- Academic Editor
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Osteoarthritis (OA) is now considered as a multifaceted disease affecting
various articular tissues, including cartilage, bone, synovium, and surrounding
ligaments. The pathophysiology strongly implicates intricate chemical
communication, primarily through cytokines, leading to the production of
degradative enzymes in cartilage, inflammatory peptides in synovium, and
structural changes in bone, resulting in characteristic clinical features such as
joint deformities and loss of cartilage space seen on X-rays. Recent studies
highlight the previously underestimated role of subchondral bone in OA, revealing
its permeability to cytokines and raising questions about the influence of
abnormal perfusion on OA pathophysiology, suggesting a vascular component in the
disease’s etiology. In essence, alterations in bone perfusion, including reduced
venous outflow and intraosseous hypertension, play a crucial role in influencing
the physicochemical environment of subchondral bone, impacting osteoblast
cytokine expression and contributing to trabecular remodeling, changes in
chondrocyte phenotype, and ultimately cartilage matrix degeneration in OA.
Dynamic contrast (gadolinium) enhanced magnetic resonance imaging (DCE-MRI) was
used to quantify perfusion kinetics in normal and osteoarthritic subchondral
bone, demonstrating that decreased perfusion temporally precedes and spatially
correlates with cartilage lesions in both young Dunkin-Hartley (D-H) guinea pigs
and humans with osteoarthritis. Pharmacokinetic analysis of DCE-MRI generated
data reveals decreased tracer clearance and outflow obstruction in the medial
tibial plateau of osteoarthritic guinea pigs, coinciding with progressive
cartilage degradation, loss of Safranin O staining, and increased expression of
matrix metalloproteinases and interleukin-1. Positron emission tomographic (PET)
scanning using