From a biological perspective, stiffness is a function of tissue quality (rigidity) and is defined as the resistance of a tissue structure to deformation under applied load. It is dependent on the shape and boundary conditions of the structure, not on the material itself (whereas elasticity is a property of the tissue material, independent of the shape or boundary conditions). For the rotator cuff, stiffness, in linear tension, is a function of the cross-sectional area and the Young modulus (of tendon tissue) and is inversely proportional to the length of the tissue. The architectural and associated biochemical alterations that occur in the tendons of the rotator cuff as a result of damage were elegantly demonstrated in an animal model: the addition of neuromuscular impairment appeared to severely exacerbate the structural deterioration in muscle and bone quality after simulated tendon tear1. Muscle stiffness appears to be due to the deposition of extracellular collagen, causing impairment of function in muscle fiber bundles, rather than by a mechanism affecting single muscle fibers alone. Age is known to be associated with fatty infiltration, or atrophy, of rotator cuff muscles (possibly due to associated neurological compromise, e.g., cervical spondylopathy) as well as with increasing incidence of rotator cuff tearing, diminished capacity for healing of torn tendons, and thus, higher failure rates for attempted repairs. It is also recognized that acute rotator cuff tears, largely limited to younger and more active patients, have a different prognosis. This is a function of the health of the pre-tear tendon, the capacity to mount an appropriate vascular response to the trauma and the biological capacity to achieve a healed tendon, the anatomical location of the tear (with such tears being more prevalent outside the “privileged” crescent zone), the quality of the bone at the enthesis, and the quality of the remaining tendon bounding the tear.
It follows that conflating the management and prognosis of acute traumatic tears with that of chronic degenerative (and acute-on-chronic) tears risks hiding essential and important differences that become important to the logical treatment of this wide range of conditions. In the study by McNamara et al., all primary tears that underwent arthroscopic repair have been brought together and considered as a single group, with patient age at presentation ranging from 18 to 91 years and tear size ranging from <2 cm2 (i.e., very small) to 64 cm2 (i.e., massive), and with an average operative time of just over 20 minutes for all tears and an average of 2 anchors per repair (most tears were small). Preoperative stiffness in the youngest patient (almost certainly a traumatic tear, one of the 32% of tears in this study that were traumatic) will have had notably different causes (hemorrhage and edema) and potential treatment than those in the eldest (almost certainly a degenerative tear, one of the other 68% of tears, with fibrosis and weakness as potential causes). It was interesting to note that patient-ranked shoulder stiffness at 6 months was associated with a smaller anteroposterior tear size and lower preoperative strength in external rotation, both of which would characterize the older degenerative tear, while operative time, operative technique, and no specific preoperative injury were the best predictors of postoperative stiffness at 6 weeks. Stiffness, in the sense of a change in tissue quality, is inevitable after surgery. Edema and hemorrhage will create tissue rigidity. The patients’ perception of this will be governed by internal mechanisms such as prior expectation (cultural effects) and pain levels (personal tolerance), and external mechanisms, such as the demands of the exercise program. The output—the range of motion achieved—can be measured but will not necessarily (and almost never does) equate to the patients’ assessment, at least until the later stages of recovery as pain diminishes in importance.
This article describes the condition of stiffness as judged by the patients’ subjective estimation of function (on a Likert scale) and measured in terms of passive range of motion by clinicians (with unknown observational error), and places this in the context of the preoperative biological quality of the tendon and the consequences of surgery: failure to heal, or retear. The assessment of stiffness by the patient and by the clinician are different, but are reported to be moderately correlated in this study, at least in the postoperative phase. This is similar to comparing the Constant Score with the American Shoulder and Elbow Surgeons (ASES) assessment: both measure a similar quality but with different methods and outputs, so concordance is likely, but they are not necessarily equivalent.
