No significant differences in cartilage damage were found between the two groups of mice that were fed a normal diet. However, a slight increase in synovial thickening was found in the ApoE deficient mice compared to the control mice (1.9 vs. 1.1 respectively; p<0.05), suggesting an activated status of synovial lining cells.
The ApoE deficient mice on a normal diet had shown markedly higher LDL levels than the control mice (8.90 mmol/L and 0.40 mmol/L, respectively; p<0.001).
A second analysis investigated the impact of a cholesterol-rich diet on joint pathology after induction of OA was investigated. In contrast to when the two groups of mice were fed a normal diet, the cholesterol-rich diet increased LDL levels even further in the ApoE deficient mice: a 2.1-fold increase compared to ApoE deficient mice on a normal diet (p<0.001).
Adding a cholesterol-rich diet to the ApoE deficient mice resulted in significant histological differences becoming apparent at day 28. Synovial thickening was increased four times (p<0.001), and also ectopic bone formation in the medial collateral ligament was strongly increased at this early time point (2.7-fold increase; p<0.01).
Interestingly, the addition of a cholesterol-rich diet to ApoE deficient mice did not enhance ectopic bone formation at day 54. In fact, it decreased by 40% in the medial collateral ligament compared to those ApoE deficient mice fed a normal diet. However, cartilage damage at the medial side of the femoral condyle was strongly increased compared to the ApoE deficient mice receiving a normal diet (1.6-fold increase; p<0.05).
According to lead author, Dr. Wouter de Munter of the Department of Experimental Rheumatology, Radboud University Medical Centre, Nijmegen, Netherlands, a relationship between OA and metabolic syndrome, the medical term for a combination of diabetes, high blood pr
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