Osteoarthritis (OA) is a common multifactorial and heterogeneous degenerative joint disease, and biochemical changes in cartilage matrix occur during the early stages of OA before morphological changes occur. Thus, it is desired to measure regional biochemical changes in the joint. High-resolution magic angle spinning (HRMAS) NMR spectroscopy is a powerful method of observing cartilaginous biochemical changes ex vivo, including the concentrations of alanine and N-acetyl, which are markers of collagen and total proteoglycan content, respectively. Previous studies have observed significant changes in chondrocyte metabolism of OA cartilage via the altered gene expression profiles of ACAN, COL2A1 and MMP13, which encode aggrecan, type II collagen and matrix metalloproteinase 13 (a protein crucial in the degradation of type II collagen), respectively. Employing HRMAS, this study aimed to elucidate potential relationships between N-acetyl and/or alanine and ACAN, COL2A1 and/or MMP13 expression profiles in OA cartilage. Thirty samples from the condyles of five subjects undergoing total knee arthroplasty to treat OA were collected. HRMAS spectra were obtained at 11.7 T for each sample. RNA was subsequently extracted to determine gene expression profiles. A significant negative correlation between N-acetyl metabolite and ACAN gene expression levels was observed; this provides further evidence of N-acetyl as a biomarker of cartilage degeneration. The alanine doublet was distinguished in the spectra of 15 of the 30 specimens of this study. Alanine can only be detected with HRMAS NMR spectroscopy when the collagen framework has been degraded such that alanine is sufficiently mobile to form a distinguished peak in the spectrum. Thus, HRMAS NMR spectroscopy may provide unique localized measurements of collagenous degeneration in OA cartilage. The identification of imaging markers that could provide a link between OA pathology and chondrocyte metabolism will facilitate the development of more sensitive diagnostic techniques and will improve methods of monitoring treatment for patients suffering from OA.

Purpose

To quantitatively evaluate longitudinal changes in water and lipid in knee bone marrow with and without bone marrow edema-like lesions (BMELs) in subjects with acutely ruptured anterior cruciate ligaments (ACLs) or osteoarthritis (OA) using three-dimensional magnetic resonance spectroscopic imaging (3D MRSI).

Material and methods

Ten ACL and 10 OA subjects who presented with BMEL and seven BMEL-free controls were scanned at 3T. All ACL and OA subjects had one-year follow-up scans. 3D MRSI was acquired in BMEL and adjacent bone marrow, and water content (WC) and unsaturated lipid index (UI) were calculated in each region of interest.

Results

At baseline, ACL BMEL WC was significantly higher than ACL non-BMEL, OA BMEL, and control WC; ACL non-BMEL WC, ACL BMEL UI, and OA BMEL WC were significantly higher than control. ACL BMEL WC decreased significantly one year post-reconstruction; UI decreased non-significantly (p=0.09). No significant changes in OA BMEL or ACL and OA non-BMEL WC and UI were observed.

Conclusion

3D MRSI is a powerful method of quantitatively assessing the biochemical composition of bone marrow in OA and ACL-injured knees, which may serve as imaging markers to improve comprehension of primary and secondary OA pathology.

Altered knee kinematics following ACL reconstruction may predispose patients to the development of early onset post-traumatic osteoarthritis. The goal of our study was to examine the longitudinal interrelationship between altered tibial position relative to the femur and cartilage health measured by quantitative T1ρ MRI. Twenty-five patients with isolated unilateral ACL injury underwent kinematic and cartilage T1ρ MRI at baseline prior to ACL reconstruction and then at 1-year post-reconstruction. Tibial position relative to the femur in the anterior-posterior plane was calculated as well as cartilage T1ρ relaxation values in the injured and uninjured knee. At baseline prior to ACL reconstruction, the tibia was in a significantly more anterior position relative to the femur in the ACL deficient knee compared to the healthy contralateral knee. This difference was no longer present at 1-year follow-up. Additionally, the side-side difference in tibial position correlated to increased cartilage T1ρ relaxation values in the medial compartment of the knee 1-year post-reconstruction. Altered tibial position following ACL reconstruction is correlated with detectable cartilage degeneration as soon as 1 year following ACL reconstruction.