26 August 2020

Cartilage regeneration in vivo

In laboratory studies, scientists managed to restore cartilage tissue inside the joint

Marina Astvatsaturyan, Echo of Moscow

Researchers from Stanford University (Stanford University School of Medicine) caused the regeneration of articular cartilage cushion in experimental mice and published an article about it in the journal Nature Medicine (Murphy et al., Articular cartage regeneration by activated skeletal stem cells).

"In adulthood, the ability of cartilage tissue to regenerate is almost zero, and if it is damaged or degraded, our ability to do something for the patient is very limited ..., and therefore finding a way to help the body restore this important tissue is extremely gratifying," says one of the authors of the study, associate professor at Stanford University Charles K.F. Chan).

The work being published now is based on a previous study by the same authors, in which the development of skeletal stem cells was studied. These are self-renewing cells responsible for the formation of bone and cartilage tissues, as well as the production of cells of a special type that contribute to the transformation of blood cells into bone marrow.

Articular cartilage is a complex and specialized tissue from which an elastic "cushion" with a sliding surface is formed inside the joint between the bones. If it is damaged as a result of injury or simply becomes thinner with age, the bones begin to rub against each other, which causes not only painful sensations and inflammation, but also leads eventually to arthritis.

There is a way to treat damaged articular cartilage by creating micro–injuries - tiny holes are made on the surface of the joint and this stimulates the body to create new articular cartilage tissue. But such a new tissue is not quite cartilage, it is the so-called fibrocartilage, more like scar tissue and does not have the elasticity and elasticity of natural cartilage, moreover, it degrades relatively quickly, explains Chan.

To improve the process, scientists decided to try to divert stem cells from the path of transformation into fibrocartilage. First, they used a molecule called bone morphogenetic protein 2 (BMP2) to initiate the formation of bone tissue after micro–injuries, and then stopped the process halfway with a molecule that blocks another signaling molecule important for bone formation, namely vascular endothelial growth factor (VEGF).

As a result, cells similar to the cells of natural cartilage tissue were formed. Osteoratric mice, which were injected with these signaling molecules after micro-injuries of the joints, began to move normally. In another series of experiments, human bone stem cells were injected into mouse joints, which, thanks to the same molecules, turned into normal cartilage tissue. 

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