Dynamic changes in compressive and shear plantar tissue properties during gait and rest in people living with and without diabetes

This pilot study utilized a novel PlantarSense tool to demonstrate that people with diabetes exhibit impaired plantar tissue thermoregulation and reduced recovery of shear and compressive energy dissipation ratios after walking compared to non-diabetic controls, highlighting dynamic tissue adaptations relevant to diabetic foot ulceration risk.

The Gist

The Big Picture: Why Do Diabetic Feet Get Ulcers?

Imagine your foot is like a high-tech shock absorber on a car. Every time you take a step, your foot's soft tissues (fat pads and skin) squish down to cushion the impact, then spring back up to get ready for the next step. This "squish and spring" action is crucial. If the shock absorber breaks or gets too stiff, the car (your foot) takes a beating, leading to damage.

For people with diabetes, this shock-absorbing system often starts to malfunction. They are at high risk for Diabetic Foot Ulcers (painful sores that won't heal). While doctors know that this happens, they haven't fully understood how the tissue changes when you are actually walking around. Most previous studies only looked at feet while they were sitting still (static), which is like testing a car's suspension while the car is parked in a garage.

The New Tool: "PlantarSense"

The researchers built a new gadget called PlantarSense. Think of it as a smart, high-tech stethoscope that doesn't just listen; it pushes and pulls on your foot while measuring exactly how the tissue reacts.

• How it works: It uses an ultrasound camera to see inside the foot and force sensors to feel the pressure.
• What it measures: It checks two things:
  1. Compression: How much the tissue squishes down (like pressing a sponge).
  2. Shear: How the tissue slides or stretches sideways (like rubbing your hand back and forth on a table).
• The Goal: To see how the foot's "shock absorbers" behave during a walk and after a rest, comparing people with diabetes to healthy people.

The Experiment: A Day in the Life of a Foot

The researchers recruited two groups:

1. The Control Group: Healthy people without diabetes.
2. The Diabetes Group: People living with diabetes (but without severe nerve damage or existing sores).

They put everyone in a lab and did three things:

1. Baseline: Measured the feet while resting.
2. The Walk: Everyone walked on a treadmill for 15 minutes.
3. The Recovery: Everyone sat down and rested their feet for 15 minutes.

During all three stages, they measured the temperature of the foot and the energy the tissue absorbed (called the Energy Dissipation Ratio, or EDR).

The Findings: What Happened?

Here is what the "smart stethoscope" found, using some simple metaphors:

1. The "Overheating Engine" (Temperature)

• The Healthy Foot: When healthy people walked, their feet got a little warm (like a car engine warming up), but they cooled down pretty quickly once they stopped.
• The Diabetic Foot: When people with diabetes walked, their feet got significantly hotter, especially at the heel. Even after resting, their feet stayed warmer than the healthy group.
• The Analogy: Imagine two cars driving for 15 minutes. The healthy car has a good cooling system and returns to normal temperature quickly. The diabetic car has a clogged radiator; it gets hotter faster and stays hot for a long time after the engine is off. This "stuck heat" suggests the tissue is inflamed or struggling to circulate blood properly.

2. The "Sticky Sponge" (Energy Dissipation)

• The Concept: When you squeeze a sponge, some energy bounces back (elastic), and some is lost as heat (dissipated).
• The Healthy Foot: Their tissues were like a bouncy rubber ball. They absorbed energy efficiently and bounced back well.
• The Diabetic Foot: Their tissues, especially at the ball of the foot, acted more like a sticky, water-logged sponge. They absorbed more energy (dissipated it) rather than bouncing back.
• The Twist: Interestingly, after walking, both groups' tissues got "tired" and lost some of their bounce (energy dissipation went down). However, the healthy group bounced back to normal quickly after resting. The diabetic group stayed "tired" and didn't recover their bounce as well.
• The Analogy: Think of a trampoline. A healthy trampoline springs back perfectly after you jump. A diabetic trampoline is like one that has been used too much; it sags a bit more and takes longer to return to its original shape.

