Recurrent tears after rotator cuff repair are common. Postoperative rehabilitation after rotator cuff repair is a modifiable factor controlled by the surgeon that can affect re-tear rates. Some surgeons prefer early mobilization after rotator cuff repair, whereas others prefer a period of immobilization to protect the repair site. The tendon-healing process incorporates biochemical and biomechanical responses to mechanical loading. Healing can be optimized with controlled loading. Complete load removal and chronic overload can be deleterious to the process. Several randomized clinical studies have also characterized the role of postoperative mobilization after rotator cuff repair.
Key points
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Tendon is a mechanically sensitive tissue. Biochemical and biomechanical properties of the repair site are altered by mechanical load.
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Tendon-to-bone healing likely responds best to controlled loading. Complete removal of load may understimulate the healing process, while excessive loading can cause microtrauma, gap formation, and repair failure.
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Clinically, numerous randomized controlled trials have shown no difference in healing rates between early mobilization and delayed rehabilitation protocols.
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In the early postoperative period, range of motion and function may be better with early mobilization compared with delayed rehabilitation. However, this benefit is transient, and there is no difference 1 year after surgery.
Introduction
The rate of rotator cuff tears is high in the increasingly aging population, and rotator cuff repair has become one of the most commonly performed orthopedic procedures. However, re-tear rates after rotator cuff repair is reported to be around 20% and even greater than 90% in massive tears. Age, tear size, and chronicity are all important factors affecting healing rates after repair but are inherent to the patient and disease. Two important and modifiable factors that the surgeon can control are the surgical technique and the postoperative rehabilitation protocol. There is an abundance of literature concerning surgical approach and techniques for rotator cuff repair. Unfortunately, despite advances in both techniques and technology, the rate of recurrent tearing after rotator cuff repair remains substantial. Surgeons may potentially improve outcomes after rotator cuff repair by controlling and optimizing the mechanical environment after rotator cuff repair, but until recently, literature regarding postoperative rehabilitation and mobilization was relatively scarce.
There is significant variation in the postoperative rehabilitation for patients undergoing rotator cuff repair. Some surgeons may choose to immobilize the shoulder for a period of time after surgery. Immobilization protects the repair site from excessive force that may damage the repair construct and lead to early failure. This approach, however, risks increased postoperative shoulder stiffness and decreased shoulder function. Other surgeons prefer to mobilize early in order to improve early shoulder function. Early mobilization may potentially put the repair construct and tendon-to-bone healing potential at risk.
In the past decade, in vitro studies, animal studies, and clinical investigations have helped to guide the understanding of the role of mechanobiology, early mobilization, and immobilization after rotator cuff repair. The objective of this article is to review the basic science and clinical evidence behind mobilization after rotator cuff repair. The effects of mechanical loading on tendon-to-bone healing are outlined. The most recent evidence investigating the effects of immobilization on tendon healing in animal models are reviewed. Finally, recent high-quality randomized clinical trials are summarized. This information can help surgeons formulate a postoperative rehabilitation protocol.
Introduction
The rate of rotator cuff tears is high in the increasingly aging population, and rotator cuff repair has become one of the most commonly performed orthopedic procedures. However, re-tear rates after rotator cuff repair is reported to be around 20% and even greater than 90% in massive tears. Age, tear size, and chronicity are all important factors affecting healing rates after repair but are inherent to the patient and disease. Two important and modifiable factors that the surgeon can control are the surgical technique and the postoperative rehabilitation protocol. There is an abundance of literature concerning surgical approach and techniques for rotator cuff repair. Unfortunately, despite advances in both techniques and technology, the rate of recurrent tearing after rotator cuff repair remains substantial. Surgeons may potentially improve outcomes after rotator cuff repair by controlling and optimizing the mechanical environment after rotator cuff repair, but until recently, literature regarding postoperative rehabilitation and mobilization was relatively scarce.
There is significant variation in the postoperative rehabilitation for patients undergoing rotator cuff repair. Some surgeons may choose to immobilize the shoulder for a period of time after surgery. Immobilization protects the repair site from excessive force that may damage the repair construct and lead to early failure. This approach, however, risks increased postoperative shoulder stiffness and decreased shoulder function. Other surgeons prefer to mobilize early in order to improve early shoulder function. Early mobilization may potentially put the repair construct and tendon-to-bone healing potential at risk.
In the past decade, in vitro studies, animal studies, and clinical investigations have helped to guide the understanding of the role of mechanobiology, early mobilization, and immobilization after rotator cuff repair. The objective of this article is to review the basic science and clinical evidence behind mobilization after rotator cuff repair. The effects of mechanical loading on tendon-to-bone healing are outlined. The most recent evidence investigating the effects of immobilization on tendon healing in animal models are reviewed. Finally, recent high-quality randomized clinical trials are summarized. This information can help surgeons formulate a postoperative rehabilitation protocol.
