Cobalt ions from some orthopaedic implants induce a dose-dependent cytotoxic and pro-inflammatory response. However, this new paper from Prof Knight and Prof Shelton's groups shows that low levels of cobalt are in fact beneficial and block pro-inflammatory signalling in cartilage.
The authors showed that sub-toxic levels of cobalt (50uM) prevented the action of the pro-inflammatory cytokine, interleukin-1 beta (IL-1B), and that this stopped the degradation of the cartilage extracellular matrix and the resulting loss of biomechanical properties that is observed in arthritis. The effect of cobalt was associated with modulation of tiny cellular structures, known as the primary cilia, which Knight's group have shown to be involved in pro-inflammatory signalling.

These observations provide new insight into the interaction between orthopaedic implants and the body. Furthermore, understanding the potential beneficial role of cobalt and the mechanism through which this occurs may lead to novel therapies for controlling cartilage inflammation and arthritis.

The experimental work was led by Su Fu, who recently completed his PhD in Prof Knight's group funded by a grant from the China Scholarship Council. In addition the project was supported by two medical students, Fran Freer and Chloe Kwon, who completed their intercallated BSc biomedical engineering project in Prof Knight's lab.

The paper was published in a special issue of the Journal of Biomechanics.

Updated by: Martin Knight