Modeling the Effects of Vasoactive Intestinal Peptide on Pre-Osteoblast Differentiation

Multiple Sclerosis (MS) is a chronic, autoimmune disease of the central nervous system (CNS) that affects millions of people globally. It targets the neurons of the CNS and destroys their myelin sheaths, or the fatty layer of insulation around them. This can lead to loss of motor function, deteriorating vision, loss of balance, and muscle weakness. In addition, recent studies have shown mounting evidence of crosstalk between the cellular pathways of MS and osteoporosis, a disease of the degeneration of bone and loss of bone density. These studies have demonstrated that the risk of osteoporosis in people with MS is far higher than that of the general population (Lian et al., 2012). Osteoporosis is a disease that originates from an imbalance in the bone remodeling cycle. Osteoblasts, which are the cells that form new bone, cannot maintain pace with osteoclasts, which break down bone, causing a loss in bone mass and increasing the chance of fractures.

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