Spontaneous Rupture of the Anterior Tibial Tendon in a Diabetic Patient: Results of Operative Treatment

DiDomenico, Lawrence A.; Williams, Kwamee; Petrolla, Angelo F.

doi:10.1053/j.jfas.2008.05.007

Cited by 56 publications

(35 citation statements)

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“…Several clinical case reports describe thickened, fibrotic tendons and decreased range of motion in diabetic patients [22], [23], [29]. Importantly, these patients are also at increased risk for tendon rupture and have less satisfactory outcomes following surgical repair [28], [30]. In the current study, biomechanical testing in injured FDL tendons from a HF diet-induced obese, type 2 diabetic mouse model demonstrates the detrimental effect of this metabolic state on tendon repair.…”

Section: Discussionmentioning

confidence: 59%

Tendon Repair Is Compromised in a High Fat Diet-Induced Mouse Model of Obesity and Type 2 Diabetes

et al. 2014

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IntroductionThe obesity epidemic has resulted in a large increase in type 2 diabetes (T2D). While some secondary complications of T2D are well recognized and their cellular and molecular mechanisms are defined, the impact of T2D on the musculoskeletal system is less understood. Clinical evidence suggests that tendon strength and repair are compromised. Here, a mouse model of obesity and T2D recapitulates the deleterious effects of this condition on tendon repair.MethodsMale C57BL/6J mice at 5 weeks of age were placed on a high fat (HF)(60% kcal) or low fat (10% kcal) diet for 12 weeks. The flexor digitorum longus (FDL) tendon was then injured by puncturing it with a beveled needle. Progression of FDL tendon healing was assessed through biomechanical and histological analysis at 0, 7, 14 and 28 days post-injury.ResultsHF-fed mice displayed increased body weight and elevated fasting glucose levels, both consistent with T2D. No differences in biomechanical properties of the uninjured FDL tendon were observed after 12 weeks on HF versus lean diets, but decreased maximum force in uninjured tendons from HF-fed mice was observed at 24 weeks. Following puncture injury, tendons from HF-fed mice displayed impaired biomechanical properties at day 28 post injury. In support of defective repair in the HF-fed mice, histological examination of the injury site showed a smaller area of repair and lower cell content in the repair area of HF-fed mice. Insulin receptors were expressed in most cells at the injury site regardless of diet.DiscussionThe HF-diet mouse model of obesity and T2D reproduces the impaired tendon healing that is observed in this patient population. The exact mechanism is unknown, but we hypothesize that a cellular defect, perhaps involving insulin resistance, leads to decreased proliferation or recruitment to the injury site, and ultimately contributes to defective tendon healing.

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Section: Discussionmentioning

confidence: 59%

Tendon Repair Is Compromised in a High Fat Diet-Induced Mouse Model of Obesity and Type 2 Diabetes

et al. 2014

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“…Although there is human and animal evidence of abnormal tendon composition and structure in subjects with diabetes , ex vivo evidence from some animal studies of diabetes‐related mechanical failure , and individual case reports and small series suggesting an association between tendon rupture and diabetes , this is the first large‐scale longitudinal study to address this issue. The patients with Type 2 diabetes in the present study had a significant 44% greater risk of hospitalization for any tendon rupture compared with age‐ and gender‐matched community‐based control subjects.…”

Section: Discussionmentioning

confidence: 98%

Incidence and predictors of hospitalization for tendon rupture in Type 2 diabetes: the Fremantle Diabetes Study

Zakaria

Davis

2013

Diabet. Med.

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“…Case reports and epidemiological studies suggest a relationship between Diabetes Mellitus (DM) and complications and ruptures of tendons from various regions of the human body [1], [2], [3], [4], [5], [6]. To evaluate this relationship in diabetic patients, studies have stopped at structural analysis of the tendon performed through diagnostic imaging methods, such as musculoskeletal ultrasound [1], [4], [5], [7], [8], computerized tomography [6] and magnetic resonance imaging [9].…”

Section: Introductionmentioning

confidence: 99%

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

et al. 2013

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This study aims to demonstrate how the state of chronic hyperglycemia from experimental Diabetes Mellitus can influence the homeostatic imbalance of tendons and, consequently, lead to the characteristics of tendinopathy. Twenty animals were randomly divided into two experimental groups: control group, consisting of healthy rats and diabetic group constituted by rats induced to Diabetes Mellitus I. After twenty-four days of the induction of Diabetes type I, the Achilles tendon were removed for morphological evaluation, cellularity, number and cross-sectional area of blood vessel, immunohistochemistry for Collagen type I, VEGF and NF-κB nuclear localization sequence (NLS) and nitrate and nitrite level. The Achilles tendon thickness (µm/100g) of diabetic animals was significantly increased and, similarly, an increase was observed in the density of fibrocytes and mast cells in the tendons of the diabetic group. The average number of blood vessels per field, in peritendinous tissue, was statistically higher in the diabetic group 3.39 (2.98) vessels/field when compared to the control group 0.89 (1.68) vessels/field p = 0.001 and in the intratendinous region, it was observed that blood vessels were extremely rare in the control group 0.035 (0.18) vessels/field and were often present in the tendons of the diabetic group 0.89 (0.99) vessels/field. The immunohistochemistry analysis identified higher density of type 1 collagen and increased expression of VEGF as well as increased immunostaining for NFκB p50 NLS in the nucleus in Achilles tendon of the diabetic group when compared to the control group. Higher levels of nitrite/nitrate were observed in the experimental group induced to diabetes. We conclude that experimental DM induces notable structural, inflammatory and vascular changes in the Achilles tendon which are compatible with the process of chronic tendinopathy.

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Spontaneous Rupture of the Anterior Tibial Tendon in a Diabetic Patient: Results of Operative Treatment

Cited by 56 publications

References 10 publications

Tendon Repair Is Compromised in a High Fat Diet-Induced Mouse Model of Obesity and Type 2 Diabetes

Tendon Repair Is Compromised in a High Fat Diet-Induced Mouse Model of Obesity and Type 2 Diabetes

Incidence and predictors of hospitalization for tendon rupture in Type 2 diabetes: the Fremantle Diabetes Study

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

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