Development of immunomodulatory biomaterial in tissue repair
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According to International Osteoporosis Foundation, osteoporosis causes more than 8.9 million bone fractures annually worldwide. In other words, a person suffers a fracture every three seconds. Many different surgeries can be performed depending on the type of fracture. For example, bone grafting helps severe trauma and commuted fracture. Nevertheless, regardless of the surgery performed, the primary goal after injury is to return the damaged tissue back to its original state. Bone healing is very complicated process involving proliferation of tissue cells and stem cell differentiation. A complex cascade of chemical signals and cells, such as growth factors, inflammatory cytokines, osteoclasts (cells that break down bone), and osteoblast (bone-forming cell), work as a team to perform a compact task. Seems like our body has a mysterious program that cell and chemical present in the certain stages in order. The injury site initiates inflammation and spreads a signal to recruit inflammatory monocytes. The inflammatory monocytes infiltrate the injury site and work to effectively defend and clear the virus, bacterial, and other infection from an external source. However, the functionality of inflammatory can also lead pathogenesis of inflammation and degenerative disease. Therefore, anti-inflammatory monocytes patrolling in the vasculature move from blood vessel to the tissue and differentiate into anti-inflammatory macrophage called “M2” macrophages. Anti-inflammatory macrophages clean the inflammation and also repair damaged tissues. Ideally, if we can identify the correlation within those components and speed up the procedure, we could increase the body’s regeneration rate. Therefore, our research focuses on studying those components and developing strategies to increase the efficiency of recruitment of therapeutic cell types.