Ankle osteoarthritis (OA) is a foot and ankle disease that causes pain and chronic hindfoot disability (Thomas and Daniels, 2003, Valderrabano et al., 2009). Varus ankle OA is a subtype of OA induced by the asymmetric joint loading of the ankle resulting from varus malalignment. This condition is characterized by varus tilting of the talus relative to the tibial shaft and narrowing of the medial joint space of the ankle mortise (Takakura et al., 1995). Varus ankle OA accounts for 55% of all ankle OA cases (Valderrabano et al., 2009). A better understanding of the factors associated with this condition could enhance the current efforts to treat joint injuries and reduce the risk and severity of ankle OA.

However, mechanisms underlying the incidence and progression of varus ankle OA remain controversial. Pathological talar instability in the mortise resulting from unresolved chronic lateral collateral ligament injuries is a common cause of ankle OA and leads to varus deformity (Lofvenberg et al., 1994, Valderrabano et al., 2006). However, previous longitudinal studies have reported that less than half of patients with chronic ankle instability after sprains develop ankle OA (Lee et al., 2022, Lofvenberg et al., 1994). Additionally, some cases of ankle OA are idiopathic and have an unknown cause and are known as primary ankle OA (Valderrabano et al., 2009). Therefore, the risk of varus ankle OA is presumed to be multifactorial.

Recent evidence suggests that slight differences in joint mechanics driven by variability in hindfoot bone morphology are among the risk factors for the development and progression of various joint diseases, such as the talus and navicular bone in flatfoot deformity (Louie et al., 2014, Peeters et al., 2013) and medial malleolus and trochlea of the talus in osteochondral lesions (Teramoto et al., 2018, Tümer et al., 2016). Furthermore, bone morphological characteristics in chronic lateral ligamentous instability of the ankle have been reported in the varus tilt of the tibial plafond (Sugimoto et al., 1997) and unstable osseous joint configuration of the ankle (Frigg et al., 2007, Kanbe et al., 2002), as well as in the articular surface morphology of the talocalcaneal joint (Barbaix et al., 2000, Tümer et al., 2019b). These diseases and ankle OA are closely related epidemiologically; thus, an altered load response due to certain unique bone morphologies may further be involved in the pathogenesis of ankle OA.

Evidence on the innate (congenital) bone morphological configuration in varus ankle OA is limited. Several descriptive studies (Schaefer et al., 2012, Takakura et al., 1995, Wiewiorski et al., 2016) have reported that the characteristic bone shape of the hindfoot, such as a medially tilting plafond, medial malleolus opening medially, and flattening of the talus, could be intrinsic risk factors for the development of ankle OA. However, these previous morphological analyses of the bone morphology of OA feet and healthy feet cannot evaluate possible innate bone morphology that may be associated with the onset of ankle OA because the degenerative changes of the ankle mortise occurring in ankle OA are relatively significant (Seki et al., 2021, Seki et al., 2019), making it difficult to detect possible differences in the innate, predegenerative morphology of the hindfoot bones that may be unique in ankle OA patients. However, if we analyze the differences in the hindfoot bone morphology between the non-affected sides in patients with unilateral varus ankle OA and healthy control feet, the effect of morphological bone degeneration due to the arthritic process can be eliminated, and the innate pattern of morphological variations of the hindfoot morphology that may be associated with ankle OA can be extracted, assuming symmetry of the left and right hindfoot bones before the development of unilateral varus ankle OA (Gabrielli et al., 2020, Islam et al., 2014, Tümer et al., 2019a).

The present study aimed to investigate the innate morphological features of the hindfoot bones possibly associated with varus ankle OA by comparing the three-dimensional (3D) variations of the hindfoot bones between the non-affected side of participants with unilateral varus ankle OA and controls using 3D geometric morphometrics (Adams et al., 2004, O’Higgins, 2000). Such information on the innate morphological features of hindfoot bones associated with varus ankle OA could be used as an indicator of increased risk of developing ankle OA, possibly contributing to the development of preventive interventions for ankle OA.