This study investigates if there is a significant difference in this angle as measured on MRI between a study cohort with early AMG (partial thickness cartilage damage and intact ACL) and a comparator control cohort of patients (no cartilage damage and ACL rupture).
The results of mobile bearing Oxford unicompartmental knee replacement (UKR) in the lateral compartment have been disappointing (five-year survival: 82%). Therefore, it is recommended that mobile bearings should not be used for lateral UKR. This low survivorship is primarily due to a high dislocation rate. A detailed analysis confirmed the elevated lateral tibial joint line to be a contributory factor to bearing dislocation. A new surgical technique was therefore introduced in which care was taken neither to remove too much bone from the distal femur nor to over tighten the knee and therefore ensure that the tibial joint line was not elevated. Other modifications included use of a domed tibial component. The aim of this study is to compare the outcome of these iterations: the original series (series I), those with improved surgical technique (series II) and the domed tibial component (series III). The primary outcome measure was bearing dislocation at one year. One year was chosen as all the dislocations in the first series occurred within a year. In the original series (n=53), implanted using a standard open approach, there were six dislocations in the first year, the average flexion 110°, and 95% had no/mild pain on activity. In the second series (n=65), there were 3 dislocations, the average flexion was 117°, and 80% had no/mild pain on activity. In the third series with the modified technique and a convex domed tibial plateau, there was one dislocation, average flexion was 125° and 94% had no/mild pain on activity. At four years the cumulative primary dislocation rates were 10%, 5% and 0% respectively, and were significantly different (p=0.04). The improved surgical technique and implant design has reduced dislocation rate to an acceptable level so a mobile bearing can now be recommended for lateral UKR.
About ten years ago we introduced sophisticated instrumentation and an increased range of component sizes for the Oxford unicompartmental knee replacement (UKR) to facilitate a minimally invasive surgical (MIS) approach. The device is now routinely implanted through an incision from the medial pole of the patella to the tibial tuberosity. This has resulted in a more rapid recovery and an improved functional result. As the access to the knee is limited there is a concern that the long term results may be compromised. The aim of this study was to determine the 10 year survival. A prospective follow up of all Phase 3 minimally invasive Oxford UKR implanted by two senior authors (DWM &
CAFD) has been undertaken. So far 1015 UKRs have been implanted for anteromedial osteoarthritis. All patients received a cemented implant through a MIS approach and were followed up prospectively by an independent observer. The data was collected prospectively regarding pre-operative status, complications and clinical as well as functional outcome at predetermined intervals. The average age of patients was 66.4 years (range: 33 – 88) with mean Oxford Knee Score 41 (SD: 7.9) at the time of last follow up, Knee Society Score (objective) of 84 (SD: 13) and Knee Society Score (functional) of 83 (SD: 21). At ten years the survival of this cohort is 96%. There were 22 revisions including 7 for progression of arthritis, 5 for infection, 5 for bearing dislocation, 4 for unexplained pain and one for rupture of ACL secondary to trauma. We conclude that the Oxford Knee can be implanted reliably through a minimally invasive approach, giving excellent long term results.
90% of lateral compartments were normal and none had full thickness cartilage loss. However 10% showed high signal in the tibial plateau. There was a highly reproducible pattern of osteophyte formation; 94% posteromedial and posterolateral aspect of medial femoral condyle; 90% medial tibial; 80% medial femoral and 84% lateral intercondylar notch.
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.
Inflammatory changes in synovial tissues occur commonly in knee osteoarthritis (OA) and are termed “inflammatory OA”. The pathogenic significance of this inflammatory OA is uncertain. It is also not known whether inflammatory changes in the synovial membrane are reflected in the synovial fluid (SF) and whether the SF contains a similar inflammatory cell infiltrate. This study examined 34 cases of knee joint OA and cytologically and immunohistochemically characterised inflammatory cells in the synovial membrane and SF. Specimens of SF and synovial membrane were taken at the time of knee arthroplasty. All cases of inflammatory OA synovium contained (CD68+) macrophages; several cases also contained a scattered, focally heavy (CD3+) lymphocytic infiltrate and occasional lymphoid aggregates. Inflammatory changes in OA SF reflected this cell composition with numerous CD68+ macrophages and CD3+ lymphocytes being noted in inflammatory OA cases. The SF volume was greater (>
5ml) in cases of inflammatory OA. Non-inflammatory OA knee joints contained very few inflammatory cells, which were mainly macrophages, in both the synovial membrane and SF. Our findings indicate that inflammatory changes in the synovial membrane of OA knee joints are reflected in the SF and that the volume of SF is commonly increased in cases of inflammatory OA. Both macrophages and lymphocytes in the inflammatory infiltrate of knee joint SF may contribute to joint destruction in OA by providing mononuclear phagocyte osteoclast precursors and the production of inflammatory cytokines and growth factors that promote osteoclastogenesis. In conclusion, the cytology of SF and synovitic membrane are similar in inflammatory OA. With knee effusions of greater than 5mls and inflammatory synovitic membrane consideration of total knee arthoplasty in the presence of single compartment disease should be considered because of the risk of further joint destruction.
100% of medial compartments showed full thickness anteromedial loss with preservation of the posteromedial cartilage. When present, the meniscus was extruded in 96% of cases. 90% of lateral compartments were normal and none had full thickness cartilage loss. However 10% showed high signal in the tibial plateau. There was a highly reproducible pattern of osteophyte formation; 94% posteromedial and posterolateral aspect of medial femoral condyle; 90% medial tibial; 80% medial femoral and 84% lateral intercondylar notch.
Kinematic data from in-vivo fluoroscopy measurements during a step-up activity was used to determine the relative tibial-femoral position as a function of knee flexion angle for each model. Medial and lateral force distribution was adapted from loads measured in-vivo with an instrumented implant during a step-up activity. The affect that varying the bearing thickness has on the stresses in the bearing was investigated. In addition, varus-valgus mal-alignment was investigated by rotating the femoral component through 10 degrees.
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.