Rotator cuff pathology is a common finding in patients with shoulder pain.1,2 Although the etiology of rotator cuff pathology is likely complex and multifactorial, it is generally believed that repeated tendon deformation (i.e., mechanical impingement) during shoulder motion contributes to degenerative tears.3,4 One form of tendon impingement – internal impingement – occurs when the undersurface of the rotator cuff is entrapped against the superior glenoid.5,6 It was originally identified in overhead athletes when the shoulder is placed in a combination of abduction and external rotation.5 However, recent evidence suggests that internal impingement may also occur during more functional arm raising tasks.7-10 Diverse study methodologies including in vivo assessment,7,10 modeling,8 and arthroscopic evaluation,9 all show the distance between the glenoid and the supraspinatus tendon insertion (i.e., footprint) to steadily decrease during humeral elevation. Furthermore, contact between the glenoid and rotator cuff footprint may be prevalent.8-10 Taken together, this evidence suggests that internal impingement may be a mechanism of rotator cuff injury in non-athletic populations.

When a potential mechanism of injury has been identified, it is important to understand the extent to which movement factors may impact the mechanism so that more targeted prevention and rehabilitation strategies can be developed.11 For example, Saini et al.8 hypothesized that decreased scapulothoracic upward rotation (UR) may increase the incidence of contact between the glenoid and rotator cuff footprint as it would presumably orient the superior glenoid rim downwards and closer to the rotator cuff tendon insertion (i.e., footprint). If decreased scapulothoracic UR does indeed increase the incidence of glenoid-to-footprint contact and internal impingement is suspected to be underlying the patient's symptoms, then it may be prudent to focus rehabilitation on increasing scapulothoracic UR. However, the impact of decreased scapulothoracic UR on internal impingement remains unknown. Therefore, the purpose of this study was to compare the distance between the glenoid and rotator cuff footprint between two groups classified based on scapulothoracic UR magnitude (i.e., low, high) at 90° humerothoracic elevation. It was hypothesized that the low scapulothoracic UR group would have smaller glenoid-to-footprint minimum distances.

This study investigated the kinematic mechanisms of rotator cuff internal impingement by calculating the distance between the glenoid and rotator cuff footprint during scapular plane abduction and comparing this distance between groups classified based on scapulothoracic UR. In all participants, the glenoid-to-footprint distance steadily decreased during the motion trial and in 75%, the distance fell below the estimated labral thickness, suggesting glenoid-to-footprint contact. Moreover, contact typically occurred at an average of 133.6° (3.2°) humerothoracic elevation, which was an average of 20° below the maximum humerothoracic elevation. This finding suggests that contact occurs well-within available range of motion, is consistent with previous investigations,8-10 and provides further evidence that internal impingement could be a more prevalent mechanism of rotator cuff injury or symptom provocation than what is currently believed. Unfortunately, the angle at which pain was provoked during the motion trial in symptomatic participants was not recorded, which would have allowed for correlation with symptoms. However, the high prevalence of pain in symptomatic individuals in overhead elevation angles28 suggests it may be prudent for clinicians to carefully consider how to counsel patients regarding how much pain to tolerate if internal impingement is suspected (e.g., whether to “push through” pain).

Although glenoid-to-footprint minimum distances decreased consistently in all participants, individuals in the low UR group tended to have smaller distances than those in the high UR group (Fig. 2) and made contact at a lower humerothoracic elevation angle. However, these effects did not achieve statistical significance despite modest mean differences due to high between-subject variability. One factor that likely contributed to the inconclusive findings of the current study was the manner in which groups were classified. For example, the angle at which participants were classified (i.e., 90° humerothoracic elevation) is arguably subjective; however, the results of the sensitivity analysis suggest that classifying participants based on other relevant humerothoracic elevation angles (i.e., 100°, 110°, 120°) would not have substantially altered the results of the study (Supplementary Material 1). This is likely because over 65% of participants remained in the same group classification regardless of the angle. Additionally, we chose to investigate glenoid-to-footprint distances and contact centers between 100°−140° humerothoracic elevation as it coincides with when the supraspinatus tendon approximates the glenoid.8 However, the statistical effect may have been underestimated by including the 100° angle, when glenoid-to-footprint distances remained large and variable between participants.

But perhaps a more important consideration when interpreting the inconclusive findings is that the analysis was likely confounded by attempting to assess the effect of a single kinematic variable (i.e., UR) within the complex three-dimensional, multi-joint system of the shoulder girdle. For example, group differences in glenohumeral kinematics were also observed despite being classified based on scapulothoracic kinematics. Specifically, individuals in the low UR moved more inferiorly on the glenoid and tended to have decreased glenohumeral external rotation (Fig. 1). Therefore, it is possible the effect of decreased UR was offset by the effect of other kinematic variables and by the influence of anatomical morphology (e.g., glenoid version, inclination, footprint shape). Herein lies a major challenge when assessing the effect of a single movement variable within a complex system, and why dismissing the importance of UR based on the results of this study may be premature. Instead, it may be beneficial in future studies to first investigate the effect of a single movement variable on mechanisms of rotator cuff pathology so that confounding variables can be controlled. Once those effects are elucidated, then the investigation can be broadened to determine how these effects manifest within the more complex in vivo movement system. Finally, translational studies would be needed to develop and validate techniques to identify and quantify relevant movement patterns within a clinical environment.

