Australian scientists have identified a specific type of stem cell they believe to be responsible for the progression of osteoarthritis – a degenerative joint disease caused by tissues in the body’s joints wearing down over time.
The researchers from the University of Adelaide ‘believe this finding may provide new avenues for treatment and even reversal of the disease’ (the most common type of arthritis), reported medicalnewstoday.com.
Their study, published in Nature Communications, found loss of a specific type of stem cell is responsible for the progression of osteoarthritis, via a mouse model. They say this finding may provide new avenues for treatment and even reversal of the disease – and ‘challenges the idea of osteoarthritis just being a ‘wear-and-tear’ condition’.
Co-lead author Dr Jia Ng commented: ‘Most treatments for osteoarthritis concentrate on treating the symptoms and improving the quality of life instead of targeting the disease, which leads ultimately to joint replacement surgery. This inevitable prospect also significantly impacts a patient’s mental health.’
She added: ‘The original concept of osteoarthritis being a ‘wear-and-tear’ condition implies the disease itself may not have pharmacological intervention to treat it and reverse the pathology. Wear-and-tear indicates progression of the disease is a matter of time and inevitable.
‘By reimagining the disease, we provide an opportunity and, more importantly, a pharmaceutical target for the medical community to discover new drugs to reverse and treat osteoarthritis.’
Using a mouse model of osteoarthritis, her team identified a specific population of stem cells marked by the Gremlin 1 gene (a family of bone morphogenic protein which has a role in regulating organogenesis, body patterning and tissue differentiation) that they believe are responsible for the progression of osteoarthritis.
They found treatment with fibroblast growth factor 18 (FGF18) vitalised the rapid production of Grem1 cells in the joint cartilage of mice, which led to ‘a significant recovery of cartilage thickness and reduced osteoarthritis’.
Dr Ng added: ‘This opens the door to other pharmaceutical options beyond FGF18.’
