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Expression of hyaluronan synthase 3 in deformed human temporomandibular joint discs: in vivo and in vitro studies

T. Matsumoto, M. Inayama, I. Tojyo, N. Kiga, S. Fujita
  • M. Inayama
    Affiliation not present
  • I. Tojyo
    Affiliation not present
  • N. Kiga
    Affiliation not present
  • S. Fujita
    Affiliation not present

Abstract

The present study aimed at investigating the expression of a hyaluronan synthase (HAS) 3 in tissue samples of deformed human temporomandibular joint (TMJ) discs and cells obtained from the discs. Fifteen adult human TMJ discs (twelve diseased discs and three normal discs) were used in this study. The twelve diseased discs were obtained from twelve patients with internal derangement (ID) of TMJ. These patients all had anteriorly displaced discs and deformed discs. The tissues were immunohistochemically stained using HAS3 antibodies. In addition, the subcultured TMJ disc cells under both normal and hypoxic conditions (O2: 2%) were incubated for 3, 6, 12, and 24 h after addition of interleukin-1ß (IL-1ß) (1ng/mL). Subsequently, the expression of HAS3 was examined using real-time reverse transcription-polymerase chain reaction (RT-PCR). The control group showed from negative to weak positive reactions for HAS3 on immunohistochemical staining. The discs extracted from twelve cases with ID presented from moderate to strong positive reactions for HAS3. The quantity of HAS3 mRNA was compared with a control group, and showed a 204-fold increase at 3 h, a 26-fold increase at 6 h, a 2.5-fold increase at 12 h and a 32-fold increase at 24 h under hypoxia with the addition of IL-1ß. The expression of HAS3 mRNA was significantly enhanced at 3 h and 24 h. The results obtained suggest that HAS3 is related to the pathological changes of human TMJ discs affected by ID.

Keywords

Temporomandibular joint disc; Internal derangement; Hyaluronan synthase 3 (HAS3); Human; Hypoxia

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Submitted: 2010-09-14 16:10:45
Published: 2010-12-15 11:26:52
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Copyright (c) 2010 T. Matsumoto, M. Inayama, I. Tojyo, N. Kiga, S. Fujita

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