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<!--  FILE :  lemaire_model_2004.xml

CREATED :  25th July 2007

LAST MODIFIED : 25th July 2007

AUTHOR :  Catherine Lloyd
          Bioengineering Institute
          The University of Auckland
          
MODEL STATUS :  This model conforms to the CellML 1.1 Specification.

DESCRIPTION :  This file contains a CellML description of Lemaire et al's 2004 mathematical model of the interactions between osteoblast and osteoclast activities in bone remodelling.

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  <title>Modeling the interactions between osteoblast and osteoclast activities in bone remodeling</title>
  <author>
    <firstname>Catherine</firstname>
          <surname>Lloyd</surname>
    <affiliation>
      <shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
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  <sect1 id="sec_structure">
  <title>Model Structure</title>

<para> 
Please note that the CellML model presented here (variant 8) represents an extension of the core model (version 1) such that the receptor activator of NF-kB ligand (RANKL) is being added at a constant rate from day 20 and osteoprotegerin (OPG) is subsequently added 60 days later, also at a constant rate.
</para>

<para>
Bone is a dynamic, living tissue whose structure and shape are continually adjusting to provide a structural framework.  In addition to its supporting function, bone also represents the principal site of hematopoiesis.  Bone comprises a unique composite of living cells embedded within a three dimensional, mineralised, honeycomb like structure.  Even after the skeletal growth is complete, bone remodelling continues.  This complex process is carried out by two types of cells; osteoclasts and osteoblasts.  Osteoclasts are responsible for the resorption of mineralised bone, while osteoblasts are responsible for the synthesis of bone matrix.  The interaction between osteoblasts and osteoclasts is known as coupling, and it is essential for maintaining a balance between the rates of bone loss and gain.  Metabolic bone diseases occur when a biochemical or cellular link in this regulated network is disrupted.  One such disease is osteoporosis, characterised by rapid bone loss together with the spontaneous fracturing of the remaining bone.
</para>

<para>
In the paper described here, Lemaine <emphasis>et al.</emphasis> 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. 
</para>

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<caption>Schematic diagram of the basic structure of the model.</caption>
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<para>
The complete original paper reference is cited below:
</para>

<para>
<ulink url="http://www.sciencedirect.com/science?_ob=ArticleURL&amp;_udi=B6WMD-4CMYKWX-1&amp;_user=140507&amp;_coverDate=08%2F07%2F2004&amp;_rdoc=1&amp;_fmt=summary&amp;_orig=search&amp;_cdi=6932&amp;_sort=d&amp;_docanchor=&amp;view=c&amp;_acct=C000011498&amp;_version=1&amp;_urlVersion=0&amp;_userid=140507&amp;md5=a3964b39cf2abde280a34432329a29fd">Modeling the interactions between osteoblast and osteoclast activities in bone remodeling</ulink>, Vincent Lemaire, Frank L. Tobin, Larry D. Greller, Carolyn R. Cho, and Larry J. Suva, 2004, <ulink url="http://www.sciencedirect.com/science/journal/00225193">
            <emphasis>Journal of Theoretical Biology</emphasis>
          </ulink>, 229, 293-309.  (<ulink url="http://www.sciencedirect.com/science?_ob=ArticleURL&amp;_udi=B6WMD-4CMYKWX-1&amp;_user=140507&amp;_coverDate=08%2F07%2F2004&amp;_rdoc=1&amp;_fmt=full&amp;_orig=search&amp;_cdi=6932&amp;_sort=d&amp;_docanchor=&amp;view=c&amp;_acct=C000011498&amp;_version=1&amp;_urlVersion=0&amp;_userid=140507&amp;md5=6bf1bf00fd87b7470356662140c858e7">Full text</ulink> and PDF versions of the article are available to journal subscribers on the <emphasis>Journal of Theoretical Biology</emphasis> website.)  <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&amp;cmd=Retrieve&amp;dopt=AbstractPlus&amp;list_uids=15234198&amp;query_hl=1&amp;itool=pubmed_docsum">PubMed ID: 15234198</ulink>
</para>



</sect1>
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Source
Derived from workspace Lemaire, Tobin, Greller, Cho, Suva, 2004 at changeset 5023c6be53d8.
This exposure was expired. A more up-to-date exposure is available, or view related resources.
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License

This work is licensed under a Creative Commons Attribution 3.0 Unported License.