Journal of Electron Microscopy 52(6): 503-513 (2003)
© Japanese Society of Microscopy
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Defective bone remodelling in osteoprotegerin-deficient mice
1 Division of Oral Anatomy, 2 Division of Pediatric Dentistry, 3 Division of Oral and Maxillofacial Surgery and 4 Division of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, 2-5274 Gakkochodori, Niigata 951-8514, Japan, 5 Center for Transdisciplinary Research, Niigata University, Niigata 951-8514, Japan, 6 Center for Bone and Periodontal Research, McGill University Health Centre, Royal Victoria Hospital, Montréal, Québec H3A 1A, Canada, 7 Department of Pharmacology, Jichi Medical University, Yakushiji 329-0498, Japan and 8 Institute for Dental Science, Matsumoto Dental University, Shiojiri 399-0704, Japan
* To whom correspondence should be addressed. E-mail: amizuka{at}dent.niigata-u.ac.jp
Abstract
Previous studies have reported enhanced osteoclastogenesis, increased bone resorption and osteoporosis in osteoprotegerin (OPG)-deficient mice. In the present study, we show that the tibial epiphyses contain abundant, thin trabeculae lined with numerous osteoclasts and cuboidal osteoblasts. The increase in osteoblasts and osteoclasts was associated with a dramatic increase in calcein labelling of the mineralization fronts and replacement of much of the intertrabecular marrow with numerous alkaline phosphatase-positive preosteoblasts. Furthermore, the discrete, linear cement lines seen in wild-type mice were replaced by a randomly oriented meshwork of cement lines that were stained intensely for tartrate-resistant acid phosphatase and osteopontin in the OPG-/- mice. These indices of accelerated bone remodelling in mutant bone were associated with irregular trabecular surfaces, a disorganized collagen matrix interspersed with amorphous ground substance and numerous fissures between old and new bone. In total, these observations indicate that enhanced osteoclastic activity in OPG-/- epiphyses led to a coupled increase in osteoblast differentiation and activity and an increase in bone remodelling. The high bone turnover, disorganized matrix and impaired attachment of new to old bone in the cement lines in OPG-/- mice appear to cause bone fragility.
Keywords osteoclast, osteoblast, osteoprotegerin, bone remodelling, ultrastructure, bone matrix
Received 22 July 2003, accepted 25 August 2003
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