Risk Factors

 

Little is understood about the pathogenesis of tendon pain in the early stages. Tendinopathic changes are frequently asymptomatic. Many patients present themselves to physicians and physiotherapists when they are symptomatic. This presentation may be precipitated by an increase in tendon loading (Scott et al. 2013).

 

A recent systematic review summarised the main histological and molecular findings in human and animal models of rotator cuff overuse (Dean et al. 2012). The paper concluded that intrinsic, extrinsic and environmental factors in combination or isolation have a role in the disordered tendon homeostasis of rotator cuff disease.  The paper outlines a number of degenerative mechanisms, some related to inflammatory pathways (interleukin-1, substance P) and others related to altered loading conditions or systemic influences (aging). The paper noted the disparity of the level of degenerative change and the extent of symptoms.

 

The mechanisms of the development of rotator ruff tendinopathy are multi factorial. Outlined in Figure 3.1 are the extrinsic and intrinsic mechanisms of rotator cuff Tendinopathy as proposed by Seitz et al (2011). This review attempted to identify subgroups of patients potentially affected by rotator cuff tendinopathy based on these mechanisms. By developing a clearer understanding of the mechanism involved in the aetiology of rotator cuff tendinopathy it is postulated that a better suite of targeted interventions can be used by therapists and clinicians. Lewis (2010) used the continuum model of tendinopathy to describe how rotator cuff pathology can oscillate between the three stages of  reactive, disrepair and degenerative tendinopathy (Lewis 2010).

 

Fig 3.1: Extrinsic and intrinsic mechanisms of Rotator Cuff Tendinopathy. Lines indicate non directional evidence of these relationships (Seitz et al. 2011).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Extrinsic Factors

Extrinsic mechanisms of rotator cuff tendinopathy are those relating to the external compression of the tendons due to anatomical or biomechanical factors. Neer proposed an extrinsic mechanism to the development of Rotator Cuff tendinopathy with compression of the RC tendons and associated tissues within the subacromial space (Lewis et al. 2001). This compressive load may not describe all rotator cuff tendinopathies accurately. A novel extrinsic mechanism, internal impingement, has been described in overhead athletes (Burkhart et al. 2003).  Internal impingement occurs due to compression of the articular side rather than the bursal side of the rotator cuff tendons, between the posterior superior glenoid rim and humerus when the arm is in full external rotation, abduction and extension. The rotator cuff tendons are thought to become impinged between the posterior glenoid rim and the greater tuberosity of the humeral head, leading to tendon degeneration and labral damage (Manske et al. 2004).

 

The evidence in relation to the association between acromial shape and rotator cuff tendinopathy is conflicting. Whilst some studies suggest linkages between the presence of a hooked (Type III) or sloped acromion and rotator cuff tears, other studies suggest that the prevalence of altered acromial shape is similar among those with and without rotator cuff tendon pathology (Hirano et al. 2002). There is evidence from a number of studies that altered acromial shape is resultant of the development of spurs on the coraco-acromial arch, as a secondary consequence of rotator cuff tendinopathy or stresses on the coracroacromial ligament (Chambler et al. 2003).

 

While anatomical differences or degenerative bony change of the coraco-acromial arch have been proposed as a static source of subacromial impingement, kinematic abnormalities of scapular and shoulder girdle motion have been suggested as a possible source of dynamic reduction of the subacromial space during shoulder overhead motion (Ludewig and Cook 2000). A recent systematic review exploring the relationship between scapular orientation and subacromial impingement demonstrated that studies that suggest causation are confounded by very small sample sizes and the use of healthy shoulders in young people as comparisons (Ratcliffe et al. 2014).

 

A potential dynamic mechanism of subacromial space reduction is superior migration of the humeral head, which has been extensively  described to contribute to rotator cuff dysfunction (Keener et al. 2009) . The mechanism of this upward humeral head displacement is not clearly understood, lack of inferior stabilisation by the rotator cuff, relative to a normal or increased upward pull of the deltoid muscle, is an explanation that has been postulated (Kim et al. 2010). Electromyographic studies of rotator cuff activation in people with rotator cuff tendinopathy have reported reduced activation levels in supraspinatus and infraspinatus muscles (Bandholm et al. 2008).

 

Intrinsic Factors

Intrinsic mechanisms of rotator cuff tendinopathy describe factors which influence tendon health and quality, causing degeneration that exceeds the tendon’s capacity to heal and repair, and includes factors such as overload of tendons capacity, ageing, genetics, vascular changes and adiposity (Seitz et al. 2011).

 

Evidence would suggest that the onset of rotator tendinopathy increase with advanced age. Both symptomatic and asymptomatic prevalence rates of degenerative rotator cuff changes increase from middle age (Tempelhof et al. 1999).

 

A high prevalence rate of rotator cuff tears and tendinopathy has been observed amongst siblings which could indicate that there is a genetic component to the disease process (Tashjian et al. 2014). Results showed that 32.3% of patients in the rotator cuff tear group studied reported that family members had a history of rotator cuff problems or surgery compared to only 18.3% of the controls.

 

Links between waist circumference, metabolic syndrome and smoking and the prevalence of rotator tendinopathy have been observed (Rechardt et al. 2010). In a large study conducted in the Finnish population, the authors suggest that altered glucose metabolism and vascular pathology caused by increased adiposity and smoking may contribute to tendon damage.

 

Consistent loading beyond the physiological capacity of a tendon is considered to be an important factor in the aetiology of tendinopathy (Scott et al. 2013). In a study of Elite swimmers 73/80 (91%) swimmers reported shoulder pain. Most (84%) had a positive impingement sign, and 69% of those examined with MRI had supraspinatus tendinopathy (Sein et al. 2010).

 

 

KEY REFERENCE

• Seitz, A. L., McClure, P. W., Finucane, S., Boardman, N. D. and Michener, L. A. (2011) 'Mechanisms of rotator cuff tendinopathy: Intrinsic, extrinsic, or both?', Clinical Biomechanics, 26(1), 1-12.