Document Detail

Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis.
MedLine Citation:
PMID:  24072604     Owner:  NLM     Status:  MEDLINE    
Osteoarthritis (OA) is a whole joint disease, in which thinning and disappearance of cartilage is a critical determinant in OA progression. The rupture of cartilage homeostasis whatever its cause (aging, genetic predisposition, trauma or metabolic disorder) induces profound phenotypic modifications of chondrocytes, which then promote the synthesis of a subset of factors that induce cartilage damage and target other joint tissues. Interestingly, among these factors are numerous components of the inflammatory pathways. Chondrocytes produce cytokines, chemokines, alarmins, prostanoids, and adipokines and express numerous cell surface receptors for cytokines and chemokines, as well as Toll-like receptors. These receptors activate intracellular signaling pathways involved in inflammatory and stress responses of chondrocytes in OA joints. This review focuses on mechanisms responsible for the maintenance of cartilage homeostasis and highlights the role of inflammatory processes in OA progression.
Xavier Houard; Mary B Goldring; Francis Berenbaum
Related Documents :
12421674 - Cytokine regulation of liver development.
9252144 - Role of ischemia in causing apoptosis, atrophy, and nodular hyperplasia in human liver.
20887844 - Changes in interleukin-1β and 6 after hepatic microwave tissue ablation compared with ...
15578514 - Innate immune system plays a critical role in determining the progression and severity ...
24067614 - Temperature triggers immune evasion by neisseria meningitidis.
16152704 - Hiv protease inhibitors prevent mitochondrial hyperpolarization and redox imbalance and...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current rheumatology reports     Volume:  15     ISSN:  1534-6307     ISO Abbreviation:  Curr Rheumatol Rep     Publication Date:  2013 Nov 
Date Detail:
Created Date:  2013-09-27     Completed Date:  2014-03-31     Revised Date:  2014-04-17    
Medline Journal Info:
Nlm Unique ID:  100888970     Medline TA:  Curr Rheumatol Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  375     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Adipokines / physiology
Cartilage, Articular / pathology,  physiopathology*
Chemokines / physiology
Homeostasis / physiology*
Inflammation / complications*,  physiopathology
Mechanotransduction, Cellular / physiology
Osteoarthritis / etiology,  pathology,  physiopathology*
Signal Transduction / physiology
Toll-Like Receptors / physiology
Grant Support
Reg. No./Substance:
0/Adipokines; 0/Chemokines; 0/Toll-Like Receptors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Measuring bone quality.
Next Document:  Mechanistic insights from animal models of psoriasis and psoriatic arthritis.