Arthroscopic Transosseous Rotator Cuff Repair: Tips and Tricks

By Claudio Chillemi, Alessandro Castagna and Marcello Osimani

The book offers a comprehensive and up-to-date guide to the cutting edge arthroscopic transosseous techniques for the treatment of rotator cuff tears, which are gradually taking over from the common open surgical approach, defined as the gold standard for RCR. With the help of numerous figures, it presents step by step a novel all-arthroscopic anchorless transosseous suture technique that is less invasive and easier to perform. After discussing the etiopathogenesis, histopathology and radiological classification of rotator cuff tears, the book reviews all possible arthroscopic procedures and explores in detail suture management, describing single and double tunnel options. It also examines the complications and post-operative rehabilitation and imaging, while the closing chapter addresses the economic aspects of daily use. Intended primarily for arthroscopic surgeons interested in the field of shoulder joint repair, this exhaustive guide is also a valuable resource for residents and shoulder specialists.

• Language: English
• Publisher: Springer
• Release date: Jun 29, 2018
• ISBN: 9783319761534

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© Springer International Publishing AG, part of Springer Nature 2018

Claudio Chillemi, Alessandro Castagna and Marcello OsimaniArthroscopic Transosseous Rotator Cuff Repairhttps://doi.org/10.1007/978-3-319-76153-4_1

1. Rotator Cuff Tear: Etiopathogenesis and Histopathology

Claudio Chillemi¹ , Alessandro Castagna² and Marcello Osimani³

(1)

Department of Orthopaedics and Traumatology, Istituto Chirurgico Ortopedico Traumatologico (ICOT), Latina, Italy

(2)

Shoulder Unit, Istituto Clinico Humanitas, Milan, Italy

(3)

Department of Radiological Sciences, Oncology and Pathology, Sapienza - University of Rome (ICOT Latina), Rome, Italy

With the invaluable contribution of Prof. Antonio Gigante, MD.

Rotator cuff (RC) is a complex of four tendons (supraspinatus, SSP; infraspinatus, ISP; teres minor, TM; and subscapularis, SSC) together wrapping the humeral head (Fig. 1.1).

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Fig. 1.1

Rotator cuff (RC) tendon insertion into the humeral head (legends: SSP supraspinatus, IS infraspinatus, TM teres minor, SSC subscapularis)

RC tears (RCT) represent the most common source of shoulder pain and disability in people older than 50 years (Oliva et al. 2016). Patients affected with RCT may complain a variety of symptoms ranging from absent or minimal discomfort without any functional deficits to severe pain, weakness, and marked disability (Longo et al. 2011, 2017). Anyway approximately one third of asymptomatic RCT can become symptomatic over time leading to pain and decreased shoulder function (Liem et al. 2014; Oliva et al. 2016). For this reason it is difficult to ascertain the true incidence and prevalence of RCT in the general population (Liem et al. 2014).

RCT prevalence was firstly reported in cadaveric studies, ranging from 8% (for partial tear) to 11% (for full-thickness tear) (Hijioka et al. 1993). Recent studies based on radiologic examination of patients (with and without symptoms) report different numbers, establishing an overall prevalence of 38.9% for asymptomatic and 41.4% for symptomatic tears detected by ultrasound (Reilly et al. 2006). Moreover these rates tend to rise when the patient’s age increase, reaching the 65% in person older than 70 years.

Etiopathogenesis

The etiopathogenesis of RCT remains still unclear and considered as multifactorial. Currently, the most accepted theory explains the presence of tears of the rotator cuff as a combination of extrinsic and intrinsic factors (Chillemi et al. 2011).

Among the extrinsic factors, the most accredited theory is the chronic impingement syndrome described by Charles Neer in 1972 (Neer 1972). Tendon tears occur because of the impingement of the RC against the undersurface of the acromion and coracoacromial (CA) ligament (Fig. 1.2).

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Fig. 1.2

Arthroscopic view. Lateral decubitus. Subacromial space. The scope is posterior. Isolation of the hooked acromion (A) before performing acromioplasty

The acromial morphology described by Bigliani (Bigliani et al. 1986) is in support of Neer’s theory (Neer 1972). Three types of acromion are reported according to its shape: type I or flat (17%), type II or curved (43%), and type III or hooked acromion (40%) (Fig. 1.3). Nowadays, many authors believe that type III acromion is the result of degenerative changes of the CA ligament. In fact, in the presence of a RCT, the humeral head migrates superiorly (dynamic instability) increasing tensile stress to the CA ligament so to form a reactive traction spur at its insertion into the anteromedial corner of the acromion (Uhthoff et al. 1988).

