Type 2 Diabetes mellitus (T2D) is a chronic condition that affects over 30 million people in the United States alone. Those with T2D have increased bone fragility compared to healthy adults. One suspected cause of this risk is the accumulation of Advanced Glycation End-Products (AGEs), non-enzymatic crosslinks that alter the collagen matrix and ultimately affect bone quality. Pentosidine is an AGE that is easily detected and measurable in bone and has been known to alter the structure and function of bone tissue. The buildup of AGEs can also affect bone cells, specifically osteocytes. Osteocytes are multifunctional bone cells, and alterations in these functions can lead to osteocyte apoptosis and alterations in bone repair. The bone resorption and remodeling processes are crucial to bone health, and largely regulated by two important proteins, sclerostin and receptor activated nuclear factor kappa beta (RANKL). The combination of AGE buildup and a hyperglycemic environment lead to alterations in the expression of these proteins. Our goal is to examine the protein and gene expression in Ocy-454 osteocytes grown in either hyperglycemic media or media supplemented with pentosidine to better understand the link between T2D and skeletal fragility. We hypothesize that osteocytes in both high sugar media and pentosidine supplemented media will have an increase in sclerostin and RANKL production.