Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation?

Abstract

Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases. Although strong efforts have been made to regenerate degenerated joint cartilage, OA is a progressive and irreversible disease up to date. Among other factors the dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis. Here, only little data are available about the mediation and interaction between different joint compartments. The article provides a review of the current literature regarding the influence of oxidative stress on cellular aging, senescence and apoptosis in different joint compartments (cartilage, synovial tissue and subchondral bone). Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA. ROS induced by exogenous factors such as overload, trauma, local intraarticular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.

<i>Sargassum serratifolium</i> attenuates RANKL-induced osteoclast differentiation and oxidative stress through inhibition of NF-κB and activation of the Nrf2/HO-1 signaling pathway

“…However, they certainly play important signaling roles in the process of osteoclastogenesis (21,22). Many previous studies have shown that ROS accumulation can increase the expression of RANKL in osteoclasts and enhance their survival and proliferation (19,23,24).…”

“…Excessive ROS can also cause bone destruction by exerting oxidative damage to all cellular biomolecules such as proteins, lipids and nucleic acids (21,22). In addition, the overproduction of ROS has been demonstrated to increase the expression of RANKL by osteoclasts, thereby activating osteoclasts and enhancing bone resorption capacity, indicating that ROS play an important role in osteoclastogenesis (19,23,24).…”

Myrtol improves post‑traumatic knee osteoarthritis by regulation of reactive oxygen species, transforming growth factor β1 and apoptosis in a mouse model

“…Damaged mitochondria can lead to cell senescence and death. However, ROS generation has an important effect on the over-proliferation of PTKO and synovial membrane (23). Previous studies have suggested that ROS can regulate cell proliferation, differentiation, programmed cell death and aging.…”

The role of Mediterranean diet and it’s components on the progress of osteoarthritis

“…Τhese biomarkers are affecting the onset of OA, through the rise of levels of collagen type II, while increasing the expression of aggrecan and inhibit the apoptosis of proteins related to the protection of cartilage 46,47 . The MD components hydroxytyrosol, resveratrol and oleuropein show antioxidant action in vitro, as they constrain the activation of transcription NF-kB factors and AP-1 and decrease the expression of endothelial adhesion molecules 48 .…”