The long-term objective of this research is to determine the muscle and joint factors associated with metatarsophalangeal joint deformity, a primary contributor to neuropathic plantar ulceration and lower extremity amputation in individuals with diabetes mellitus and peripheral neuropathy. Hyperextension at the metatarsophalangeal joint is a forefoot deformity associated with excessive peak plantar pressures under the metatarsal heads that can lead to skin breakdown on an insensate foot. The prevalence of metatarsophalangeal joint deformity in individuals with a history of ulceration and amputation has been found to be as high as 85%. Potential risk factors of deformity are neuropathic intrinsic foot muscle deterioration and limited joint mobility at the ankle. Weakened intrinsic foot muscles are thought to result in joint hyperextension from a muscular imbalance between the intrinsic flexor and extrinsic extensor muscles. Advanced glycation end-product accumulation also increases collagen cross-linking in tissues, and decreased ankle mobility is thought to lead to extrinsic toe extension compensation. This cross-sectional study will recruit two groups: 1) diabetic and neuropathic without metatarsophalangeal joint hyperextension, and 2) diabetic and neuropathic with metatarsophalangeal joint hyperextension. The groups will be compared utilizing quantitative measures of intrinsic foot muscle deterioration, advanced glycation end-products, and intersegmental joint kinematics over three aims.
Aim 1 will determine group differences in intrinsic foot muscle structure (magnetic resonance- based volumetric analysis of lean muscle and adipose content) and function (strength measured by cuff dynamometry, range of motion from 3D motion capture).
Aim 2 will determine the relationships between advanced glycation end-product accumulation (skin intrinsic fluorescence score from SCOUT DS device), peripheral neuropathy (neuropathy disability score and vibration perception threshold) and limited joint mobility at the ankle (3D motion capture).
Aim 3 will determine the contribution of intrinsic foot muscle structure and limited joint mobility to metatarsophalangeal joint angle (multiple regression analysis). We hypothesize that the proposed research will identify the muscular and joint impairments associated with metatarsophalangeal joint deformity in people with diabetic neuropathy. Understanding the factors involved in the development and progression of this forefoot deformity will lead to early and targeted interventions for the prevention of neuropathic ulceration and lower extremity amputations.
Knowledge gained from this study will help identify the muscle and joint impairments associated with forefoot deformity in people with diabetes and neuropathy. Understanding the risk factors involved in the development and progression of forefoot deformities will lead to early and targeted interventions for the prevention of neuropathi plantar ulceration and lower extremity amputations.