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BME PhD Proposal Seminar: Sara Nowacki

Tuesday, April 29, 2014
2:00 p.m.
MC 2-6408 (K-207)

"Parathyroid Hormone (1-34) in Conjunction with Cartilage-Derived Matrices as a Potential Treatment Method for Articular Cartilage Defects"

Supervised by Professor Hani Awad


Current articular cartilage defect treatments result in a compositionally and mechanically inferior cartilage tissue termed fibrocartilage. Fibrocartilage is detrimental as the stiffness mismatch and lack of integration with surrounding cartilage alters joint biomechanics during articulation, resulting in accelerated catabolic cartilage degradation. This leads to osteoarthritis (OA), an irreversibly degenerative disease that affects 27 million Americans with an annual cost of $89.1 billion.

The clinical gold standard treatment for articular cartilage defects is microfracture. Upon microfracture, mesenchymal stem cells (MSC) infiltrate the defect site and proliferate, leading to secretion of the primary extracellular matrix (ECM) components of cartilage - glycosaminoglycans and type II collagen. Short-term, microfracture improves knee functionality, however long-term the incidence of OA increases due to poor integration and chondrocyte hypertrophy. This indicates a clinical need for a treatment method that results in long-term maintenance of resultant articular cartilage tissue, reducing the need for potential revision surgery thus improving patient quality of life.

Matrices derived from natural or synthetic materials offer an alternative for cartilage repair. Results from microfracture in a rabbit osteochondral defect combined with an implanted cartilage-derived matrix (CDM) developed in our lab indicates that the CDM induced and maintained MSC chondrogenic differentiation up to 16 weeks post-surgery, however with incomplete integration. PTH(1-34) has recently been linked to chondroregeneration and suppression of chondrocyte hypertrophy in OA. We believe the CDM in conjunction with PTH(1-34) has exciting potential for repair of articular cartilage defects. In this proposal, we will utilize PTH(1-34) as an adjuvant to CDM and explore how it modulates chondroregeneration in vitro and in a rabbit osteochondral defect model. Our global hypothesis is this dual-treatment method with microfracture will result in neocartilage recapitulating the compositional and biomechanical properties of native cartilage with complete integration to surrounding healthy cartilage tissue.