Though a characteristic of OA, the use of inflammatory cytokines such as IL-1β and TNF-α to induce a chondrocyte disease state is more appropriate to the study of rheumatoid arthritis (RA), not OA [20–24]. And, while mechanical disruption using high strain dynamic loading (up to 25% at 1 Hz) has been shown to induce OA-like cell responses in MSC-laden hydrogel [19], these models do not generate the etiology of PTOA because they do not use acute loads to initiate the onset of OA. This evidence concerns the gene TNF and rheumatoid arthritis.