Another approach to investigating the impact of movement impairments on mechanisms of rotator cuff pathology may be to adopt another method of classification entirely. The ideal movement-based classification system identifies impairments that presumably contribute to or result from a patient's pain or dysfunction,29 which may be better suited when classification is performed within an individual using movement modification tests (e.g., scapular assistance test)30,31 instead of by interpreting kinematics based on normative or distributive values. For example, the current study classified individuals as “low” or “high” UR based on the magnitude of UR at 90° humerothoracic elevation, and it is possible that individuals in the low UR group had other kinematic or anatomical factors (e.g., high glenoid inclination) that allowed the low UR to be sufficient, even if it was considered “low” across the study's sample. In other words, it is possible that the objective magnitude of UR is not as important to a movement-based classification as the effect of modifying the movement on the patient's symptoms. Future research attempting to elucidate the effect of movement impairments on mechanisms of pathology may benefit from a within-subject classification as it may be more consistent with the goals of a movement-based classification system, and thus has a higher potential for clinical translation.

Although glenoid-to-footprint minimum distances were not significantly different between scapulothoracic UR groups, differences were observed in the proximity center location on the glenoid and footprint surfaces. Between 100–140° humerothoracic elevation, the proximity center remained more centralized within the anterior footprint and posterosuperior glenoid in individuals with low UR compared to those with high UR (Fig. 3). The consistent localization is an interesting finding. Presumably, a larger distribution of contact would help distribute the stress within the tissue, which may help prevent (or delay) any associated tissue microtrauma. However, this supposition is highly speculative in the absence of measures of tendon deformation and longitudinal analyses. In all participants, the proximity center was located an average of 11.7 mm posterior to the biceps groove at initial contact, which corresponds to the region where tears are thought to originate,26,27 and may help to explain the occurrence of undersurface tears.1,2,5,32,33 While these findings may suggest that internal impingement is a potential mechanism for degenerative rotator cuff tears, causation cannot be inferred from the results of this study. Future work that aims to longitudinally assess kinematics and proximity center locations in combination with diagnostic imaging may help clarify the role of internal impingement in rotator cuff pathology.

The findings that glenoid-to-footprint contact was observed in most participants without a significant difference between individuals with and without shoulder pain raises the question of whether internal impingement is pathological. However, several factors preclude the ability of this study to address the question including the study's cross-sectional nature, relatively young sample, and lack of diagnostic imaging. Furthermore, other factors that may contribute to rotator cuff tendon degeneration were not assessed (e.g., genetics,34 comorbidities,26,35 exposure36,37). Consequently, it is possible that contact between the rotator cuff and glenoid itself is not outright pathological, but the consequences likely depend on the frequency and nature of contact, and the ability of the tissues to withstand the associated stresses.38 More research is needed to understand how a combination of these factors (and others) may contribute to the etiology of rotator cuff pathology.

The following limitations need to be considered when interpreting the results of this study. First, single-plane fluoroscopy likely resulted in out-of-plane kinematic tracking errors.14 However, kinematic tracking was performed blinded; therefore, errors are not expected to influence group comparisons. Second, the relatively small and young sample may limit the generalizability of the results. Third, 7 participants did not achieve 140° humerothoracic elevation during the motion trial. It is possible that the seated posture may have limited range of motion; however, the average maximum elevation angle in this group (152.4°) agrees with studies using similar methodologies.10 Fourth, this study calculated bone-to-bone distances to investigate a potential mechanism of soft tissue pathology, and it is likely that the measure is an oversimplification of a complex phenomenon. More complex methodologies (e.g., finite element analysis) are likely necessary to better elucidate the role of internal impingement in rotator cuff pathology. Fifth, an average labral thickness was used to estimate the incidence of glenoid-to-footprint contact given the labrum was not well-visualized in the MRI images. However, a prior sensitivity analysis suggests that the estimated thickness did not significantly alter the prevalence of contact.10 Ultimately, our understanding of potential mechanisms of rotator cuff injury would benefit from methodology that can simultaneously account for soft tissue deformation, kinematics, and morphology.

The results of this study suggest that groups classified based on scapulothoracic UR at 90° humerothoracic elevation exhibit differences in the glenoid-to-footprint proximity center location, but not in the magnitude of the minimum distance when considered between 100 and 140° humerothoracic elevation. However, the effect of UR on glenoid-to-footprint distances may be confounded by concurrent group differences in glenohumeral kinematics. Glenoid-to-footprint contact was identified in most participants and well-within their humeral elevation range of motion. Taken together, these findings provide further evidence that glenoid-to-footprint contact likely occurs during functional overhead motions and could therefore be a more prevalent mechanism of rotator cuff injury than what is currently believed.