Objective:
Knee osteoarthritis (KOA) is the most common form of arthritis, but the biomolecular involvement of its onset and progression is controversial. Several studies have shown that the alterations of N-glycans on proteins contribute to the pathophysiology and progression of various diseases. However, the biomolecular distribution of N-glycans on KOA cartilage-bone tissue is poorly understood. Thus, the aim of this study was to spatially compare N-glycans from formalin-fixed paraffin-embedded (FFPE) cartilage-bone tissue of KOA patients and cadaveric controls (CTL).
Methods:
Human FFPE cartilage-bone tissue from end-stage KOA patients (2-Female; aged 58 and 79 years) and CTL individuals (2-Female; 44 and 54 years) was analysed by matrix‐assisted laser desorption/ionisation mass spectrometry imaging (MALDI‐MSI). In order to do so, we have developed and applied a novel and cost-effective sample preparation workflow in which commercial conductive ITO slides are pre-coated with gelatin and chromium potassium sulfate dodecahydrate to improve the adherence of tissue sections. Based on the theoretical masses, N-glycan peaks were manually selected, and ion intensity maps were generated using FlexImaging and SCiLS Lab software. Putative N-glycan structures were annotated using the following tools: GlycoMod, which calculates the theoretical monosaccharide composition, and Glycoworkbench to create individual N-glycan structures.
Results:
MALDI-MSI revealed differential N-glycan profiles between KOA patients and CTL individuals within the cartilage region only. Overall, 13 N-glycans were identified in KOA cartilage compared to 9 N-glycans in CTL cartilage, with approximately a 3-fold increase in the signal intensity. Interestingly, ion intensity maps of KOA cartilage-specific hybrid/complex-type N-glycans, m/z 1501.7 ± 0.5 Da, m/z 1647.2 ± 0.5 Da, and m/z 1663.4 ± 0.5 Da, showed higher intensity localisation to the superficial fibrillated area of degraded cartilage (cartilage histological grade 2-2.5) with underlying bone sclerosis, compared to the adjacent region with less damaged cartilage tissue (cartilage histological grade 0-1), associated with non-sclerotic bone.
Conclusion:
Our preliminary results demonstrate the novel application of MALDI-MSI to identify and localise KOA cartilage‐specific N-glycans. The alterations of these hybrid/complex-type N-glycans could evolve into a potential cartilage degradation marker and may play an important role in the development of underlying bone sclerosis. This could also mean that N-glycans are a possible new target for treatment of cartilage degradation in patients with KOA.