Abstract
Introduction
Osteoarthritis (OA) occurs due to a multi-scale degradation of articular cartilage (AC) surface which aggravates the disease condition. Investigating the micro-scale structural alterations and mechano-tribological properties facilitates comprehension of disease-mechanisms to improve future injectable-therapies. This study aims to analyze these properties using various experimental and analytical methods to establish correlations between their morpho-physiological features.
Method
In this study, Raman-spectroscopy was used to investigate microscale changes in AC constituents and categorize OA damage regions in knee-joint samples from joint replacement patients (Samples = 5 and Regions = 40). Following, microscale indentation and sliding tests were performed on these regions to evaluate variations in aggregate-modulus (AM) and elastic-modulus (EM), with coefficient of friction (COF). Finally, scanning electron microscopy (SEM) was employed to analyze these morphological variations.
Result
Raman spectroscopy revealed degree of collagen-damage (Amide-3 α-helix to random-coil ratio I-1250/I-1280), proteoglycan-damage (Sulphated bonds SO3- to CH2 twist ratio I-1065/I-1206), amount of bone exposure (Phosphated-hydroxyapatite PO43- to Amide-1 ratio I-959/I-1669) and increased crystallinity (Carbonated hydroxyapatite CO32- to Amide-1 ratio I-1075/I-959) in ECM. Subsequently, these regions were categorized into different groups (G) based on these damages; G1 (Proteoglycan); G2 (Collagen + Proteoglycan); G3 (Collagen + Proteoglycan + Carbonated crystallinity) G4 (Collagen or Proteoglycan + bone exposure); and G5 (Collagen + Proteoglycan + Bone exposure). Further experimentation revealed the differences in mechano-tribological properties (AM, EM, and COF) between the different groups. G5 displayed the highest values of AM (1.5 ± 0.2MPa), EM (0.3 ± 0.01MPa) and COF (0.39 ± 0.08), compared to other groups. These altered properties were confirmed via SEM that revealed micro-asperity junctions, superficial fronding, fibrillations and bone exposure at these damaged regions.
Conclusion
This study demonstrated micro-scale changes in AC among OA patients commensurate to the degree of tissue damage, which correlates with disease progression altering joint structure and function particularly in regions with high COF.
