YAMATO Masayuki
   Department   Research Institutes and Facilities, Research Institutes and Facilities
   Position   Professor
Article types Original article
Language English
Peer review Peer reviewed
Title Polydactyly-derived allogeneic chondrocyte cell-sheet transplantation with high tibial osteotomy as regenerative therapy for knee osteoarthritis.
Journal Formal name：NPJ Regenerative medicine
Abbreviation：NPJ Regen Med
ISSN code：20573995/20573995
Domestic / ForeginForegin
Volume, Issue, Page 7(1),pp.71
Author and coauthor HAMAHASHI Kosuke, TOYODA Eriko, ISHIHARA Miya, MITANI Genya, TAKAGAKI Tomonori, KANESHIRO Nagatoshi, MAEHARA Miki, TAKAHASHI Takumi, OKADA Eri, WATANABE Ayako, NAKAMURA Yoshihiko, KATO Reiko, MATOBA Ryo, TAKAGI Takehiko, AKUTSU Hidenori, UMEZAWA Akihiro, KOBAYASHI Hiroyuki, AKAMATSU Tadashi, YAMATO Masayuki, OKANO Teruo, WATANABE Masahiko, SATO Masato
Publication date 2022/12
Summary Allogeneic cell therapies are not fully effective in treating osteoarthritis of the knee (OAK). We recently reported that transplantation of autologous chondrocyte cell-sheets along with open-wedge high tibial osteotomy promoted hyaline cartilage repair in humans. Here we describe our regenerative therapy for OAK using polydactyly-derived allogeneic chondrocyte cell-sheets (PD sheets) and temperature-responsive culture inserts. Ten patients with OAK and cartilage defects categorized arthroscopically as Outerbridge grade III or IV received the therapy. Cartilage viscoelasticity and thickness were assessed before and after transplantation. Arthroscopic biopsies obtained 12 months after transplantation were analyzed histologically. Gene expression was analyzed to evaluate the PD sheets. In this small initial longitudinal series, PD sheet transplantation was effective in treating OAK, as indicated by changes in cartilage properties. Gene marker sets in PD sheets may predict outcomes after therapy and provide markers for the selection of donor cells. This combined surgery may be an ideal regenerative therapy with disease-modifying effects in OAK patients.
DOI 10.1038/s41536-022-00272-1
PMID 36522336