Knee joint injuries are typically related to sports, such as football, rugby or ice hockey, but people often do not know that such injuries may lead to joint inflammation and post-traumatic osteoarthritis. In advanced post-traumatic osteoarthritis, joint cartilage breaks down completely, causing severe joint pain, lack of mobility and even social isolation. However, the mechanisms leading to osteoarthritis are not known.
Currently, it is not possible for a physician examining a patient to predict future joint condition and possible development of osteoarthritis. In the future, however, this may be possible, as a new study from the University of Eastern Finland and Massachusetts Institute of Technology now shows that articular cartilage degenerates specifically around injury areas when the fluid flow velocity becomes excessive. The findings were reported in Scientific Reports.
The study presents a new mechanobiological model for cartilage degeneration by implementing tissue deformation and fluid flow as mechanisms for cartilage breakdown when a normal dynamic loading, such as walking, is applied to the joint. The results were compared to experimentally observed degradation of articular cartilage. Ultimately, the new model could be used to predict osteoarthritis in personal medicine, to suggest optimal rehabilitation protocols, and to improve the quality of life.
The researchers found that different mechanisms, such as fluid flow and tissue deformation, can cause cartilage degradation after a knee injury. The results obtained using the novel algorithm agreed well with the experimentally observed proteoglycan content and cell death in cartilage samples. According to the researchers, a numerical analysis shows that both fluid flow and tissue deformation are plausible mechanisms leading to osteoarthritis, but increased fluid flow from cartilage seems to be better in line with the experiments.
“Our findings indicate that after an injury in the knee and subsequent tissue loading, osteoarthritis is caused by easy leakage of proteoglycans through the injury surface by high fluid outflow,” says Gustavo A. Orozco from the University of Eastern Finland.
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