Aims

The aim of this to study was to compare the previously unreported long-term survival outcome of the Oxford medial unicompartmental knee arthroplasty (UKA) performed by trainee surgeons and consultants.

Introduction

A common question posed by adolescents undergoing corrective scoliosis surgery is, “How much taller will I be after my operation?” This study aims to help answer this question, and quantify the gain in height that might be expected.

Aim

To evaluate the effect of corrective surgery for adolescent idiopathic scoliosis on pelvic morphology.

Introduction

It is becoming increasingly more accepted that Patient Reported Outcome Measures (PROMs) should be used to assess surgical interventions. We report on a pilot study of a generic database with complete pre and post-operative data sets in a UK hospital.

Aim

This aim of this study was to investigate apoptosis, reactive oxygen species (ROS), and their upstream markers in Anteromedial Gonarthrosis (AMG).

Our aim was to investigate the molecular features of progressive severities of cartilage damage, within the phenotype of Anteromedial Gonarthrosis (AMG).

Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements. The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O and H& E staining) and immunohistochemical analysis (Type I and II Collagen, proliferation and apoptosis). Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had an OARSI grade of 0 (normal). The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (p< 0.0001). There was no significant difference in the Collagen II content or gene expression between areas. The Collagen I immunohistochemistry showed increased staining within chondrocyte pericellular areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (p< 0.0001). Furthermore, real time PCR showed a significant increase in Collagen I expression in the macroscopically normal areas compared to the damaged areas (p=0.04).

In AMG there are distinct areas, demonstrating progressive cartilage loss. We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

Introduction: Anteromedial gonarthrosis (AMG) is a distinct phenotype of osteoarthritis (OA), with a specific pattern of disease. There is full thickness cartilage loss anteromedially, progressing to an area of damaged cartilage, and then to an area of macroscopically and histologically normal cartilage posteriorly. It can be considered to be a spatial model of OA progression. Apoptosis, or chondrocyte cell death, has been shown to be a feature of OA cartilage, however the triggers are poorly understood; similarly, reactive oxygen species (ROS) have been implicated in OA. They have never been studied in a replicable topographical model of OA. This study characterises the regional levels of cell death and implicated ROS in AMG using a number of immunohistochemical studies.

Method: Ten tibial resection specimens were obtained from patients undergoing unicompartmental knee arthroplasty. Eight above knee amputations (from patients with peripheral vascular disease) were used as age matched controls. Cross sections taken through all regions were paraffin embedded. Routine histology was performed and immunohistochemical studies were conducted for Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), Active Caspase 3, Cytochrome C, Active Bax, Bim, 3-Nitrotyrosine and Forkhead Box O3A (FOXO 3A).

Results: Cell death, as detected by TUNEL appeared predominantly in the surface layer of chondrocytes of damaged cartilage (p< 0.001). Median values were 23% in superficial cartilage (range 0 – 51) compared to 0% in deeper cartilage (range 0 – 15). There was a significant difference in TUNEL staining between regions (p=0.001). This ranged from 26% (most damaged) to 4% (undamaged). There was a good correlation with degree of cartilage damage (ρ=0.66, p< 0.001) asdefined by histological grade and TUNEL was significantly higher (p< 0.001) in AMG compared to the control samples which showed an average of 2% TUNEL overall. Upstream markers of apoptosis (Active Caspase 3, Cytochrome C, Active Bax), assessed qualitatively, were present in a similar distribution to that of TUNEL staining. 3-Nitrotyrosine was also shown to be a predominantly surface phenomenon. There was a significant difference (p< 0.001) between regions, ranging from 58% (most damaged) to 10% (undamaged). Again, this was significantly higher that the control samples (p< 0.001). In line with indicators of ROS mediated damage, Bim and FOXO3A were also detected.

Discussion: The mechanism of apoptosis in OA cartilage has not been studied in depth, and understanding the biochemical and molecular responses of ‘stressed’ chondrocytes may provide invaluable information about the specific causes of cell death. Such cellular responses may provide targets for disease modification, thus delaying or preventing the need for joint arthroplasty. We conclude that AMG is a phenotype demonstrating cartilage at progressive stages of disease. Apoptosis involves the intrinsic mitochondrial pathway and ROS appear to be implicated. Further work is needed to provide evidence of what lies further upstream of markers demonstrated in this study.

Anteromedial Osteoarthritis of the Knee (AMOA) is a distinct phenotype of OA. Within this pattern of disease, the anterior third of the medial tibial plateau exhibits full thickness cartilage loss. The middle third has damaged partial thickness cartilage, and the posterior third has retained cartilage, which is seen on macroscopic visual assessment to be normal. This study investigates the molecular features of progressive severities of cartilage damage within this phenotype.

Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements. The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O) and immunohistochemical analysis (Type I and II Collagen, proliferation and apoptosis). Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had a grade of 0 (normal). The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (p< 0.0001). Proliferation and apoptosis, as expected, were increased in the more damaged areas. There was no significant difference in the Collagen II content or gene expression between areas. The Collagen I immunohistochemistry showed increased staining within chondrocyte pericellular areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (p< 0.0001). Furthermore, real time PCR showed a significant increase in Collagen I expression in the macroscopically normal areas compared to the damaged areas (p=0.04).

We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

Purpose: To compare the site of lesions in medial and lateral unicompartmental osteoarthritis (OA) of the knee.

Methods: Patients with medial (n=35) and lateral (n=15) OA, having unicompartmental knee arthroplasty, were recruited. Intra-operatively, the distance between the anterior, posterior, medial and lateral margins of the full-thickness lesion and reference lines dividing the condyles was measured. The midpoints of lesions were calculated and groups were compared. Lateral radiographs were used to determine the relationship between the lesion site and knee flexion angle (KFA).

Results: Femoral lesion: In lateral OA, the midpoint of lesions was 25.0mm (SD:8.8) posterior to the reference line passing transversely through the apex of the inter-condylar notch. This was significantly different (p< 0.001) from midpoint in medial OA, which was 10.7mm (SD:9.4) posterior to the reference line.

Tibial lesion: In lateral OA, the midpoint of lesions was 2.0mm (SD:6.5) posterior to the reference line passing through the mid-coronal plane of the resected tibia. This was located significantly more posterior (p=0.038) than midpoint in medial OA, which was 2.2mm (SD:5.7) anterior to the reference line.

Knee Flexion Angle: In lateral OA, the midpoint of lesions was on average at 40° flexion and sites of smaller lesions were very variable. The lesion expanded both anteriorly and posteriorly. In medial OA, smaller femoral lesions occurred in full extension and extended further posteriorly with disease progression.

No significant difference was demonstrated in medial and lateral localisation of the lesions.

Conclusion: Medial OA begins near full extension, progresses in a predictable manner and is perhaps initiated by events occurring at heel strike. Lateral OA begins in flexion in a less predictable manner, at KFA above that seen during the gait cycle. The different sites of lesions in medial and lateral OA suggest different aetiology and pathophysiology. Therefore, prevention and treatment strategies should be different.

Aim: The aim of this study was to asses the accuracy of skyline radiographs in the assessment of the patellofemoral joint, when compared to open intraoperative assessment.

Methods: Eighty nine patients undergoing knee replacement surgery were included in the study. Skyline radiographs were obtained preoperatively. These radiographs were assessed and graded by an experienced musculoskeletal radiologist using the Altman and Ahlbäck classifications. The grades were calculated for both the medial and lateral facets of the PFJ. Intraoperative assessment of the Patellofemoral joint was undertaken at the time of surgery. The damage was graded using the modified Collins classification (0: Normal, 1: Superficial damage, 2: Partial thickness cartilage loss, 3: Focal Full thickness cartilage loss < 2cm2, 4: Extensive full thickness cartilage loss < 2cm2). Data was obtained for the Medial Facet, Lateral Facet and Trochlea.

Results: Spearman’s rank correlation coefficient between the radiographic and macroscopic changes within the lateral PFJ were poor with both the Altman 0.22 (p=0.0350) and Ahlbäck 0.24 (p=0.018). The correlation of the medial PFJ was slightly better with a coefficient for Altman 0.42 (P< 0.0001) and Ahlbäck 0.34 (P> 0.001).

Conclusion: In conclusion skyline radiographs provide a poor to moderate preoperative assessment of the degree of osteoarthritis within the patella-femoral joint. This has significant implications for establishing radiographic criteria for planning patella-femoral joint replacement.

Purpose: The aim of this study is to compare the long-term survival results of TKA in patients under the age of 60, using

revision surgery and

Method: From our knee database we identified a cohort of 60 total knee replacements that had been performed over 15 years previously. We identified those who had died, those who had been revised and established the Oxford Knee Score (OKS) for all those still surviving.

Results Using the following endpoint criteria the cumulative 15-year survival was (A) revision surgery alone = 78% (CI 12), (B) revision surgery or an OKS less than or equal to 24 (50% of total OKS) = 63% (CI 13), and (C) revision surgery or moderate pain = 48% (CI 14).

Conclusion The functional survival of TKA in patients under the age of 60 decreases in the second decade following implantation with a significant number of prostheses failing the patient due to knee pain

Aim: To investigate the molecular features of progressive severities of cartilage damage, within the phenotype of Anteromedial Osteoarthritis of the Knee (AMOA).

