Aims

The evidence demonstrating the superiority of early MRI has led to increased use of MRI in clinical pathways for acute wrist trauma. The aim of this study was to describe the radiological characteristics and the inter-observer reliability of a new MRI based classification system for scaphoid injuries in a consecutive series of patients.

Aims

To determine the role of early MRI in the management of suspected scaphoid fractures.

Introduction

Osteoarthritis (OA) involves pathological change in all joint tissues, including cartilage degradation and synovitis. Synovial inflammation is significantly associated with pain severity and incidence in knee OA. It is becoming evident that synovitis also plays an active role in the initiation and progression of cartilage erosion in OA, through direct secretion of catabolic enzymes as well as factors that stimulate chondrocyte catabolic activity. Therapeutic agents that target both synovitis and cartilage pathology are likely to be maximally beneficial in treating pain and slowing cartilage breakdown in OA. We have previously shown that an amide-derivative of HA (HYMOVIS™) was superior to native HA of the same MW in improving gait, and reducing synovial hyperplasia in a sheep OA model. In the present study the mechanisms whereby the chemically modified HA may be beneficial were examined using chondrocytes and synovial fibroblasts from knees of OA patients.

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.

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 [1]. Previous research in our laboratory has shown that aggrecanase expression is markedly up-regulated by stress deprivation. This finding in combination with the results of the present study suggest that the aggrecanase molecules may provide a future therapeutic target for the treatment tendinopathy.

Introduction: The aetiology of dystrophic disc calcification in adult humans is unknown but a well-described clinical disorder with hydroxyapatite as the single mineral phase. Comparable but age-related pathology in the sheep could serve as a model for the human disorder. The objective of this study was to investigate the mineral phase, its mechanisms of formation/association with degeneration in a naturally-occurring animal model of disc calcification.

Methods: Adult sheep lumbar intervertebral discs (n=134) from animals aged 6 (n=4), 8 (n=12) and 11 years (n=2) were evaluated using radiography, morphology, scanning and transmission electron microscopy, energy dispersive X-ray spectroscopy, X-ray powder diffraction, histology, immunohistology and proteoglycan analysis.

Results: Half of the 6 yr, 84% of the 8 yr and 86% of the 11 yr old discs had calcific deposits. These were not well delineated by plain radiography. They were either:

punctate deposits in the outer annulus,

Their maximal incidence was in the lower lumbar discs (L4/5-L6/7) with no calcification seen in the lumbosacral or lower thoracic discs. All deposits were hydroxyapatite with large crystallite sizes (800–1300 angstrom) compared to cortical bone (300–600 angstrom). No type X-collagen, osteopontin or osteonectin, were detected in calcific deposits although positive staining for bone sialoprotein was evident. Calcified discs had less proteoglycan of smaller hydrodynamic size than non-calcified discs.

Discussion: Disc calcification in ageing sheep is due to hydroxyapatite deposition. The variable but large crystal size, lack of protein markers indicate that this does not occur by an ordered endochondral ossification-like process. The decrease in disc proteoglycan content and size suggests an association between calcification and disc degeneration in ageing sheep. There are notable dissimilarities between hydroxyapatite deposition disorder in humans and sheep. No mechanistic explanation can be offered for the different spinal distributions, thoracic and upper lumbar in the former and lumbar in the latter; hydroxyapatite deposition disorder has occasionally been seen in the lumbar spines of four year old sheep during the course of other studies but not at an earlier age. Diffferences in spinal biomechanics may be implicated but hydroxyapatite deposition does not primarily affect the most or least mobile discs in either species. Neither can an explanation be offered for the apparent immunity of the ovine lumbosacral disc to calcification. However, it is known that proteoglycan turnover is faster at this spinal level than at more proximal lumbar discs. While we have been unable to elucidate the mechanism of hydroxyapatite deposition disorder in sheep, clearly it is different from that in normal osteogenesis. We contend this animal provides a useful, naturally-occurring model for investigation of the aetiology and pathogenesis of human hydroxyapatite deposition disorder, notwithstanding obvious differences between sheep and man.

Introduction: Surgery and the use of pneumatic tourniquets lead to an increase in the activity of the fibrinolytic system, which in turn may accentuate the blood loss during knee arthroplasty. Drugs that inhibit the fibrinolytic system may thus be used to reduce blood loss. Tranexamic acid (TA) acts by binding to one of the enzymes at the start of the coagulation cascade, so inhibiting the fibrinolytic system. A concern is that this inhibition may have the side effect of increasing thromboembolic disease, a common complication of joint replacement surgery. We aim to confirm the reductions in blood loss and to assess the impact of TA usage on clinical and sub-clinical DVT.

Method: We performed a prospective, randomised, double blind, controlled trial, using patients due to undergo primary unilateral total knee arthroplasty. Patients were randomised to receive either 15mg/kg of tranexamic acid or a similar volume of normal saline at the time of cementing of the prosthesis. Perioperative blood loss was recorded and patients were screened for DVT with duplex ultrasound assessment of both legs on the fifth post-operative day.

Results: A statistically significant (p=0.006) decrease in blood loss in the early post operative period was noted in the group receiving tranexamic acid. This was not associated with a significant difference in total blood loss (p=0.55) or in transfusion requirements. There was no evidence of DVT in either group on duplex ultrasound screening of the lower limbs.

Interpretation: One injection of 15mg/kg of tranexamic given at the time of cementing the prosthesis in total knee arthroplasty, before deflation of the tourniquet, significantly decreases the amount of blood loss in the early post operative period. The treatment was not associated with an increase in thromboembolic complications.

Aims: To assess the value of hip arthrography in planning definitive treatment for children with DDH and Perthes’ disease.

