R Appleyard, Murray Maxwell Biomechanics Lab, Royal North Shore Hospital, Sydney The fundamental mechanisms that underlie tendon breakdown are ill understood. There is an emerging hypothesis that altered mechanical strain modulates the metabolism and/or phenotype of tenocytes, disrupting the balance of matrix synthesis and degradation, and that rupture then occurs through an abnormal tendon matrix. The critically regulated genes have not yet been determined. We have developed sheep model in sheep where both stress-deprived and over-stressed areas can be examined in the one tendon, to evaluate the pathological and molecular changes over time. We have also used ‘wild type’ and genetically modified mice to determine the role of specific enzymes and proteoglycans in tendon degeneration. Stress-deprived and over-stressed regions showed classical changes of increased cellularity and vascularity, rounded tenocytes and interfascicular matrix infiltration. These structural changes resolved for up to one year after injury. Resolution was more rapid in over-stressed regions. Irrespective of the initiating stress, proteoglycan staining and chondroid metaplasia increased in tendon with time. There were distinct molecular and temporal differences between regions, which are reviewed here. While tendon degeneration has traditionally been regarded as a single field of change, our studies show that at a molecular level, the injured tendon may be regarded as a number of distinct regions—overloaded and underloaded, adjacent to bone or adjacent to muscle. Each region manifests distinct molecular changes, driven by relevant gene expression. While collagen metabolism in pathological tendon has received much attention, accumulation of proteoglycan is also consistently induced by altered mechanical loading. We suggest that ADAMTS enzymes, which cleave aggrecan, versican and small proteoglycans, may play a significant role in tendon homeostasis and pathology. Regulating proteoglycan turnover may represent a novel target for treating tendon degeneration. We have initiated studies using mesenchymal stem cells (MSC), not to directly augment healing but to modify the molecular pathology in tendon resulting from altered loading. Preliminary data indicates that injection of MSC into an acute tendon defect significantly abrogates the increase in expression of aggrecan and collagen degrading metalloproteinases in the adjacent over-stressed tendon. This may decrease the resultant degeneration. The effects of MSC in treating tendon degeneration are reviewed here, as are the possible benefits of radiofrequency microtenotomy.
Thirty years ago, rotator cuff surgery was exceedingly uncommon and shoulder arthroplasty almost unknown. Surgery for shoulder instability was largely empirical, non-anatomical and frequently unsuccessful. With the help of arthroscopy and MR scanning, a complex array of labral, ligament and tendon pathologies can now be recognised and treated, precisely and predictably. Anatomy-restoring arthroscopic techniques have largely replaced open stabilisation surgery. As life expectancy rises and citizens remain active into their seventh and eighth decades, the call for rotator cuff surgery has risen dramatically. Complex tendon transfers have expanded the indications for cuff surgery. Open repair has in part been supplanted by increasingly sophisticated arthroscopic techniques. The potential use of orthobiologics and stem cells promises further advances in the foreseeable future. Following the successful development of humeral hemiarthroplasty, and later of total shoulder replacement, surgical techniques and clinical indications for arthroplasty are now well refined. Predictable outcomes have been further enhanced by the present generation of ‘anatomic’ prostheses. More recently, the ‘rediscovery’ and improvement of semi-constrained (reverse) prostheses has transformed the previously dismal outlook for sufferers of cuff arthropathy and similar conditions. Many Australian Orthopaedic Association trainees undertake post-specialisation fellowships in shoulder surgery, both at home and abroad, and there is a steady flow of young overseas fellows through Australian shoulder units. The Shoulder and Elbow Society of Australia, founded in 1990 as a loose grouping of interested colleagues, now boasts over 70 active members. Australian surgeons and researchers are well represented in the prestigious Journal of Shoulder and Elbow Surgery and Australian shoulder surgery has come of age.
The morbidity associated with tendinopathy is a costly burden on our health system. Recent investigations in our laboratory have shown that alterations in mechanical stress cause significant changes in tendon expression of key matrix molecules and proteolytic enzymes including the aggrecanase molecules, (e.g. ADAMTS-5). Here, we investigate the biomechanical consequences of such altered tensile stress in tail tendons from mice with and without deletion of the ADAMTS-5 gene. Tail tendons from 12 week old C57BL6 wild type and ADAMTS-5 knock-out mice were immediately snap frozen (ex vivo), or cultured stress deprived for 120 hours in DMEM/10% FCS (eight tendons per group). Material properties including maximum stress, strain and elastic modulus were determined for each tendon in uniaxial tension to failure at a constant strain rate of 1.0 mm/second (10% strain/second) on an Instron 8874 servo-hydraulic testing apparatus. Significant differences between groups were determined with Kruskal-Wallis one-way analysis of variance, followed by Mann-Whitney U test with Benjamini-Hochberg post-hoc corrections for multiple comparisons. Stress deprivation for 120 hours led to a significant increase in maximum stress for both the wild type (~150% increase, p = 0.0008) and ADAMTS-5 deficient (~100%, p = 0.0033) mice when compared to ex vivo tendon. Stress deprivation led to a 100% increase in elastic modulus compared to ex vivo for the wild type tendons (p = 0.0033) but failed to increase this parameter in the ADAMTS-5 deficient mice. When the effect of stress deprivation of the ADAMTS-5 deficient mice was directly compared to the wild type stress deprived tendons, a 35% decrease in elastic modulus was found (p = 0.021). We have shown for the first time that deletion of an aggrecanase molecule significantly decreases the material properties of tendon. Alterations in the expression of the aggrecanase molecules may play a role in the development and progression of tendinopathy through their ability to modulate the metabolism of aggrecan [
Surgeons often protect Tendon-bone reconstructions such as rotator cuff repairs by off loading them. We investigated the effect of limb position and boundary conditions in an in-vitro rabbit patella tendon-bone repair model. Patella tendons were repaired back to the tibia in eight hindlimb cadavers with 2 mitek anchors(Mitek, Westwood, MA) and 3-0 Ethibond (Ethicon, Sommerville, NJ) using two techniques, one involving simple sutures and the other involving crossing over between the sutures. A loading mechanism through the patella tendon was constructed using static weights over a pulley mechanism. The contact area and force at the PT-bone interface were measured using a TekScan pressure sensor (6911, TekScan, South Boston, MA). The contact footprint (area and normal force) was acquired under four configurations: (1) knee full extension with interface unloaded, (2) knee 45° flexion with interface unloaded, (3) knee full flexion with interface loaded by limb weight alone, (4) tendon loaded with limb weight and 20N force applied through tendon loading mechanism. The contact area force footprint changed substantially between the different suture techniques and loading configurations. Crossing over of sutures appears to provide an increased and more evenly distributed force across the tendon-bone interface. Repair off-loading was accompanied by a decrease in the contact footprint force and pressure. The force in both suture techniques increased with increasing flexion angle and was substantially increased by both bearing the weight of the dependent limb and by an axial load in the patellar tendon. Off loading a repair may not provide optimal environment for healing.
The surgical technique involved an arthrodesis at the acromio-clavicular joint and coraco-clavicular space using autogenous iliac crest bone graft and fixation with both tension band wires and a cancellous screw.
The fusion rate was 75% (six out of eight). Pain, measured using a Visual Analogue Scale (0 to 10), was reduced from 8.5 pre-operatively to 3.1 post-operatively. The patient’s perception of instability reduced from an average of 9.0 to an average of 1.0. The range of motion increased in five patients, decreased in two and remained the same in one. All of the patients would have the operation again and seven out of eight were very satisfied. The complications included the two non-unions, mild sterno-clavicular pain in two cases and a need to remove K-wires in seven instances.