Aim: The aim of this study was to examine foot function in the presence of diabetes-induced alterations of the anatomical and biomechanical unit formed by the Achilles tendon, plantar fascia and metatarso-phalangeal joints. More specifically, we focused on the Windlass mechanism, the physiological mechanism which entails stiffening of the foot during propulsion.
Methods: Sixty-one diabetic patients, with or without neuropathy, and 21 healthy volunteers were recruited. The thickness of Achilles tendon and plantar fascia was measured by ultrasound. The main biomechanical parameters of foot-floor interaction during gait were acquired by means of dedicated platforms. The range of motion of the 1st metatarso-phalangeal joint was measured passively.
Results: The plantar fascia (PF) and Achilles tendon (AT) were significantly thickened in diabetic patients [control subjects: PF 2.0+/-0.5 mm, AT 4.0+/-0.5 mm; diabetic patients without neuropathy: PF 2.9+/-1.2 mm (P=0.002), AT 4.6+/-1.0 mm (P=0.016); diabetic patients with neuropathy: PF 3.0+/-0.8 mm (P<0.0001), AT 4.9+/-1.7 mm (P=0.026)]. Joint mobility was significantly reduced [control subjects: 100.0+/-10.0 degrees; diabetic patients without neuropathy: 54.0+/-29.4 degrees (P<0.0001); diabetic patients with neuropathy: 54.9+/-17.2 degrees (P<0.0001)]. Loading times and force integrals under the heel and the metatarsals increased [metatarsal loading time (% stance phase): control subjects 88.2+/-4.1%; diabetic patients without neuropathy 90.1+/-4.7% (P=0.146); diabetic patients with neuropathy 91.7+/-6.6% (P=0.048)].
Conclusions: Increased thickness of Achilles tendon and plantar fascia, more evident in the presence of neuropathy, may contribute to an overall increase of tensile force and to the occurrence of an early Windlass mechanism, maintained throughout the whole gait cycle. This might play a significant role in the overall alteration of the biomechanics of the foot-ankle complex.