BIOLOGY OF THE ROTATOR CUFF TENDON

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STRUCTURE AND BIOLOGY OF TENDONS

Tendons are a complex composite material composed primarily of water (∼55% of wet weight) and type I collagen (∼85% of dry weight), along with lesser amounts of other collagens, proteoglycans, and cells. The molecular and macromolecular structure is organized to facilitate transmission of tensile loads from muscle to bone. Although many aspects of tendon biology have been known for a long time (e.g., triple helical arrangement of polypeptides in the type I collagen molecule), very basic aspects

STRUCTURE AND BIOLOGY OF ROTATOR CUFF TENDONS

Rotator cuff tendons have not been studied as extensively and are not as wellcharacterized as flexor tendons. Investigations have demonstrated that several aspects of the structure and biology of rotator cuff tendons are unique. These characteristics undoubtedly reflect the rotator cuff's unique function of stabilizing and assisting in motion of the most mobile and unstable joint in the body.

Mechanisms of Injury

The underlying mechanisms by which the rotator cuff tendons become injured have been a subject of debate for some time.34 Extrinsic and intrinsic mechanisms of injury have been described. Extrinsic mechanisms include macrotrauma (e.g., a fall onto the shoulder), repetitive microtrauma (e.g., pitching), primary subacromial impingement (due to variations in acromial morphology), secondary impingement (due to kinematic abnormalities), and internal impingement (undersurface of the cuff against

CONCLUSIONS

Techniques developed in the disciplines of biochemistry and molecular biology are opening up important new areas of research into the biology of rotator cuff tendon injury and repair. Information from this research, as well as from biomechanical investigations, will help clinicians develop and refine therapeutic interventions for rotator cuff disease. These are exciting times for orthopedic surgeons and scientists interested in the rotator cuff.

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      The inclusion of PCL microfibers can increase the roughness of the 3D-printed frame and provide an aligned topography. The diameter of the PCL microfiber is around 30 µm, which is similar to the diameter of type I collagen fiber in the rotator cuff tendon [57]. For the mechanical properties of the frames, Fig. 2I illustrates the representative force-displacement curves of the one-layer or double-layer frames with or without direct writing microfibers.

    • Preoperative tendon retraction, not smoking, is a risk factor for failure with continuity after rotator cuff repair

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      With national smoking rates of 17%, it is important to understand the potential effects of smoking on patients undergoing arthroscopic rotator cuff repair (RCR).5 The lateral edge of the rotator cuff tendon is relatively hypovascular, which is made worse by poorer blood supply in chronically torn tendons with myxoid changes.6,7 Nicotine, a key component of cigarettes, is a potent vasoconstrictor and is thought to further impair the tenuous blood supply to the rotator cuff.8

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      While extrinsic factors include mechanical stress from impingement, intrinsic factors arise from biologic alterations of the tendon itself. The degeneration of collagen structures in degenerative rotator cuff tears has been observed extensively in histopathological research [1–4]. The decay of tendon tissue is promoted by subacromial inflammation which has been linked to degenerative rotator cuff tears by multiple studies demonstrating an increase of IL-1, IL6, TNF-alpha, matrix-metallo proteases and cyclooxygenases [5–8].

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      However, tendon detachment remains the primary cause of surgical failure, as the restoration of the native tendon-bone insertion is not adequately achieved. Like the ACL, tendons insert into subchondral bone through a fibrocartilage transition or direct insertion [21,22,32]. Focusing on this fibrocartilaginous interface, Moffat et al. designed a biphasic interface scaffold consisting of contiguous layers of aligned PLGA and PLGA-HA nanofibers joined via electrospinning, which are intended to mimic the non-calcified and calcified fibrocartilage regions, respectively [33].

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    Address reprint requests to Field T. Blevins, MD, Department of Orthopaedics, University of New Mexico Medical Center, 2211 Lomas NE, Albuquerque, NM 87131

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