Contributing Factors to Forefoot Deformity in the Diabetic, Neuropathic Foot

Author's School

Graduate School of Arts and Sciences

Author's Department/Program

Movement Science


English (en)

Date of Award

Summer 8-15-2015

Degree Type


Degree Name

Doctor of Philosophy (PhD)

Chair and Committee

Michael Mueller

Committee Members

Mary Hastings, Gretchen Meyer, David Sinacore, Linda Van Dillen, Samuel Ward


The primary goal of this dissertation was to determine the contribution of proposed risk factors to the severity of metatarsophalangeal joint (MTPJ) deformity. People with diabetic neuropathy (DMPN) are likely to have advanced glycation end product (AGE) accumulation, intrinsic foot muscle deterioration, and limited joint mobility at the ankle, contributing to an increased risk for deformity and progression down the impairment cascade of ulceration and amputation. We hypothesized the interaction of PN and AGEs leads to intrinsic foot muscle deterioration and limited ankle joint mobility, which produces a habitual MTPJ hyperextension movement pattern during tasks that require active dorsiflexion, which causes MTPJ deformity. Understanding the etiology of MTPJ deformity would improve techniques to manage and treat diabetic, neuropathic foot deformity, reducing the risk of lower extremity amputation in this high risk population.

In chapter 2, we developed a semi-automated program that would segment subcutaneous fat and intrinsic foot muscles based on signal intensities of a MR image. We found our program could quantify subcutaneous fat, lean muscle, and adipose tissue volume in the foot with excellent reliability and minimal root mean square error for all phantoms. In chapter 3, we determined the effects of intrinsic foot muscle deterioration and limited ankle joint mobility on the severity of MTPJ deformity, and determined the relationships between these contributing factors and indicators of diabetic complications. The methods developed and tested in chapter 2 were applied to assess intrinsic foot muscle deterioration in the forefoot. Remaining lean muscle volume and maximum ankle dorsiflexion were correlated with severity of MTPJ deformity, and together they explained a significant amount of the variance of MTPJ angle. Skin intrinsic fluorescence, a proxy measure of AGEs, was correlated to severity of neuropathy but not maximum ankle dorsiflexion, or deterioration measures when controlling for neuropathy. Neuropathy was correlated with forefoot muscle deterioration. In chapter 4, we characterized a MTPJ movement pattern in persons with diabetic neuropathy and a broad spectrum of MTPJ deformity. We found MTPJ hyperextension deformity severity was associated with a pattern of motion characterized by an increase in MTPJ extension during active ankle dorsiflexion in persons with DMPN. The amount of MTPJ extension excursion during daily tasks was related to the severity of resting MTPJ extension alignment.

The results of this dissertation have identified potentially modifiable causal factors leading to MTPJ deformity. These factors are excessive AGEs, intrinsic foot muscle deterioration, limited ankle dorsiflexion range of motion, and a MTPJ hyperextension movement pattern. Determining the interaction of these factors and their contribution to the progression of deformity would help clinicians develop targeted interventions to best improve patient outcomes. A comprehensive examination of the contributors to MTPJ deformity in a prospective study, using the methods developed and tested in this dissertation, would have profound implications for understanding how the interplay of these factors predicts deformity progression over a multi-year period. A foot-specific intervention targeting these same factors would best show whether muscle volume, strength, ankle dorsiflexion range of motion, MTPJ hyperextension movement pattern, and MTPJ alignment could be improved noninvasively in the short term and maintained in the long term.