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Osteocytic cells exposed to titanium particles increase sclerostin expression and inhibit osteoblastic cell

Hao Chai1, Zai Hang Zhang1, Jing Yi Fang2

  • 1Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.

Journal of Cellular and Molecular Medicine
|June 28, 2022
PubMed

Insights

Titanium particles induce osteocyte cell death and inflammation, while inhibiting bone cell differentiation. Silencing sclerostin (SOST) mitigates these negative effects, highlighting SOST

Area of Science:

  • Biomaterials Science
  • Cell Biology
  • Orthopedic Research

Background:

  • Periprosthetic osteolysis, a significant complication of artificial joint replacements, is often induced by wear particles.
  • The precise cellular mechanisms by which these particles, particularly titanium (Ti), trigger osteolysis remain incompletely understood.
  • Osteocytes, embedded within the bone matrix, play a critical role in bone remodeling and response to mechanical stimuli and injury.

Purpose of the Study:

  • To elucidate the role of osteocytes in titanium particle-induced periprosthetic osteolysis.
  • To investigate the impact of titanium particles on osteocyte function and viability.
  • To determine the involvement of sclerostin (SOST) in the cellular crosstalk between osteocytes and osteoblasts under titanium particle exposure.

Main Methods:

  • In vitro culture of MLO-Y4 osteocytic cells and MC3T3-E1 osteoblastic cells.
  • Exposure of osteocytic cells to varying concentrations of titanium particles.
  • Manipulation of SOST expression using silencing techniques.
  • Co-culture systems to assess intercellular communication effects.
  • Analysis of cell apoptosis, gene/protein expression (SOST, IL-6, TNF-α, connexin 43, ALP, OCN, Runx2), and osteoblastic differentiation markers.

Main Results:

  • Titanium particles increased SOST expression, induced apoptosis, and elevated inflammatory markers (IL-6, TNF-α) and connexin 43 in osteocytes in a dose-dependent manner.
  • SOST silencing ameliorated titanium particle-induced osteocyte apoptosis and inflammation.
  • Titanium-treated osteocytes significantly inhibited osteoblastic differentiation of MC3T3-E1 cells, primarily via cell-to-cell contact.
  • SOST silencing attenuated this inhibitory effect, restoring osteoblastic differentiation markers (ALP, mineralization, OCN, Runx2).

Conclusions:

  • Titanium particles exert detrimental effects on osteocytes, impacting their viability and function.
  • Osteocyte dysfunction induced by titanium particles contributes to the inhibition of osteoblastic differentiation, mediated significantly through intercellular communication.
  • Sclerostin (SOST) plays a crucial role in mediating the negative effects of titanium particles on osteocytes and their subsequent impact on osteoblasts, suggesting it as a potential therapeutic target in periprosthetic osteolysis.
Keywords:
SOST/sclerostinosteoblastosteocyteosteolysiswear debris

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