Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.

Autor:	Dilley JE; Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA., Bello MA; Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA., Roman N; Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA., McKinley T; Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA., Sankar U; Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.; Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Jazyk:	angličtina
Zdroj:	Bone reports [Bone Rep] 2023 Jan 30; Vol. 18, pp. 101658. Date of Electronic Publication: 2023 Jan 30 (Print Publication: 2023).
DOI:	10.1016/j.bonr.2023.101658
Abstrakt:	Post-traumatic osteoarthritis (PTOA) develops secondary to a joint injury and accounts for 12 % of all osteoarthritis. These injuries, often of the lower extremity joints, occur due to trauma or accidents related to athletic or military activities. They primarily affect younger individuals although PTOA can occur across the spectrum of age. Pain and functional disability caused by PTOA confer a heavy economic toll on patients, in addition to detrimentally affecting their quality of life. Both high energy injuries that cause articular surface fracture with or without subchondral bone disruption and low-energy injuries involving joint dislocations or ligamentous injury cause PTOA, albeit through different mechanisms. Regardless, chondrocyte death, mitochondrial dysfunction, reactive oxygen species production, subchondral bone remodeling, inflammation and cytokine release in the cartilage and synovium play integral roles in the pathogenesis of PTOA. Evolving surgical methods are focused on stabilizing articular surface and joint structure congruity. However, to date there are no disease modifying medical therapies against PTOA. Increased recent understanding of the pathogenesis of the subchondral bone and synovial inflammation as well as that of chondrocyte mitochondrial dysfunction and apoptosis have led to the investigation of new therapeutics targeting these mechanisms to prevent or delay PTOA. This review discusses new advances in our understanding of cellular mechanisms underlying PTOA, and therapeutic approaches that are potentially effective in reducing the self-propagating cycle of subchondral bone alterations, inflammation, and cartilage degradation. Within this context, we focus therapeutic options involving anti-inflammatory and anti-apoptotic candidates that could prevent PTOA. Competing Interests: Julian Emerson Dilley, Margaret Anne Bello and Uma Sankar have no financial disclosures or conflicts of interest in relation to this study. Roman Natoli receives consultation fees from Quince. Todd McKinley receives royalties from Innomed. (© 2023 The Author(s).)
Databáze:	MEDLINE
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