| dc.description.abstract | The various forms of joint loading have been found to differentially influence anatomical and molecular responses, which together are
aimed to maintain the joint homeostasis. To elucidate these mechanisms of mechanotransduction, we review the roles of the distinct joint
components, as well as numerous in vitro studies that have been performed to unravel chondrocyte responses in changing environments.
The main signalling pathways in transduction of load signals are initiated by integrins sensing matrix deformation and by altered interstitial
pH, influencing ion fluxes through membrane channels. Downstream signalling after static compression occurs mainly via the MAPK
pathways of ERK1/2, SAPK (Jnk) and p38, which directly influence transcription factors of genes involved in cartilage breakdown. In
contrast, cyclic compression and mild shear forces lead to membrane hyperpolarisation and subsequently stimulates cartilage matrix
synthesis. These findings add further comprehension with regard to the satisfactory clinical outcomes of joint distraction in osteoarthritic
(OA) joints. It has been shown that these joints contained repaired cartilage after treatment in animal models. Using improved in vivo
models in further research would allow a more thorough understanding of the underlying molecular processes of this reparative capacity of
damaged cartilage, which could lead to improved arthropathy treatment options. | |