Basic science evidence
Tendon-to-Bone Healing
The tendon-bone junction represents a crucial area that is most commonly affected in rotator cuff disease. The structural and mechanical properties in this complex area of transition are the focus of both laboratory and clinical investigations on rotator cuff healing. The rotator cuff has a direct fibrocartilaginous insertion that incorporates 4 different but continuous zones of tissue composition ( Fig. 1 ). Zone 1 is predominantly type I collagen similar to that found in the midsubstance of the tendon. The transition from zone 1 to 2 constitutes a change in the collagen composition (predominantly types II and III) as well as a change in extracellular matrix composition. In zone 3, the collagen and extracellular matrix composition is similar to cartilage. Zone 4 completes the transition with constituents similar to bone. This gradation from tendon to fibrocartilaginous tissue to bone assists in efficiently transferring and dissipating load between 2 tissue structures with very different mechanical properties.
In some patients, tearing at this tendon-bone junction causes shoulder pain and dysfunction and necessitates repair. After a torn rotator cuff is repaired back down to its insertion, a scar-forming process ensues. However, the healing process does not recapitulate the normal transition from tendon to bone, and therefore, even a healed rotator cuff repair is structurally and mechanically inferior to a healthy native enthesis. The enthesis of a normal rotator cuff insertion is already typically weaker in tension than the midsubstance of a healthy tendon. The significant re-tear rate seen after repair may be due to formation of disorganized reactive scar tissue rather than organized tendon with a fibrocartilaginous intermediary zone.
Tendon healing follows 3 phases. During the first 4 to 7 days, inflammatory cells including macrophages and neutrophils remove tissue debris. Callous is formed through deposition of types I and III collagen. The second phase is the proliferative or reparative phase in which collagen and other extracellular matrix components are deposited. The last phase is the remodeling phase, which starts approximately 6 to 8 weeks after injury. This phase is characterized by increased order of collagen structure in a linear orientation, presumably in response to stress along the longitudinal axis of the tendon.
During this remodeling phase, mechanical traction, in addition to many other elements such as growth factors, plays a role in the generation of organized tissue at the repaired tendon site. Tendon-to-bone healing, like healing of many other musculoskeletal tissues such as bone and ligament, is affected by an increased transmission of force across the healing interface. This force transmission may promote the formation of collagen in a more organized fashion and may increase the strength of the repair over time.
Mechanobiology in Tendon Healing
Rotator cuff healing is a mechanosensitive process and therefore can be altered by adjusting the mechanical load to the repair site. Tendons have biochemical and biomechanical properties that respond and adjust to mechanical loading. Many studies have supported the theory that appropriate exercise-related loading can enhance tendon mechanical properties, while removal of load from the tendon can lead to deterioration. Adequate mechanical loading can also help to reverse deteriorating mechanical properties in aging tendon.
When mechanical load is imparted onto tendon, biochemical changes within tenocytes are evident, along with increased collagen deposition and upregulation of growth factors important in collagen synthesis. Expression of transforming growth factor-β and scleraxis, both of which are involved in differentiation and proliferation, is altered with varying mechanical load. On the other hand, chronic, repetitive loads on tendon (overuse/overload) can lead to microtrauma and production of inflammatory mediators, including prostaglandin 2 and leukotriene 4 ; this can lead to further degeneration of tendon and soft tissue edema. Literature suggests that repetitive mechanical load can have 2 opposite effects that are dependent on the magnitude of load. A smaller magnitude decreases matrix metalloproteinase-1 (MMP-1), cyclo-oxygenase-2, and interleukin1β and has an anti-inflammatory effect, while the opposite is seen with larger magnitudes.
Disuse and immobilization can decrease stiffness and tensile strength of tendon. Deprivation of stress at the repair site can induce a catabolic state. Arnoczky and colleagues have shown that mRNA expression of collagenase (MMP-1) is markedly increased in load-deprived tendon cells but significantly inhibited with increasing load to the tendon cells. This finding suggests that upregulation of MMP-1 expression can be inhibited through a cytoskeletally based mechanotransduction pathway. A subsequent study by the same group has suggested that load deprivation decreases the mechanoresponsiveness of tendon cells.
Animal Studies of Immobilization and Load Removal
A large portion of the literature pertaining to tendon-to-bone healing has been carried out in the rat rotator cuff model initially described by Soslowsky and colleagues. Subsequent studies using the rat animal model have been shown to be a good animal model to evaluate overuse activity and treatment modalities of rotator cuff injuries. Because of the similarities in soft tissue and bony anatomy between the rat and the human, the rat model has been one of the primary animal models to study rotator cuff disease and tendon-to-bone healing.
The rat rotator cuff model has been commonly used to investigate the role of immobilization on rotator cuff healing. Thomopoulos and colleagues initially investigated tendon-to-bone healing under a variety of loading conditions. After detachment and immediate repair of the supraspinatus tendon, rats were divided into 3 different groups based on activity level: immobilization in a cast, cage activity, and exercise. At 8 weeks, they noted that the tendons in the immobilized group had superior material properties, better tendon organization, and higher type I to type III collagen ratio when compared with the exercise group. These results supported the clinical practice of decreased activity and immobilization after surgical repair. In a subsequent study, Gimbel and colleagues investigated the length of immobilization and activity on the mechanical properties of the supraspinatus tendon of the rat using a similar method. They found that decreased activity level had the greatest positive effect on elastic properties over time. Further studies by the same group have shown that the joint stiffness that resulted from immobilization was only transient and that exercise after a short period of immobilization was detrimental to tendon properties.
