A comorbidity of inflammatory bowel disease (IBD) is inflammation-induced bone loss characterized by elevated bone resorption and decreased bone formation. Fracture incidence is resultantly elevated. Using a TNBS rat model, we have found osteocytes, cells embedded in the bone matrix, have high TNF-α prevalence. Two proteins TNF-α regulates – RANKL, a driver of bone resorption, and sclerostin, an inhibitor of bone formation – were elevated concurrent with TNF-α. These alterations in osteocyte proteins correlated with changes in bone turnover.