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Fig. 1.3

Acromion morphology: Bigliani classification. Three types of acromion are reported according to its shape: type I or flat, type II or curved, and type III or hooked acromion

Among the intrinsic factors, the most ancient theory in the pathogenesis of RCT is the degenerative theory proposed by Codman (Codman 1934). Different histopathological changes commonly occur in the tendon before tearing, with the involvement also of its insertion (i.e., enthesopathy) (Uhthoff et al. 2003). Obviously a degenerated tendon is weaker to resist stress, so that tear may easily occur (degenerative-microtraumatic theory) (Yadav et al. 2009).

Also tendon vascularity represents a weak point for tendon degeneration. Histologically, at 10–15 mm medial to the rotator cuff, tendon insertion was described a hypovascular zone (Lohr and Uhthoff 1990) characterized by a 30% reduction of both vessel diameter and number (Brooks et al. 1992) which may affect tendon degenerative changes.

Among these changes was also recognized an increase of apoptosis of the supraspinatus cells (Yuan et al. 2002). The consequent reduced number of functioning cells (i.e., fibroblasts-fibrocytes) may impair collagen metabolism so to culminate in tendon degeneration increasing the risk of rupture.

The structural integrity of tendons is also guaranteed by a healthy extracellular matrix (ECM), the substrate to which cells adhere, migrate, and differentiate (Chiquet 1999). The normal ECM turnover of tendon is mediated by different proteins, such as matrix metalloproteinases (MMPs) (Choi et al. 2002). After tendon rupture was encountered, the upregulation of MMP-1 is associated with a downregulation of MMP-2 and MMP-3 (Riley et al. 2001). An excess of the activity of MMPs can lead to progressive weakening of the extracellular matrix of tendons. Normally, the activity of endogenous MMPs is inhibited by endogenous tissue inhibitors of MMPs (TIMPS), and the relative balance between MMPs and TIMPS is relevant in the development, morphogenesis, and normal tendon remodeling. Tenocytes of tendinopathic tendons show increased expression of MMPs and decreased expression of TIMP mRNA (Castagna et al. 2013).

Another possible pathogenetic mechanism of rotator cuff tendon tear is the development of fibrous cartilage inside the tendon tissue (Fig. 1.4). It can arise because of repeated stimulation in compression that may reduce oxygen tension activating the system supported by tenascin-C. Moreover, by inhibiting angiogenesis, cartilage glycosaminoglycans could give rise to a poorly vascular tissue. This aspect, whether an adaptive or pathologic process, clearly involves an altered pattern of matrix synthesis and a remodeling of the existing matrix. This could result in a tendon more resistant to compressive stress but, in the long term, less resistant to traction, predisposing it to rupture (Gigante 2004).

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Fig. 1.4

Histopathology. Human rotator cuff torn tendon – supraspinatus. Numerous areas of cartilage (i.e., chondral metaplasia) – detected at the edge of torn tendon – consisted of rounded cells surrounded by disorganized matrix. These chondrocyte-like cells appear either clustered in groups or randomly dispersed in the matrix (H&E – original magnification 100×)

Histopathology

Tendon. Tendons consist of collagens, mostly type I collagen (Fig. 1.5) (Transmission Electron Microscopy) however, other collagens II, III, V, VI, IX, and XI are also present (Fukuta et al. 1998; Ottani et al. 2002; Kjaer 2004) and elastin embedded in a proteoglycan-water matrix with collagen accounting for 65–80% and elastin (Fig. 1.6) approximately 1–2% of the dry mass of the tendon (Kannus 2000). The cellular components (i.e., tenoblasts and tenocytes, which are the elongated fibroblasts and fibrocytes) (Fig. 1.7) produce the matrix and lie between the collagen fibers and ground substance surrounding the collagen including proteoglycans, glycosaminoglycans, structural glycoproteins, and other small molecules. Inorganic components represent less than 0.2% of dry tendon mass, being calcium the most abundant inorganic tendon component (Weinreb et al. 2014). Proteoglycans are primarily responsible for the viscoelastic behavior of tendons, but do not make any major contribution to their tensile strength (Puxkandl et al. 2002; Robinson et al. 2004). The principal role of the collagen fibers is to resist tension, although they still allow for a certain degree of compliance (i.e., reversible longitudinal deformation) (Benjamin et al. 2008).

