Handy way to beat clawed fingers
BriTiSh scientists have identified the cells that trigger a common hand condition, paving the way for new and more effective treatments. Some 2.6 million Britons have Dupuytren’s disease, an age-related condition in which the fingers curl in towards the palm.
it occurs when knots of scar tissue form in the palmar fascia, the thin layer of tissue that lies under the skin of the palm, making it tougher. These knots eventually link together to form a thick cord that pulls one or more fingers over towards the palm.
This can lead to ‘clawed’ fingers, making it difficult for people to carry out day-to-day activities, such as doing up buttons.
With no drugs to treat the disease and physiotherapy unable to release ‘clawed’ fingers, surgery — in which the knotted cords are removed under general anaesthetic — is the main treatment.
recovery, though, is lengthy (two weeks during which the hand is in a splint, followed by two months of physiotherapy). Moreover the condition recurs in up to half of cases because the diseased tissue simply grows back.
Surgery can also be risky if the diseased tissue is wrapped around nerves and arteries.
now scientists have found a specialised cell type only present in the diseased tissue, which they believe is responsible for the scarring that leads to the ‘knots’ developing in the first place.
These cells could now be the target of drug treatments for the disease in its earliest stages.
What causes Dupuytren’s isn’t known. as well as having a genetic component, studies suggest it is more common in people with diabetes. high blood sugar levels are known to damage blood vessels and one theory is that some of these damaged blood vessel cells break away and form scar tissue.
The first sign of the condition is thickening or pitting of the skin of the palm. in severe cases people can lose the use of all their fingers within two or three years.
Dr ross Dobie, a biologist at the University of Edinburgh and a researcher with the study, used single-cell rna sequencing to analyse the function of thousands of cells taken from diseased fascia from patients with Dupuytren’s and from healthy tissue — this revealed the specialised cell type in the diseased tissue. Further experiments on these cells revealed a protein on their surface was key to scar formation.
The researchers found they could stop the protein from working using monoclonal antibodies — man-made proteins that mimic the role of antibodies to fight diseases. This led to changes in the cells that should prevent them from producing scar tissue, the Journal of investigative Dermatology has reported. More studies are planned to learn how to stop the cells producing scar tissue.
‘Dupuytren’s is massively debilitating and we urgently need better treatments that can help slow, stop and prevent the problems that it causes,’ says Chris West, a consultant plastic surgeon at Leeds Teaching hospitals nhS Trust and co-author of the study.
neal Millar, a professor of orthopaedic surgery and musculoskeletal science at the University of Glasgow, adds: ‘These data are crucial in developing new targeted treatments to radically change the options available to patients suffering from Dupuytren’s.’