Orthopedic & Muscular System: Current Research
Open Access

Abstract

Pentosidine Deposition Affects Biomechanical Properties of Achilles Tendon in Diabetic Rats

Yoshimasa Sakoma, Takayuki Furumatsu and Toshifumi Ozaki

Pentosidine, a biomarker for advanced glycation end products (AGEs), accumulates in vessels, kidney, skin, and bone and induces serious pathological conditions in diabetic patients. However, the relationship between AGE deposition and biomechanical weakness in tendons has not been elucidated. We hypothesized that diabetic status might induce excessive pentosidine deposition in tendon tissue and that accumulated pentosidine might modify the biomechanical properties of the diabetic tendon. In this study, we assessed the effect of pentosidine on cellular viability, senescence, and gene expression of type I/III collagens in NIH3T3 fibroblasts. Pentosidine deposition and the biomechanical properties of diabetic Achilles tendon were investigated using a diabetic rat model. Pentosidine induced cellular senescence of NIH3T3 fibroblasts in a dose-dependent manner without affecting cellular viability. Moreover, pentosidine decreased gene expression of type I/III collagens in NIH3T3 fibroblasts. Diabetic rats showed a higher level of pentosidine deposition in their Achilles tendons compared with that in normal rats. In addition, the toughness and ultimate stress of the Achilles tendon were lower in diabetic rats. Our results suggest that pentosidine may induce cellular senescence and inhibit collagen synthesis in tendon fibroblasts. Moreover the accumulated pentosidine may alter the biomechanical properties of the Achilles tendon in the diabetic rats. Hence the suppressed collagen synthesis may cause the deterioration of the tendon mechanical properties. These phenomena might be one of the reasons of the tendon deterioration in the diabetic patients.