Pathogenesis

The pathogenesis of RCTs is multifactorial and is still not completely clear.⁴ Many theories have been proposed, and tears are traditionally classified into ‘extrinsic’ and ‘intrinsic’ (Table 44.1). Chronic impingement, as described by Neer in his chronic impingement syndrome theory, is the best known extrinsic pathological factor in RCTs.⁵ Excessive load, repetitive load or loads applied from different directions have been implicated in the process of tendinopathy. Other theories include localized hypoxia produced by tensile load, hyperthermic injury as the tendon heats up with exercise, tenocyte apoptosis, and cytokines or proteolytic enzymes released as a result of applied stress. The release of nitrous oxide has also been implicated in the tendinopathy process. Currently, RCTs are considered to be of multifactorial etiology, and the relative contributions of these factors remain to be determined.

Any process that impairs tissue healing may be implicated in rotator cuff disease. Nicotine exerts deleterious effects on tendon healing,⁶ and smokers are less likely to respond favorably to cuff repair operations, with reduced postoperative function and satisfaction compared to non-smokers.⁷ In the current literature, factors such as patient age, sex and fatty muscle infiltration are highly correlated to the presence of RCTs and the prevalence of recurrence of tears.⁴

Many studies emphasize the importance of extracellular matrix (ECM) for the homeostasis of connective tissue. ECM is the substrate to which cells adhere, migrate and differentiate. ECM imparts information to cells and tissues by providing cell-binding motifs in its own proteins or by presenting growth factors and morphogens to the cells. Physiological and pathological modifications of the ECM seem to be the most important intrinsic factors involved in tendinopathies and tendon ruptures.⁸ Transglutaminases (TGs) have been implicated in the formation of hard tissue development, matrix maturation and mineralization and have been shown to be down-regulated in human supraspinatus tendon ruptures.⁹

The roles of hormonal and metabolic diseases have recently been investigated.¹⁰ The relationship between thyroid disorders and shoulder pain has been suspected since the late 1920s¹¹ but has not been systematically investigated. The thyroid hormones, T3 and T4, play an essential role in the development and metabolism of many tissues and organs. Thyroxine is important for both collagen synthesis and ECM metabolism. A recent study demonstrated that thyroid hormone nuclear receptors are present in healthy and pathologic rotator cuff tendons, and that, in vitro, thyroid hormones enhance tenocyte growth and counteract apoptosis in healthy tenocytes isolated from tendon in a dose- and time-dependent manner.¹² Hypothyroidism causes accumulation of glycosaminoglycans in the ECM, which may, in turn, predispose to tendon calcification.¹⁰ Diabetes is also a risk factor for RCTs.¹³ In a study on asymptomatic subjects, age related rotator cuff tendon changes were more common in diabetic subjects.¹⁴ Diabetic patients show a restricted shoulder range of motion, a higher prevalence of recurrent tears after surgical repair and a higher rate of complications and infections after open and arthroscopic repair of RCTs.¹⁵ An association between obesity and RCTs has also been proposed.¹⁶

Physical examination

The clinical diagnosis is not always easy. Painful conditions of the long head of the biceps or the acromioclavicular joint may result in a high false positive rate. The clinical presentation of rotator cuff pathology is extremely variable. A recent review concluded that RCTs are frequently asymptomatic.⁷ Such variation in clinical features remains unexplained. Physical examination should include inspection, palpation, the evaluation of active and passive range of motion and the execution of strength and provocative tests. Many specific clinical tests are available to test the muscles forming the rotator cuff. Patients with shoulder pain who test positive for supraspinatus weakness, weakness in external rotation and impingement have 98% chance of having an RCT. If none of these clinical features are present, the chance of having a tear decreases to 5%.⁴

Rotator cuff healing

Tendon healing is a complex and well-orchestrated series of physiological events involving synthesis, migration and degradation of ECM components. The ability of tendons to heal is controversial: tendon tissue can repair but not regenerate.¹³ Tissue adjacent to an RCT (2.5 mm) appears to be histologically viable in both microvasculature and cellular synthesis of type I procollagen. Therefore, many authors advise avoiding wide excision of the edges of the torn rotator cuff before reattachment.⁴ This is supported by the observation of Jost et al.¹⁷ who, in a long-term follow-up after structural failure of rotator cuff repairs, observed compelling evidence that small reruptures have a potential to heal.

It is very important to provide the tendon with the best conditions to heal. The subacromial bursa seems to play an important role. In normal conditions, the subacromial bursa has three functions. It facilitates gliding between two layers of tissue, provides blood supply to the cuff tendons and provides cells and vessels to aid healing after surgical repair. Mobilization after repair promotes cellular activity, improves tensile properties and enhances gliding function. A fine balance exists between the progression of tendon healing and postoperative mobilization.

Treatment of rotator cuff tears

Both arthroscopic and mini-open techniques are effective for rotator cuff repair, but there is still considerable debate over the benefits of these procedures. Many improvements have been made since the first completely arthroscopic rotator cuff repair described by Johnson,¹⁸ and arthroscopists state that the main advantages of all-arthroscopic repairs are less postoperative pain and shorter rehabilitation time. However, when the outcome of arthroscopic and mini-open repair are compared, no significant differences are found. Functional outcome, pain, range of motion and complications do not significantly differ between all arthroscopically repaired patients and those treated with mini-open repair in the first year after surgery.¹⁹ Pearsall et al.²⁰ and Kim et al.,²¹ in retrospective studies, found no differences in outcome for small and medium sized tears of the rotator cuff at mid-term follow-up. A systematic review showed decreased pain at short-term follow-up in patients treated arthroscopically.²² However, massive tears remain difficult to treat arthroscopically, and the mini-open surgical technique could be a good choice in the elderly patient. Another difference between the two different methods is the re-tear rate, which is higher in patients treated arthroscopically at 24-month follow-up.²³ In reality, there is no evidence about which is the best treatment.

