Histological examination on osteoblastic activities in the alveolar bone of transgenic mice with induced ablation of osteocytes.
The purpose of this study was to examine histological alterations on osteoblasts from the alveolar bone of transgenic mice with targeted ablation of osteoctyes. Eighteen weeks-old transgenic mice based on the diphtheria toxin (DT) receptor-mediated cell knockout (TRECK) system were used in these experiments. Mice were injected intraperitoneally with 50 µg/kg of DT in PBS, or only PBS as control. Two weeks after injections, mice were subjected to transcardiac perfusion with 4% paraformaldehyde in 0.1M phosphate buffer (pH 7.4), and the available alveolar bone was removed for histochemical analyses. Approximately 75% of osteocytes from alveolar bones became apoptotic after DT administration, and most osteocytic lacunae became empty. Osteoblastic numbers and alkaline phosphatase (ALP) activity were markedly reduced at the endosteum of alveolar bone after DT administration compared with the control. Osteoblastic ALP activity in the periodontal ligament region, on the other hand, hardly showed any differences between the two groups even though numbers were reduced in the experiment group. Silver impregnation showed a difference in the distribution of bone canaliculi between the portions near the endosteum and the periodontal ligament: the former appeared regularly arranged in contrast to the latter's irregular distribution. Under transmission electron microscopy (TEM), the osteoblasts in the periodontal ligament showed direct contact with the Sharpey's fibers. Thus, osteoblastic activity was affected by osteocyte ablation in general, but osteoblasts in contact with the periodontal ligament were less affected than endosteal osteoblasts.
Department of Bone Metabolism, School of Stomatology, Shandong University, Jinan, China. li_min_qi@hotmail.com
Minqi
M
Li
Tomoka
T
Hasegawa
Hiromi
H
Hogo
Sawako
S
Tatsumi
Zhusheng
Z
Liu
Ying
Y
Guo
Muneteru
M
Sasaki
Chihiro
C
Tabata
Tsuneyuki
T
Yamamoto
Kyoji
K
Ikeda
Norio
N
Amizuka
D055011:Ablation Techniques / Q000379:methods*; D000135:Acid Phosphatase / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000378:metabolism; D016301:Alveolar Bone Loss / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D000539:Alveolar Process / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects; D004167:Diphtheria Toxin / Q000494:pharmacology; D004195:Disease Models, Animal; D007527:Isoenzymes / Q000378:metabolism; D008336:Mandibular Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008822:Mice, Transgenic; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010011:Osteocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D010513:Periodontal Ligament / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D053245:RANK Ligand / Q000378:metabolism; D016622:Silver Staining; D000071681:Tartrate-Resistant Acid Phosphatase
D015415:Biomarkers; D004167:Diphtheria Toxin; D007527:Isoenzymes; D053245:RANK Ligand; C505689:Tnfsf11 protein, mouse; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase