New insights into tendon injury
Susan H. Taylor, Sarah Al-Youha, Tom Van Agtmael, Yinhui Lu, Jason Wong, Duncan A. McGrouther, Karl E. Kadler. (2011). Tendon Is Covered by a Basement Membrane Epithelium That Is Required for Cell Retention and the Prevention of Adhesion Formation. PLoS One, 6:e16337. PLoS
As a result of surgery or injury our organs may become damaged, causing internal bleeding and clotting. As the organ heals, cells move into the blood clot which is gradually replaced by unwanted fibrous tissue known as an ‘adhesion’. Adhesions cause organs to stick together. This is extremely painful and distressing for the patient and often requires more surgery and rehabilitation. Adhesions are also a common problem when the tendons become injured by sharp objects such as glass or by overuse in sporting activities. Scientists in the Wellcome Trust Centre for Cell-Matrix Research at the University of Manchester have studied tendons and discovered how the adhesions are formed.
Tendons attach our muscles to bone and are essential for movement. To perform this function, tendons must be able to move freely. When an adhesion forms movement of the tendon is restricted. This produces pain, stiffness and reduced mobility. If the affected tendons are in the hand this makes even the simplest of tasks very difficult. The estimated cost of treating and managing adhesion related problems ~£100m each year.
To understand how tendon adhesions form, scientists in Prof. Karl Kadler’s lab studied the surface of tendons. They reasoned that the surface of the tendon must contain a special cell that stops adhesions from forming in healthy people. Dr. Susan Taylor discovered that the tendon is covered by a thin layer of epithelial cells. These cells are usually found in skin, so effectively the tendon is covered by a thin skin that protects it from damage. Undamaged tendons do not form adhesions, however, when the tendon ‘skin’ is damaged, the cells inside the tendon make the unwanted adhesions. These cells gradually make the tendon stick to nearby tissues.
In collaboration with scientists from Glasgow University, Kadler’s group showed that mice with defective cells at the surface of their tendons appear to have difficulty walking. They also spontaneously develop tendon adhesions, even in the absence of surgery or injury.
The work described in this paper shows that the integrity of the surface of a tissue is critical in preventing adhesions. Furthermore, the discovery of this completely new layer of tendon cells changes the way we are thinking about how tendons are made during embryonic development and maintained in adulthood. Future research is aimed at finding ways of protecting the tendon epithelium and thus preventing debilitating adhesions particularly in patients with tendon injuries and athletes.
Susan H. Taylor