The study tries to explain an improvement in outcome for the repair of a tendon tear through the mechanism of stiffness in the early postoperative phase and relate this to the preoperative state of the shoulder. Statistical analysis demonstrated a small or medium correlation between retear (present or absent) and postoperative examiner assessment of range (the continuous variable), and a small correlation between preoperative patient-ranked stiffness (on a Likert scale) and examiner assessment of range postoperatively (a continuous variable). It is self-evident that preoperatively stiff shoulders will be stiffer postoperatively, unless the cause for stiffness is also addressed. The authors have discussed this previously and showed that concurrent release of capsular contractures did, in fact, enhance the rate of healing and maintenance of a healed tendon 2 years after surgery2. Stiffness, a biological reality, appears to be a requisite for the early healing response to be successful, but equally appears to be detrimental if it is prolonged or inappropriate. The difficulty is knowing, for any individual patient, when the transition between relative rest and active loading should occur, which must, in the future, be determined by biological markers rather than by imprecise assessments and subjective reports. Healing tissues go through a well-characterized process consistent through evolutionary time. We cannot enhance the rate and completeness of healing easily, other than by accurate apposition and maintenance of that position for a minimum gap, but we can certainly delay or interrupt the process readily. Permitting a rest period for the duration of cellular migration after the immediate inflammatory response makes sense, but we do not know how long that period should be in any one individual given that the healing potential of an individual’s tear varies according to genetic and environmental influences, albeit within a rather limited time frame. It might be logical to think that a smaller gap might require a shorter duration of rest, but the cellular response to surgery is the same however large the gap, and the interval of rest (cellular proliferation and migration) might actually be the same for any size of tear, given consistency in the healing gap achieved (that is, the effectiveness of the surgical technique). While an attempt has been made to demonstrate that stiffness (whether defined by the patient, by the clinician, or in biological terms) is correlated with a better outcome for the torn tendon after repair, the study flaws do not permit us to rely on this for all rotator cuff tears.
In a shoulder consultation, the term stiffness is used by patients to describe an awareness of loss of active movement(s) in daily function. It is often conflated with the other descriptors of dysfunction: pain and weakness. It is a symptom, which, with relevant other symptoms and signs, helps the clinician to diagnose the anatomical and functional state of the shoulder and formulate a prognosis. The evolution of symptoms helps us to understand how the condition impacts on the patient’s daily life, and guides judgment when determining whether operative intervention might confer benefit. Symptoms contain substantial experiential and cultural connotations. Preoperative patient experiences of stiffness are likely due to a natural reluctance to move (i.e., distort tissues) into the ranges of pain-generating positions.
From the clinician’s perspective, the term stiffness is often equated with loss of passive range of motion in an affected shoulder when compared with a normal (the contralateral or an experientially defined) shoulder, at a specific point in time. When weakness is present, the passive range of motion of a joint (clinician-defined) is greater than the active range of motion (patient-defined) unless there are fixed contractures (checkreins). Chronic rotator cuff tears frequently present with fixed contractures, often asymmetric, leading to obligate translations, which are perceived by the clinician as abnormal humeral head motion during rotational motion and by the patient as (often painful) humeral head displacement (symptomatic abnormal motion, i.e., “instability”) during activities of daily life, for example, the painful “hitch” when raising the hand above shoulder level. The implication is that a qualitative structural change has occurred in the tissues of the rotator cuff and capsule.
The use of the term stiffness, therefore, has specific meaning when used by a patient, a clinician, or a biomechanics scientist. We should be careful how we use the term. The patient describes the sensation of resistance to or loss of active motion, while the clinician observes a limitation of assisted or passive movement, thus eliminating the variable of weakness. The terms here are not synonymous.
↵* Disclosure: The author indicated that no external funding was received for any aspect of this work. On the Disclosure of Potential Conflicts of Interest form, which is provided with the online version of the article, the author checked “yes” to indicate that he had a relevant financial relationship in the biomedical arena outside the submitted work.
- Copyright © 2016 by The Journal of Bone and Joint Surgery, Incorporated