Methods: Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements.

The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O and H& E staining) and immunohistochemical analysis (Type I and II Collagen, proliferation and apoptosis).

Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

Results: There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had an OARSI grade of 0 (normal).

The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (ANOVA P< 0.0001).

There was no significant difference in the Collagen II content or gene expression between areas.

The Collagen I immunohistochemistry showed increased staining within chondrocyte pericellular areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (ANOVA P< 0.0001). Furthermore, real time PCR showed that there was a significant difference in Collagen I expression between the damaged and macroscopically normal areas (p=0.04).

Conclusion: In AMOA there are distinct areas, demonstrating progressive cartilage loss. We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

The aim of this study was to investigate the molecular features of progressive severities of cartilage damage, within the phenotype of Anteromedial Osteoarthritis of the Knee (AMOA).

Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements. The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O and H& E staining) and immunohistochemical analysis (Type I and II Collagen). Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had an OARSI grade of 0 (normal).

The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (ANOVA P< 0.0001). There was no significant difference in the Collagen II content or gene expression between areas. The Collagen I immunohistochemistry showed increased staining within chondrocyte territorial areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (ANOVA P< 0.0001). Furthermore, real time PCR showed that there was a significant increase in Collagen I expression in the macroscopically normal areas (p=0.04).

In AMOA there are distinct areas, demonstrating progressive cartilage loss. We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

Introduction: The first line treatment in our centre for Morton’s neuroma (MN), sufficient to warrant intervention, is a peri-neural Ultrasound guided injection of corticosteroid (USI).

The NHS will soon implement 18 week referral to treatment targets.

A prospective study was performed whereby from 2004–6, referral letters from General Practitioners suggesting a diagnosis specifically of Morton’s neuroma, resulted in randomised assignment to either direct referral for USI or to the specialist Foot and Ankle outpatient clinic.

Patients with less specific referral letters were evaluated in clinic and referred for USI as appropriate.

A comparison was made of the sensitivity and specificity of the referral pathways, financial implications and the time to treatment (TTT).

Results: 121 patients were referred for USI.

Of 57 patients for whom the GP had diagnosed a MN, 40 (70%) had the diagnosis confirmed on USI (other diagnoses were: 7 NAD, 3 ganglions, 2 bursae, 2 degenerative change, 1 glomus tumour, 1 angioleiomyoma, 1 SOL); this was comparable to the overall number referred to radiology with a suspected MN (69%).

In the directly referred group, the mean TTT was 115 days (95%CI = 89 – 141), compared to 241 days (95%CI = 223 – 259) for those patients who went via a Foot and Ankle clinic. P< 0.0001.

Conclusion: For patients with features highly suggestive of a Morton’s neuroma, direct referral from primary care for USI has a similar sensitivity and specificity to referral from a specialist hospital clinic and the TTT is significantly shorter.

The mean wait of this group is within the 18 week government target without any changes to our current radiology protocols. Using this direct referral protocol we saved 29 outpatient appointments; if followed for all eligible patients we would have saved 57 outpatient appointments.

Anteromedial osteoarthritis is a distinct phenotype of osteoarthritis. The arthritic lesion on the tibia is localised to the anteromedial quadrant with an intact ACL. Deficiency of the ACL leads to a progression to tricompartmental disease. Within the spectrum of intact ACL a varying degree of ligament damage is seen. Our aim was to correlate the progression of ACL damage to the geographical extent of disease and the degree of cartilage loss on the tibial plateau.

We systematically digitally mapped 50 tibial plateau resection specimens from clinical photographs of patients undergoing unicompartmental arthroplasty, additionally the damage to their ACL was graded (0: normal, 1:synovium loss, 2:longitudinal splits)

These images were imported into image analysis software. Accurate measurements were made of the dimensions of the specimen. Measurements included the AP distance to the anterior and posterior aspect of the lesion, and the distance to the start of the macroscopically non damaged cartilage. The areas of cartilage damage and full thickness loss were also recorded. The results were represented as a % of total area to account for variation in size of the resection specimens. We compared % of full thickness loss in patients with normal to those with damaged, but functionally intact ligaments.

All specimens had a similar macroscopic appearance. A significant difference was seen with the progression of ACL damage and area of eburnation of bone. Using an unpaired t test, a significant difference in area of % full thickness cartilage loss (P=0.047) was seen between patients with a normal and longitudinal splits within their ACL. No correlation between the clinical status of the ACL and start or finish point of cartilage loss on the tibial plateau

We surmise that the progression from anteromedial to tricompartmental osteoarthritis of the knee may be related to the graduated damage of the ACL.