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MR Vol.13 No.1 indexに戻る
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MODERN RHEUMATOLOGY
Vol.13 No.1 |
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Subchondral bone sclerosis in osteoarthritis:
not just an innocent bystander |
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| D. Lajeunesse1 , F. Massicotte1 , J.-P. Pelletier1
, J. Martel-Pelletier1 |
| (1)Unite de recherche en Arthrose, Centre Hospitalier
de l'Universite de Montreal, Hopital Notre-Dame, 1560 rue Sherbrooke
Est, Montreal,
Quebec H2L 4M1, Canada |
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| 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-#
(TGF-#) interleukin 1# (IL-1#), 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. |
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| Key words |
| Key words Cytokines ・ Insulin-like growth
factor-1 (IGF-1) ・ Osteoarthritis (OA) ・ Subchondral bone sclerosis
・ Transforming growth factor-&bgr;
(TGF-&bgr;) |
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