Metatarsal Phalangeal Joint Deformity Progression - R01

The long term goal of this research is to reduce the incidence of lower extremity amputation
in people with diabetes mellitus and peripheral neuropathy. It is hypothesized that muscle,
joint, and movement deterioration associated with diabetes and peripheral neuropathy
contribute to metatarsophalangeal joint (MTPJ) hyperextension deformity. MTPJ deformity
results in excessive plantar stress on the insensitive forefoot, leading to ulceration and
amputation. However, the specific cause of MTPJ deformity is not clear. The overall goal of
this proposal is to identify the causes of MTPJ deformity and examine the ability of a
targeted foot specific intervention to de-couple diabetes related mechanisms from MTPJ
deformity and progression, following participants for 3 years. The investigators hypothesize
that the cause of MTPJ deformity is an interaction of the accumulation of advanced glycation
end products, muscle deterioration, limited joint mobility and compensatory movement
strategies.

The specific aims are to determine:

1. relationships between advanced glycation end products, intrinsic foot muscle volume,
limited ankle dorsiflexion joint mobility, MTPJ hyperextension movement pattern, and
MTPJ alignment;

2. estimate the effect of a foot specific intervention on the MTPJ extension alignment and

3. determine progression of MTPJ deformity and the predictors of progression over three
years.

The following will be collected on participants with diabetes mellitus and peripheral
neuropathy and monitored over three years to understand the causes and progression of MTPJ
deformity:

1. Skin intrinsic florescence to measure advanced glycation end product accumulation which
increases collagen cross-linking and is associated with peripheral neuropathy, limited
joint mobility, and muscle deterioration.

2. Magnetic resonance images to measure intrinsic foot muscle deterioration that precedes
extrinsic foot muscle deterioration as a result of distal to proximal peripheral
neuropathy. The muscle imbalance of weak intrinsic foot muscles, the only muscles able
to flex the MTPJ, in the presence of relatively stronger extrinsic toe extensors,
results in a force couple that hyperextends the MTPJ.

3. Kinematic and computed tomography measurement of foot and ankle joint positions to
examine mobility and movement patterns that contribute to repeated and extreme MTPJ
hyperextension during daily activities.

The investigators believe advanced glycation end products lead to limited ankle joint
dorsiflexion. As a result, there is increased reliance on the extensor digitorum longus to
assist in dorsiflexing the stiff ankle joint during activities like sit to stand. This study
will have profound implications for reducing risk for skin breakdown and amputation by
helping to understand and treat the causes of acquired neuropathic foot deformities. A
successful foot specific intervention that improves MTPJ alignment will provide a
non-invasive option to halt or slow the cascade of events leading to major lower extremity
amputation, while improving function and minimizing disability.

Inclusion Criteria:

- Type 2 DM and duration of diagnosed DM > 10 years

- Type 2 DM and presence of positive prayer sign OR shoulder flexion <150 degrees;

- Disability of arm, shoulder and hand (DASH) scores < 70

Exclusion Criteria:

- Currently diagnosed adhesive capsulitis; diagnosed rotator cuff tear; recent (6
months) upper extremity injury and/or fractures; surgery in the upper extremity or
thorax; cervical radiculopathy; thoracic outlet syndrome; stroke with residual upper
extremity involvement; severe skin allergies in area to be tested; rheumatic
conditions; known connective tissue diseases; carpal tunnel syndrome; use of a cane;
individuals who engage in heavy upper extremity/ overhead use because they are likely
to have a different mechanism of injury than those with low shoulder activity