[Diffusion of ulcers in the diabetic foot is promoted by stiffening of plantar muscular tissue under excessive bone compression].
The abnormally elevated plantar pressures under the bony prominences of the diabetic foot (mainly under the medial metatarsal heads and calcaneus) were associated with intensified internal stresses in the deep soft tissues padding these bones. In this study, we tested changes in mechanical properties of muscular tissue after exposure to the internal stress levels typically developing under the first and second metatarsal heads in the load bearing diabetic foot (40-80 KPa). The gracilis muscles of anesthetized rats were subjected to constant external pressures of 35 and 70 KPa for 2 h, which caused average internal compression stresses of 40 and 80 KPa, respectively, within the living gracilis. The animals were then killed and the tangent elastic moduli of the harvested gracilis were measured in uniaxial tension at strains of 2.5%, 5% and 7.5%. Tangent moduli of gracilis muscles exposed to internal compression of 40-80 KPa in vivo ( n=6) were 1.6-fold stiffer ( p<0.05) than those of controls ( n=6). These abnormally stiff mechanical properties were incorporated into a finite element (FE) model of the plantar tissue under the second ray of the foot, and were shown to increase the magnitude of deep internal stresses and project elevated stresses to larger regions. Hence, the integration of animal model data with FE simulations indicates a mechanism of plantar tissue deterioration in the diabetic foot, where muscles exposed to critical stresses respond with increased stiffness which then further intensifies the deep plantar stresses. This suggests a new positive feedback mechanism for the diffusion of ulcers and the atrophy of intrinsic plantar muscles in the diabetic foot, where the injury spreads from deep muscles to the skin surface by an evolving mechanical stress wave.