Etiology of acquired hammertoe deformity.

The most important feature of acquired hammertoe deformity is hyperextension of the proximal phalanx. The position of the proximal phalanx at the normal metatarsophalangeal joint is subject to the antagonistic action of the extensors and intrinsic flexors. The plantar joint capsule and the attached extensions of the plantar aponeurosis make an important contribution to the dynamic balance of this joint. The balance is distrubed in acquired hammertoe deformity because of age-related inefficiency of the plantar structures (the intrinsic flexors, the plantar joint capsule, and the plantar aponeurosis). This concept evolved from clinical obervations and measurements from roentgenograms of the feet of patients from different age groups. Hyperextension of the toes can be corrected by increasing tension on plantar structures. Dorsiflexion of the lesser toes, as measured on lateral weightbearing roentgeograms, is significantly increased in older age groups as compared with younger ones (means of 33 degrees, 33 degrees, 39 degrees 37, degrees vs 23 degrees, 24 degrees, 25 degrees, 25 degrees). These observations suggest elongation of the plantar structures beyound physiological length. Higher-heeled shoes worn for many years may be responsible because they maintain dorsiflexion of the toes and stretching of the plantar structures even during the foot flat interval of the walking cycle. Hyperextension of the proximal phalanx may be the primary deformity. In this position, the long extensor loses its tendodesing effect and flexion deformity of the proximal interphalangeal joint results.