Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Mechanical injury is the most important risk factor in osteoarthritis (OA) development. Although once considered a passive disease of mechanical attrition, injury drives active mechanosensitive intracellular signalling which affects the structural and symptomatic course of disease. Mechanosensitive signalling in cartilage has been elucidated over the years and two principal responses emerge: those that cause the release of growth factors from the matrix and which stimulate repair, and those that drive inflammatory signalling, a process that we have termed "mechanoflammation". The up-stream activator of mechanoflammation remains unknown, but it results in rapid activation of NFkB and the inflammatory mitogen activated protein (MAP) kinases and this controls the bioavailability of aggrecanase and regulation of nerve growth factor (NGF), causing pain. The precise relationship between mechanoflammation and cartilage repair is currently unclear but it is likely that chronic mechanoflammation will contribute to disease by also suppressing intrinisic tissue repair.

Original publication

DOI

10.1016/j.semarthrit.2019.09.018

Type

Journal article

Journal

Semin Arthritis Rheum

Publication Date

12/2019

Volume

49

Pages

S36 - S38

Keywords

Animals, Cartilage, Articular, Humans, Osteoarthritis, Signal Transduction, Stress, Mechanical