Macro, Micro, and Molecular. Changes of the Osteochondral Interface in Osteoarthritis Development

Abstract

Osteoarthritis (OA) is a long-term condition that causes joint pain and reduced movement. Notably, the same pathways governing cell growth, death, and differentiation during the growth and development of the body are also common drivers of OA. The osteochondral interface is a vital structure located between hyaline cartilage and subchondral bone. It plays a critical role in maintaining the physical and biological function, conveying joint mechanical stress, maintaining chondral microenvironment, as well as crosstalk and substance exchange through the osteochondral unit. In this review, we summarized the progress in research concerning the area of osteochondral junction, including its pathophysiological changes, molecular interactions, and signaling pathways that are related to the ultrastructure change. Multiple potential treatment options were also discussed in this review. A thorough understanding of these biological changes and molecular mechanisms in the pathologic process will advance our understanding of OA progression, and inform the development of effective therapeutics targeting OA.

3D Printed Multiphasic Scaffolds for Osteochondral Repair: Challenges and Opportunities

“…In the native tissue, the articular cartilage is continuous, with an average pore size of only 6 nm, calcified cartilage has pores within the unmineralized areas which accounted for ≈22% of the tissue and subchondral bone has an overall porosity of 64-94% [42,52,63].…”

“…The calcified zone is made up of ≈22% unmineralized tissue which contains porous structures and then ≈88% mineralized tissue and, along with the subchondral bone, assists with shock absorption in the joint [52][53][54]. A few chondrocytes present in the calcified zone have limited metabolic activity and synthesize collagen type X, which can calcify the ECM [55].…”

Molecular Classification of Knee Osteoarthritis

“…However, the current view is that KOA is a whole-joint disease, or even a systemic disorder since it could be affected by various local and systemic risk factors. The major pathogenesis in KOA contains the molecular crosstalk between articular cartilage, synovium, subchondral bone, meniscus, tendon, muscle and infrapatellar fat pad (IFP) (Loeser et al, 2012;Fan et al, 2021). For instance, the accumulation of M1 macrophage in synovium is responsible for the secretion of proinflammatory cytokines, which facilitates the formation of inflammation microenvironment and aggravates cartilage degradation and synovitis (Robinson et al, 2016;Zhang et al, 2020).…”

Tert-Butylhydroquinone Prevents Oxidative Stress-Mediated Apoptosis and Extracellular Matrix Degradation in Rat Chondrocytes

“…Moreover, excessive generation of reactive oxygen species induces oxidative damage in chondrocytes, which leads to chondrocyte apoptosis and degradation of the ECM. This in turn causes irreversible damage to the articular cartilage, which contributes to the progression of OA [ 7 – 9 ]. Therefore, inhibiting the oxidative stress-induced apoptosis of chondrocytes and ECM degradation may be an effective means of preventing cartilage degeneration and progression of OA.…”