|Disorders of The Rotator Cuff|
With age the normal elasticity of tendons is diminished. Signal change on MRI correlates with this age related change which is considered pathological when it occurs in the extreme or prematurely. Mechanically, the altered tissue is stiffer. Injury is most likely to occur where the muscle is functioning in an eccentric mode, lengthening of the muscle tendon unit, while the muscle contracts as in the late follow through phase of throwing in which the cuff contributes to the coordinated deceleration of the arm. The greater stiffness of the elastin depleted tendon leads to failure. The elastin normally functions like a snubber on a mooring line which dampens the sudden jolt as the stucture of the rope reaches the limit of it's abliity to stretch. The location of the failure varies with rate of load. Episodic near failure at the tuberosity may result in remodeling changes at the tendon bone interface as an adaptive response to shore up the tendon insertion. Rotator cuff tears can occur through normal tendon with an acute injury of sufficient force and mechanism. In most cases however the pathophysiology is more complex and tears generally are found to have occurred through tendon that is not normal but rather through tendon that has deteriorated for lack of a better term. A degenerative process is another term that we use to describe the changes in the structure of the tendon that are present and which predispose to the development of a tear. These changes in the tendon can be accompanied by pain but may also be clinically silent thus despite a lack of reported symptoms after age 50 the likelihood of identifying a rotator cuff tear in a random individual is roughly 20% at age 50 and 40% at age 70. It has been a natural presumption that a small assymptomatic tear can develop into a larger symptomatic tear and that over the course of this evolution the degree of difficulty in repair is increased due to the retraction of the muscle tendon unit. Furthermore long established tears in the tendon can be accompanied by atrophy and fatty infiltration of the muscles at which point simply reestablishing the physical connection between the tendon and the bone will not necessarily restore the functional role of the structure in the overall kinematics and biomechanics of the shoulder. It is further apparent that the tendon connection to bone that results from repair of a rotator cuff differs from that of a normal tendon insertion. One feature that is lacking in the repaired tendon are Sharpies fibers which in a normal tendon anchor into the structure of the bone imparting greater resistence to tear. Lacking this feature therefore a repaired tendon is more subject to retear although as the results tally it may be possible to have successfully alleviated the complaint despite evidence on post operative imaging that the tendon has either failed to heal, or has retorn.
The net benefit that is seen in 85% of rotator cuff repairs however suggests that a successful repair is not incompatable with a residual tendon defect. On net then with our present techniques we can hope at least to convert a symptomatic tear into an assymptomatic tear. Since we know by recent studies that a small tear need not progress this may nonetheless be an favorable outcome which is sustained. It is possible that a residual tear in the watershed zone at the junction of the supraspinatus and infraspinatus where many assymptomatic rotator cuffs are noted to occur at inconsequential to the result and represent the majority of residual tears that are assymptomatic. Despite this hope we are driven to improve our results by restoring anatomy and function. One strategy is to improve tendon fixation strength to the point where early motion is feasible. If we can justifiably extrapolate from the experience of tendon repair in the hand, a post operative environment that allows some degree of controlled active motion is optimum for healing if gaps can be prevented in the repair interface. Thusfar the predominant practice following rotator cuff repair is for no motion or very limited motion designed to be passive characterize the rehabilitation protocols following rotator cuff repair. This approach presumes that the frequency of residual defects are due to repair failure and that this results more frequently when motion is allowed. It seems as though our present methods of fixation as varied as they may be between double row and single row repairs arthroscopic or open, we have optimized the strength of fixation and it is insufficient to allow unsupervised active motion. The second strategy that is being pursued is to augment the healing process with biological adjuncts to stimulate and speed the process of healing if not to qualitatively improve the healing to better reiterate the ultrastucture of the normal tendon insertion. The possibility of one day augmenting the repair process is suggested by animal studies which show a promising effect of FGF-2 which stimulates fibroblasts. Impregnated in suture this has been shown to augment tendon healing and improve motion following flexor tendon repair in the hand. In has also been show to promote the development of sharpies fibers in some experimental models, thus this represents a promising line of future research. Early clinical efforts using PRP which contains a variety of growth factors are thusfar on no demonstrable benefit when applied within a collagen carrier to augment rotator cuss repair. The potential however is there and the devil as usual is in the details. Other pharmacological interventions are of course promising including smoking sessation, avoidance of NSAIDs and the potential that doxycycline as a MMP inhibitor thereby moderating breakdown of nacent neotendon perhaps permitting more productive healing. The latter incidentally is a suitable antibiotic against P Acne which has a predilection to produce infection especially around the shoulder.
Whether through failure of through periodic contractile inhibition secondary to pain, the rotator cuff becomes functionally insufficient even before failure of its substance leads to a loss to the normal head centering function with glenohumeral abduction. Eventually there is cephalad migration under the influence of the deltoid. The acromion and AC ligament receive compressive loads and adaptive changes occur leading to thickening of the anterior inferior acromion and ossification of the AC ligament. This abnormal boney structure then creates a secondary mode of injury by abrading the dorsal surface of the tendon acting like a wood plane. Osteophytes at the inferior surface of the A-C joint have a similar effect contributing to the process of outlet impingement. As part of the procedure for repairing the rotator cuff tear then measures are required to alter the potential for extrinsic abrasion by adjacent bony structures even if they are not as previously thought always the cause for the original tear. The bony changes that occur secondary to the tear and the altered biomechanics do however present a threat to the integrity of the repair if they abrade the structure of the healing tendon. These spurs can occur anteriorly through ossification of the coracoacromial ligament with a resultant anterior inferior prominence of the acromion, which in some cases is already curved downward anteriory. The spurs that form inferiorly at the acromioclavicular joint also potentially threaten the integrity of the repaired supraspinatus which must glide beneath this joint in the course of active shoulder motion. Failing to address these spurs but resection of the distal 8mm or so of clavicle can presumably contribute to retear. Certainly the persistence of shoulder pain following rotator cuff repair is often found to be due to AC joint arthritis which has not been addressed at the primary surgery. Indeed it seems that this pain and subsequent response to subsequent distal clavicle resection is not necessarily evident as a feature of the chief complaint. This may be due to the pain limited motion at the time of initial presentation, if may also be that the repaired tendon being bulkier is more subject to the abrading effect of the AC joint spurs, thus a relatively low threshold for concomitant resection of the distal clavicle is warranted especially if there is evidence of superior impingement on the rotator cuff by inferiory protruding osteophytes.
Rotator cuff injury in the throwing athelete has a different mechanism. The throwing athelete may develop excessive external rotion and a restricted internal rotation as a consequence of mechanical stresses on the shoulder capsule which occur with the throwing motion. The anterior capsule stretches in late cocking phase and the posterior capsule strethces in follow.
The loss of elasticity of tendons happens by an unknown mechanism. An abnormal pattern of remodeling with the rotator cuff tendon appears to be the net effect of an altered gene expression triggered by the extreme mechanical demands. Abnormally high levels of metalloproteinases implying altered collagen processing are noted in assays of torn rotator cuffs.