Macrophage-Driven Inflammation in Metabolic Osteoarthritis: Implications for Biomarker and Therapy Development

Abstract

Osteoarthritis (OA) is a common and debilitating joint disorder that leads to progressive joint breakdown and loss of articular cartilage. Accompanied by a state of low-grade inflammation, its etiology extends beyond that of a wear-and-tear disease, and the immune system might have a role in its initiation and progression. Obesity, which is directly associated with an increased incidence of OA, alters adipokine release, increases pro-inflammatory macrophage activity, and affects joint immune regulation. Studying inflammatory macrophage expression and strategies to inhibit inflammatory macrophage phenotype polarization might provide insights into disease pathogenesis and therapeutic applications. In pre-clinical studies, the detection of OA in its initial stages was shown to be possible using imaging techniques such as SPECT-CT, and advances are made to detect OA through blood-based biomarker analysis. In this review, obesity-induced osteoarthritis and its mechanisms in inducing joint degeneration are summarized, along with an analysis of the current developments in patient imaging and biomarker use for diagnostic and therapeutic strategies.

Autophagy in Osteoarthritis: A Double-Edged Sword in Cartilage Aging and Mechanical Stress Response: A Systematic Review

“…Persistent inflammation in the joint worsens the deterioration of cartilage, with inflammatory cytokines playing a role in causing discomfort [4]. Metabolic variables such as obesity and dyslipidemia elevate the risk of osteoarthritis by stimulating joint inflammation and causing the breakdown of cartilage [5]. Genetic variations impact an individual's vulnerability to osteoarthritis by altering the metabolism of cartilage and the occurrence of inflammation [6].…”

Analysis of anti-rheumatic activity of Nyctanthes arbor-tristis via in vivo and pharmacovigilance approaches

“…Increased oxidative stress, along with an increase in pro-inflammatory cytokines, is thought to be a significant risk factor for joint deterioration in RA. When inflammatory cells like macrophages and neutrophils stimulate cytokine production, they release reactive oxygen species (ROS) and may damage tissues ( Warmink et al, 2023 ).…”