Metabolic triggered inflammation in osteoarthritis.

X Wang, D Hunter, J Xu, C Ding

Journal: Osteoarthritis and cartilage 2015;23(1):22-30

PMID: 25452156

Free Full Text on Elsevier Science View on PubMed

Abstract

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-triggered inflammation and its components are anticipated to have potential for the treatment of OA.

Address: Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia.; Institute of Bone and Joint Research, Kolling Institute and Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia.; Department of Rheumatology and Arthritis Research Institute, 1st Affiliated Hospital, Anhui Medical University, Hefei, China.; Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia; Institute of Bone and Joint Research, Kolling Institute and Royal North Shore Hospital, University of Sydney, Sydney, NSW, Australia; Department of Rheumatology and Arthritis Research Institute, 1st Affiliated Hospital, Anhui Medical University, Hefei, China. Electronic address: [email protected].

DOI: 10.1016/j.joca.2014.10.002