Background: It is sometimes unclear whether children with DDH and Perthes’ disease need an operation. Surgeons are guided by the clinical symptoms and signs together with the radiographic appearances of the affected hip. In our Unit children on whom an operation is considered undergo an examination under anaesthetic (EUA) and a hip arthrogram. This prospective study was developed to assess whether treatment was modified by the arthrogram.

Methods: All patients who underwent an EUA and hip arthrogram for DDH or Perthes’ disease over a 10 month period were entered into this prospective study. Prior to arthrography a Consultant Children’s Orthopaedic Surgeon formulated a treatment plan. A standard arthrogram was performed which included anteroposterior, frog lateral, Von Rosen and oblique views. Traction axial loading views were taken to assess stability. Following EUA and arthrogram the Consultant Surgeon formulated a definitive treatment plan. Three Children’s Consultants were then invited subsequently to review the preoperative and arthrographic appearances blindly to monitor reproducibility. Twenty-one patients with DDH and 19 with Perthes’ disease were entered into the study.

Results: In the DDH group of patients the treatment plan was modified in 12 of the 21 patients as a consequence of the arthrogram. Six of the 19 patients (31.6 %) of the Perthes’ affected patients had their treatment modified. When it was felt likely prior to EUA a conservative treatment was indicated. The correlation of intra-observer Consultant agreement was high but inter-observer Consultant agreement was moderate only. In both groups of patients the range of hip motion was significantly greater under anaesthesia.

Conclusion: Static and dynamic arthrography helps decision making in patients with DDH and Perthes’ disease.

A systematic review of the English language literature has suggested that the performance of linked and unlinked elbow replacement implants differ in terms of function, survival and mode of failure; however, in this review, only one comparative series using contemporary implants was identified. We have performed a cohort study of Kudo, Souter-Strathclyde and Coonrad-Morrey elbow replacements performed at a single centre by or under the direct supervision of a single Consultant shoulder and elbow surgeon to see if these findings were reflected in clinical practice. The first forty implantations in patients with Rheumatoid arthritis for each device have been reviewed with respect to surgical complications, elbow function and implant survival. The follow-up was shorter for the Coonrad-Morrey cohort. In terms of pain relief and range of motion, the performance of the implants was comparable. The mode of failure was different, with no dislocations/ instability seen with the linked Coonrad-Morrey implants. The loosening rate of the Coonrad-Morrey implants (both clinical and radiographic) was lower, albeit with a shorter follow-up period. The loosening rates seen in this series were higher than those previously reported in the English language literature. We conclude that the functional performance of the implants, at similar stages of the surgical learning curves, are similar in patients with Rheumatoid arthritis, but that use of a linked implant removes the risk of post-operative instability and may reduce the risk of the radiographic and clinical loosening.

There is an increasing interest amongst surgeons and demand from patients for hip resurfacing. One concern regarding resurfacing is the incidence of femoral neck fracture post operatively. McMinn and Treacy report an incidence of 0.4% in their series, our finding was of an incidence of over four times as high (1.9%). We looked at our database of hip resurfacings and tried to identify the risk factors for fracture.

We identified 11 fractures and compared these with 22 controls selected by choosing the cases performed by the surgeon immediately before and after the fracture case. We analysed their medical notes and x-rays. Statistical analysis was performed using a package in ™Excel. The implants were either Birmingham Hip (Midland Medical Technologies) or Cormet (Corin) resurfacings.

No statistically significant correlation was found for sex, age or body mass index. We found that fracture was twice as likely in the presence of possible or probable osteopenia. We did not find that fracture was more likely to occur in patients with a previous diagnosis of Perthes, DDH, SUFE and avascular necrosis (AVN).

We found patients with a superior overhang of the femoral component on the neck did not risk fracture, however we could not demonstrate that notching in itself increased the risk of fracture.

There was no correlation with neck-shaft and stem-shaft angle or neck lengthening and offset and subsequent neck fracture.

In 13 bilateral cases there was fracture in 3 (incidence 23%). Apart from one fracture that occurred at 18 weeks post-operatively all the others occurred before eight weeks. Five fractures occurred in patients who subsequently on histological analysis were found to have avascular necrosis.

We conclude that bilateral surgery is probably unwise. That a superior overhang seems to protect against fracture as long as this is not at the expense of creating an inferior notch. Finally, we find AVN in a number of retrieved heads, what is the true incidence of AVN and does the approach adopted cause the avascular process and if so why do we see so few fractures?

Aims: To determine the pathological changes in the femur following resurfacing hip arthroplasty and identify possible causes of early failure. Methods: Bone samples from 8 femoral heads at several levels were examined histologically following removal of cemented femoral head surface replacement following aseptic early failure: 4 neck fractures (no history of fall), 3 persistent severe pain and 1 cup loosening. Intra-operatively no obvious macroscopic causes of failure (including notching the neck) were noted. In all patients, the initial diagnosis had been osteoarthritis. None had known risk factors for osteonecrosis. Results: In the patients who had recent fracture, the bony changes were suggestive of relatively longstanding osteonecrosis with degenerative, necrotic and þbrotic changes in the bone marrow and loss of osteocyte nuclei in the trabeculae. There was appositional new bone formation at the surface of the necrotic bone trabeculae. The changes were consistent with osteonecrosis of more than 2 weeks duration and probably preceded the fracture in all cases. In the patients who underwent revision for non-fracture, some osteonecrosis was seen, but this was a lot less than when a fracture had occurred. Conclusion: Osteonecrosis of the femoral head is seen following resurfacing hip arthroplasty and may be a predisposing factor in patients who subsequently fracture.