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Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_XXIII | Pages 121 - 121
1 May 2012
Sonnabend D Smith M Little C
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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.


Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_XXIII | Pages 8 - 8
1 May 2012
Sonnabend D
Full Access

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.