This article is part of the supplement: 1st Congress of the International Foot & Ankle Biomechanics (i-FAB) community

Oral presentation

Clawed toes in the diabetic foot: neuropathy, intrinsic muscle volume, and plantar aponeurosis thickness

William R Ledoux^3,1,2*, Jason Schoen¹, Matthew Lovell¹ and Elizabeth Huff¹

• * Corresponding author: William R Ledoux wrledoux@u.washington.edu

Author Affiliations

¹ RR&D Center of Excellence, Department of Veterans Affairs, Seattle, WA, USA

² Departments of Mechanical Engineering, University of Washington, Seattle, WA, USA

³ Orthopaedic & Sports Medicine, University of Washington, Seattle, WA, USA

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Journal of Foot and Ankle Research 2008, 1(Suppl 1):O2 doi:10.1186/1757-1146-1-S1-O2

Published: 26 September 2008

First paragraph (this article has no abstract)

Clawed toes, defined as extension of the metatarsophalangeal joint (MTPJ) and flexion of the proximal and distal interphalangeal joints (IPJ), have been associated with the diabetic foot. One theory states that this deformity is caused by an imbalance between the extrinsic and intrinsic foot muscles [1,2]. However, Bus et al. found a 73% decrease in intrinsic muscle cross sectional area between diabetic neuropathic patients and controls, but only 2 of 8 neuropathic patients had toe deformities [3]. Anderson et al. found that diabetic neuropathic patients had a little more than 50% of the intrinsic muscle volume of either controls or non-neuropathic diabetic patients, but none of the diabetic neuropathic patients had toe deformities [4]. Others have found a link between plantar apo-neurosis (PA) dysfunction and clawed toes [5,6] and between diabetes and a thicker PA [7-9]. The purpose of this study was to explore the relationship between claw toes, neuropathy, intrinsic muscle volume and PA thickness.