Arthritis is marked by joint deterioration that affects articular cartilage and subchondral
bone. Though cartilage degradation does the major damage during arthritis, subsequent bone degeneration
cannot be neglected. Recent progress in arthritis research has identified the clinical importance of
bone erosion in destructive arthritis. Studies have showed the key role played by osteoclasts and receptor
activator of nuclear factor kappaB ligand (RANKL) signaling in bone erosion. Cathepsins and tartrate
resistant acid phosphatase (TRAP) are considered key enzymatic factors contributing to bone erosion.
Further, reactive oxygen species (ROS) formed at the ruffled border of osteoclasts also causes
bone resorption and matrix degradation. Besides, severe inflammation during arthritis induces bone
erosion by aiding in Ca2+ removal and activating osteoclastogenesis. The inflammatory cytokines and
ROS influence osteoclast differentiation by regulating osteoclast-lineage cells or by acting on other
cells to regulate the expression of RANKL and osteoprotegerin (OPG). The enhanced production of
pro-inflammatory cytokines and ROS in arthritis stimulates tissue injury by means of oxidative damage
leading to vital organ damage and synovial and circulatory cell apoptosis. Thus, blocking enzymatic
and non-enzymatic factors responsible for bone erosion and inflammation is considered a prime
strategy in the management of arthritis. In this review we provide an overview of the mechanisms of
bone erosion, inflammation and associated oxidative stress/damage during arthritis perpetuation along
with shedding light on potential targets. The article also describes the possible natural therapeutic
agents that could prevent bone loss and inflammation, and related secondary complications of arthritis.
Keywords: Arthritis, bone erosion, inflammation, oxidative damage, secondary complications, therapeutic targets.
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