The T1ρ parameter reflects the slow motion interactions between motion-restricted water molecules and their local macromolecular environment. The extracellular matrix (ECM) in articular cartilage provides a motion-restricted environment for water molecules, so changes to the ECM, therefore, may be reflected in measurements of T1ρ. T1ρ relaxation rate (1/T1ρ) has been shown to decrease linearly with decreasing PG content in ex vivo bovine patellae12
and in trypsinized cartilage.13
In vivo studies have also shown increased cartilage T1ρ values for patients with OA.25,26
Delayed contrast-enhanced MRI of cartilage (dGEMRIC) represents another technique that can also be used to study cartilage glycosaminoglycan (GAG) content and distribution in the knee.27–29
In diseased cartilage, the contrast agent is easily absorbed because of the lack of GAG. However, compared with T1ρ technique, the dGEMRIC is invasive in the imaging protocol as suggested by Burstein et al;27
the contrast agent being injected intravenously, the subject exercises for approximately 10 minutes, and imaging is performed after about 2 to 3 hours.
Several studies ex vivo14
and in vivo15
investigated the relationship between T1ρ and T2 relaxation times in human OA, suggesting that both T1ρ and T2 increase with the degree of OA, but that T1ρ has a higher dynamic range for detecting early cartilage degeneration and, in consequence, is more sensitive than T2. Li et al30
reported significantly increased T1ρ values in OA patients compared with controls, whereas the increase in T2 was not significant, demonstrating that patients with similar average T2 may have different T1ρ, or vice versa. They suggested that the average T1ρ may be used to distinguish OA cartilage from healthy cartilage, whereas T2 may not be able to.
Therefore, in this study, T1ρ mapping technique was performed to examine patients with acute ACL tears within 2 months of injury and to quantitatively assess the articular cartilage overlying and surrounding the BMEL. We also studied the regional T1ρ variations of the normal and ACL-injured knees.
The results of our study are consistent with previous studies where BMELs were found predominantly on the lateral side of the joint, commonly identified in T2-weighted fat-saturated FSE images.4,31–33
For the BMEL located at the LT only, significant elevated T1ρ values were found in cartilage overlying BMEL when compared with surrounding cartilage. The significant elevation of T1ρ within the cartilage overlying BMEL at the LT suggests that early cartilage breakdown may have taken place at the time of injury. For the BMEL located in LFC only, no significant differences in T1ρ values were found between cartilage overlying BMEL and surrounding cartilage. Different hypotheses are discussed to explain this aspect. The lateral femoral notch sign described as an indirect sign of ACL tear might play an important role to answer these questions. It is known that, during the acute ACL injury, the cartilage is highly compressed, and this causes a pattern of injuries known as “kissing contusions.” These contusions are caused by a “pivot-shift” mechanism of injury whereby excessive valgus stress tears the ACL, resulting in anterior tibial translation with relative external rotation of the femur, allowing the LFC to impact the posterolateral tibial plateau. As a consequent, the cartilage becomes compressed and its thickness at the central site of the lateral femur decreases. The GAGs have a high propensity to attract and hold water (about 75% of weight) which, when the cartilage is load bearing as on the bone surface of joints, can be squeezed out into the joint space to assist synovial fluid in lubrication (weeping lubrication). Different studies reported regional tissue response to physiologic joint loading in the human knee, suggesting that a change in superficial collagen fiber orientation is likely the mechanism for the observed T2 shortening.34
Also, previous T1ρ studies have shown that the relaxation times were reduced in the presence of mechanical loading of cartilage.35
This might explain the fact that there were no significant increased T1ρ values within the cartilage overlying BMEL at the LFC.
In a previous study, Johnson et al7
performed biopsies in patients with acute ACL rupture and have demonstrated histologic changes (chondrocyte and matrix degeneration) and biochemical variations in the cartilage overlying BMEL. Another study reported histologic and immunostaining assessment for cartilage oligomeric matrix protein–an abundant noncollagenous ECM protein in cartilage–performed in cartilage biopsies overlying MRI-detected BMEL associated with acute ACL tears.36
The authors demonstrated scattered chondrocyte necrosis or apoptosis and altered distribution of PG in cartilage tissue adjacent to the cartilage overlying BMEL. A more recent study33
investigated GAG content using dGEMRIC in ACL-injured patients. The authors found significant loss of GAG in the LFC of patients with isolated BMEL when compared with controls. The findings of the recent study are consistent with those of previous studies demonstrating that cartilage overlying BMEL has already undergone degeneration after acute injury.
The weight-bearing (wb) and nonweight-bearing (nwb) portions of LFC and MFC were also investigated using T1ρ relaxation time techniques in both healthy controls and ACL-injured patients. Significantly elevated T1ρ values were found in ant-nwb and postnwb portions of the LFC and MFC when compared with wb portions of either condyle. For ACL-injured patients, the results demonstrated a similar distribution and no significant differences were found when comparing with the control data. Our data suggested that in wb portions there is higher concentration of PG when compared with the nwb portions. This finding is consistent with a previous ex vivo37
study that demonstrated, using spectrophotometric measurements, significantly increased concentration in GAG and, therefore, PG in wb portion compared with nwb portion from human cartilage specimens. Also, a very interesting point were the significant increased T1ρ values in LT compared with MT for the ACL-injured patients (), reinforcing the fact that in the acute stage of ACL injuries, the major changes occur at the lateral side of the knee, especially at the posterior location of the LT, as emphasized recently.38
Currently, the natural history of the ACL-injured knee is unknown. A few prospective studies have assessed the long-term outcome of the condition.4,39,40
Further studies evaluating the longitudinal course of BMEL are needed. It has been speculated that BMEL present on MRI scans might represent irreversible injury to the articular cartilage,32,41
and may continue to deteriorate despite ligament reconstruction and develop clinical symptoms of OA.7
Therefore, better understanding of cartilage and bone injuries are extremely important for the future noninvasive development with regard to cartilage repair tissue evaluation, as reported recently.42
This current cohort of ACL-injured patients will be followed up to examine the longitudinal cartilage changes in these compartments postsurgery. We expect that cartilage overlying BMEL in the lateral compartment will show more significant abnormalities than the medial compartment if no cartilage repair is present. However, the medial compartment is more susceptible to kinematic abnormalities and may develop cartilage degeneration sooner despite less initial injury.43
In conclusion, quantitative T1ρ assessment of cartilage overlying BMEL compared with surrounding cartilage and wb portions compared with nonwb portions demonstrated pathologic changes related to ACL injuries. The ability to correlate MRI appearance of BMEL with pathologic findings on cartilage would ideally offer clinicians the opportunity to monitor the early course of cartilage degeneration and to predict the clinical outcome of different treatments. Quantitative MRI can be a more valuable and direct tool to study nonoperative and operative interventions to prevent the development of OA.