Exercise ameliorates diabetes-induced osteoarthritis in rats

Abbas Elkarib

doi:10.21608/eajbsc.2014.16035

Abstract

Introduction: Osteoarthritis secondary to diabetes is one of the common public health problems arising from diabetic complications in humans. Exercise was reported to alleviate cardiovascular diabetic complications. We sought to determine whether exercise can also ameliorate diabetes-induced osteoarthritis condition. Material and methods: Using basic histological staining, I studied the morphological changes in the articular cartilage of diabetic rats with and without swim exercise and compare it with the control, untreated rats. In addition, interleukin-6 (IL-6), a biomarker that is known to be elevated in osteoarthritis was assayed in the blood of the three rat groups by enzyme-linked immunosorbent assay (ELISA). Results: Compared to the control group, induction of type I diabetes mellitus (T1DM) in Wistar rats caused a profound damage to the knee joint cartilage as demonstrated by disrupted lacunae, condensing of the matrix and enlargement of the chondrocytes and its nucleus with the disappearance of both, the euchromatin staining and the discrete cytoplasmic vacuoles. Furthermore, there was a four-fold increase in IL-6 in the T1DM group that was significantly (p<0.01) reduced in the diabetic group with exercise. More interestingly, exercise resolved diabetes-induced cartilage damage by restoring the chondrocytes spherical intact nucleus and vaculated cytoplasms with regular lacunae. Conclusion: In this report, we have demonstrated a model of diabetes-induced osteoarthritis in rats where swim exercise was able to ameliorate both articular cartilage damage and IL-6 inflammatory biomarker in T1DM rats.

Highlights

Osteoarthritis secondary to diabetes is one of the common public health problems arising from diabetic complications in humans
This modestly low bone marrow density (BMD) caused an increase in hip fracture risk of about 2-fold (Hofbauer et al 2007), yet prospective studies indicate that postmenopausal women with T1DM have about 10 times greater risk of hip fracture compared with age-matched non- diabetics (Forsen et al 1999)
Animal model As previously reported by our group (Haidara et al 2004), Wistar rats were injected with a single dose of streptozotocin (65 mg/kg) and T1DM was induced with a blood sugar level reached 220 mg/dl compared to 80 mg/dl in the control group injected with citrate buffer

Summary

Introduction

Osteoarthritis secondary to diabetes is one of the common public health problems arising from diabetic complications in humans. People with type 1 (juvenile) diabetes (T1DM) tend to have mild osteopenia as adults, with bone marrow density (BMD) values around 10% lower than normal (Bouillon 1991) This modestly low BMD caused an increase in hip fracture risk of about 2-fold (Hofbauer et al 2007), yet prospective studies indicate that postmenopausal women with T1DM have about 10 times greater risk of hip fracture compared with age-matched non- diabetics (Forsen et al 1999). Osteoarthritis (OA) is a degenerative joint disease that involves degradation of joints including articular cartilage leading to pain, swelling and reduce joints movement (Manen et al 2012; Pottie et al 2006) It affects millions of people worldwide and regarded as one of the most prevalent condition leading to disability in elderly population as a consequence of the knee OA and/or hip OA (Grazio and Balen 2009). Knee OA is more important for its high prevalence rate compared with other types of OA and for its presentation at earlier age groups in younger age groups of obese women (Bliddal and Christensen 2009; Hayami 2008)

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