MRI-identified bone marrow lesions (BMLs) are frequently seen beneath cartilage, in the subchondral bone, and are used to interrogate early knee osteoarthritis (KOA). BMLs are closely associated with joint pain and progression of cartilage loss and subchondral trabecular bone (SCTB) structural change. However, a full understanding of the nature of BMLs at the tissue level is lacking. Thus, the main aim of this study was to examine the biochemical properties of BML and No-BML SCTB tissue from KOA patients and compare this to cadaveric controls without KOA.
Tibial plateau (TP) specimens were collected from 19 KOA arthroplasty patients (6-Male, 13-Female; aged 56-74 years). BMLs were identified by MRI using PDFS- and T1-weighted sequences and categorized into OA-BML (n=12) and OA No-BML (n=7). Non-OA cadaver TPs with no BMLs and no macro-/micro-scopic appearance of OA (n=8; 4-Male, 2-Female; aged 44-80 years) were collected as controls. There were two control cases where both the right and left TP were taken from the same individual. Raman spectroscopy with high spatial resolution was used to quantify the biochemical properties of non-fixed, acetone treated (for lipid removal), SCTB tissue sampled from both the medial and lateral compartment of each TP.
Measures of mineralization, the mineral:matrix ratios of Phosphate(v1):Amide I, Proline, Amide III; Phosphate(v2):Amide I, Proline, Amide III and Phosphate(v4):Amide I were all significantly lower for OA-BML compared to Non-OA within the medial compartment only (p<0.002, p<0.014, p<0.038, p<0.004, p<0.027, p<0.028, p<0.002; respectively). Further, there were no group or compartment differences for Carbonate:Phosphate(v1,v2,v4), Amide III(α-helix):Amide III(random-coil), Hydroxyproline:Proline, or Crystallinity.
These data demonstrate that SCTB tissue is significantly less mineralized in BML areas for patients with KOA. This finding has implications for both the etiology of BMLs, their biomechanical properties and the mechanical interaction between subchondral bone and articular cartilage in OA disease development and progression.