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Abstract
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<h5 class="section-title" id="d5113277e177">Objective</h5>
<p id="P2">Anterior cruciate ligament (ACL) injury initiates a cascade of events often
leading
to osteoarthritis. ACL reconstruction does not alter the course of osteoarthritis,
suggesting that heightened osteoarthritis risk is likely due to factors in addition
to the joint instability. We showed that torn ACL remnants express periostin (
<i>POSTN</i>) in the acute phase of injury. Considering that ACL injury predisposes
to osteoarthritis
and that
<i>POSTN</i> is associated with cartilage metabolism, we hypothesize that ACL injury
affects chondrocytes
via
<i>POSTN</i>.
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<h5 class="section-title" id="d5113277e191">Design</h5>
<p id="P3">Cartilage was obtained from osteoarthritic patients and ACL remnants were
collected
from patients undergoing ACL reconstruction. Crosstalk between remnants and chondrocytes
was studied in a transwell co-culture system. Expression of
<i>POSTN</i> and other anabolic and catabolic genes was assessed via real-time PCR.
Immunostaining
for periostin was performed in human and mouse cartilage. The impact of exogenous
periostin and siRNA-mediated ablation of periostin on matrix metabolism and cell-migration
was examined. Furthermore, the effect of anabolic (TGF-β1) and catabolic (IL-1β) factors
on
<i>POSTN</i> expression was investigated.
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<h5 class="section-title" id="d5113277e202">Results</h5>
<p id="P4">ACL remnants induced expression of
<i>POSTN</i>,
<i>MMP13</i> and
<i>ADAMTS4</i>. Periostin levels were significantly higher in osteoarthritic compared
to normal
cartilage. Exogenous periostin induced
<i>MMP13</i> expression and cell-migration, repressed
<i>COL1A1</i> expression while
<i>POSTN-</i>knockdown inhibited expression of both anabolic and catabolic genes and
impeded cell-migration.
TGF-β1 and IL-1β treatment did not alter
<i>POSTN</i> expression but influenced chondrocyte metabolism as determined by anabolic
and catabolic
genes.
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<h5 class="section-title" id="d5113277e229">Conclusions</h5>
<p id="P5">ACL remnants can exert paracrine effects on cartilage, altering cellular
homeostasis.
Over time, this metabolic imbalance could contribute to osteoarthritis development.
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