Subchondral bone sclerosis in osteoarthritis: not just an innocent bystander.

Abstract:

:Abstract  Osteoarthritis (OA) is considered to be a complex illness in which the tissues of the joint play a significant role in the initiation and/or progression of the pathophysiology. We still do not completely understand what initiates the degradation and loss of cartilage. However, it has been suggested that increased catabolism due to elevated cytokines and growth factors in OA joints plays a significant role. Recent evidence suggests a key role for the subchondral bone tissue in the progression and/or initiation of OA. Indeed, the subchondral bone tissue produces a number of similar proinflammatory cytokines, and growth factors are involved in cartilage tissue remodeling. Interestingly, studies have shown the presence of clefts or channels in the tidemark that appears early in OA, indicating a possible way to traffic cytokines and growth factors from the subchondral compartment to the overlying cartilage. Therefore, it is possible that certain bone-derived products drive cartilage metabolism. Potential candidates include insulin-like growth factor-1 (IGF-1), transforming growth factor-β (TGF-β) interleukin 1β (IL-1β), and interleukin-6 (IL-6). Demonstrating that the subchondral bone plays a role in the initiation of OA would greatly contribute to furthering our knowledge of this pathology and provide new insights for therapeutic approaches.

journal_name

Mod Rheumatol

journal_title

Modern rheumatology

authors

Lajeunesse D,Massicotte F,Pelletier JP,Martel-Pelletier J

doi

10.3109/s101650300001

subject

Has Abstract

pub_date

2003-03-01 00:00:00

pages

7-14

issue

1

eissn

1439-7595

issn

1439-7609

journal_volume

13

pub_type

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