标题：Histochemical Examination on Periodontal Tissues of Klotho-Deficient Mice Fed With Phosphate-Insufficient Diet
作者：Hikone, Kumiko; Hasegawa, Tomoka; Tsuchiya, Erika; Hongo, Hiromi; Sasaki, Muneteru; Yamamoto, Tomomaya; Kudo, Ai; Oda, Kimimitsu; Hara 更多 作者机构：[Hikone, Kumiko; Hasegawa, Tomoka; Tsuchiya, Erika; Hongo, Hiromi; Yamamoto, Tomomaya; Kudo, Ai; Haraguchi, Mai; Amizuka, Norio] Hokkaido Univ, Grad S 更多
通讯作者地址：[Amizuka, N]Hokkaido Univ, Grad Sch Dent Med, Dept Dev Biol Hard Tissue, Kita Ku, Kita 13,Nishi 7, Sapporo, Hokkaido 0608586, Japan.
来源：JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
关键词：alpha Klotho-deficient mice; DMP-1; osteopontin; periodontal tissue;; phosphate
摘要：To elucidate which of elevated serum concentration of inorganic phosphate (Pi) or disrupted signaling linked to alpha klotho/fibroblast growth factor 23 (FGF23) is a predominant regulator for senescence-related degeneration seen in alpha Klotho-deficient mice, we have examined histological alteration of the periodontal tissues in the mandibular interalveolar septum of alpha Klotho-deficient mice fed with Pi-insufficient diet. We prepared six groups of mice: wild-type, kl/kl, and alpha Klotho(-/-) mice with normal diet or low-Pi diet. As a consequence, kl/kl(norPi) and alpha Klotho(-/-norPi) mice showed the same abnormalities in periodontal tissues: intensely stained areas with hematoxylin in the interalveolar septum, dispersed localization of alkaline phosphatase-positive osteoblasts and tartrate-resistant acid phosphatase-reactive osteoclasts, and accumulation of dentin matrix protein 1 in the osteocytic lacunae. Although kl/kl(lowPi) mice improved these histological abnormalities, alpha Klotho(-/-lowPi) mice failed to normalize those. Gene expression of alpha Klotho was shown to be increased in kl/kl(lowPi) specimens. It seems likely that histological abnormalities of kl/kl mice have been improved by the rescued expression of alpha Klotho, rather than low concentration of serum Pi. Thus, the histological malformation in periodontal tissues in alpha Klotho-deficient mice appears to be due to not only increased concentration of Pi but also disrupted alpha klotho/FGF23 signaling.