PhD Fellow Moustafa Hamada

After traumatic injuries, the knee joint is at a greater risk of developing post-traumatic osteoarthritis (PTOA). A major concern is usually devoted to the articular cartilage, given its likely irreversible degradation after the injury. A comprehensive understanding of the early-phase structural and compositional cartilage changes that arise after injury is critical for gathering insights into the underlying biomechanical and biochemical disease mechanisms. In this project, Moustafa aims to understand better the separate and combined role of biomechanical and biochemical degradation factors promoting the progression of cartilage tissue damage and degradation.

To achieve this goal, he establishes experimental in vitro PTOA models of PTOA to mimic the early biomechanical (i.e., abnormal physiological loading) and biochemical (i.e., inflammatory challenge) factors that could influence the onset of PTOA. In such models, cartilage explants of young bovine knee joints are harvested and subjected to these factors separately and in combination. Next, tissue- and cell-level measurements will investigate location- and time-dependent biochemical changes (e.g., collagen and proteoglycan content, cell viability, reactive oxidative species production) and tissue mechanical responses (e.g., regional shear strain in compressed cartilage measured with phase-contrast synchrotron x-ray tomography).

Through such experiments, understanding the mechanistic link between the mechanical (such as level of shear strain)/biochemical (inflammation) and compositional changes will be crucial to find reliable markers for early disease progression.

The general outcome of this work will be critical as a step forward to endorse our understanding of the early disease progression, which could extend our frontiers for effective interventions of PTOA. Additionally, the obtained experimental data will validate computational tissue-level models developed in the biophysics group at the University of Eastern Finland.