In addition, some reservations regarding this mechanism were provided by results from recent studies. But when the intrinsic muscles are atrophic and overpowered by the extrinsic muscles, this stabilizing action is lost, which eventually may result in clawing of the toes.ĭespite the existence of numerous anecdotal and observational reports on this mechanical theory of claw toe pathogenesis and despite wide acceptance of this mechanism in the diabetic foot literature, experimental data to support this theory do not exist. If the intrinsic muscles (i.e., the lumbricals and interossei) function correctly, they compensate for this mechanical advantage by flexing the MTP joint while extending the interphalangeal joints. The long extrinsic flexors have a greater mechanical advantage over the extensors at the interphalangeal joints, and the extensors have a greater mechanical advantage over the flexors at the MTP joint ( 6, 12). However, the most commonly reported cause of claw toe deformity is intrinsic muscle atrophy and weakness due to motor neuropathy, leading to an imbalance between intrinsic and extrinsic muscles across the MTP and interphalangeal joints ( 9, – 11). There are some suggestions that rupture of the plantar fascia or ligament contractures at the MTP joints may be involved ( 7, 8). Ill-fitting footwear, in particular cramped toe boxes in patients who lack protective sensation, may externally force the toes in a clawed position ( 6). There are several theories that may explain why claw toes develop in diabetic patients.

Extrinsic foot muscles