Knee cartilage is an important structure in the human body and plays a pivotal role in knee joint activity. It is known that cartilage morphology is influenced by many factors, such as age, gender, genetics, BMI, level of physical activity, osteoarthritis, pain and ACL or meniscal injuries. Among these factors, meniscal damage appears to be an important factor to induce cartilage morphological changes. Meniscal damage or loss alters the in vivo cartilage contact biomechanics by shifting the contact location to smaller regions of thinner cartilage, and by increasing the magnitude of the cartilage contact deformation. It is presumed that cartilage morphological alteration is accelerated in the knees with meniscal pathology; with altered knee joint kinematics, the mechanical demand eventually exceeds the ability of the joint to repair itself, setting the stage for OA development.
In this study the mechanism of injury was non-significant trauma in 50% of patients. This finding is in agreement with previous studies that reported that 52–92% of patients with symptomatic knee melatonin receptor agonist present with meniscal damage when assessed by MRI to the contralateral normal knees.
Quantitative MRI (qMRI), like 3D-WS-bSSFP sequence used in this study, provides non-invasive and reliable data on cartilage morphology in healthy subjects with different age groups and different genders. Comprehensive knowledge of the biochemical and biomechanical changes that occur with OA may require a combination of various qMRI techniques. The application of these qMRI techniques to the identification and monitoring of cartilage damage in individual patients for the early diagnosis and treatment of OA would be clinically significant. However, assessment of other joint structures is not possible. In fat-suppressed 3D-WS-bSSFP, the articular cartilage has very high signal intensity, joint fluid has an intermediate to low signal intensity, and subchondral bone and bone marrow are dark. Reported sensitivity and specificity for detection of cartilage loss are 75–85% and 95–97%, respectively.
The cartilage morphology (including cartilage volume by MRI and thickness by US) was investigated in the meniscectomized knees and the contralateral intact knees with a mean injury time of 6.4months. Using the 3D cartilage models (Fig. 1), the mean total cartilage volume was calculated for the femur and tibia. The cartilage thickness was measured within the weight-bearing area by US. In this study, the contralateral knees were used as the control side for analyzing the cartilage morphological changes in the post-meniscectomy knees. It was found that the meniscectomized side demonstrated a statistically significant lower total knee cartilage volume compared with the control side. The percentage of decrease in the total knee cartilage volume post-operatively from pre-operatively was >10% in 13 patients (65%), this value progressors of cartilage loss based on MRI measurements of the cartilage volume as a biomarker. However, this did not correlate with KOOS scores. As the articular cartilage is avascular and aneural, early changes could be asymptomatic or affecting the functional knee activity. Significant rates of cartilage loss are seen also in other studies; in subjects of post partial meniscectomy compared with healthy controls (difference 6.5% per year, 95% CI 3.7–9.3% per year; P<0.001). Even greater losses were observed at the central medial tibial cartilage and medial femoral condyle (15% and 12% respectively). Greater losses are observed in this cohort of Egyptian adults, this may have a genetic basis. The same genes that promote healing after cartilage damage also appear to protect against OA due to wear-and-tear processes. Osteoarthritis, like several other disorders, involves many genes that each contribute in a small way to the disease process. It is proved that there is a subtle genetic influence on OA risk, while other genes are protective.