Prostaglandin E2 enhances cortical bone mass and activates intracortical bone remodeling in intact and ovariectomized female rats

Jee, Webster S. S.; Mori, Satoshi; Li, X.J.; Chan, Shu-Park

doi:10.1016/8756-3282(90)90078-d

Cited by 236 publications

(109 citation statements)

References 31 publications

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“…However, the area of alveolar bone at the buccal aspect adjacent to the mesial root of the first molar in the mandible of those animals treated with the two highest doses of PGE 2 (0.1 and 0.05 mg/day) was significant greater than that observed in animals treated with 0.025 PGE 2 mg/day or placebo. These results showed that PGE 2 induced localized alveolar bone formation in the mandible similar to that observed in long bones [3,6,7], and were consistent with the effect of PGE1 in the mandible [10,11,14,17]. It should be noted that the mandible was not injured during pellet implantation, there was no evidence of inflammation in the soft tissues following healing and at the end of the experimental period.…”

Section: Discussionsupporting

confidence: 85%

“…Prostaglandin E 2 is known to stimulate bone formation in long bones [3,6,7], and the dose required to produce this positive effect may be as low as 0.3 mg/kg per day in load-bearing bones [15]. The animals used in this experiment weighed about 200 g. If the dose locally delivered to the mandible is associated with the animals' weight, 0.1 and 0.05 mg correspond to 0.5 and 0.25 mg/kg applied daily.…”

Section: Discussionmentioning

confidence: 99%

“…Particularly as local delivery of prostaglandin E1 (PGE1) has been shown to enhance the formation of mandibular alveolar bone, reorganization of adjacent cells in the periodontal ligament and cementum formation [11,13,18]. The positive effect of PGE 2 on bone deposition has been reported with doses as low as 1 mg/kg per day delivered subcutaneously into different animal models over extended periods of time [1,6,9,20]. In load-bearing bones, PGE 2 has an anabolic effect when administered either systemically or locally [7].…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Ramirez-Yañez

Seymour

Walsh

et al. 2004

Bone

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Prostaglandin E 2 (PGE 2 ) induces bone formation in stress-bearing bones. The mandible, a stress-bearing bone, is loaded daily during mastication. The aim of this study was to determine if PGE 2 delivered locally to the mandible over 20 days enhances alveolar bone deposition. In 18 Lewis rats, controlled-release pellets containing PGE 2 were implanted on the buccal aspect on the left-hand side of the mandible, mesial to the root of the first molar. Controlled-release pellets locally delivered 0.1, 0.05, or 0.025 mg/day of PGE 2 . The right side of the mandible was used as a matched control for each animal. Six sham-treated animals were implanted with a placebo pellet. On days 7 and 19, animals were injected with the bone markers tetracycline and calcein, respectively. On day 21, animals were sacrificed and undecalcified tissues obtained for morphometrical analysis. Morphometrical measurements were analyzed by paired t test to determine differences between the matched samples and one-way ANOVA to compare the different treatment groups. A significant increase in alveolar bone area was observed in mandibles treated with 0.1 and 0.05 mg/day when compared with matched controls and the placebo group. This was accompanied by a significant increase in alveolar bone height and width. The proportions of double-labeled surface (dLS), the mineral apposition rate (MAR), and bone formation rate (BFR) were significantly increased in mandibles treated with the two higher doses of PGE 2 . The proportion of resorptive surface (RS) was significantly reduced in these two groups. It is concluded that PGE 2 induces alveolar bone formation in the mandible when locally delivered at a dose of 0.1 or 0.05 mg/day for 20 days.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Ramirez-Yañez

Seymour

Walsh

et al. 2004

Bone

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“…Prostaglandins also have catabolic effects on bone and have been shown to stimulate osteoclastic bone resorption and osteoclast formation and activation (28,(31)(32)(33)(34). In addition, prostaglandins activate intracortical bone remodeling in both intact and ovariectomized female rats in vivo (35). The differential effects of PGE 2 are thought to be mediated through multiple subtypes of PGE 2 receptors designated as EP 1 , EP 2 , EP 3 , and EP 4 (36,37).…”

mentioning

confidence: 99%

Effects of Mechanical Strain on the Function of Gap Junctions in Osteocytes Are Mediated through the Prostaglandin EP2 Receptor

Cherian

Cheng

et al. 2003

Journal of Biological Chemistry

191

146

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Fluid flow conditioned medium and PGE 2 stimulated cAMP production and PKA activity suggesting that PGE 2 released by mechanically stimulated cells is responsible for the activation of cAMP and PKA. The adenylate cyclase activators, forskolin and 8-bromo-cAMP, enhanced intercellular connectivity, the number of functional gap junctions, and Cx43 protein expression, whereas the PKA inhibitor, H89, inhibited the stimulatory effect of PGE 2 on gap junctions. These studies suggest that the EP 2 receptor mediates the effects of autocrine PGE 2 on the osteocyte gap junction in response to fluid flow-induced shear stress. These data support the hypothesis that the EP 2 receptor, cAMP, and PKA are critical components of the signaling cascade between mechanical strain and gap junction-mediated communication between osteocytes.

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“…Ac-cording to results from in vivo studies (Jee et al [13]), prostaglandins, e.g. prostaglandin E 2 (PGE 2 ), stimulate osteoblast activity.…”

Section: Introductionmentioning

confidence: 99%

Strain driven transport for bone modeling at the periosteal surface

Banks‐Sills

Ståhle

Svensson

et al. 2011

Mathematical Biosciences

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Bone modeling and remodeling has been the subject of extensive experimental studies.There have been several mathematical models proposed to explain the observed behavior, as well. A different approach is taken here in which the bone is treated from a macroscopic view point. In this investigation, a one-dimensional analytical model is used to shed light on the factors which play the greatest role in modeling or growth of cortical bone at the periosteal surface. It is presumed that bone growth is promoted when increased amounts of bone nutrients, such as nitric oxide synthase (NOS) or messenger molecules, such as prostaglandin E 2 (PGE 2 ), seep out to the periosteal surface of cortical bone and are absorbed by osteoblasts. The transport of the bone nutrients is assumed to be a strain controlled process. Equations for the flux of these nutrients are written for a one-dimensional model of a long bone. The obtained partial differential equation is linearized and solved analytically. Based upon the seepage of nutrients out of the bone, the effect of loading frequency, number of cycles and strain level is examined for several experiments that were found in the literature. It is seen that bone nutrient seepage is greatest on the tensile side of the bone; this location coincides with the greatest amount of bone modeling.

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Prostaglandin E2 enhances cortical bone mass and activates intracortical bone remodeling in intact and ovariectomized female rats

Cited by 236 publications

References 31 publications

Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Effects of Mechanical Strain on the Function of Gap Junctions in Osteocytes Are Mediated through the Prostaglandin EP2 Receptor

Strain driven transport for bone modeling at the periosteal surface

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