Inhibition of T-Cell-Mediated and infection-Induced periodontal bone resorption by TACE blockade

Hiroyuki Kanzaki, Xiaozhe Han, Yukiko Asami, Maiko Suzuki, Toshihisa Kawai, Martin Taubman

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations


Host immune responses trigger promotion of bone resorption in periodontitis, and infiltrated lymphocytes express abundant RANKL, the essential factor for osteoclastogenesis. Since RANKL is initially produced as a membrane- bound protein, cell-to-cell contact can be required for osteoclastogenesis. However, distance between lymphocytes and active osteoclasts is generally observed. This observation presume released cytokine(s) from activated lymphocytes might induce osteoclastogenesis in periodontitis. Previously, we reported that cleavage of RANKL and TNF-α by TNF-α converting enzyme (TACE) from lymphocytes can play a role in human periodontitis. Herein, we further examined function of TACE in two experimental periodontitis models in rats: (1) Aggregatibacter actinomycetemcomitans-reactive T-cell adop- tive transfer and (2) Porphyromonas gingivalis infection. Anti-TACE antibody was injected into the gingivae to probe the role of TACE in bone destruction. Our data suggested that TACE blockade could inhibit alveolar bone destruction. TACE might be a potentially therapeutic target for periodontitis amelioration.

Original languageEnglish (US)
Title of host publicationInterface Oral Health Science 2011
PublisherSpringer Japan
Number of pages3
ISBN (Electronic)9784431540700
ISBN (Print)9784431540694
StatePublished - Jan 1 2012


  • Osteoclastogenesis
  • Periodontitis
  • TACE
  • TNF-α
  • sRANKL

ASJC Scopus subject areas

  • Dentistry(all)


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