Abstract
The degeneration of articular cartilage (AC) occurs in osteoarthritis (OA), which is a leading cause of pain and disability in middle-aged and older people. The early disease-related changes in cartilage extra-cellular matrix (ECM) start with depletion of proteoglycan (PG), leading to an increase in tissue hydration and permeability. These early compositional changes are small (<10%) and hence difficult to register with conventional non-invasive imaging technologies (magnetic resonance and ultrasound imaging). Here we apply Brillouin microscopy for detecting changes in the mechanical properties and composition of porcine AC. OA-like degradation is mimicked by enzymatic tissue digestion, and we compare Brillouin microscopy measurements against histological staining of PG depletion over varying digestion times and enzyme concentrations. The non-destructive nature of Brillouin imaging technology opens new avenues for creating minimally invasive arthroscopic devices for OA diagnostics and therapeutic monitoring.
Highlights
articular cartilage (AC) is a highly organized connective tissue, comprising a single type of specialized cell - the chondrocyte - within an extra-cellular matrix (ECM) [1]
After enzymatic digestion all 10 samples were washed in phosphate buffered saline (PBS) to quench the digestion process and sectioned in 2 equal parts using a surgical scalpel along the plane perpendicular to the articular surface
We have applied Brillouin microscopy for studying the relationship between the tissue’s longitudinal modulus and the depletion of a solid component of the ECM in porcine AC exposed to enzymatic digestion
Summary
AC is a highly organized connective tissue, comprising a single type of specialized cell - the chondrocyte - within an ECM [1]. Abnormal load distribution, accelerated mechanical wear of the cartilage surface and overproduction of matrix-degrading components all can trigger pathological processes in chondrocytes and ECM, leading to disease and irreversible degradation of articular cartilage [1,2,3]. The protein cores of PGs are lined by covalent attachments of glycosaminoglycans (GAGs), which confer negative charge due to the abundance of carboxyl and sulfate groups This property fixes PGs to the ECM and attracts cations, such as sodium, which draw water into the tissue to generate the swelling pressure of cartilage. The progression of OA is classified into three stages: 1) proteoglycan degradation followed by degradation of type II collagen, 2) the fibrillation and erosion of the cartilage surface, and 3) the onset of the synovial inflammation [4] The progression starts from the molecular level (PGs depletion), evolves to the architectural changes within ECM (collagen network erosion) and ends up at irreversible structural and functional damage
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