Posterior ankle impingement (PAI) is a painful syndrome in the posterior aspect of the ankle, and it is a mechanical conflict that arises in forced plantar flexion.

The talus extends posteriorly with a bony process that can cross laterally the midline in case of hypertrophy: it is called the posterolateral process, and in about 7 % of the adult population, it appears as a distinct accessory bone for a failed union of this ossification center [17]. This center is normally separated from the ossification center of the body of the talus until 8–10 years of life. In adults this distinct ossicle, if present, is called os trigonum, and it is usually linked to the talus through a fibrous synchondrosis. Medially to the posterolateral process, there is another smaller bony prominence of the talus, the medial tubercle: between these two bony prominences, there is a sulcus that is transformed in an osteofibrotic channel by a fibrous retinaculum that takes insertion on the tip of the two tubercles. The flexor hallucis longus (FHL), the most posterior of the posteromedial tendons, slides in this channel. At this level the channel acts as a pulley where the FHL changes its direction of sliding, from vertical to nearly horizontal: this is a point of weakness of the tendon, and pathologies that can involve the posterolateral talar process (or the os trigonum, if present) can also involve the tendon itself and cause a FHL tendinitis. The posterolateral process also gives insertion to the posterior talofibular ligament (PTFL), the strong and most posterior ligament of the lateral ligamentous complex of the ankle. This ligament is lax in plantar flexion and taut in maximal dorsal flexion, and for this reason, it can detach the process (or the os trigonum) from the talus during forced and sudden movements.

PAI can be caused by trauma or overuse, and it has been typically associated with ballet dancers for the frequent “en pointe” or “demi-pointe” position assumed by these athletes. However, any sport that requires or any trauma that provokes forced plantar flexion or more rarely forced dorsal flexion can determine this syndrome. Running (especially downhill running), soccer, basketball, volleyball, and jumping (high, long, and triple jump) are the sports more frequently involved in this kind of pathology. Rarely the detachment of the posterior bony process can be caused by a sudden traction of the PTFL during a trauma in forced dorsal flexion. More frequently a forced plantar flexion of the ankle, sometimes in association with supination or pronation of the hindfoot, provokes a crush of the os trigonum or of the posterolateral process between the posteroinferior edge of the tibia and the calcaneus. The mechanism of this crush has been compared to a nut (the os trigonum) in a nutcracker (tibia and calcaneus). This kind of trauma can be acute and can determine the fracture of the posterior talar process or the sudden mobilization of the os trigonum. Other times the trauma can be repetitive during a long period of time and can cause an overuse syndrome. This different etiology is not academic, but it is of practical interest because of better prognosis of PAI in overuse syndromes compared to traumatic cases [18]. The presence of the os trigonum or of a hypertrophic posterolateral process is neither sufficient nor essential to determine this syndrome. If the bony process or the ossicle is present, they are not sufficient to determine the pain syndrome: sometimes the pain is caused only by the traumatic event or by efforts beyond the anatomical limit. In other patients the painful syndrome is caused by a soft tissue impingement: a thickened joint capsule, a rupture of the PTFL, and a bump of hypertrophic tissue may cause a PAI syndrome without bony prominence.