Restoring the Broken Balance Anacardic acid mediated regulation of bone homeostasis

Abstract

Bone, a specialized connective tissue in conjunction with cartilage provides mechanical support, protection for vital organs, and is a source of ions for the body, especially calcium and phosphate. Maintaining healthy bones requires constant bone remodelling throughout life. A number of cells within the microenvironment form a vital role in sustaining the balance of the skeletal system. Osteoclasts and osteoblasts are the major types of cells that play prominent roles in bone remodelling by performing opposing functions of removing bone and replacing it respectively. The imbalance between osteoblasts and osteoclasts brings about bone destruction in several bone-devouring diseases. Inflammatory responses in the bones and joints can be caused by infections, localized dysfunctions, or immune-mediated disorders. Despite the importance of local inflammation in the healing process, an unrestrained inflammatory response can produce a cascade of inflammatory cytokines that damage the fundamental link between osteogenesis and bone resorption, subsequently leading to bone loss. A pathologic bone loss caused by inflammation is characterized by the simultaneous inhibition of bone formation and the stimulation of bone resorption [1, 2]. In most cases, these aberrations result from impaired differentiation or survival of osteoblastic cells, accompanied by increased activity of osteoclast cells [2]. An infection of the musculoskeletal system, such as osteomyelitis, is a devastating condition on survivors, physicians, and medical care service providers as a whole. Microorganisms, in addition to causing infection, also sustain inflammation, which usually destroys bone and joint tissues severely. In addition to causing pain and fever, these infections are often chronic, hard to eradicate, and present a high morbidity rate [3]. Most cases of osteomyelitis are caused by Staphylococcus aureus, which accounts for roughly 80% of all cases of osteomyelitis [4, 5]. However, as antimicrobial resistance and virulence factors have evolved,