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Related Experiment Video

Updated: Apr 20, 2026

Author Spotlight: Advancements in Cell and Tissue Engineering for Tendon Repair
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In Vitro Modulation of Murine Tenocyte Behavior by Hyperbaric Oxygen Therapy.

Afton K Limberg1, Lily M Giurleo1, Victoria Ruiz1

  • 1Thayer School of Engineering at Dartmouth College, Hanover, New Hampshire, USA.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|April 19, 2026
PubMed
Summary
This summary is machine-generated.

Hyperbaric oxygen therapy (HBOT) impacts tendon cells by increasing collagen and mitochondrial activity, but may hinder healing in inflammatory conditions. Further research is needed for therapeutic applications in tendon repair.

Keywords:
hyperbaric oxygenscar tissuetendontendon healingtenocytes

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Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Regenerative Medicine

Background:

  • Tendon injuries cause prolonged healing and scarring due to poor perfusion and hypoxia.
  • Hyperbaric oxygen therapy (HBOT) is used for wound healing and may benefit tendon repair by addressing hypoxia.
  • The cellular effects of HBOT on tenocytes (tendon cells) are not well understood.

Purpose of the Study:

  • To investigate the in vitro effects of HBOT on tenocytes under normal and inflammatory conditions.
  • To assess HBOT's impact on tenocyte wound healing, mitochondrial activity, viability, collagen production, and gene expression.

Main Methods:

  • Murine Achilles tenocytes were cultured and exposed to HBOT (2.5 ATA for 30, 60, or 90 minutes).
  • Interleukin-1 beta (IL-1β) was used to induce inflammatory conditions.
  • Assays included scratch assay for wound healing, mitochondrial activity, cell viability, collagen deposition, and gene expression analysis at 24 and 72 hours.

Main Results:

  • HBOT increased collagen deposition and mitochondrial activity (especially with longer exposure).
  • HBOT transiently suppressed collagen type I and III gene expression and reduced HIF-1α expression.
  • Under inflammatory conditions (IL-1β), HBOT significantly reduced tenocyte wound closure compared to controls.
  • Cell viability remained high, though some visual increase in dead cells was noted with HBOT.

Conclusions:

  • HBOT modulates tenocyte mitochondrial activity, ECM production, and gene expression.
  • The effects of HBOT on tenocytes differ in the presence of inflammation, potentially impairing wound closure.
  • Findings provide insights into HBOT's cellular mechanisms in tendon biology, supporting further investigation for tendon repair therapies.