Osteoarthritis (OA) is a common chronic joint disorder with a multifactorial etiology including genetic
and environmental factors. Metabolic triggered inflammation, induced by nutrient overload and metabolic
surplus, consists of components such as obesity, pro-inflammatory cytokines and adipokines,
abnormal metabolites, acute phase proteins, vitamin D deficiency, and deregulated microRNAs that may
play a role in OA pathophysiology. Obesity-related metabolic factors, especially adipokines, contribute to
OA development by inducing pro-inflammatory cytokines and degradative enzymes, leading to cartilage
matrix impairment and subchondral bone remodeling. Ectopic metabolite deposition and low-grade
systemic inflammation can contribute to a toxic internal environment that exacerbates OA. Complement
components highly expressed in osteoarthritic joints have also been proposed as causative factors.
Vitamin D deficiency has been associated with obesity and is implicated to be associated with cartilage
loss in OA. Metabolic microRNAs may explain the inflammatory link between obesity and OA. Therapies
targeting metabolic