The Effects of Autologous Fat Transfer in an In Vitro Model of Basal Joint Osteoarthritis

Basal joint osteoarthritis (OA) is a highly prevalent and debilitating condition. Recent clinical evidence suggests that autologous fat transfer (AFT) may be a promising, minimally invasive treatment for this condition. However, the mechanism of action is not fully understood. It is theorized that AFT reduces inflammation in the joint, functions to regenerate cartilage, or acts as a mechanical buffer. The purpose of this study was to better understand the underlying mechanism of AFT using an in vitro model. We hypothesize that the addition of stromal vascular fraction (SVF) cells will cause a reduction in markers of inflammation. Articular chondrocytes were expanded in culture. Liposuction samples were collected from human subjects and processed similarly to AFT protocols to isolate SVF rich in adipose-derived stem cells. A control group was treated with standard growth media, and a positive control group (OA group) was treated with inflammatory cytokines. To mimic AFT, experimental groups received inflammatory cytokines and either a low or high dose of SVF. Expression of relevant genes was measured, including interleukin (IL)-1ß, IL-1 receptor antagonist, and matrix metalloproteinases (MMP). Compared to the OA group, significant decreases in IL-1ß, MMP3, and MMP13 expression on treatment day 3 were found in the high-dose SVF group, while MMP13 expression was also significantly decreased in the low-dose SVF group on day 3. In this study, we found that SVF treatment reduced expression of IL-1ß, MMP3, and MMP13 in an in vitro model of OA. These results suggest that an anti-inflammatory mechanism may be responsible for the clinical effects seen with AFT in the treatment of basal joint OA. An anti-inflammatory mechanism may be responsible for the clinical benefits seen with AFT for basal joint arthritis.