We compared the early complication rates of total hip (THA) and total knee (TKA) arthroplasty carried out at a regional orthopaedic hospital (AOC) and two Independent Sector Treatment Units (ISTUs) (WGH and CNH). After THA, reoperation rates were higher at CNH (9%) than AOC (0.6%) or WGH (1.4%). After TKA, reoperation rates at CNH were (8%) higher than AOC (1%) and WGH (1.9%).

5% of patients undergoing TKR at CNH underwent 2 stage revision for deep infection.

After THA, dislocation rates at CNH (6%) were higher than AOC and WGH (1.8%). Readmission from CNH (13%) was higher than AOC (1.2%) and WGH (0.6%).

Major wound problems at CNH (20%) were higher than WGH (3.8%) and AOC (0.4%).

After TKA, major wound problems were higher at CNH (19%) compared to WGH (1.9%) and AOC (1.1%). Readmission rates not requiring surgery from CNH (13%) were higher than AOC. (1.1%) and WGH (1%). AOC and WGH audited their outcomes. None were available from CNH. WGH initially missed many of their complications because they presented at base hospitals elsewhere.

ISTUs performed approximately 2/3rds of procedures for which patients had been referred from base hospitals.

At CNH, 23% were rejected on grounds of potential co-morbidity. Audit from ISTUs is inferior to NHS hospitals and the results in one of those audited significantly worse.

Patients offered surgery at ISTUs should be told that the audited outcome of the surgeon who will be treating them is not known and that, in some, results are inferior to surgery in the NHS.

Purpose of Study: Fixed bearing unicompartmental knee replacement (UKR) has become popular since several series have now shown good 10 year survivorship and excellent function. However little is known about survival during the second decade.

Method: From the Bristol database of over 4000 knee replacements 203 St. Georg Sled UKR’s which had already survived 10 years were identified. The mean age at surgery was 67 years (48–85), with 64% being female. This cohort has been further reviewed at an average of 14.8 years (10–30) from surgery to determine survivorship and function.

Results: Survivorship during the second decade was 87.5%. 58 patients (69 knees) had died with implant in situ and only 2 after revision. A further 15 UKR’s have been revised at an average of 13 years post op; 7 for progression of disease in the opposite compartment, 4 for tibial loosening, 3 for polyethylene wear, 2 for femoral component fracture and 2 for infection.

99 knees were followed for 15 years, 21 knees for 20 years and four for 25 or more years. The average Bristol knee score of the surviving knees fell from 86 to 79 during the second decade, largely as a result of aging.

A previous study of the St Georg. Fixed bearing UKR showed an 89% 10 year survivorship and this is now extended to 82% at 15 years and 76.5% at 20 years.

Conclusion: Satisfactory survival of fixed bearing UKR can be achieved in the second decade suggesting that the indications for mobile bearings require careful definition since there is a higher incidence of complications in many people’s hands.

We examined the vasoconstrictive actions of neuropeptide Y (NPY) in the intact medial collateral ligament (MCL) of normal and anterior cruciate ligament (ACL) -deficient rabbit knees. Blood flow to the surgically exposed MCL was measured using high-resolution laser speckle imaging (LSI) before and after topical administration of NPY and the α₁-adrenoreceptor agonist phenylephrine. In control rabbit knees, dose-dependent vasopressor responses were significantly greater than those in ACL-deficient knees, where there was little or no vasoconstrictor response. We conclude that chronic ACL deficiency markedly changes the vascular physiology and pharmacology of the surrounding articular tissues.

To determine the effect of chronic ACL-deficiency on the physiologic responses to the potent sympathetic vasoconstrictor NPY.

Abrogation of the vasoconstrictor response to both NPY and phenylephrine indicates that chronic ACL deficiency induces major changes in the vascular physiology of associated articular tissues.

This study is the first to examine the vasoregulatory role of NPY in the MCL of unstable knee joints using LSI.

In control rabbits, topical administration of NPY produced dose-dependent vasopressor responses (maximal effect at 10⁻¹⁰mol NPY). In ACL-transected knees there was little or no response to NPY (Figure 1). BIBP 3226 (selective NPY-Y1 receptor antagonist) did not affect the constrictor response to NPY in normal tissue, indicating that a receptor other than Y-1 mediates the response.

Many neuropeptides participate in the post-traumatic inflammatory response. The sympathetic-derived NPY helps regulate inflammatory responses, is a vasoconstrictor and stimulates angiogenesis. Rupture of the ACL induces inflammation, hyperaemia and angiogenesis in the MCL. These changes in vascular physiology induced us to study the effect of ACL-deficiency on the actions of NPY in the MCL.

Unoperated control (n=6) and 6-week ACL-transected (n=5) adult rabbits were used. Under anaesthesia, the MCL was surgically exposed and tissue blood flow was measured in real time using LSI as various doses and combinations of NPY, phenylephrine, and BIBP 3226 were administered topically.

Possible causes of the reduced vasoconstrictive response to both NPY and phenylephrine in the MCL after 6wk of ACL-deficiency include change in the distribution or functionality of their specific receptors or inactivation of the associated down stream signalling pathways.

Funding: This work was supported by funding from the CIHR and the Alberta Heritage Foundation for Medical Research.

Please contact author for tables and/or graphs.

Our aim was to determine the effect of denervation on repair-associated mRNA levels in the MCL after partial tear.

Cohorts of rabbits underwent partial MCL tear with or without concomitant femoral nerve transection. Ligaments were harvested, RNA extracted and RT-PCR was performed using rabbit-specific primers for repair-associated molecules at three days, two wks, six wks and sixteen wks post-injury.

