Cell phenotypic variation in normal and damaged tendons.
Injuries to tendons are common in both human athletes as well as in animals, such as the horse, which are used for competitive purposes. Furthermore, such injuries are also increasing in prevalence in the ageing, sedentary population. Tendon diseases often respond poorly to treatment and require lengthy periods of rehabilitation. The tendon has a unique extracellular matrix, which has developed to withstand the mechanical demands of such tensile-load bearing structures. Following injury, any repair process is inadequate and results in tissue that is distinct from original tendon tissue. There is growing evidence for the key role of the tendon cell (tenocyte) in both the normal physiological homeostasis and regulation of the tendon matrix and the pathological derangements that occur in disease. In particular, the tenocyte is considered to have a major role in effecting the subclinical matrix degeneration that is thought to occur prior to clinical disease, as well as in the severe degradative events that occur in the tendon at the onset of clinical disease. Furthermore, the tenocyte is likely to have a central role in the production of the biologically inadequate fibrocartilaginous repair tissue that develops subsequent to tendinopathy. Understanding the biology of the tenocyte is central to the development of appropriate interventions and drug therapies that will either prevent the onset of disease, or lead to more rapid and appropriate repair of injured tendon. Central to this is a full understanding of the proteolytic response in the tendon in disease by such enzymes as metalloproteinases, as well as the control of the inappropriate fibrocartilaginous differentiation. Finally, it is important that we understand the role of both intrinsic and extrinsic cellular elements in the repair process in the tendon subsequent to injury.
Clegg
Peter D
PD
Department of Veterinary Clinical Science, University of Liverpool Veterinary Teaching Hospital, Leahurst, Neston, UK. p.d.clegg@liverpool.ac.uk
Strassburg
Sandra
S
Smith
Roger K
RK
D000818:Animals; D002454:Cell Differentiation; D019902:Chondrocytes / Q000502:physiology; D006734:Horse Diseases / Q000201:enzymology / Q000473:pathology; D006736:Horses; D006801:Humans; D010447:Peptide Hydrolases / Q000502:physiology; D052256:Tendinopathy / Q000201:enzymology / Q000473:pathology* / Q000662:veterinary; D013710:Tendons / Q000166:cytology* / Q000473:pathology
D010447:Peptide Hydrolases
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