3. The "Sideways Slip" (Shear Force)

• The study found that the foot's tissues react much more dramatically to sideways forces (shear) than just straight-down pressure.
• The Analogy: If you push a block of jelly straight down, it squishes. If you push it sideways, it slides and stretches. The study showed that the diabetic foot's "jelly" is much more sensitive to that sideways sliding, which is a major cause of skin breakdown and ulcers.

Why Does This Matter?

This study changes the way we might think about preventing foot ulcers:

1. It's Not Just About Pressure: We used to think ulcers were caused only by high pressure (standing on a rock). This study shows that heat and recovery time are huge clues. If your foot stays hot and "tired" after a short walk, it's a warning sign.
2. The "Hidden" Damage: Even if a person with diabetes walks normally and doesn't feel pain (because of nerve damage), their tissues are working harder, heating up more, and failing to recover. They are accumulating "micro-damage" with every step.
3. New Prevention Strategies: Instead of just telling people to "walk less," doctors might need to focus on:
   • Cooling: Helping the feet cool down faster.
   • Recovery: Giving feet more time to rest between activities.
   • Shear Protection: Using socks or shoes that stop the foot from sliding inside the shoe (reducing that sideways friction).

The Bottom Line

The researchers built a cool new tool that proved diabetic feet are like overheated, slow-to-recover shock absorbers. They get hotter than healthy feet when you walk, and they take longer to cool down and "bounce back."

This study is a "pilot" (a small test run), so they need to test more people to be 100% sure. But the message is clear: To keep diabetic feet safe, we need to watch not just how hard they are pressed, but how hot they get and how well they recover after a day's walk.

Technical Summary

1. Problem Statement

Diabetic foot ulcers (DFUs) are a severe complication of diabetes, often resulting from altered plantar tissue mechanics, repetitive loading, and impaired thermoregulation. While existing literature acknowledges that plantar soft tissue becomes stiffer and less compliant in diabetes, current assessment methods have significant limitations:

• Static vs. Dynamic: Most studies rely on quasi-static measurements, failing to capture the time-dependent, viscoelastic behavior of tissue during actual gait.
• Loading Modes: Research predominantly focuses on compressive loading, neglecting shear stress, which is a critical factor in tissue breakdown and ulceration.
• Thermal-Mechanical Link: There is a lack of integrated systems that simultaneously quantify mechanical energy dissipation and thermal responses (temperature changes) during activity and recovery to understand tissue adaptation.
• Gap: No existing in vivo system simultaneously quantifies plantar tissue properties under both normal (compressive) and shear loading conditions while monitoring dynamic temperature changes in people with and without diabetes.

2. Methodology

A. Novel Measurement System: PlantarSense

The authors developed PlantarSense, a custom in vivo measurement device integrating:

• Ultrasound Imaging: A high-resolution B-mode ultrasound probe (L15-6L25N) to measure tissue deformation.
• Force Measurement: Three load cells (LCEB-10) mounted to capture compressive and shear forces applied to the probe head.
• Data Acquisition: Signals digitized at 60 Hz via a 24-bit ADC and processed in real-time (LabVIEW) and post-processed (MATLAB).
• Thermal Monitoring: An infrared thermometer (RS-8806S) measured skin temperature at the first metatarsal head (1stMTH) and calcaneus.

Key Metrics:

• Energy Dissipation Ratio (EDR): Calculated from the hysteresis loop of stress-strain curves ($EDR = (E_L - E_U) / E_L \times 100\%$), representing the proportion of mechanical energy absorbed (dissipated) rather than elastically returned.
• Loading Protocols: Both quasi-static (ramped steps) and dynamic (sinusoidal at 1 Hz) loading were applied in compression (0–40 N) and shear (0–10 N under 15 N preload).

B. Validation

The system was validated in vitro using:

• Silicone Phantom (Ecoflex 00-10): To test repeatability and accuracy.
• Porcine Tissue (Pork belly): To simulate biological tissue.
• Comparison: Results were benchmarked against a standard mechanical test machine (Instron).
• Outcome: Accuracy of 96–97% for silicone and 92–95% for porcine tissue; intra-sample variability <10%.

