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April 12th

  • Modeling the interactions between osteoblast and osteoclast activities in bone remodeling ? CellML: In the paper described here, Lemaine et al. present a mathematical model of the interactions which occur between osteoblasts and osteoclasts in the process of bone remodelling. Using this model the authors were able to simulate skeletal disease by inserting dysfunctional connections in the coupling network to explore different disease hypotheses.
  • ScienceDirect - Journal of Theoretical Biology : Modeling the interactions between osteoblast and osteoclast activities in bone remodeling: The model results corroborate all behaviors of the bone remodeling system that we have simulated, including the tight coupling between osteoblasts and osteoclasts, the catabolic effect induced by continuous administration of PTH, the catabolic action of RANKL, as well as its reversal by soluble antagonist OPG. The model is also able to simulate metabolic bone diseases such as estrogen deficiency, vitamin D deficiency, senescence and glucocorticoid excess. Conversely, possible routes for therapeutic interventions are tested and evaluated. Our model confirms that anti-resorptiv e therapies are unable to partially restore bone loss, whereas bone formation therapies yield better results.

April 11th

April 10th

  • IL-17 in synovial fluids from patients with rheuma...[J Clin Invest. 1999] - PubMed Result: Osteoclastogen esis inhibitory factor (OCIF), a decoy receptor of ODF, completely inhibited IL-17-induced osteoclast differentiatio n in the cocultures. Levels of IL-17 in synovial fluids were significantly higher in rheumatoid arthritis (RA) patients than osteoarthritis (OA) patients. Anti-IL-17 antibody significantly inhibited osteoclast formation induced by culture media of RA synovial tissues. These findings suggest that IL-17 first acts on osteoblasts, which stimulates both COX-2-dependen t PGE2 synthesis and ODF gene expression, which in turn induce differentiatio n of osteoclast progenitors into mature osteoclasts, and that IL-17 is a crucial cytokine for osteoclastic bone resorption in RA patients.
  • Differential modulation of RANKL isoforms by human...[Bone. 2008] - PubMed Result: CONCLUSION: Our findings showed that the normal, L- and H-OA subchondral bone osteoblasts differentially express membranous RANKL and RANKL isoforms, and that treatment with osteotropic factors generally favours increased membranous localization of RANKL on L-OA compared to H-OA osteoblasts. This phenomenon appears to take place through differential modulation of each RANKL isoform.
  • Differential modulation of RANKL isoforms by human...[Bone. 2008] - PubMed Result: CONCLUSION: Our findings showed that the normal, L- and H-OA subchondral bone osteoblasts differentially express membranous RANKL and RANKL isoforms, and that treatment with osteotropic factors generally favours increased membranous localization of RANKL on L-OA compared to H-OA osteoblasts. This phenomenon appears to take place through differential modulation of each RANKL isoform.
  • The differential expression of osteoprotegeri n (OP...[Clin Exp Rheumatol. 2008 Mar-Apr] - PubMed Result

March 28th

March 24th

  • The differential expression of osteoprotegeri n (OP...[Clin Exp Rheumatol. 2008 Mar-Apr] - PubMed Result: CONCLUSION: OPG and RANKL levels, and consequently the OPG/RANKL ratio, differed according to human OA subchondral bone osteoblast classification ; it is decreased in L and increased in H OA. These findings, in addition to those showing that L OA osteoblasts have a reduced subchondral bone mass and induce a higher level of osteoclast differentiatio n, strongly suggest that the metabolic state of the L OA osteoblasts favours bone resorption.

June 16th

December 17th

July 23rd

July 10th

  • The development of a long bone.: Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter
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