Acquired flatfoot deformity caused by dysfunction of the posterior tibial tendon is a common clinical problem. Treatment, which depends on the severity of the symptoms and the stage of the disease, includes non-operative options, such as rest, administration of anti-inflammatory medication, and immobilization, as well as operative options, such as tendon transfer, calcaneal osteotomy, and several methods of arthrodesis.

The posterior tibial muscle forms part of the deep posterior compartment of the calf. It originates from the proximal third of the tibia and the interosseous membrane and passes immediately posterior to the medial malleolus, where it changes direction acutely23. A groove in the posteromedial aspect of the distal part of the tibia holds the posterior tibial tendon but is not deep enough to keep the tendon from bow-stringing or dislocating after an injury45. The flexor retinaculum, which is adjacent to the medial malleolus, tethers the tendon and keeps it in the groove, preventing dislocation. Distally, this retinaculum blends with the sheath of the posterior tibial tendon and the superficial deltoid ligament. The posterior tibial tendon does not have a mesotenon, and there is an area of relative hypovascularity immediately distal to the medial malleolus that may contribute to degenerative changes of the tendon15. The posterior tibial tendon divides anterior to the tuberosity of the navicular. An anterior slip, which is in direct continuity with the main tendon, inserts onto the tuberosity of the navicular, the inferior aspect of the capsule of the medial naviculocuneiform joint, and the inferior surface of the medial cuneiform. A second slip attaches to the plantar surfaces of the middle and lateral cuneiforms and the cuboid as well as to the bases of the corresponding metatarsals56.