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Fig. 1.5

Collagen fibrils (arrows) (TEM)

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Fig. 1.6

Elastic fiber: the amorphous core of elastin (E) is surrounded by microfibrils (arrows) (TEM)

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Fig. 1.7

Tendon cellular components are immersed in the ECM rich in collagens. The cells appear elongated (TEM)

Tendon structure follows a complex hierarchical scheme. Collagen molecules consist of polypeptide chains, and three such chains combine together to form a densely packed, helical tropocollagen molecule. Soluble tropocollagen molecules form cross-links to create insoluble collagen molecules. Five tropocollagens then aggregate progressively into microfibrils, and microfibrils aggregate together to form collagen fibrils (Benjamin et al. 2008). A bunch of collagen fibrils forms a collagen fiber, which is the basic unit of a tendon. A fine sheath of connective tissue (the endotenon) encloses each collagen fiber and binds fibers together. The number of collagen fibers in each subfasicle may vary considerably from tendon to tendon (Kannus 2000). A bunch of collagen fibers forms a primary fiber bundle, and a group of primary fiber bundles forms a secondary fiber bundle. A group of secondary fiber bundles, in turn, forms a tertiary bundle, and the tertiary bundles make up the tendon. Externally, the entire tendon is surrounded by a fine connective tissue sheath (the epitenon). The spatial orientation of tendon fibers and fiber bundles is complex. The fibrils of one collagen fiber are oriented not only longitudinally but also transversely and horizontally. The longitudinal fibers do not run only parallel to the major axis of the tendon but also cross each other, forming spirals. This complex organization permits the tendon to solve its function: transmit the force created by the muscle to the bone, and, in this way, make joint movement possible (Kannus 2000).

Enthesis. The normal insertion (i.e., site of attachment, osteotendinous junctions) of tendon into bone is named enthesis (Fig. 1.8). Enthesis (i.e., insertion sites, osteoligamentous junctions) is a site of stress concentration at the region where tendons attach to bone (Benjamin et al. 2008).

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Fig. 1.8

Macroscopic view. Human rotator cuff enthesis. The enthesis is the insertion (i.e., site of attachment) of tendon (T) into bone (B)

Entheses were distinguished into two broad categories and classified in fibrous and fibrocartilaginous according to the type of tissue present at the attachment site (Benjamin and Ralphs 1998, 2001). They correspond, respectively, to the well-known indirect and direct attachments (Apostolakos et al. 2014). Fibrous entheses attach directly to bone or periosteum primarily via fibrous tissue, which is similar in structure to the tendon midsubstance. Fibrocartilaginous entheses attach to bone through a layer of fibrocartilage which acts as a transition from the fibrous tendon tissue (Lu and Thomopoulos 2013; Benjamin and McGonagle 2001; Benjamin et al. 2002).

Fibrous entheses are characterized by dense fibrous connective tissue at the tendon-bone interface and are common in tendons that attach to diaphyses of long bones (Benjamin et al. 2002). These entheses typically occur over large surface areas and are characterized by perforating mineralized collagen fibers (Lu and Thomopoulos 2013). Furthermore, these entheses can be either bony or periosteal depending on whether the tendon inserts directly into bone or periosteum, respectively (Benjamin et al. 2002). This type of enthesis is found in muscles such as the deltoid, which inserts into the humerus, and the muscles attaching to the linea aspera of the femur, such as the adductor magnus (Lu and Thomopoulos 2013; Angeline and Rodeo 2012). Fibrous entheses have received relatively little attention in the literature compared to fibrocartilaginous entheses, likely due to the fact that overuse injuries are more common in fibrocartilaginous tendon-to-bone insertions such as those of the rotator cuff.

Fibrocartilaginous entheses are characterized by fibrocartilage at the tendon-bone interface and are typical of epiphyses and apophyses (Benjamin et al. 2002). These types of entheses are more common than fibrous entheses and are prone to overuse injuries such as those of the rotator cuff and Achilles tendons (Lu and Thomopoulos 2013; Benjamin et al. 2002). A typical fibrocartilaginous enthesis has four distinct zones that create a structurally continuous gradient from uncalcified tendon to calcified bone (Fig. 1.9) (Benjamin et al. 2002; Lu and Thomopoulos 2013; Apostolakos et al. 2014). These zones, in order, are distinguished in:

1.

Dense fibrous connective tissue: is composed of pure tendon and is heavily populated by fibroblasts1. The mechanical properties of this zone are similar to those of midsubstance tendon, with its composition consisting mainly of linearly arranged type I collagen as well as some type III collagen, elastin, and proteoglycans within the ground substance surrounding the cells (Lu and Thomopoulos 2013; Angeline and Rodeo 2012).

