Influence of asymptomatic rotator cuff pathology on in-vivo shoulder motion and clinical outcomes

Document Type

Conference Proceeding

Publication Date

6-20-2017

Publication Title

Journal of orthopaedic research

Abstract

INTRODUCTION: Rotator cuff tears are common, affecting up to 50% (or more) of individuals over age 60 and accounting for an economic burden of $3- 5 billion per year in the U.S. alone [1,2]. Although many rotator cuff tears are painful, the incidence of asymptomatic rotator cuff tears has been reported to range from 15-39% [3]. However, the influence of asymptomatic rotator cuff pathology on shoulder function is not particularly well understood. Thus, the objective of this study was to assess the effects of asymptomatic rotator cuff pathology on shoulder kinematics, strength, and patient-reported outcomes. METHODS: Following IRB approval, 25 asymptomatic subjects (age: 59±5.5, range: 51-74) with normal shoulder function underwent a clinical ultrasound exam to evaluate their rotator cuff. The ultrasound imaging identified subjects as having an intact rotator cuff (CNTL, n=9, age: 58.1 ± 5.4, range: 51-69) or having asymptomatic rotator cuff pathology ranging from tendinosis to a full-thickness tear (PATH, n=16, age: 59.6 ± 5.7, range: 51-74). For all subjects, in-vivo shoulder motion during frontal-plane elevation was measured using a biplane x-ray system. The 3D position and orientation of the humerus, scapula, and ribs 3 and 4 were measured from biplane x-ray images using model-based tracking (±0.4, 0.5°) [4]. From these data we measured humerothoracic, glenohumeral, and scapulothoracic kinematics [5], glenohumeral joint contact patterns [6], and acromiohumeral distance [7]. Conventional clinical outcomes were assessed by measuring: 1) isometric shoulder strength during abduction (ABD), elevation (ELEV), internal rotation (IR), and external rotation (ER), 2) active and passive ROM during ABD, ELEV, IR, and ER, and 3) patient-reported outcomes using the Western Ontario Rotator Cuff (WORC) score and a visual-analog pain scale (VAS). The effects of rotator cuff pathology on measures of shoulder motion, strength, ROM, and patientreported outcomes were assessed with an unpaired t-test. Significance was set at p=0.05 and statistical trends were set at p=0.10. RESULTS: Conventional clinical outcomes: No significant differences were detected between the CNTL and PATH subjects in average age (p=0.76), composite WORC score (p=0.18), VAS score (p=0.47), or any measure of active or passive ROM (p>0.32). Subjects with rotator cuff pathology had significantly less ABD strength (p=0.03) and a trend for lower ELEV and ER strength (p=0.08), but no difference in IR strength (p=0.22, Fig. 1A). Joint kinematic outcomes: Compared to the CNTL subjects, there were statistical trends for the subjects with asymptomatic rotator cuff pathology a more inferiorly positioned humerus on their glenoid (p=0.06, Fig. 1B) and a more anteriorly tilted scapula (p=0.10, Fig. 1C). No statistically significant differences were detected between the CNTL and PATH subjects in scapulothoracic internal/external rotation ROM (p=0.47), scapulothoracic anterior/posterior tilt ROM (p=0.77), or scapulothoracic upward rotation ROM (p=0.69). Similarly, no significant differences were detected between the CNTL and PATH subjects in the average scapulothoracic internal/external rotation (p=0.56) or average scapulothoracic upward rotation (p=0.92). No differences were detected between the CNTL and PATH subjects in the average (p=0.57) or range (p=0.56) of acromiohumeral distance. DISCUSSION: Although the study failed to detect statistically significant differences between PATH and CNTL subjects in many of the outcome measures, the subtle differences and statistical trends that were observed together suggest a plausible progression of rotator cuff pathology. First, intrinsic supraspinatus tendon degeneration - typically identified clinically as tendinosis - appears to be one of the earliest indications of rotator cuff pathology. We suspect that the degenerated/torn supraspinatus tendon is structurally compromised in a way that prevents it from fully transmitting muscle forces, thus contributing to a decrease in shoulder strength (Fig. 1A). Next, the decrease in sup aspinatus tendon forces leads to subtle GHJ instability, as evidenced by the humerus positioned more inferiorly on the glenoid (Fig. 1B). This subtle instability further exacerbates the issue of decreased shoulder strength, since the GHJ is no longer in an optimal configuration to provide a stable base of support necessary to generate high muscle forces. At some point during the progression of rotator cuff pathology the scapula becomes tilted more anteriorly (Fig. 1C), though it is still unknown if abnormal scapular motion contributes to the development of rotator cuff pathology or is the result of rotator cuff pathology. There is evidence that anterior tilting of the scapula decreases the acromiohumeral distance and, presumably, increases the likelihood of symptoms due to subacromial impingement, but the data reported here suggest that the humerus positioned more inferiorly on the glenoid appears to maintain the acromiohumeral distance. Consequently, the on-going biologic processes associated with rotator cuff tendon degeneration and/or tear propagation are able to proceed in the absence of impingement-related symptoms. Although this mechanism is speculative, it may help to explain why such a high number of rotator cuff tears remain asymptomatic. This mechanism would also suggest that exercises designed to restore normal scapular motion may increase the acromiohumeral distance sufficiently to minimize or eliminate impingementrelated symptoms and the need for surgery. Furthermore, it is possible that some measure of scapular kinematics may be the best predictor of the presence/absence of symptoms in individuals with a rotator cuff tear. Clearly, further research is needed to more precisely understand the relationships between tendon pathology, GHJ motion, scapulothoracic motion, acromiohumeral distance, and the development of symptoms. (Figuer Presented).

Volume

35

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