Extracellular Matrix Protection Factor-1 Treatment in a Rat Model of Osteoarthritis Slows the Progress of Cartilage and Bone Destruction Associated with the Pathology
Location
Philadelphia Campus
Start Date
7-5-2014 1:00 PM
Description
Osteoarthritis (OA) is a disease of the joints caused by an imbalance between extracellular matrix destruction and production. We have developed an innovative disease modifying therapeutic technology to treat OA. Extracellular matrix protection factor (ECPF-1) is a novel, safe and effective intra-articular injection effective in alleviating tissue pathology associated with OA. Knees of rats in an OA model were treated with ECPF-1 peptide or BMP-7 protein as a control because BMP-7 has been shown to be chondroprotective in a rabbit model of OA. Micro computed tomography (uCT) indicates the amount of bone volume present in the samples and the areas of mineralization. Since healthy cartilage is not normally mineralized, one would expect a low bone volume in these samples and a higher bone volume in cartilage of OA. ECPF-1 treated OA joints contained the lowest bone volume after four weekly injections of peptide. Trabecular thickness indicates the strength of the bone, and the ECPF-1 treated animals had the best trabecular thickness numbers following 4 weekly injections of peptide. This data provides critical proof of concept that ECPF-1 acts as a disease modifying therapeutic in a rat model of OA. This work was supported in part by intramural funding.
Extracellular Matrix Protection Factor-1 Treatment in a Rat Model of Osteoarthritis Slows the Progress of Cartilage and Bone Destruction Associated with the Pathology
Philadelphia Campus
Osteoarthritis (OA) is a disease of the joints caused by an imbalance between extracellular matrix destruction and production. We have developed an innovative disease modifying therapeutic technology to treat OA. Extracellular matrix protection factor (ECPF-1) is a novel, safe and effective intra-articular injection effective in alleviating tissue pathology associated with OA. Knees of rats in an OA model were treated with ECPF-1 peptide or BMP-7 protein as a control because BMP-7 has been shown to be chondroprotective in a rabbit model of OA. Micro computed tomography (uCT) indicates the amount of bone volume present in the samples and the areas of mineralization. Since healthy cartilage is not normally mineralized, one would expect a low bone volume in these samples and a higher bone volume in cartilage of OA. ECPF-1 treated OA joints contained the lowest bone volume after four weekly injections of peptide. Trabecular thickness indicates the strength of the bone, and the ECPF-1 treated animals had the best trabecular thickness numbers following 4 weekly injections of peptide. This data provides critical proof of concept that ECPF-1 acts as a disease modifying therapeutic in a rat model of OA. This work was supported in part by intramural funding.