Angiogenesis genes MMP3, MMP13, matrix components Collagen I and III and growth factors TGF-ß and NGF mRNA levels were increased in the denervated group at two-weeks post-injury (p< 0.05).

Denervation significantly alters mRNA levels during the early stages of rabbit MCL healing.

To determine the effect of denervation on repair-associated mRNA levels in the injured medial collateral ligament (MCL). Previous experiments revealed that denervation impairs healing of the MCL. We hypothesized that denervation would decrease repair-associated mRNA levels in the injured MCL when compared with normally innervated injured MCL.

Adult, skeletally mature female rabbits were assigned to one of four groups: unoperated control, femoral nerve transection alone (denervated controls), MCL partial tear and denervated MCL partial tear. At three days, two weeks, six weeks or sixteen weeks post-surgery, cohorts of six rabbits from each experimental group were killed. Control rabbits were assessed at two weeks. Ligaments were harvested, RNA extracted and RT-PCR was performed using rabbit-specific primers.

In the denervated injury group, mRNA levels of angiogenesis genes MMP-3 and MMP-13, matrix components Collagen I and III and growth factors TGF-ß and NGF had all increased at two-weeks post-injury, in comparison to non-denervated (p< 0.05). We also found increased levels of MMP-3 and NGF mRNA in the denervated group at sixteen weeks post injury (p< 0.05). The mRNA levels of the housekeeping gene GAPDH were increased in the denervated group only at three days post injury (p< 0.05). Of note, TGF-ß mRNA levels were significantly decreased in the denervated group at three days post injury (p< 0.05).

Contrary to our initial hypothesis, denervation increases mRNA levels for many important molecules during the early stages of MCL healing. Additional research will be required to explain how and why denervation impairs ligament healing.

No previous study has shown that innervation regulates mRNA levels in healing ligament.

Joint instability was induced by posterior cruciate ligament (PCL) transection. This resulted in significant changes in medial collateral ligament (MCL) gene expression as early as three days after injury that persisted as long as 6 weeks. We noted substantial changes in expression of matrix-metalloproteinases (MMPs) −1, −3 and -13, with reciprocal effects on their specific inhibitors TIMP-1 and −3. Sustained changes in expression of these angiogenesis-associated matrix-degrading enzymes likely account for the observed degradation of the mechanical properties of secondary stabilizers in chronically unstable joints.

To determine changes in gene-expression induced by traumatic instability.

Instability activates aberrant expression of angiogenesis-associated matrix metalloproteinases.

PCL transection induces a significant increase in the expression of MMP-3 and decrease in its specific inhibitor TIMP-3 with opposite effects on MMP-1 and TIMP-1 as early as three days after injury.

Understanding the changes in gene expression induced by instability may lead to specific treatments that could prevent the “collateral damage” to secondary stabilizing structures.

Under anaesthesia, four cohorts of six adult rabbits underwent surgical transection of the PCL. Three days, and two, six and sixteen weeks later, the MCL was harvested and the relative expression of TGF-β, MMP-1, -3, and −13, and their tissues inhibitors, and urokinase-type plasminogen activator (uPA) was measured using semi-quantitative RT-PCR.

Previous work revealed increased in blood flow by two weeks and increased vascular volume by six weeks in the MCL of PCL-deficient joints. These changes are preceded by substantial changes in expression of mRNA for matrix degradation enzymes involved in the early stages of angiogenesis. This aberrant expression of matrix metalloproteinases likely accounts for the progressive degradation of the mechanical properties of secondary stabilizing structures seen in chronic instability.

Funding: This work was supported by funding from the CIHR and the Alberta Heritage Foundation for Medical Research.

Please contact author for figures and/or graphs.

Ten New Zealand White rabbits underwent anterior cruciate ligament transection (ACLX), then reconstruction using a mersiline tape graft and mitek mini anchors. Animals were divided into two groups and sacrificed at six and fourteen week after surgery. Medial collateral ligament (MCL)-complexes were evaluated for joint laxity, and periarticular tissues evaluated for changes in vascular volume. Both reconstructed groups showed significantly reduced MCL-complex laxity and inflammatory angiogenesis compared to ACLX controls. This reconstructive method (using an artificial graft) provided transient restabilization out to 6 and 14 wk after ACLX in the rabbit, with a high 80% success rate of intact grafts.

To refine a method of ACL reconstruction in the New Zealand White (NZW) rabbit to study angiogenic adaptations in a restabilized knee joint.

The artificial graft approach provided transient restabilization out to six and fourteen week post ACLX with an 80% success rate, and reduced MCL-complex laxity and inflammatory angiogenesis.

Addressing joint instability after ACLX reduces inflammatory angiogenesis and mechanical deterioration in peri-articular tissues, and delays the progression of OA.

Compared to normal control tissues, loss of the ACL resulted in marked joint instability, and significantly increased vascular volumes in all periarticular tissues examined six and fourteen week post-ACLX. However, following transient restabilization using reconstructive surgery, MCL-complex laxity and periarticular tissue vascular volume were significantly reduced at both the six and fourteen week intervals compared to ACLX controls.

ACL reconstructive surgery was performed on the right knee of ten skeletally mature NZW rabbits using a mersiline tape graft and mitek mini anchors, immediately after the ACL had been transected. MCL-complex laxity was measured in all joints using established biomechanical procedures. To assess the effect of joint restabilization six and fourteen week after ACL reconstruction, limbs were infused with a 5% carmine red dye/5% gelatin solution, and the vascular volume of periarticular tissues was detemined.

The artificial graft approach to rabbit ACL reconstruction resulted in a high success rate of intact grafts 6 and 14 wk post-ACLX. The transient restabilization of an ACLX knee joint results in less inflammatory angio-genesis in periarticular tissues.

Funding: CIHR