Person: Gomoll, Andreas H.
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Publication Aarhus Regenerative Orthopaedics Symposium (AROS): Regeneration in the ageing population
(Taylor & Francis, 2017) Foldager, Casper B; Bendtsen, Michael; Berg, Lise C; Brinchmann, Jan E; Brittberg, Mats; Bunger, Cody; Canseco, Jose; Chen, Li; Christensen, Bjørn B; Colombier, Pauline; Deleuran, Bent W; Edwards, James; Elmengaard, Brian; Farr, Jack; Gatenholm, Birgitta; Gomoll, Andreas H.; Hui, James H; Jakobsen, Rune B; Joergensen, Natasja L; Kassem, Moustapha; Koch, Thomas; Kold, Søren; Krogsgaard, Michael R; Lauridsen, Henrik; Le, Dang; Le Visage, Catherine; Lind, Martin; Nygaard, Jens V; Olesen, Morten L; Pedersen, Michael; Rathcke, Martin; Richardson, James B; Roberts, Sally; Rölfing, Jan H D; Sakai, Daisuke; Toh, Wei Seong; Urban, Jill; Spector, MyronThe combination of modern interventional and preventive medicine has led to an epidemic of ageing. While this phenomenon is a positive consequence of an improved lifestyle and achievements in a society, the longer life expectancy is often accompanied by decline in quality of life due to musculoskeletal pain and disability. The Aarhus Regenerative Orthopaedics Symposium (AROS) 2015 was motivated by the need to address regenerative challenges in an ageing population by engaging clinicians, basic scientists, and engineers. In this position paper, we review our contemporary understanding of societal, patient-related, and basic science-related challenges in order to provide a reasoned roadmap for the future to deal with this compelling and urgent healthcare problem.
Publication Cellular senescence in aging and osteoarthritis: Implications for cartilage repair
(Taylor & Francis, 2016) Toh, Wei Seong; Brittberg, Mats; Farr, Jack; Foldager, Casper Bindzus; Gomoll, Andreas H.; Hui, James Hoi Po; Richardson, James B; Roberts, Sally; Spector, MyronIt 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.