Subsequent studies by other groups have shown that complete removal of load from the repair site is detrimental to healing. By using botulunim toxin (Botox) to inhibit contraction of skeletal muscle, multiple investigators have shown that completely unloading the repair site is deleterious to the healing tendon. This finding was investigated by Galatz and colleagues using the same rat rotator cuff model. Cuff healing in 3 different groups were investigated: Botox and immobilization, Botox and free range of motion, and saline-injected and immobilization. Rats that were immobilized and injected with botulinum toxin A into the supraspinatus muscle belly had inferior structural properties compared with saline-injected, immobilized rats. Hettrich and colleagues performed a similar study using Botox without immobilization and suggested that stress deprivation from the tendon-bone interface leads to decreased mechanical properties. It should be noted that in the study by Galatz and colleagues, the material properties were not different between any of the groups; the increased structural properties in the saline/casted group were due to increased volume of scar tissue formation. This finding suggests that, regardless of method for load removal, reparative rather than regenerative scar tissue is generated. Leading the repair site down a regenerative pathway rather than a reparative pathway remains a challenge.
Both complete removal of load and chronic overload are detrimental to tendon healing. Removing load will understimulate the repair site, whereas chronic overload can damage the repair site and may activate a catabolic environment that is detrimental to healing. Clinically, controlled mobilization after rotator cuff repair must balance between understimulation and overload of the repair site.
Clinical Evidence
Until recently, clinicians relied heavily on personal experience and intuition when formulating postoperative rehabilitation protocols after rotator cuff repair; literature on this topic was almost nonexistent. Fortunately, multiple prospective, randomized trials investigating various postoperative rehabilitation protocols have recently been published. A summary of the characteristics and results of these studies are summarized in Tables 1 and 2 , respectively. The data from these studies pertaining to healing of the rotator cuff, pain, range of motion, strength, and function have been helpful in formulating postoperative rehabilitation protocols. Although the important details of each study are summarized in this section, it is important to realize that the postoperative protocols in each of these studies vary greatly, and the reader should be familiar with the details and variations of each of the randomized studies in order to draw his or her own conclusion regarding the role of immobilization after repair.
| Study | Rehabilitation Protocol | No. of Patients | Average Age (y) | Tear Size | Repair Technique | Key Elements of Rehabilitation Protocol | Follow-Up (mo) | % Follow-up |
|---|---|---|---|---|---|---|---|---|
| Lee et al, 2012 | Early aggressive therapy | 30 | 54.5 | 21 medium, 8 large | Single row | 0–6 wk: manual therapy w/out limitation & self-directed passive ROM | 12 | 70% (30/43) |
| Early limited therapy | 34 | 55.2 | 20 medium, 14 large | 0–3 wk: FE <90° w/CPM 3–6 wk: FE >90° w/CPM & passive ER | 12 | 81% (34/42) | ||
| Cuff and Pupello, 2012 | Early therapy | 33 | 63.0 | N/A | Suture bridge | 0–6 wk: pendulums & therapist-guided passive FE/ER | 12 | N/A |
| Delayed therapy | 35 | 63.5 | N/A | 0–6 wk: pendulums only | 12 | N/A | ||
| Kim et al, 2012 | Early passive motion | 56 | 60.1 | All <3 cm | 9 single row 1 double row 46 suture bridge | 0 to 4–5 wk: passive FE, abduction, ER day after surgery | 12 | 93% (56/60) |
| Immobilization × 4–5 wk | 49 | 60.0 | All <3 cm | 8 single row 1 double row 40 suture bridge | 0 to 4–5 wk: no passive ROM | 12 | 86% (49/57) | |
| Keener et al, 2014 | Early passive motion | 61 | 56.1 | All <3 cm | Double row | 0–1 wk: pendulums only 2–6 wk: therapist-guided passive ROM 7–12 wk: active & active-assist ROM | 24 | 91% (61/67) |
| Immobilization × 6 wk | 53 | All <3 cm | 0–6 wk: immobilization 6–12 wk: therapist-guided passive ROM | 24 | 85% (53/62) | |||
| Koh et al, 2014 | Immobilization × 4 wk | 40 | 59.9 | 2–4 cm | Single row | 0–4 wk: immobilization 5–10 wk: gentle passive ROM, progression to active, & active-assist ROM | 24 | 85% (40/47) |
| Immobilization × 8 wk | 48 | 2–4 cm | 0–8 wk: immobilization 9–14 wk: gentle passive ROM, progression to active, & active-assist ROM | 24 | 91% (48/53) |
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