Mechanisms of tendon injury and repair

Abstract

Tendon disorders are common and lead to significant disability, pain, healthcare cost, and lost productivity. A wide range of injury mechanisms exist leading to tendinopathy or tendon rupture. Tears can occur in healthy tendons that are acutely overloaded (e.g., during a high speed or high impact event) or lacerated (e.g., a knife injury). Tendinitis or tendinosis can occur in tendons exposed to overuse conditions (e.g., an elite swimmer's training regimen) or intrinsic tissue degeneration (e.g., age-related degeneration). The healing potential of a torn or pathologic tendon varies depending on anatomic location (e.g., Achilles vs. rotator cuff) and local environment (e.g., intrasynovial vs. extrasynovial). Although healing occurs to varying degrees, in general healing of repaired tendons follows the typical wound healing course, including an early inflammatory phase, followed by proliferative and remodeling phases. Numerous treatment approaches have been attempted to improve tendon healing, including growth factor- and cell-based therapies and rehabilitation protocols. This review will describe the current state of knowledge of injury and repair of the three most common tendinopathies--flexor tendon lacerations, Achilles tendon rupture, and rotator cuff disorders--with a particular focus on the use of animal models for understanding tendon healing.

Keywords: animal models; healing; inflammation; tendinopathy.

Figure 1

(a) Macrophages can differentiate into specific subpopulations with distinct phenotypes and functions. (b) In acute inflammation, macrophage phenotypes such as M2 and Mreg are usually beneficial for immunosuppression, scar resolution, and remodeling. In chronic inflammation, macrophage phenotypes such as M2 and M2a can stimulate excessive tissue remodeling resulting in fibrosis. [Reproduced, with permission, from ]

Figure 2

To achieve effective healing, a balance must be reached between loads that are too low (leading to increased adhesions, retarded repair tissue maturation, and/or joint stiffness) and loads that are too high (leading to repair site gapping or rupture).