title: Lithium chloride prevents interleukin-1β induced cartilage degradation and loss of mechanical properties.
abstract: Osteoarthritis is a chronic degenerative disease that affects the articular cartilage. Recent studies have demonstrated that lithium chloride exhibits significant efficacy as a chondroprotective agent, blocking cartilage degradation in response to inflammatory cytokines. However, conflicting literature suggests lithium may affect the physicochemical properties of articular cartilage and thus long-term exposure may negatively affect the mechanical functionality of this tissue. This study aims to investigate the effect of lithium chloride on the biomechanical properties of healthy and interleukin-1β treated cartilage in vitro and examines the consequences of long-term exposure to lithium on cartilage health in vivo. Bovine cartilage explants were treated with lithium chloride for 12 days. Chondrocyte viability, matrix catabolism and the biomechanical properties of bovine cartilage explants were not significantly altered following treatment. Consistent with these findings, long term-exposure (9 months) to dietary lithium did not induce osteoarthritis in rats, as determined by histological staining. Moreover, lithium chloride did not induce the expression of catabolic enzymes in human articular chondrocytes. In an inflammatory model of cartilage destruction, lithium chloride blocked interleukin-1β signaling in the form of nitric oxide and prostaglandin E2 release and prevented matrix catabolism such that the loss of mechanical integrity observed with interleukin-1β alone was inhibited. This study provides further support for lithium chloride as a novel compound for the treatment of osteoarthritis.
authors.affiliation: Institute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
authors.forename: Clare L
authors.initials: CL
authors.lastname: Thompson
authors.affiliation: Institute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
authors.forename: Habiba
authors.initials: H
authors.lastname: Yasmin
authors.affiliation: Institute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
authors.forename: Anna
authors.initials: A
authors.lastname: Varone
authors.affiliation: Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
authors.forename: Anna
authors.initials: A
authors.lastname: Wiles
authors.affiliation: Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
authors.forename: C Antony
authors.initials: CA
authors.lastname: Poole
authors.affiliation: Institute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
authors.forename: Martin M
authors.initials: MM
authors.lastname: Knight
mesh_terms: D000818:Animals; D002358:Cartilage, Articular / Q000187:drug effects* / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D004353:Drug Evaluation, Preclinical; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism; D018021:Lithium Chloride / Q000494:pharmacology* / Q000627:therapeutic use*; D008297:Male; D010003:Osteoarthritis / Q000139:chemically induced* / Q000188:drug therapy*; D017208:Rats, Wistar
chemical_list: D053583:Interleukin-1beta; D018021:Lithium Chloride
keywords: cartilage; lithium chloride; mechanics