The role of prostaglandins in bone in vivo

Norrdin, R. W.; Jee, Webster S. S.; High, Wanda B.

doi:10.1016/0952-3278(90)90081-u

Cited by 182 publications

(79 citation statements)

References 80 publications

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“…Furthermore, PGs have a direct effect on bone resorption through increased osteoclastic activity [15,38,42,46,56] and also increase the replication and differentiation of the osteoblasts resulting in enhanced bone formation [42 , 46]. Thus, PGs are involved in regulation of the balance between bone resorption and bone formation [18,36,47].…”

Section: Discussionmentioning

confidence: 99%

Parecoxib and Indomethacin Delay Early Fracture Healing: A Study in Rats

Dimmen

Nordsletten

Madsen

2009

Clinical Orthopaedics &Amp; Related Research

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Nonsteroidal antiinflammatory drugs (NSAIDs) are used to reduce inflammatory response and pain. These drugs have been reported to impair bone metabolism. Parecoxib, a specific COX-2 inhibitor, exerts an inhibitory effect on the mineralization of fracture callus after a tibial fracture in rats. Decreased bone mineral density (BMD) at a fracture site may indicate impairment of early healing, casting doubt on the safety of using COX-2 inhibitors during the early treatment of diaphyseal fractures. Fortytwo female Wistar rats were randomly allocated to three groups. They were given parecoxib, indomethacin, or saline intraperitoneally for 7 days after being subjected to a closed tibial fracture stabilized with an intramedullary nail. Two and 3 weeks after surgery, the bone density at the fracture site was measured using dual energy xray absorptiometry (DEXA). Three weeks after the operation the rats were euthanized and the healing fractures were mechanically tested in three-point cantilever bending.Parecoxib decreased BMD at the fracture site for 3 weeks after fracture, indomethacin for 2 weeks. Both parecoxib and indomethacin reduced the ultimate bending moment and the bending stiffness of the healing fractures after 3 weeks. These results suggest COX inhibitors should be avoided in the early phase after fractures.

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Section: Discussionmentioning

confidence: 99%

Parecoxib and Indomethacin Delay Early Fracture Healing: A Study in Rats

Dimmen

Nordsletten

Madsen

2009

Clinical Orthopaedics &Amp; Related Research

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“…In orthodontics, there seems to be a consensus on the fact that PGE2 injections increase the rate of tooth movement (Bao, Zhao & Rao, 1995;Chao et al, 1988;Kale et al, 2004;Kokkinos et al, 1993;Leiker et al, 1995;Seifi, Eslami & Saffar, 2003). In contrast to orthopedic studies, which typically show anabolic effects of PGE2 (Norrdin, Jee & High, 1990), studies have reported increase in bone resorption alone (Boekenoogen et al, 1996;Chao et al, 1988;Kale et al, 2004;Leiker et al, 1995;Seifi et al, 2003;Yamasaki, Shibata & Fukuhara, 1982). For ERR, there are studies that report an increase (Boekenoogen et al, 1996;Leiker et al, 1995), but there are also studies that report no significant effect of this molecule (Brudvik & Rygh, 1991).…”

Section: Biological Factors In Rate Of Tooth Movement and Errmentioning

confidence: 99%

Orthodontic mechanotransduction and the role of the P2X7 receptor

Viecilli

Katona

Chen

et al. 2009

American Journal of Orthodontics and Dentofacial Orthopedics

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DEDICATIONTo my parents, who have supported my education. iv ACKNOWLEDGMENTSOne of the most important things I have learned during my PhD is the necessity of the existence of a working network of people that can help you achieve your goals. The more effectively this network functions, the higher the chance you will achieve the goals quickly.I would first like to thank my parents, who have unconditionally supported my decision to abandon a profitable private practice in Orthodontics, and return to humble student conditions while aiming for a full time academic career.I also thank my girlfriend Laura Kruter who has (almost always) been ok with my, some might say, not very sane ideas. Sometimes they do turn out fine, though (like this "PhD" one).I can hardly think of anyone else that could have complemented my work and ideas during this Program as well as Dr. Thomas Katona. While I was passionately conditioned to an idea, he was always rational and careful. While I was sometimes furious with a shortcoming, he was always temperate and humorous. When I ran into his office with some news about a project, he would always listen and almost never seem too busy to see me. While I was working and something went wrong, he would listen and wonder with me about the "whys" and "hows", instead of telling me what to do or express disappointment. He was even subject to some of my home culinary experiments. I was extremely fortunate to find someone that thought about science the same way I did, and that actually helped me with my project instead of just telling me what to do. I felt like we worked as a team, and that helped to increase my motivation during my studies. The third part of this project tested the role of the P2X7 receptor in the dentoalveolar morphology of C57B/6 mice. P2X7R KO (knockout) mice were compared to C57B/6 WT to identify differences in a maxillary molar and bone. Tooth dimensions viii were measured and 3D bone morphometry was conducted. No statistically significant differences were found between the two mouse types. P2X7R does not have a major effect on alveolar bone or tooth morphology.The final part examines the role of the P2X7 receptor in a controlled biomechanical model. Orthodontic mechanotransduction was compared in wild-type (WT) and P2X7R knock-out (KO) mice. Using Finite Element Analysis, mouse mechanics were scaled to produce typical human stress levels. Relationships between the biological responses and the calculated stresses were statistically tested and compared.There were direct relationships between certain stress magnitudes and root resorption and bone formation. Hyalinization and root and bone resorption were different in WT and KO. Orthodontic responses are related to the principal stress patterns in the PDL and the P2X7 receptor plays a significant role in their mechanotransduction.

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“…inflammation (1)(2)(3)(4)(5). PGE 2 production from arachidonic acid, which is released by phospholipase A 2 from membrane glycerophospholipids (6), is controlled by two rate-limiting steps.…”

mentioning

confidence: 99%

Transcriptional Regulation of the Membrane-associated Prostaglandin E2 Synthase Gene

Naraba¹,

Yokoyama²,

Tago³

et al. 2002

Journal of Biological Chemistry

126

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Membrane-associated prostaglandin (PG) E 2 synthase (mPGES) is an inducible terminal enzyme in the biosynthetic pathway for prostaglandin E 2 , which participates in many biological processes. In this study, we investigated the molecular mechanism controlling the inducible expression of mPGES. The mouse mPGES gene consisted of three exons, and its 5-proximal promoter contained consensus motifs for the binding of several transcription factors. Transgenic expression in mice of the mouse mPGES promoter flanked by a reporter gene resulted in stimulus-dependent induction of the reporter in tissues where mPGES was intrinsically induced. Deletion and site-specific mutation analyses of the 5-flanking region demonstrated that stimulus-inducible expression of mouse and human mPGES required tandem GC boxes adjacent to the initiation site. The stimulus-induced GC box binding activity was present in nuclear extracts of cells, in which the proximal GC box was essential for binding. An 80-kDa stimulusinducible nuclear protein that bound to this GC box was identified as the transcription factor Egr-1 (for early growth response-1). These results suggest that Egr-1 is a key transcription factor in regulating the inducible expression of mPGES.

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The role of prostaglandins in bone in vivo

Cited by 182 publications

References 80 publications

Parecoxib and Indomethacin Delay Early Fracture Healing: A Study in Rats

Parecoxib and Indomethacin Delay Early Fracture Healing: A Study in Rats

Orthodontic mechanotransduction and the role of the P2X7 receptor

Transcriptional Regulation of the Membrane-associated Prostaglandin E2 Synthase Gene

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