title: A histological assessment on the distribution of the osteocytic lacunar canalicular system using silver staining.
abstract: Giving the complexity that characterizes the mechanisms of bone remodeling and the number of events that have to be in absolute harmony for it to occur flawlessly, the postulation that temporospatial distribution of osteocytes and their lacunar canalicular system might influence and be influenced by bone remodeling can be regarded, at least, as feasible. In this study, using Schoen's silver staining, we have examined the distribution of the osteocytic lacunar canalicular system (OLCS) in bones of developing mice. Trabecular bones of 3-day-old, 2-week-old, and 3-week-old mice displayed osteocytic cytoplasmic processes without any perceptible alignment. Also, many plump osteocytes were embedded in the mineralized bone matrix in a disorderly manner. At 4 weeks of age, however, mice bones showed some osteocytic processes that reached the bone surface on a right angle, while other osteocytes displayed the same features seen on 3-week specimens. Samples at 8 weeks of age featured osteocytes with their usual spindle shape, organized so as to parallel the longitudinal axis of trabecular bone. They also extended their cytoplasmic processes perpendicularly to the bone surface. However, several osteocytes immersed in older bone, i.e., a residual mix of cartilage and bone matrices, still showed a random pattern of distribution of their cytoplasmic processes. Up to 12 weeks of age, the majority of the osteocytes became flattened and were shown to be aligned with their long axis paralleling the bone surface. This tendency for such a gradual arrangement was also observed in cortical bones. We have further demonstrated that 8-week-old osteoprotegerin-deficient mice, which demonstrated histological evidence of higher than average bone turnover, revealed a disorganized OLCS. Given the data gathered in this work, the OLCS appears to assume an organized, probably function-related spatial distribution as normal bone remodeling goes on.
authors.affiliation: Division of Reconstructive Surgery for Oral and Maxillofacial Region, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hirose
authors.forename: Minqi
authors.initials: M
authors.lastname: Li
authors.forename: Taku
authors.initials: T
authors.lastname: Kojima
authors.forename: Paulo Henrique Luiz
authors.initials: PH
authors.lastname: de Freitas
authors.forename: Sobhan
authors.initials: S
authors.lastname: Ubaidus
authors.forename: Kimimitsu
authors.initials: K
authors.lastname: Oda
authors.forename: Chikara
authors.initials: C
authors.lastname: Saito
authors.forename: Norio
authors.initials: N
authors.lastname: Amizuka
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D005269:Femur / Q000166:cytology / Q000196:embryology; D006253:Haversian System / Q000166:cytology*; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010006:Osteoblasts / Q000166:cytology; D010010:Osteoclasts / Q000166:cytology / Q000201:enzymology; D010011:Osteocytes / Q000166:cytology*; D053244:Osteoprotegerin / Q000172:deficiency; D016622:Silver Staining / Q000379:methods*; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D053244:Osteoprotegerin; C506031:Tnfrsf11b protein, mouse; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase