OBJECTIVE: The infrapatellar fat pad (IPFP) has been identified as a source of anterior knee pain. Fibrosis and marked inflammatory infiltrate in the IPFP of patients with arthritis of the knee and reduction in pain post knee replacement in patients following resection of the IPFP have been observed. We have investigated changes in the IPFP of rats undergoing the monoiodoacetate (MIA) model of degenerative joint disease, a model that exhibits some histopathological similarities to osteoarthritis (OA). METHODS: Rats were injected intra-articularly with MIA and the development of weight bearing asymmetry was followed for 21 days as compared to vehicle-injected animals. In addition, IPFPs were removed from both ipsilateral and contralateral joints. Both inflammatory infiltrate and histopathological changes were analysed. RESULTS: MIA injection caused marked weight bearing asymmetry. Ipsilateral IPFP wet weights were significantly increased on days 1 and 3 in MIA-treated animals. MIA treatment also resulted in significant increases in IPFP total white blood cells and monocytes on days 1, 3, and 7 and neutrophils on days 1 and 3. This was supported by histopathological findings at early time points which progressed to adipocyte necrosis, IPFP fibrosis, patellar cartilage and subchondral bone necrosis with synovial hyperplasia at later timepoints. CONCLUSIONS: The current study clearly demonstrated that marked inflammatory changes in the IPFP occur during the early stage of the MIA model of OA which may contribute to the pain observed at this early stage. The role of the IPFP in later stages of the model needs to be further explored.
OBJECTIVE: The infrapatellar fat pad (IPFP) has been identified as a source of anterior knee pain. Fibrosis and marked inflammatory infiltrate in the IPFP of patients with arthritis of the knee and reduction in pain post knee replacement in patients following resection of the IPFP have been observed. We have investigated changes in the IPFP of rats undergoing the monoiodoacetate (MIA) model of degenerative joint disease, a model that exhibits some histopathological similarities to osteoarthritis (OA). METHODS:Rats were injected intra-articularly with MIA and the development of weight bearing asymmetry was followed for 21 days as compared to vehicle-injected animals. In addition, IPFPs were removed from both ipsilateral and contralateral joints. Both inflammatory infiltrate and histopathological changes were analysed. RESULTS: MIA injection caused marked weight bearing asymmetry. Ipsilateral IPFP wet weights were significantly increased on days 1 and 3 in MIA-treated animals. MIA treatment also resulted in significant increases in IPFP total white blood cells and monocytes on days 1, 3, and 7 and neutrophils on days 1 and 3. This was supported by histopathological findings at early time points which progressed to adipocyte necrosis, IPFP fibrosis, patellar cartilage and subchondral bone necrosis with synovial hyperplasia at later timepoints. CONCLUSIONS: The current study clearly demonstrated that marked inflammatory changes in the IPFP occur during the early stage of the MIA model of OA which may contribute to the pain observed at this early stage. The role of the IPFP in later stages of the model needs to be further explored.
Authors: Nathan M Solbak; Bryan J Heard; Yamini Achari; May Chung; Nigel G Shrive; Cyril B Frank; David A Hart Journal: Inflamm Res Date: 2015-06-20 Impact factor: 4.575