Irreparable RCTs in elderly patients are a challenging problem. There are several treatment options, but determining the correct treatment for each patient is difficult. Reverse shoulder arthroplasty (RSA) is an emerging solution for these patients in whom anatomic shoulder arthroplasty or hemiarthroplasty has failed. Many mid-term studies showed early encouraging results, and the first long-term studies show good survivorship. Favard et al.²⁴ retrospectively reviewed 527 arthroplasties in 506 patients and found 89% survivorship at 10 years. Similar results have been reported by Guery et al.,²⁵ who demonstrated deteriorating function and increasing pain after 6 years. Boileau et al.²⁶ reported improved shoulder function and restored active elevation in patients with cuff-deficient shoulders treated with RSA. Supported by these encouraging results, original indications for RSA were expanded. Originally, the reverse shoulder prostheses were designed for rotator cuff arthropathy, and massive RCTs with arthritis and massive irreparable RCTs were considered appropriate indications. Recently, displaced three- or four-part neck of humerus fractures in older patients, RCTs with fatty infiltration of infraspinatus or subscapularis muscles, sequelae of fracture, rheumatoid arthritis, revision arthroplasty and tumors are becoming common indications for RSA.²⁷ RSA combined with latissimus dorsi and teres major tendon transfer has been developed to improve external rotation and spatial control in patients with no functional teres minor and infraspinatus with early promising results.²⁸ However, a high rate of complications is still reported after RSA and progressive functional and radiographic deterioration continue to be of concern.²⁹ Scapular notching is one of the most important complications of RSA.²⁵

Future perspectives

Several strategies have been proposed to enhance tendon healing. Recently research focused on regenerative therapies such as growth factors (GFs) and plasma rich platelet (PRP) which have become a popular treatment for tendon injuries. However, the efficacy of PRP treatment is highly controversial. In vitro studies showed that the addition of PRP to human tenocytes resulted in cell proliferation, collagen deposition, well-ordered angiogenesis and improved gene expression for matrix degrading enzymes and endogenous growth factors.^30,31 More recently, two studies demonstrated that PRP induced in vitro tendon mesenchymal stem cells (T-MSCs) to differentiate into active tenocytes, and that PRP has an anti-inflammatory function by suppressing the levels of prostaglandin E (PGE) biosynthetic pathway components (COX-1, COX-2 and PGE synthase-1 [PGES-1] expression) and PGE2 production.³² These results have important clinical implications because high levels of PGE2 cause pain, decrease cell proliferation and collagen production and induce degenerative changes in rabbit tendons.³³ But the same authors also reported that, even if PRP is able to induce the differentiation of T-MSCs into tenocytes under regular culture conditions, PRP injection in clinics may not be able to effectively reverse the degenerative conditions of late-stage tendinopathy.³⁴

However, clinical studies do not report any substantial benefit using PRP for rotator cuff lesions. A few studies demonstrated that the application of PRP for large to massive rotator cuff repairs significantly improved structural outcomes with a decreased re-tear rate.³⁵ Gumina found that the platelet-leukocyte membrane improved structural repair integrity, but without improvement in functional outcome.³⁶ Other works did not report better results with the use of PRP. Randelli et al.³⁷ found that PRP reduces pain in the short term, making it possible to mobilize the patient earlier, but they did not find long-term improvement in functional scores. No differences in rotator cuff healing or improvements in function were found at 1-year follow-up.³⁸ No statistically significant difference in the recurrent tear rate between patients treated with or without the addition of PRP was found.³⁸ Castricini et al.³⁹ performed a randomized double blind controlled trial with 88 patients and there were no statistically significant differences at 16-month follow-up. They stated that the study does not support the use of PRP in small to medium sized RCTs. There results were confirmed in a further RCT by Rodeo et al.⁴⁰

Percutaneous Achilles tendon repair: surgical technique

A 1-cm transverse incision is made over the defect using a size 11 blade. Four longitudinal stab incisions are made lateral and medial to the tendon 6 cm proximal to the palpable defect. Two further longitudinal incisions on either side of the tendon are made 4–6 cm distal to the palpable defect. Forceps are then used to mobilize the tendon from beneath the subcutaneous tissues. A 9 cm Mayo needle is threaded with two double loops of Number 1 Maxon, and this is passed transversely between the proximal stab incisions through the bulk of the tendon (Figure 44.1). The bulk of the tendon is surprisingly superficial. The loose ends are held with a clip. In turn, each of the ends is then passed distally from just proximal to the transverse Maxon passage through the bulk of the tendon to pass out of the diagonally opposing stab incision. A subsequent diagonal pass is then made to the transverse incision over the ruptured tendon. To prevent entanglement, both ends of the Maxon are held in separate clips. This suture is then tested for security by pulling with both ends of the Maxon distally. Another double loop of Maxon is then passed between the distal stab incisions through the tendon (Figure 44.2), and in turn through the tendon and out of the transverse incision starting distal to the transverse passage (Figure 44.3). The ankle is held in full plantar flexion, and in turn opposing ends of the Maxon thread are tied together with a double throw knot, and then three further throws before being buried using the forceps. A clip is used to hold the first throw of the lateral side to maintain the tension of the suture. We use 3-0 Vicryl sutures to close the transverse incision and Steri-Strips to close the stab incisions (Figure 44.4). A non-adherent dressing is applied. A full plaster cast is applied in the operating room with the ankle in physiologic equinus. The cast is split on both medial and lateral sides to allow for swelling. The patient is discharged on the same day of the operation.

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