There are two types of tears: traumatic or chronic. The traumatic tear has a defined origin, which by the name is the result of a traumatic episode; while chronic tears may have multiple factors involved in their onset (Bassett and Cofield 1983). This thesis will focus on chronic tears, which are more frequent, more complex to describe in terms of causative mechanisms and require better evidence for optimal rehabilitation. Currently, there are two categories to classify different factors that can explain the injury mechanism behind a chronic lesion, i.e. extrinsic and intrinsic. Extrinsic factors are those external to the tendon itself; in this category are included those related to the anatomy of other structures, such as acromion and presence of spurs (Maffulli et al., 2011; Seitz et al., 2011; Pandey and Willems 2015). The link between the acromial shape and rotator cuff tears was first explored by Neer (1972), where the author described that the majority of tendinopathies and tears that required surgical intervention occurred in the supraspinatus tendon, mainly in the area close to the
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coracohumeral ligament, followed by the area of the anterior region of the acromion and acromioclavicular joint. Based on this classic work, further studies classified the
acromion in three different shapes: flat, curved and hooked or type 1,2 and 3,
respectively (Bigliani et al., 1991) (Figure 2.10). Based on the literature, it may seem that the acromion shape has a significant influence on rotator cuff tears. Individuals with type 3 are thought to present a narrow subacromial space, which consequently would cause compression of the supraspinatus tendon and abrasion between muscle and bone. Even though correlations have been found mainly for the hooked form, it is still not possible to confirm that the acromion shape, or its size, is the main or sole cause of the disorder (Balke et al., 2013). In contrast to the view that the acromion shape causes a tear, other studies have raised the question that the acromion shape may be the
consequence, not the cause, of an already injured tendon (Sarkar, Taine, and Uhthoff, 1990; Maffulli et al., 2011). For instance, when the supraspinatus is impaired, the force pulling the humeral head downwards during elevation will be reduced; in turn, it will induce an upward migration of the humeral head provoking compensations that may lead to dyskinesis. The dysfunctional shoulder would put additional stress over the coracoacromial ligament, especially on the acromion side, that has a smaller area of insertion in relation to the coracoid process due to its trapezoid shape. Therefore, the increased tension on the coracoid process would stimulate bony growth, potentially creating osteophytes or in a long-term the continuum traction could result in a deformed acromion ( Maffulli et al., 2011; Lewis, 2016). Spurs can also be found on the
acromioclavicular joint, which may also contribute to narrowing the subacromial space and compression of underlying structures (Pandey and Willems, 2015).
Figure 2.10. Classification of acromion types. From Pandey and Willems (2015).
Intrinsic factors are those with origin related to the tendon, such as microtrauma, mechanical properties, morphology and vascularity. The main intrinsic factor is
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microtrauma, this theory explains degenerative changes of the tendon based on the history of chronic cumulative microtraumas during life. The damage occurs when humeral elevation is required with greater activity, especially if it exceeds overhead height, where the tendon is more exposed to injury. In addition, the repetitive cycle of small injuries results in a modification of the cells biological environment due to the continuous activity of inflammatory mediators and oxidative stress (Nho et al., 2008).
Consequently, mechanical alterations are also observed, the fibres that suffer consecutive microruptures do not have enough time to heal before further injury; therefore, the remaining intact fibres have to sustain higher loads and are then more exposed to ruptures (Seitz et al., 2011). The healing process becomes deficient because of the short time available for recovery, making the collagen arrangement disorganised and leading to decreased quality of the tendon’s mechanical property; the faulty
mechanical property reduces the fibres loading capacity, making them more prone to injury (Seitz et al., 2011).
Another intrinsic factor, the vascular pattern of the supraspinatus, has been the theme of debate for a long time. First described by Codman in 1934, the supraspinatus was depicted as having an area of hypovascularity about 10 to 15 mm proximal to the tendon insertion. The critical zone, as it is called, was believed to be a fragile point of the tendon that contributed to a higher incidence of the number of supraspinatus cases (Lohr and Uhthoff, 1990). However, later studies showed no differences in vascularity or perfusion when compared to other parts of either supraspinatus or infraspinatus (Brooks, Revell, and Heatley, 1992). The question that is still not clear is whether the pressure caused by the inappropriate position of the humeral head may decrease
supraspinatus blood supply and therefore contribute to tendon degeneration (Nho et al., 2008).
A few other factors that are not classified in the two main categories also need to be mentioned. Smoking habits have been associated with poorer outcomes of patients with rotator cuff disease. Baumgarten et al. (2010) administered a questionnaire to 586 patients who were diagnosed with shoulder pain and had an ultrasound to confirm if a rotator cuff tear was present. They found a strong relationship between smoking and cuff tears, and that a dose-dependent relationship exists between the number of
cigarettes per day and risk of rotator cuff tears. Patients who complain of shoulder pain and who smoke less than one pack per day have an odds ratio of 1.08 of having a rotator
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cuff tear, between 1 and 2 packs the ratio rises to 1.66 and a further sharp increase to 3.35 is denoted in the subgroup of more than 2 packs a day. Nicotine has been shown to provoke chronic inflammation and significantly reduces the amount of Type-I collagen expression and cellular proliferation, the consequence is a weaker tendon, with poorer tensile properties (Galatz, 2006).
The glycaemic and lipid profiles also seem to influence on chronic tears and tendon healing, high level of glucose may change collagen cross-links and
hypercholesterolemia may decrease tendon’s vascularity, however, more studies in the area are needed (Maffulli et al., 2011).
The development of a chronic rotator cuff tear is likely to be a combination of factors. It is important to understand the mechanisms that cause the disorder as it may help with tailoring the treatment plan of a patient. For instance, the use of non-steroidal anti-inflammatory drugs will improve inflammation or acromioplasty arguably
decreasing pain, but they do not resolve biomechanical imbalances presented by muscle incoordination nor improve proprioception or maybe improving patient’s lifestyle, which may contribute to a faster tendon healing.