Determination the role of apoptosis on cartilage injury (osteoarthritis) in human KNEE joint chondrocytes through diabetes and mechanical loading

Determination The Role of Apoptosis on Cartilage Injury (Osteoarthritis) in Human Knee Joint Chondrocytes Through Diabetes and Mechanical Loading Osteoarthritis (OA), which is the most common cause of chronic disability in humans, especially in the elderly, occurs when the balance between joint disintegration and repair is disrupted Although apoptosis of chondrocyte is the main factor in the development of osteoarthritis, its mechanism is unknown yet. Therefore, the main aim of the present study was to determine apoptotic signal pathways by biomolecular markers in osteoarthritis caused by diabetes and mechanical loading (obesity) in human articular cartilage and to define the relationship between apoptosis and osteoarthritis through the amount of load on cartilage. In the present study, samples with excision material from total knee replacement were used. OA patients were divided into groups according to their body mass index (BMI). In addition, samples belong to diabetes (DM) patients were also taken in our study, and a positive control group was formed for apoptosis. Then, patients with diabetes were also separated according to their BMIs and four different groups were constructed as Light Weight (LW), DM+LW, Obese and LW+Obese. In the study, lysates were prepared from tissues, and Bcl-2, caspase-3 and CAMK II protein activations were measured by western blot method. Changes in gene expression levels encoding CAMKII protein were determined by real-time PCR method. In our thesis study, it was observed that caspase-3 protein expression increased in all groups compared to the LW group. In addition, Bcl-2 and CAMK proteins were also increased in all groups (DM, DM+Obese, Obese), but the increase in the Obese and DM+Obese groups were highest. In the light of these data, we observed that chondrocyte apoptosis was increased by metabolic diseases in human knee cartilage osteoarthritis. However, the increase in Bcl-2 and CAMKII activation showed that anabolic processes against apoptosis still continue despite catabolic processes in diseases such as DM and obesity. The fact that Bcl-2 and CAMKII activation is higher in obesity than in DM indicates that there is a more active anabolic process in OA caused by mechanical loading. Keywords: Apoptosis, CAMK, Chondrocytes, Obesity, Osteoarthritis