlying aetiology in this cohort was post-traumatic ankle OA in 78% of cases, secondary arthritis in 13% of cases and primary OA in 9% of cases. Of the 78% of cases of post-traumatic OA, 62% were attributable to fracture events and 16% had ligamentous post-traumatic ankle OA.⁷ Malleolar fractures and tibial plafond fractures were the two most common causes of fracture-related post-traumatic ankle OA.⁸ Studies indicate that severity of the initial injury and adequacy of reduction may play a role in the development of post-traumatic ankle OA.^8–10 Other studies revealed that subsequent post-traumatic OA development correlates with the initial cartilage damage.¹¹ Research has also shown that ligament lesions are a significant cause of post-traumatic OA.^12–15 Inadequate ligament healing after the initial ankle sprain likely leads to the development of chronic ankle instability,¹⁶ which then progresses to ankle OA.¹⁵ The low overall incidences of ankle OA and in particular primary OA is surprising considering the small articular contact area compared with the knee,^17–19 in conjunction with the high loads sustained during standing, walking and running. This phenomenon is thought to be caused by the unique anatomic, biomechanical and cartilage characteristics of the ankle.²⁰ Functionally, the ankle acts mainly as a rolling joint with high congruency.²¹ Further, ankle cartilage is thinner compared to knee or hip cartilage^22,23 but shows a higher compressive stiffness and proteoglycan density,²⁴ lower matrix degradation25 and a lower response to catabolic stimulations.^26,27 These properties might make ankle cartilage more resistant against primary degeneration.