Ankle & Midfoot OA

Ankle and midfoot osteoarthritis (OA) causes activity-related pain, stiffness and loss of function, and unlike hip and knee OA, ankle OA usually follows previous trauma.

In a large series 70% of ankle OA was post-traumatic, mostly after rotational ankle fractures, and 7% was primary. Midfoot OA affects the tarsometatarsal (TMT) and naviculocuneiform joints and may be primary or follow a Lisfranc injury, inflammatory arthritis or Charcot neuroarthropathy.

Management follows current NICE osteoarthritis guidance: therapeutic exercise, weight management and information first, with footwear changes and selective orthoses. Arthrodesis and total ankle replacement are the main options for end-stage ankle disease.

The ankle (talocrural joint) is a highly congruent hinge between the tibial plafond, the malleoli and the talar dome. Load is spread over a large contact area, and ankle cartilage is more resistant to degradation than knee cartilage. Both protect against primary OA.

Causes of ankle OA:

• •Previous fracture: malleolar, pilon or talar, even after good reduction
• •Chronic ankle instability with repeated abnormal loading
• •Osteochondral lesions of the talus
• •Inflammatory arthritis
• •Less often haemochromatosis, haemophilia, talar avascular necrosis and Charcot neuroarthropathy in diabetes

The midfoot comprises the TMT (Lisfranc) joints, the naviculocuneiform joints, and the talonavicular and calcaneocuboid joints. The talonavicular joint contributes much of hindfoot inversion and eversion, so OA there reduces the foot's ability to adapt to uneven ground. The 1st TMT joint is a common site of primary OA. Degeneration of the 2nd and 3rd TMT joints after trauma suggests a previous, often missed, Lisfranc injury.

Other risk factors include age, obesity and malalignment.