Rotator Cuff Injury: Pathogenesis, Biomechanics, and Repair

Abstract

Anterior Rotator cuff tears are one of the most common surgically addressed disorders, as the tears in the tendon can affect anyone regardless of risk factors or activity level. The rotator cuff is responsible for most of the shoulder motion, hence the tendon-bone interface experiences immense stress making it incredibly prone to failure. Rotator cuff tendon tears can either occur due to trauma or natural degeneration of the rotator cuff. To help mitigate effects of high stress on the rotator cuff tendon-bone interface, the rotator cuff is intrinsically designed to redistribute stress through protective mechanisms, such as the rotator crescent or coronal-transverse force. But when the tear goes through the intrinsic protective mechanisms, the glenohumeral joint is left unstable and thus is no longer capable of its normal range of motion. Location, size, and type of rotator cuff tendon tears are the strongest indicators for interventional therapy. Surgical therapies demonstrate low success rates, as seen by the significantly high recurrence rate of rotator cuff reinjury following initial repair. This is due to extrinsically healing of rotator cuff tendons, instead of the more intrinsic healing, which causes rotator cuff tendons to not undergo the necessary biomechanical remodeling to prevent reinjury leading to a mechanically and functionally inferior healed tendon. In this article, we thoroughly discussed the underlying pathophysiology of rotator cuff tears from onset to repair to healing, demonstrating that rotator cuff tendon healing is an intrinsically flawed process, irrespective of the risk factors, occurrence of rotator cuff tears, or surgical treatment. Rotator cuff healing can only be successful if rotator cuff tendon repair surgery is augmented with biologics to promote a successful intrinsic healing environment.

Keywords: Biomechanics; Inflammation; Infraspinatus tendon; Rotator cuff injury; Rotator cuff repair; Supraspinatus tendon; Tendinopathy.

Figure 1:

Coronal Force Couple showing opposite force relationship between the deltoid muscle and subscapularis-infraspinatus-teres minor muscles.

Figure 2:

Transverse Force Couple showing opposite force relationship to maintain downward stability through the motions of subscapularis and infraspinatus-teres minor.

Figure 3:

Presentation of Asymptomatic and Symptomatic Rotator Cuff Injury, underlying Pathology, and Clinical Intervention.

Figure 4:

Schematic diagram showing Rotator Cable-Rotator Crescent Relationship. The margin of the rotator crescent has thick bundles of rotator cable fibers. SS = Supraspinatus, IS = Infraspinatus, TM = Teres Minor.

Figure 5:

Schematic diagram showing Rotator Bridge Analogy to Suspension Bridge. (a) light blue shaded region = rotator crescent, dark blue line = rotator cable, light blue line = main towers of suspension bridge running in direction of muscle belly, (b) When supraspinatus and infraspinatus tendons are mechanically strained at the bone tendon interface, there is a high chance a rotator cuff tear will occur due to the plastic deformation of the tendon and rotator crescent. The rotator cable prevents this by redistributing the stress (red arrow) from the strained bone-tendon interface to the muscle belly of infraspinatus and supraspinatus. (c) If there is complete damage to either supraspinatus or infraspinatus tendons, then the rotator cable is rendered useless as there is no longer a redistribution of mechanical forces through the rotator cable into the respective muscle belly. The rotator cuff is now unstable as seen by the direction of forces (red arrow) in the torn infraspinatus.

Figure 6:

Stress/Strain Curve for Tendon. At rest, collagen fibers exist in a crimped configuration. Toe region, 0 - 2%, the collagen fibers begin to straighten. Linear region, 2 - 4%, the crimp pattern disappears, and the collagen fibers are straightened. 4% strain and below marks elastic deformation in which the tendon can still return to its original shape. Yield strength is at 4%. Strains above 4% mark the start of plastic deformation, where the tendon will undergo microscopic or macroscopic damage and can no longer return to its original shape when load is removed. 10% strain marks the fracture point and any strain beyond 10% will result in tendon rupture.