2.

Uncalcified fibrocartilage: is an avascular zone of uncalcified, or unmineralized, fibrocartilage populated by fibrochondrocytes and consisting of the proteoglycan aggrecan and types I, II, and III collagen (Lu and Thomopoulos 2013; Benjamin et al. 2002; Angeline and Rodeo 2012). The uncalcified fibrocartilage zone functions as a force damper to dissipate stress generated by bending collagen fibers in the tendon (Benjamin and McGonagle 2001). The functional impact of this zone is supported by studies reporting that the quantity of uncalcified fibrocartilage is increased at insertion sites with more variable ranges of insertion angles during joint movements (Benjamin and Ralphs 1998, 2001).

Tidemark (the line of provisional calcification) is a basophilic line that separates the uncalcified and calcified fibrocartilage zones. This is more clearly described as the mechanical boundary between soft and hard tissues. The tidemark is relatively straight which indicates the production of a flat surface during the mineralization process which is important clinically as this surface reduces the risk of damage to soft tissues during joint movement (Angeline and Rodeo 2012).

3.

Calcified fibrocartilage: is an avascular zone of calcified, or mineralized, fibrocartilage populated by fibrochondrocytes and consisting of predominantly type II collagen as well as aggrecan and type I and X collagen (Lu and Thomopoulos 2013; Benjamin and McGonagle 2001; Angeline and Rodeo 2012). This zone represents the true junction of the tendon to the bone and creates a boundary with the subchondral bone (Benjamin and Ralphs 2001). In contrast to the tidemark, this anatomical junction of tendon to bone is highly irregular. This irregularity is functionally important as the attachments of the calcified fibrocartilage layer into the bone provide the mechanical integrity of the enthesis (Benjamin and McGonagle 2001). This layer is believed to be important in allowing a gradual transition of force across the enthesis in addition to acting as a barrier against blood vessels in the bone and preventing direct cell-cell communication between osteocytes and tendon cells (Benjamin et al. 2002; Benjamin and McGonagle 2009).

4.

Bone: consists of osteoclasts, osteocytes, and osteoblasts residing in a matrix of type I collagen and carbonated apatite mineral1 (Angeline and Rodeo 2012) (Fig. 1.10).

Tendinopathy. Tendinopathy is associated with degeneration and disorganization of the collagen structure and an increase in mucoid, proteoglycan, and water content (Hodgson et al. 2012; Andres and Murrell 2008; de Mos et al. 2007; Kannus and Jozsa 1991; Khan et al. 1999; Riley et al. 1994). A 10–20-fold calcium concentration increase may also occur (Kannus 2000). Chemical and molecular changes have been described in tendon overuse (Andres and Murrell 2008), and structural and compositional changes of tendon have been described during aging (Angeline and Rodeo 2012).

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Fig. 1.9

The enthesis. A typical fibrocartilaginous enthesis has four distinct zones that create a structurally continuous gradient from tendon (up) to bone (down)

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Fig. 1.10

The enthesis. Note the basophilic line of provisional calcification (tidemark) that separates the uncalcified and calcified fibrocartilage zones (H&E, 5×)

The degenerative changes occurring in rotator cuff tendon were analyzed in details by Riley and coll. (Riley et al. 2001) which proposed a grading system based on the organization of the tendon fiber bundles, the aspect of cell nucleus, and the grade of tissue hyalinization.

In addition two different scales, originally developed for the Achilles tendon, the Movin scale (Movin et al. 1997), and the patellar tendon, the Bonar scale (Cook et al. 2004), were adopted to evaluate the rotator cuff tendon (Longo et al. 2008; Maffulli et al. 2008).

The variables included in the Movin scale are (1) fiber structure, (2) fiber arrangement, (3) rounding of the nuclei, (4) regional variations in cellularity, (5) increased vascularity, (6) decreased collagen stainability, (7) hyalinization, and (8) GAG content. Each variable is scored between 0 and 3, with 0 being normal, 1 slightly abnormal, 2 abnormal, and 3 markedly abnormal. The total semiquantitative histologic score for a given slide could vary between 0 (normal tendon) and 24 (the most severe abnormality detectable).

The variables included in the Bonar scale are (1) tenocytes, (2) ground substance, (3) collagen, and (4) vascularity. A four-point scoring system is used, where 0 indicates a normal appearance and 3 a markedly abnormal appearance (Table 1.1). Overall, the total score for a given slide could vary between 0 (normal tendon) and 12 (most severe abnormality detectable).

Table 1.1

Bonar score