C. Clinical Study Protocol

• Participants: 15 total (5 with diabetes, 10 healthy controls). Groups were matched for age, BMI, and sex.
• Settings: Gait laboratory with standardized footwear and clothing.
• Phases:
  1. Baseline: 30-min rest, followed by initial temperature and PlantarSense measurements.
  2. Walking: 15-minute treadmill walk at self-selected pace (monitored via F-scan insoles for Pressure-Time Integral).
  3. Recovery: 15-minute rest with feet elevated, followed by repeated measurements.
• Locations: Measurements taken at the 1st Metatarsal Head (1stMTH) and Calcaneus.

3. Key Contributions

1. Device Innovation: Successful development and validation of PlantarSense, the first in vivo system capable of simultaneous dynamic measurement of compressive and shear tissue properties combined with thermal monitoring.
2. Dynamic Assessment: Shifted focus from static tissue properties to dynamic, activity-induced changes in viscoelasticity (EDR) and thermoregulation.
3. Shear Loading Analysis: Provided quantitative data on how shear loading specifically affects energy dissipation, revealing that shear induces larger EDR modulation than compression.
4. Thermal-Mechanical Correlation: Linked mechanical recovery deficits (EDR) with thermal recovery deficits (temperature retention) in diabetic populations.

4. Key Results

A. Plantar Pressure (PTI)

• No statistically significant difference in Pressure-Time Integral (PTI) between diabetic and control groups during walking at either the 1stMTH or calcaneus.
• Implication: Observed tissue differences are likely due to intrinsic tissue properties rather than differences in external loading magnitude.

B. Thermal Responses

• Post-Walk Temperature: Diabetic participants showed significantly greater temperature increases at the calcaneus (11.0% vs. 6.9% in controls, p=0.03).
• Recovery: Diabetic participants exhibited incomplete thermal recovery. At the 1stMTH, residual temperature elevation was higher in the diabetic group (4.2% vs. 2.1% in controls), suggesting impaired thermoregulation and heat dissipation.

C. Energy Dissipation Ratio (EDR)

• Baseline (Compression): Diabetic group had significantly higher EDR at the 1stMTH (67.8% vs. 56.0% in controls, p=0.04), indicating a more "lossy" (viscous) tissue response.
• Activity Modulation:
  • Shear vs. Compression: EDR modulation was significantly greater under shear loading (21.5% change) compared to compression (5.4% change).
  • Post-Walk: EDR decreased in all participants immediately after walking (indicating a "conditioning" effect).
  • Recovery: The diabetic group showed less complete recovery of EDR. For example, at the 1stMTH under compression, controls recovered to within 7% of baseline, whereas the diabetic group remained 27% below baseline.
• Statistical Note: While many between-group differences were not statistically significant due to the pilot sample size (n=15), the effect sizes and directional trends were consistent with the hypotheses.

5. Significance and Conclusion

Clinical Implications:

• Early Detection: The combination of elevated post-walk temperature and incomplete mechanical recovery (EDR) may serve as early biomarkers for diabetic foot vulnerability, even before ulceration occurs.
• Mechanism of Injury: The findings suggest that diabetic tissue not only has altered baseline mechanics (higher baseline EDR at the forefoot) but also suffers from "mechanical fatigue" where tissues fail to recover their viscoelastic buffering capacity after daily activity. This leaves tissues in a compromised state for subsequent loading.
• Shear Importance: The high sensitivity of EDR to shear loading reinforces the clinical necessity of managing shear forces (e.g., via footwear design) to prevent tissue breakdown.

Limitations & Future Work:

• Sample Size: As a pilot study, the small sample size limited statistical power for some between-group comparisons.
• Loading Range: The maximum load (40 N) was capped for safety and may not fully replicate peak gait forces.
• Future Directions: Larger, adequately powered studies are needed to stratify by diabetes severity and neuropathy. Future iterations should explore multi-layer tissue modeling and extended recovery time courses to better define the kinetics of tissue adaptation.

Summary:
This study demonstrates that people living with diabetes exhibit distinct deficits in plantar tissue thermoregulation and viscoelastic recovery compared to controls. The novel PlantarSense system successfully captured these dynamic changes, highlighting that impaired tissue adaptation involves both heat retention and a failure to restore mechanical energy dissipation properties after activity, particularly under shear loading. These insights offer a new framework for understanding DFU risk beyond static pressure analysis.