PURPOSE: To review the current concepts on tendon damage and reactive oxygen species (ROS). We suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and from the tenocytes themselves. METHOD: A literature search was conducted to trace relevant literature on tendon damage and ROS. RESULTS: Tendinopathies have a complex aetiology. Tendon physiology and structure may preclude ROS involvement in various aspects of the predisposition to and participation in a failed healing response process and subsequent response to injury. However, given the ubiquitous nature of ROS production and their now accepted involvement in signal transduction, such highly active chemicals may influence signal transduction in the tendon. Therefore, the tendon is continually exposed to ROS during normal and athletic exercise which, in combination with lifestyle and possibly hereditary factors, may influence tendon integrity and orchestrate tendon repair. CONCLUSIONS: The production of ROS by tenocytes may be a response to hyperthermia and to repetitive ischaemia/reperfusion, and may influence the development of tendinopathies.

Oxygen species and overuse tendinopathy in athletes.

Oliva F;MAFFULLI, Nicola
2008

Abstract

PURPOSE: To review the current concepts on tendon damage and reactive oxygen species (ROS). We suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and from the tenocytes themselves. METHOD: A literature search was conducted to trace relevant literature on tendon damage and ROS. RESULTS: Tendinopathies have a complex aetiology. Tendon physiology and structure may preclude ROS involvement in various aspects of the predisposition to and participation in a failed healing response process and subsequent response to injury. However, given the ubiquitous nature of ROS production and their now accepted involvement in signal transduction, such highly active chemicals may influence signal transduction in the tendon. Therefore, the tendon is continually exposed to ROS during normal and athletic exercise which, in combination with lifestyle and possibly hereditary factors, may influence tendon integrity and orchestrate tendon repair. CONCLUSIONS: The production of ROS by tenocytes may be a response to hyperthermia and to repetitive ischaemia/reperfusion, and may influence the development of tendinopathies.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11386/4205678
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