Roles of hypoxia inducible factor-1α in the temporomandibular joint

Akiko Mino-Oka, Takashi Izawa, Takehiro Shinohara, Hiroki Mori, Akihiro Yasue, Shuhei Tomita, Eiji Tanaka

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


Objective Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease characterized by permanent cartilage loss. Articular cartilage is maintained in a low-oxygen environment. The chondrocyte response to hypoxic conditions involves expression of hypoxia inducible factor 1α (HIF-1α), which induces chondrocytes to increase expression of vascular endothelial growth factor (VEGF). Here, we investigated the role of HIF-1α in mechanical load effects on condylar cartilage and subchondral bone in heterozygous HIF-1α-deficient mice (HIF-1α+/−). Design Mechanical stress was applied to the TMJ of C57BL/6NCr wild-type (WT) and HIF-1α+/− mice with a sliding plate for 10 days. Histological analysis was performed by HE staining, Safranin-O/Fast green staining, and immunostaining specific for articular cartilage homeostasis. Results HIF-1α+/− mice had thinner cartilage and smaller areas of proteoglycan than WT controls, without and with mechanical stress. Mechanical stress resulted in prominent degenerative changes with increased expression of HIF-1α, VEGF, and the apoptosis factor cleaved Caspase-3 in condylar cartilage. Conclusion Our results indicate that HIF-1α may be important for articular cartilage homeostasis and protective against articular cartilage degradation in the TMJ under mechanical stress condition, therefore HIF-1α could be an important new therapeutic target in TMJ-OA.

Original languageEnglish
Pages (from-to)274-281
Number of pages8
JournalArchives of Oral Biology
Publication statusPublished - Jan 1 2017
Externally publishedYes


  • Articular cartilage degradation
  • Chondrocyte apoptosis
  • Hypoxia inducible factor-1α
  • Temporomandibular joint osteoarthritis (TMJ-OA)

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Dentistry(all)
  • Cell Biology


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