Cellular senescence in aging and osteoarthritis: Implications for cartilage repair. (16th December 2016)

• Record Type: Journal Article
• Authors: Toh, Wei Seong; Brittberg, Mats; Farr, Jack; Foldager, Casper Bindzus; Gomoll, Andreas H; Hui, James Hoi Po; Richardson, James B; Roberts, Sally; Spector, Myron
• Is Part Of: Acta orthopaedica. Volume 87(2015)Supplement 363
• Page Start: 6
• Page End: 14
• Publication Date: 2016-12-16
• Subjects: Orthopedics -- Periodicals; 616.7005
• DOI: 10.1080/17453674.2016.1235087
• Languages: English
• ISSNs: 1745-3674

Abstract

Abstract : Abstract — It is well accepted that age is an important contributing factor to poor cartilage repair following injury, and to the development of osteoarthritis. Cellular senescence, the loss of the ability of cells to divide, has been noted as the major factor contributing to age-related changes in cartilage homeostasis, function, and response to injury. The underlying mechanisms of cellular senescence, while not fully understood, have been associated with telomere erosion, DNA damage, oxidative stress, and inflammation. In this review, we discuss the causes and consequences of cellular senescence, and the associated biological challenges in cartilage repair. In addition, we present novel strategies for modulation of cellular senescence that may help to improve cartilage regeneration in an aging population.