title: Is gastrectomy-induced high turnover of bone with hyperosteoidosis and increase of mineralization a typical osteomalacia?
abstract: Gastrectomy (GX) is thought to result in osteomalacia due to deficiencies in Vitamin D and Ca. Using a GX rat model, we showed that GX induced high turnover of bone with hyperosteoidosis, prominent increase of mineralization and increased mRNA expression of both osteoclast-derived tartrate-resistant acid phosphatase 5b and osteocalcin. The increased 1, 25(OH)2D3 level and unchanged PTH and calcitonin levels suggested that conventional bone and Ca metabolic pathways were not involved or changed in compensation. Thus, GX-induced bone pathology was different from a typical osteomalacia. Gene expression profiles through microarray analysis and data mining using Ingenuity Pathway Analysis indicated that 612 genes were up-regulated and 1,097 genes were down-regulated in the GX bone. These genes were related functionally to connective tissue development, skeletal and muscular system development and function, Ca signaling and the role of osteoblasts, osteoclasts and chondrocytes. Network analysis indicated 9 genes (Aldehyde dehydrogenase 1 family, member A1; Aquaporin 9; Interleukin 1 receptor accessory protein; Very low density lipoprotein receptor; Periostin, osteoblast specific factor; Aggrecan; Gremlin 1; Angiopoietin-like 4; Wingless-type MMTV integration site family, member 10B) were hubs connected with tissue development and immunological diseases. These results suggest that chronic systemic inflammation might underlie the GX-induced pathological changes in bone.
authors.affiliation: Department of Anatomy and Cell Biology, Wakayama Medical University Graduate School of Medicine, Wakayama, Japan. tueyama@wakayama-med.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Ueyama
authors.forename: Yuta
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Kazuki
authors.initials: K
authors.lastname: Ueda
authors.forename: Aiji
authors.initials: A
authors.lastname: Yajima
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Maeda
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Yamashita
authors.forename: Takao
authors.initials: T
authors.lastname: Ito
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Tsuruo
authors.forename: Masao
authors.initials: M
authors.lastname: Ichinose
mesh_terms: D000135:Acid Phosphatase; D000818:Animals; D001835:Body Weight / Q000502:physiology; D001851:Bone Diseases, Metabolic / Q000209:etiology* / Q000378:metabolism*; D001842:Bone and Bones / Q000378:metabolism* / Q000473:pathology*; D002113:Calcification, Physiologic; D019902:Chondrocytes / Q000378:metabolism; D005743:Gastrectomy / Q000009:adverse effects*; D007527:Isoenzymes; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis; D010006:Osteoblasts / Q000378:metabolism; D015675:Osteocalcin / Q000235:genetics / Q000378:metabolism; D010018:Osteomalacia / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase; D014057:Tomography, X-Ray Computed; D014807:Vitamin D / Q000378:metabolism
chemical_list: D007527:Isoenzymes; D015675:Osteocalcin; D014807:Vitamin D; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase