Chondrocytes are responsible for the mechanical resilience of cartilage by controlling the synthesis/degradation of the extracellular matrix. In osteoarthritis (OA), increased activity of cytokines/degradative enzymes (e.g. IL-1beta, MMP-13) play a key role leading to matrix breakdown/cartilage loss. Studying early events in OA might identify targets for limiting the deleterious changes to cartilage stability. Human chondrocyte shape in situ is normally elipsoidal/spheroidal however abnormal forms within otherwise macroscopically normal cartilage are present. Changes to cell shape can alter ECM metabolism and thus these abnormal forms might be an early event in OA. We have investigated whether levels of IL-1beta and MMP-13 are altered in human chondrocytes of abnormal morphology. Tibial plateau cartilage was obtained from patients undergoing knee arthroplasty and only areas graded 0 or 0–1 studied. The shape of fluorescently-labelled in situ chondrocytes was classified by confocal scanning laser microscopy with cartilage depth, and cells characterised as normal (no cytoplasmic processes) or abnormal (one/more cytoplasmic process). Within grade 0 cartilage about 40% of the cells demonstrated abnormal morphology with a reduced proportion in deep zones. Fluorescence immunohistochemistry of antibodies for IL-1beta or MMP-13 was studied in the same cells and quantified. There was an increase in IL-1beta fluorescence with abnormal chondrocytes within the superficial (p=0.033; 21 joints >
190 cells) and deep zones (p=0.001; 8 joints >
100 cells). There were no differences between MMP-13 labelling of normal compared to abnormal chondrocytes within either the superficial or deep zones. Our results suggest that in relatively non-degenerate cartilage, a proportion of the chondrocyte population demonstrated abnormal morphology and that these cells have elevated levels of IL-1beta but not MMP-13. However, we do not know if chondrocyte shape alters cytokine levels, or vice versa. Additionally, the role of cartilage age is unclear, as although the cartilage samples were relatively normal they were obtained from aged individuals. Nevertheless these results show changes to chondrocyte morphology and increased levels of IL-1beta, and thus presumably matrix catabolism - in relatively normal human articular cartilage, raising the possibility that this is an early event in cartilage degeneration. Supported by the Wellcome Trust (075753).
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.
We report on a group of 20 metal-on-metal resurfaced hips (17 patients) presenting with a soft tissue mass associated with various symptoms. We describe these masses as pseudotumours. All patients underwent plain radiography and fuller investigation with CT, MRI and ultrasound. Where samples were available, histology was performed. All patients in this series were female. Presentation was variable; the most common symptom was pain or discomfort in the hip region. Other symptoms included spontaneous dislocation, nerve palsy, an enlarging mass or a rash. The common histological features were extensive necrosis and lymphocytic infiltration. Fourteen of the 20 cases (70%) have so far required revision to a conventional hip replacement and their symptoms have either settled completely or improved substantially since the revision surgery. Two of the three bilateral cases have asymptomatic pseudotumours on the opposite side. We estimate that about 1% of patients develop a pseudotumour in the first five postoperative years after a hip resurfacing. The cause of these pseudotumours is unknown and is probably multi-factorial, further work is required to define this; they may be manifestations of a metal sensitivity response. We are concerned that with time the incidence of these pseudotumours will increase.
The purpose of this study was to determine if a single physiotherapy intervention would enable patients to kneel following Unicompartmental knee arthroplasty (UKA). Kneeling is an important functional activity that is frequently not performed after knee arthroplasty, thus affecting a patient’s ability to carry out basic tasks of everyday life. There is however no clinical reason why patients should not kneel and many with proposed knee surgery ask about the possibility of kneeling after their operation. Sixty adults participated in a prospective randomised controlled trial with blinded assessments. At 6 weeks post-operatively UKA patients were randomised to either the Routine care group where no advice on kneeling was given or to the Kneeling intervention group where participants were taught and given advice on how to kneel and were encouraged to do so. They were re-assessed at 1 year. The primary outcome measure was Question 7 of the Oxford Knee Score which asks the question “Could you kneel down and get up again afterwards?” Pre-operatively there was no difference in the kneeling ability of the two groups. At 1 year the difference in kneeling ability between the two groups was highly significant (p<
0.05). Spearman’s correlation coefficient showed no significant association between a change in score of Question 7 at 1 year and the following factors; scar position, numbness, range of flexion, arthritic involvement of other joints and pain. Linear regression analysis also confirmed that these factors were not successful in predicting a change in kneeling ability. This study showed that the single factor predictive of kneeling ability was the physiotherapy intervention provided at 6 weeks post-operatively and it is suggested that kneeling should be incorporated into patient’s post-operative rehabilitation programmes.
revision surgery and poor functional outcome as the end-points.
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.
This study reports a clinical comparison of new and old establishing whether this modified implant has maintained the established normal kinematic profile of the Oxford UKR.
Knee kinematics were assessed by analysing the movement of the femur relative to the tibia using the PTA.