Plain language summary
Osteoarthritis (OA) is the most common and disabling joint disease worldwide and aging is the most important risk factor for its development. It was considered a ‘wear and tear’ disease for a long time, however it is now clear that low-grade inflammation is at the root of OA. This process is called ‘inflammaging’ – the presence of low-grade inflammation and decreased efficiency of the immune system with aging. This highly technical review paper describes the reaction of the immune system to small molecules that begin to circulate after cell stress or damage in the joints (known as damage-associated molecular patterns or DAMPs), causing inflammation. The paper includes a discussion on potential medication targets, including anti-inflammatory compounds such as ginger. Nutrition Practitioners working with OA and wanting to understand the inflammatory process involved will find this paper useful.
Abstract
Osteoarthritis (OA) is the most common age-related chronic and disabling joint disease. Long considered to be a "wear and tear" disease, OA is now seen as a low-grade inflammation disease that affects all tissues of the joint, involving cartilage degradation, bone remodelling, osteophytes, and synovitis. The process, called inflammaging, is characterised by the association of low-grade inflammation, profound changes in intra-cellular mechanisms, and the decreased efficiency of the immune system with ageing. The activation of innate immunity plays a critical role in the development and progression of OA. Innate immunity, including inflammasome activation, is triggered by small endogenous molecules called alarmins or damage-associated molecular patterns (DAMPs). These molecules are released in the extracellular media after cell stress or damage, bind to pathogen-recognition receptors (PRRs), such as Toll-like receptors (TLRs) and the receptor for advanced glycation end products (RAGE), and activate the secretion of pro-inflammatory factors, leading to joint inflammation. Moreover, such sterile inflammation triggers cell senescence, characterised by a senescence-associated secretory phenotype (SASP). Understanding the substantial age-related changes of joint tissues that influence the pathogenesis of OA is critical to improving the quality of life of elderly people in the context of increased life expectancy. This review will focus on age-related sterile inflammation in OA and highlight the various innovative and promising therapies targeting the mechanisms of aging.
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