Grant: Travel Awards - Institute Community Support

Osteoarthritis (OA) is commonly described by joint pain and reduced joint movement associated cartilage destructionand changes in bone formation. It is a disease that tends to get worse over time as the cartilage continues to wear away. OA is a leading cause of disability in Canada and with increasing life expectancy; OA is a major clinical and economic concern. The pathological mechanisms by which OA can be halted is still unknown. Therefore, it is utmost important to identify new targets which will help us understand the exact pathology of this disease and will further help us in stopping OA. In this context, our animal and human cell based studies suggest that a biological factor called autophagy may be an attractive target for the treatment of OA. However, we are still uncertain as to what is the exact role of autophagy in OA. Therefore, this study for the first time will investigate the specific role of autophagy in OA using mice, dog and human cells to investigate the expression pattern of autophagy markers. Te data we get from mice, dog compared to cartilage samples collected from normal human and OA patients and specifically answer the following questions: (1) What is the exact role of autophagy markers in cartilage and bone destruction associated with OA. (2) What is the exact role of autophagy on inflammation associated with OA. (3) How does autophagy control the production of harmful biological factors involved in OA. (4) What is the exact signalling mechanism by which autophagy works in OA. To answer these questions I will use a combination of techniques such as quantitative PCR and immunohistochemistry methods. I anticipate that this study will show that autophagy is the key target likely to control inflammation and damage to bone and cartilage observed in OA. Therefore, this project has the potential to generate new therapeutic strategies for the treatment of OA and related disorders.