When tendons get irritating it can lead to a serious condition called tendinosis a common class; of sports and workplace injuries which is also common in older individuals. It can take many weeks of rest for tendon irritation to heal; with no treatments, save short-term steroid injections and surgery, followed by more rest. Key molecular components of injury, opening the possibility of targeting the pathways with pharmaceutical and other interventions.
Dr. McBeath and colleagues examined tendon samples from patients who underwent surgery for tendinosis and compared tendons from elderly versus young patients. Under normal oxygen levels, the tendon cells retained a normal shape and flexibility. But when those cells grown in low-oxygen levels; mimicking the low-oxygen environment common in older people, the tendon cells changed shape and became round and more similar to tough cartilage-like cells, called fibrocartilage.
The Activity of a signaling molecule
When oxygen was low, the aged tendon cells reducing the activity of a signaling molecule called Rac1. Rac1 is in many cellular processes, including those governing cell shape, movement, and growth. With reduced Rac1, the tendon cells began to change shape; but only in low-oxygen conditions. When the researchers blocked Rac1 activity in high-oxygen conditions, tendon cells able to retain their normal shape.
The power of this study is that the results are faithfully describing the processes that occur in human tendon injury, rather than working from an animal model, says Irving Shapiro, Ph.D., Vice-Chair, Basic Science Research in Orthopedic Surgery at Jefferson. “With permission from patients; they examined human tendon tissue that was normally discarded during surgery. Analyzing human tissue provides an optimum approach to understanding events that occur during disease development.
Regrowing fibrocartilage tissue
The research also has implications for other common degenerative orthopedic diseases; where spurring cells to become fibrocartilage could equally useful. “Currently they have no way to regrow fibrocartilage tissue,” says Dr. McBeath, “so when that tissue, which keeps bones from rubbing against each other, is damaged in the knee, hip, or spine, it can cause severe pain and result in the need for joint replacement.”
“Now that we understand when and how tendon cells change shape, they might able to manipulate them to retain tendon qualities, turn them into fibrocartilage to replace what’s missing. And before they can apply these ideas in patients, they need to do more work in cell and animal models to understand how these pathways work and how to manipulate them.”