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.
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.
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.
A sibling risk study that shows a statistically significant increase in risk for anteromedial osteoarthritis of the knee. Anteromedial osteoarthritis is a distinct phenotype of osteoarthritis. Previous studies have shown a genetic aetiology to both hip and knee osteoarthritis. The aim of this study was to determine the sibling risk of antero-medial osteoarthritis of the knee. We conducted a retrospective cohort study of 132 probands with primary anteromedial osteoarthritis, who had undergone unicompartmental arthroplasty. Sibling were identified as having symptomatic knee problems by postal Oxford Knee Score (OKS). A positive OKS was defined as an OKS+/− 2SD of the mean of the proband group. Sibling spouses were used as controls. Those siblings &
spouses that were symptomatic from the OKS were invited to undergo Knee X-rays, to look for radiological signs of osteoarthritis. Osteoarthritis was diagnosed as greater than Grade II on the Kell-gren Lawrence classification. The pattern of disease was noted and it was considered if the sibling were suitable for a unicompartmental knee arthroplasty. The prevalence and sibling risk of anteromedial osteoarthritis was determined using a randomly selected single sibling per proband family. The prevalence was determined in the 103 single proband sibling pairs. There was a statistically significant risk within the sibling group P= 0.024 using the Chi square test. The relative risk of anteromedial osteoarthritis was. 3.21(95% CI 1.08 to 9.17) Genetic factors play a major role in the development of anteromedial osteoarthritis.
Antero-medial osteoarthritis of the knee displays a well recognised pattern of cartilage damage on the medial tibial plateau. Anteriorly there is a full thickness cartilage defect, with transition to a partial thickness defect, becoming full thickness in the posterior third of the plateau. The retained posterior cartilage is macroscopically normal, but no previous study has assessed its histo-logical features. This study characterises the histological changes, to examine if antero-medial OA of the knee represents a model of progressive osteoarthritic cartilage damage. Five unicompartmental resection specimens of patients with idiopathic single compartment antero-medial osteoarthritis were assessed. The samples were stained with H&
E and Saffinin-O stains and reviewed using the Mankin system, an established method for scoring osteoarthritic changes in cartilage (range 0 [normal] to 14 [grossly osteoarthritic]) Digital images of the histology were reviewed by two observers to exclude inter and intra observer error. Each specimen was assessed at 4 interval points (A,B,C,D) along the A-P axis starting from the most posterior aspect of the exposed bone to the area of macroscopically normal cartilage. Three repeat measurements were taken from the macroscopically normal region (D1,D2,D3). The scores were compared to historical age matched controls of non-osteoarthritic cartilage, where a Mankin grade of <
3 suggests normal cartilage. From anterior to posterior the H&
E staining showed a consistent decrease in structural integrity and cellularity of the cartilage, matched by a qualitative decrease in GAG content (Saffinin-O staining). Mean Mankin scores showed a progressive decrease in score; A = 14.0 (95% CI 0), B = 5.8 (95%CI 2.4), C = 4.4 (95%CI 2.5), D = 1.0 (95%CI 0.9) {p=0.04 ANOVA}. Repeated measurements at the macroscopically normal area showed the Mankin grade was maintained; D1= 1.0 (95%CI 0.9), D2 = 0.6 (95%CI 0.5), D3 = 0.6 (95%CI 0.6). The results show that the retained posterior cartilage in antero-medial arthritis has a consistently normal Mankin grade. We suggest the defect represents a model of progressive cartilage damage from near normal (posterior) to the grossly osteoarthritic state (anterior).
Polyethylene wear remains an important cause of failure in knee replacements. Retrieval studies, simulators and simple X-ray methods produce wear data that may be inaccurate or unrealistic. We have developed an accurate RSA system for measuring wear in-vivo. Using this system we have found wear rate in a fixed bearing TKR to be about 0.1mm/yr[ Four Oxford uni-compartmental knee replacements, with excellent clinical results were studied ten years after implantation. RSA X-rays were taken in double leg stance with the knee in full extension and 15 and 30 degrees flexion. Following RSA calibration, silhouettes of the components on the stereo X-rays were extracted using a Canny edge detector and were matched to silhouettes projected using CAD models to determine the 3D component position. The average minimum thickness of the bearing was determined and was compared with the measured minimum thickness of 14 unused bearings to calculate linear penetration. The average linear penetration after average 10 years implantation (range 8.5 to 10.25 years) was 0.16 mm (SD 0.13 mm). The average penetration rate was 0.017 mm/year (SD 0.011 mm/year). The maximum linear penetration rate was 0.027 mm/year. The penetration rate is similar to that obtained in a retrieval study [