Why is Osteoarthritis an Age-Related Disease?
By A. Anderson, Richard F. Loeser. Baillière's Best Practice & Research : Clinical Rheumatology, 2010
650 citations recorded by the source corpus.
Although older age is the greatest risk factor for OA, OA is not an inevitable consequence of growing old. Radiographic changes of OA, particularly osteophytes, are common in the aged population but symptoms of joint pain may be independent of radiographic severity in many older adults. Aging changes in the musculoskeletal system increase the propensity to OA but the joints affected and the severity of disease are most closely related to other OA risk factors such as joint injury, obesity, genetics, and anatomical factors that affect joint mechanics. The aging changes in joint tissues that contribute to the development of OA include cell senescence that results in development of the senescent secretory phenotype and aging changes in the matrix, including formation of advanced glycation end-products that affect the mechanical properties of joint tissues. An improved mechanistic understanding of joint aging will likely reveal new therapeutic targets to slow or halt disease progression. The ability to slow progression of OA in older adults will have enormous public health implications given the aging of our population and the increase in other OA risk factors such as obesity.
Subfields: Molecular Biology, Pharmacology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/360f316b3e362a578abff3be13c83caa832dee8e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
In Pharmacology
In Rheumatology
Citations in the corpus
- Aging, Cellular Senescence, and Cancer (2012, background): “thought to play a role in the etiology and promotion of these pathologies (124, 125).”
- Subchondral bone in osteoarthritis: insight into risk factors and microstructural changes (2013, background): “Aging is considered as a primary risk factor for OA, due to loss of normal bone structure and accumulation of bone microdamage [47].”
- Inflammation in osteoarthritis (2011, background): “The increased accumulation and expression of both advanced glycation end-products (AGEs) and the AGE receptor, RAGE, that occur in aging chondrocytes are associated with dysregulated signaling pathways, altered synthetic activity, and increased synthesis of and enhanced sensitivity to cytokines and ”