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Category: Diabetes, Hindfoot, Midfoot/Forefoot, obesity Introduction/Purpose: In recent decades, the prevalence of obesity in the United States has increased dramatically. This can be attributed in-part to the high-fat “Western Diet”. Consequentially, the economic burden of obesity to the healthcare system has rapidly increased, accounting for more than 10 percent of all medical spending in America. Furthermore, with regards to orthopedics, obesity has been shown to be a strong risk factor for musculoskeletal pain, injury, and post-operative complications. The purpose of this study was to determine the effects of high intensity cardiovascular training and controlled dietary intake on body weight, body fat percentage (BFP), and bone mineral density (BMD) in obese and non-obese mice. These results will provide a better understanding of how to optimally facilitate weight loss in obese patients. Methods: Following IAUCUC approval, 8 diet-induced obesity (DIO) C57BL/6 mice were obtained along with 6 non-obese C57BL/6 control mice. DIO mice were fed a high-fat diet (60% fat by kcal) ad libitum starting at the age of 6 weeks. Control mice were fed a standard low-fat diet (10% fat by kcal) ad libitum from birth. Starting at the age of 14 weeks, all mice underwent a controlled high intensity cardiovascular training protocol using a treadmill four times per week at 30 minute intervals. This was carried out for seven weeks including a one-week acclimation period. Speed, distance, and time spent running were all constant between groups. Mouse body weights were recorded several times per week throughout the study. Additionally, BFP and BMD were obtained bi-weekly using dual energy X-ray absorptiometry (DEXA) to assess morphophysiological changes longitudinally. Results: Preliminary investigations with a controlled exercise regimen reveal that obese mice, when fed a high-fat diet, continue to gain weight rapidly despite high intensity cardiovascular training whereas control mice maintain their weight. Following the seven-week training period, control mice gained an average of 1.25 g (p=0.41), while DIO mice gained an average of 8.55 g (p<0.001). DIO mice also showed an 8.74% increase in body fat percentage (p=0.002) while control mice showed a 0.51% decrease in body fat percentage (p=0.75). Lastly, BMD was significantly lower in DIO mice compared to controls following the exercise protocol (p<0.05). Conclusion: The results of this study support the hypothesis that a controlled exercise regimen alone is ineffective for facilitating weight loss. In fact, obese mice administered a high-fat diet actually gain weight despite undergoing a rigorous exercise program. Additionally, simple differences in dietary intake have significant effects on body weight, body fat percentage, and bone mineral density. This suggests that while exercise may play a small role in maintaining a normal weight, obesity is irreversible with exercise alone. Obese orthopedic patients should be counseled on dietary modifications before engaging in an exercise program.

Category: Diabetes, Hindfoot, Midfoot/Forefoot Introduction/Purpose: Neuroarthropathy is a progressively debilitating disease commonly affecting the lower extremity, which can lead to profound bone and joint destruction, limb deformity, and even amputation. While there are several causes, long- standing neuropathy is the most common. This leads to loss of protective sensation to the foot, which combined with repetitive micro-trauma as a result of physical activity can lead to bone and joint destruction of the lower extremity as well as major deformity. Currently there are no animal models of this disease process. The purpose of this study was to develop a novel rodent model of neuroarthropathy through the induction of the underlying neuropathic state combined with a treadmill running protocol that closely resembles local micro-trauma seen in humans. Methods: Following IAUCUC approval, 8 diet-induced obesity (DIO) C57BL/6 mice were obtained along with 6 non-obese C57BL/6 control mice. DIO mice were fed a high-fat diet (60% fat by kcal) ad libitum starting at the age of 6 weeks. Control mice were administered a standard low-fat diet (10% fat by kcal) ad libitum from birth. Starting at 14 weeks-old, all mice underwent a controlled, high-intensity cardiovascular training protocol using a rodent treadmill four times per week at 30 minute intervals. This was carried out for seven weeks including a one-week acclimation period. Speed, distance and time were held constant between groups. Weekly hind-paw sensory assessments were performed including von Frey filament and hotplate testing. Anteroposterior and mediolateral X-Rays were obtained at the beginning and conclusion of the study and radiographic analysis was performed bilaterally for all specimens. Lastly, histopathologic analysis was performed to assess musculoskeletal destructive changes to the hind-paw. Results: Baseline hotplate testing revealed that obese and non-obese mice did not differ in thermal response latency (p=0.53), however following the seven-week running protocol, obese mice demonstrated increased thermal response latency compared to controls (p=0.006). Von Frey filament testing in obese mice depicted significantly reduced hind-paw withdrawal reflexes compared to controls, both prior-to and following treadmill running (p<0.001). Comparison of initial and final radiographs for obese (figures 1.A and 1.B) and non-obese mice (figures 1.D and 1.E) showed an average increase in talo-first metatarsal angle of 7.66 degrees (p=0.007) and 0.66 degrees (p=0.75) respectively. The difference in change between groups was also significant (p<0.05). Preliminary histopathological analysis revealed significant abnormal bone remodeling in obese mice following treadmill running (figure 1.C) compared to controls. Conclusion: Obese, neuropathic animals, when challenged with a controlled exercise regimen designed to induce micro-trauma develop reliable sensory, radiographic, and histopathologic parameters reminiscent of neuroarthropathy in humans. Conversely, non-obese control animals, treated with the same exercise regimen, do not develop these neurodegenerative and musculoskeletal changes. Perhaps wild-type obese mice can be further characterized as a viable model for the development of idiopathic neuroarthropathy.