Abstract
BackgroundAdult acquired flatfoot deformity (AAFD) is caused by impaired medial ligamentous structures and posterior tibialis tendon dysfunction (PTTD). Although degeneration and trauma could separately cause AAFD, how these factors interact in the pathomechanism of AAFD is unclear. The joint capsule in the medial ankle is considered an important structure, providing passive stability by limiting joint movement. Previous reports on the joint capsule suggest its involvement in pathological changes of the ankle, but because of the high priority placed on the ligaments, few reports address the ankle joint from the joint capsule standpoint. The current study aimed to anatomically examine the medial ankle joint, focusing on the deltoid and spring ligaments in perspective of the joint capsule.MethodsWe conducted a descriptive anatomical study of 19 embalmed cadavers (mean 82.7 years, range 58 to 99). We included 22 embalmed cadaveric ankles. We detached the joint capsule in 16 ankles from the anterior to posteromedial joint, analyzed the capsular attachments of the ankle and adjacent joints, and measured the widths of the bony attachments. We histologically analyzed the joint capsule using Masson’s trichrome staining in 6 ankles.ResultsThe capsule could be separated as a continuous sheet, including 3 different tissues. The anterior capsule was composed of fatty tissue. Between the medial malleolus and talus, the capsule was strongly connected and was composed of fibrous tissue, normally referred to as the deep deltoid ligament. The tibial attachment formed a steric groove, and the talar side of the attachment formed an elliptical depressed area. On the medial part of the subtalar and talonavicular joints, the capsule covered the joints as cartilaginous tissue, normally referred to as the superomedial ligament of the spring ligament. The outer side of the cartilaginous and fibrous tissue formed the sheath floor of the posterior tibialis tendon. Histological analysis revealed three different tissue types.ConclusionsThe capsules of the ankle, subtalar, and talonavicular joints could be detached as a continuous sheet. The deltoid and the superomedial ligament of the spring ligaments could be interpreted as a part of the continuous capsule, which had different histological features.Level of evidenceDescriptive Laboratory Study.
Highlights
Adult acquired flatfoot deformity (AAFD) is caused by impaired medial ligamentous structures and posterior tibialis tendon dysfunction (PTTD)
Because of the high priority placed on the ligaments, there are very few reports addressing the ankle joint from the standpoint of the joint capsule, which should theoretically exist at the deep layer of the medial ankle joint, as is seen in other joints
Macroscopic observation of the joint capsule and its attachment in the medial ankle joint The PT tendon ran around the posterior edge of the medial malleolus and inserted into the navicular
Summary
Adult acquired flatfoot deformity (AAFD) is caused by impaired medial ligamentous structures and posterior tibialis tendon dysfunction (PTTD). Previous reports on the joint capsule suggest its involvement in pathological changes of the ankle, but because of the high priority placed on the ligaments, few reports address the ankle joint from the joint capsule standpoint. The etiology of adult acquired flatfoot deformity (AAFD) has been considered to be failure of the medial arch stabilizer, primarily posterior tibialis tendon dysfunction (PTTD) (Funk et al 1986; Kohls-Gatzoulis et al 2004). To elucidate the pathologic change underlying the initiation of AAFD, the anatomical association between the dynamic stabilizers of the medial ankle, such as the posterior tibialis tendon, and the static ones, such as the spring and deltoid ligaments, should be understood. Because of the high priority placed on the ligaments, there are very few reports addressing the ankle joint from the standpoint of the joint capsule, which should theoretically exist at the deep layer of the medial ankle joint, as is seen in other joints
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