Background
Rotator cuff tears have been reported to occur in > 50% of patients aged > 60 years [
1]. They cause chronic pain and severe dysfunction, leading to degenerative changes in the glenohumeral joint [
2,
3]. Excellent outcomes of arthroscopic rotator cuff repair for small and medium tears have been recently reported [
4,
5]. In contrast, large and massive rotator cuff tears are challenging for surgeons. Various surgical procedures, such as musculotendinous transfer [
6], autograft augmentation [
7], or synthetic materials [
8] are available for the repair of massive rotator cuff tears. However, retears have been a common complication after surgical repair of such tears. The retear rates have been reported to be 14–66% for large or massive tears [
9‐
13]. Shoulders without cuff retear had better function during daily activities and better range of motion than shoulders with retears [
3]. Retears are presumed to result from high tension and insufficient initial biological healing at the repair site [
14]. We have performed a single-row repair with graft augmentation of the fascia lata for large and massive rotator cuff tears to reduce tension at the tendon–bone repair site [
15]. However, its biological effect during the early healing period has not been clearly understood. The purpose of the study was to evaluate the biological efficacy of fascia lata augmentation during the early healing process of rotator cuff tears using a rabbit rotator cuff defect model.
Discussion
Repair site retear is a common complication of large or massive rotator cuff repairs. Several factors are considered as causes of retear, such as blood circulation disorder due to rotator cuff repair, rotator cuff degeneration, and rotator cuff retraction [
12,
19]. Furthermore, when the tear size increases, the traction force applied to the repaired site also increases, leading to weakness of initial fixation force and repaired cuff retear. Alternative therapies, such as tendon transfers, autografts, allografts, and synthetic materials, have been reported to reduce stress with the repair site after repair of massive rotator cuff tears.
We have performed fascia lata augmentation for large or massive rotator cuff tears [
15]. In a cadaveric model, rotator cuff repair with augmentation with a fascia lata patch significantly had less gap formation at the tendon–bone interface with cyclic loading compared with non-augmented repair, indicating the possibility of reducing the incidence of rotator cuff repair failure due to addition of the fascia lata patch [
20]. In our study, the mechanical strength of fascia lata augmentation was higher than that of the repaired group at 4 weeks postoperatively. Fascia lata augmentation has been suggested to provide the initial fixation strength of the repaired rotator cuff.
The main structural component of the tendon is type I collagen. However, in the early phase of tendon healing, type III collagen increases and gradually replaces type I collagen as the tissue matures. This process is essential for maintaining the structure and function of the tendon [
21,
22]. Hirose et al. found that a similar healing process occurs during the healing of rotator cuff tears. In the early phase of healing, repair tissue predominantly produces type III collagen, and type I collagen subsequently increases and replaces type III collagen [
23].
In a rat anterior cruciate ligament repair model, Mifune et al. showed that an increase in cellularity and angiogenesis was observed in augmented grafts compared with conventionally reconstructed grafts. Rat-specific type III collagen expression and biomechanical strength in augmented grafts were also significantly higher than that in the conventional reconstruction group [
24].
In the present study, picrosirius red staining was used to evaluate collagen fiber localization. In this method, the color of the collagen fiber changes depending on its thickness. As fiber thickness increases, the color changes from green to yellow to orange to red [
25]. Because type III collagen fibers are usually thinner than type I collagen fibers, type I and III collagen fibers are stained yellow and green, respectively. Picrosirius red staining revealed type I and III collagen expression in the enthesis. Type III collagen expression in the fascia lata augmentation group at 4 weeks postoperatively was higher than that in the reattachment group. The expression of type III collagen rapidly decreased in augmentation group at 8 weeks. In contrast, type I collagen expression in augmentation group at 4 weeks was higher than that in reattachment group.
Tendon maturation score of augmentation group was higher than that of reattachment group. These results suggested that fascia lata augmentation could stimulate type III collagen expression and type I collagen replacement and promote enthesis healing process in early phase. However, type I collagen expressions of both operative group at 4 and 8 weeks were lower than that of control group. The less expression of type I collagen in the operative group caused lower stiffness compared to the normal tendon.
Strong proteoglycan staining at the enthesis in the fascia lata augmentation group was observed, whereas less staining was observed in the control group in safranin O staining. Proteoglycan is a cartilage matrix produced by chondrocytes. Increased proteoglycan at the repaired enthesis has been reported to lead to increased chondrocytes at the enthesis [
26]. The anatomical structure of the enthesis consists of fibrocartilage with the following four zones: ligament substance, unmineralized fibrocartilage, mineralized fibrocartilage, and bone. Because the material properties of the special insertion zone are intermediate between the ligament and bone, a new cartilage transmits loads and decreases stress concentration at the attachment site [
18]. Leung et al. reported that new cartilage formation during the healing process was associated with the mechanical property of the tendon–bone interface [
27]. Fascia lata augmentation might promote fibrocartilage regeneration at the enthesis and contribute superior mechanical strength compared with the repair without augmentation.
Another possibility of the effectivity of fascia lata graft is its function as a scaffold. Decortication of the footprint was performed to stimulate the bone marrow after rotator cuff repair. Bone marrow stimulation is caused by the migration of bone marrow-derived mesenchymal stem cells (MSCs) [
28]. The presence of MSCs in the bone marrow provides a potential for differentiation into tendon tissues [
29]. We speculate that the fascia lata autograft over the repaired site might prevent MSCs to spread from the footprint.
The present study has several limitations. First, this rabbit model was an acute rotator cuff injury model. The animal models may differ from chronic human rotator cuff injury. Second, the anatomy between the rabbit shoulder and that of humans are different, and the short rotator cuff muscles of rabbits do not form a rotator cuff that is similar to humans. Third, because rabbits have a greater healing capacity than humans, the tendon–bone healing process in the rabbits progressed faster than that in humans.
In clinical situations, some problems such as hematoma, discomfort, and pain of donor site might be caused after graft harvest. However, Mihata et al. reported that they made autograft for arthroscopic superior capsule reconstruction (SCR) from fascia lata because the tissue is stiff enough to obtain superior shoulder stability after SCR, and no patients had any dysfunction with the harvest site at the final follow-up [
30]. Furthermore, autograft has no concern of an immune reaction, zoonosis, or foreign body reaction [
15].
The results from the present study suggest that fascia lata augmentation could stimulate biological healing and provide initial fixation strength of the repaired rotator cuff.