The ATRS is a self-administered instrument with high clinical utility, and we suggest the score for measuring the outcome, related to symptoms and physical activity, after treatment in patients with a total Achilles tendon rupture.

The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies. IntroductionPrimary disorders of tendons are common and account for a high proportion of referrals to rheumatologists and orthopedic surgeons [1]. The most commonly involved tendons are the rotator cuff (particularly supraspinatus) and biceps brachii tendons in the shoulder, the forearm extensor and flexor tendons in the forearm, the patella tendon in the knee, the Achilles tendon in the lower leg, and the tibialis posterior tendon in the ankle and foot.Historically, the term tendinitis was used to describe chronic pain referring to a symptomatic tendon, thus implying inflammation as a central pathological process. However, traditional treatment modalities aimed at modulating inflammation have limited success [2] and histological studies of surgical specimens consistently show the presence of degenerative lesions, with either absent or minimal inflammation [3,4]. As will be clear in this review, we favor the hypothesis that inflammation and degenerative changes often coexist in the course of tendon disorders, and their relative contributions are difficult to dissect. Therefore, the definition of 'tendinitis' has been largely abandoned and the terms 'tendinosis' or, more generically, 'tendinopathy' (TP) are now currently preferred [5].In this review we summarize recent findings useful for understanding the pathogenesis of primary tendon diseases. First, suggestions coming from epidemiology, histopathology and clinics are reported, then we discuss new data on biochemical changes that occur in experimental and human TPs. Finally, we propose a unifying theory, drawn from both experimental and clinical data. Anatomy and physiologyThe tendons are made up of bundles of collagen fibrils (primary, secondary and tertiary fibers), each wrapped in endotenon, which in turn is enveloped by an epitenon, forming the actual tendon. A true synovial sheath is present only in some tendons, such as tibialis posterior, peroneal, and extensor and flexor tendons of the wrist and the hand; other

BackgroundThe absence of any agreed-upon tendon health-related domains hampers advances in clinical tendinopathy research. This void means that researchers report a very wide range of outcome measures inconsistently. As a result, substantial synthesis/meta-analysis of tendon research findings is almost futile despite researchers publishing busily. We aimed to determine options for, and then define, core health-related domains for tendinopathy.MethodsWe conducted a Delphi study of healthcare professionals (HCP) and patients in a three-stage process. In stage 1, we extracted candidate domains from clinical trial reports and developed an online survey. Survey items took the form: ‘The ‘candidate domain’ is important enough to be included as a core health-related domain of tendinopathy’; response options were: agree, disagree, or unsure. In stage 2, we administered the online survey and reported the findings. Stage 3 consisted of discussions of the findings of the survey at the ICON (International Scientific Tendinopathy Symposium Consensus) meeting. We set 70% participant agreement as the level required for a domain to be considered ‘core’; similarly, 70% agreement was required for a domain to be relegated to ‘not core’ (see Results next).ResultsTwenty-eight HCP (92% of whom had >10 years of tendinopathy experience, 71% consulted >10 cases per month) and 32 patients completed the online survey. Fifteen HCP and two patients attended the consensus meeting. Of an original set of 24 candidate domains, the ICON group deemed nine domains to be core. These were: (1) patient rating of condition, (2) participation in life activities (day to day, work, sport), (3) pain on activity/loading, (4) function, (5) psychological factors, (6) physical function capacity, (7) disability, (8) quality of life and (9) pain over a specified time. Two of these (2, 6) were an amalgamation of five candidate domains. We agreed that seven other candidate domains were not core domains: range of motion, pain on clinician applied test, clinical examination, palpation, drop out, sensory modality pain and pain without other specification. We were undecided on the other five candidate domains of physical activity, structure, medication use, adverse effects and economic impact.ConclusionNine core domains for tendon research should guide reporting of outcomes in clinical trials. Further research should determine the best outcome measures for each specific tendinopathy (ie, core outcome sets).

Purpose The purpose of this study was to establish a relationship between the lengthening of the Achilles tendon post rupture and surgical repair to muscle activation patterns during walking in order to serve as a reference for post-surgical assessment. Method The Achilles tendon lengths were collected from 4 patients with an Achilles tendon rupture 6 and 12 month post-surgery along with 5 healthy controls via ultrasound. EMG was collected from the triceps surae muscles and tibialis anterior during over-ground walking. Results Achilles lengths at 6 and 12 months post-surgery were significantly longer (p < 0.05) on the involved side compared to the uninvolved side but there were no side to side differences in the healthy controls. The integrated EMG (iEMG) of the involved side was significantly higher than the uninvolved side in the lateral gastrocnemius at 6 months and for the medial gastrocnemius at 12 months in the patients with Achilles tendon rupture; no side to side difference was found in the healthy controls. The triceps surae muscles’ activations were fair to moderately correlated to the Achilles lengths (0.38 < r < 0.52). Conclusions The increased Achilles tendon length and iEMG from the triceps surae muscles indicate that loss of function is primarily caused by anatomical changes in the tendon and the appearance of muscle weakness is due to a lack of force transmission capability. This study indicates that when aiming for full return of function and strength an important treatment goal appears to be to minimize tendon elongation. Level of evidence Prognostic prospective case series. Level IV.

Published papers on anatomic anterior cruciate ligament (ACL) reconstruction often lack details in the description of the surgical procedure, and there are large variations in anatomic ACL reconstruction techniques. We aimed to develop a validated checklist to be used for anatomic ACL reconstruction. First, a list of all potential items that could be used in the checklist was generated. Thirty-four ACL experts were selected to participate in an anonymous online survey to rate the importance of these items on a scale of 1 to 4 (with a score of 4 having the most importance). The results were verified by surveying a large sample of 959 orthopaedic specialists who are peer reviewers for four major orthopaedic journals. Items were included in the final checklist if they received an importance score of 3 or 4 from at least 75% of the survey takers. The survey response rate was 79% (twenty-seven of thirty-four) of the ACL experts and 40% (379 of 959) of the peer reviewers. The final Anatomic ACL Reconstruction Checklist includes seventeen items with a maximum score of 19 points. The final checklist underwent preliminary testing for internal consistency, intertester reliability, and validity. Cronbach's alpha for internal consistency was 0.82, and the intraclass correlation coefficient (ICC) for intertester reliability was 0.65. This large survey-based study on anatomic ACL reconstruction resulted in the development of the Anatomic ACL Reconstruction Checklist; preliminary evidence for interpretation of the scores is provided.