A Study On Sequential Therapy Of PTH Therapy In EstrogenDeficient Mice Model And Its Comparison With IL-17 Neutralizing Antibody

Abstract

The global epidemic known as osteoporosis is characterized by the loss of systemic bone mass, poor bone strength brought on by low bone mineral density (BMD), and delayed bone mineralization, all of which raise the risk of non-traumatic fracture and bone fragility. Osteoporosis is the result of weakening or erosion of bone that causes the bone to become more porous. The word represents bone. Osteoporosis is mostly predicted by bone mineral density (BMD). Osteoporosis is defined as a BMD in young, healthy persons that is less than 2.5 standard deviations. According to recent research, inflammation is a major factor in the etiology of osteoporosis. T cell activation and bone loss are caused by low estrogen levels. According to a clinical study, pro-inflammatory cytokines are important factors that determine how quickly PMO women lose bone (Brincat, S. D., 2014). We can see from the literature that IL-17 cytokine is essential to the pathophysiology of osteoporosis. In this work, we have demonstrated that, in the bone defect/injury model, combination therapy (PTH (1-34) + IL-17 neutralizing antibody) increased bone regeneration potential relative to similar monotherapies. This suggested that a novel target for osteoporosis treatment drugs could be this combination therapy.