The role of bone cells in increasing metaphyseal hard tissue in rapidly growing rats treated with prostaglandin E2

Jee, Webster S. S.; Ueno, Keisuke; Kimmel, Donald B.; Woodbury, Dixon M.; Price, Paul A.; Woodbury, Lowell A.

doi:10.1016/8756-3282(87)90017-2

Cited by 124 publications

(62 citation statements)

References 31 publications

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“…In animal studies it has been suggested that eg prostaglandin E2 (PGE2) and interleukin-1 can induce a dose dependent increase in the subperiostal lamellar bone formation 90 and that subcutaneous injections of PGE2 in growing rats can induce heterotopic bone formation. 91,92 Measurement of 24-h PGE in SCI patients with NHO showed abnormal 24-h PGE2 urinary excretion as long as the bone-scan had not stabilized. 27 However, the mechanism by which prostaglandins may induce ectopic bone formation in SCI patients remains unclear and there are well-known di culties in the interpretation of PGE2 urinary excretion measurements in men presenting with a positive urinary sperm count or in patients with lower urinary tract infections.…”

Section: Local Factorsmentioning

confidence: 99%

Neurogenic heterotopic ossification in spinal cord injury

2002

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Neurogenic heterotopic ossi®cation (NHO) is a frequent complication in spinal cord injury (SCI) that is often di cult to treat. This review emphasizes the incidence, risk factors and clinical signs of NHO in SCI patients. Although the exact pathophysiology underlying NHO in neurologic patients is not yet understood, di erent pathogenic mechanisms have been proposed in the literature. A selection of the most important theories will be given and discussed. Moreover the di erent diagnostic, therapeutic, and preventive methods currently used in NHO management after SCI will be reviewed.

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Section: Local Factorsmentioning

confidence: 99%

Neurogenic heterotopic ossification in spinal cord injury

2002

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“…This dose is within the range known to be anabolic in rats (Ueno et al 1985, Jee et al 1987, 1992, Suponitzki & Weinreb 1998. Total RNA was extracted from the tibial metaphysis using a guanidinium isothiocyanate-phenol-chloroform method (Chomczynski & Sacchi 1987), after pulverizing frozen bone samples by a tissue homogenizer.…”

Section: Northern Blot Analysismentioning

confidence: 92%

“…It is now established that PGE 2 -induced bone formation results primarily from the appearance of new osteoblasts and production of new bone. Previously, others and ourselves have reported that PGE 2 is anabolic in young and aging rats (Ueno et al 1985, Jee et al 1987, 1992, Suponitzki & Weinreb 1998). In addition, we have published a detailed analysis of the effects of PGE 2 and have clarified some aspects of the mechanisms involved in the actions of PGE 2 : induction of early response genes (Weinreb et al 1997a), stimulation of osteoblast differentiation from bone marrow osteoprogenitors (Weinreb et al 1997b, Keila et al 2001) and involvement of the cAMP signaling pathway and of the EP 4 receptor (Weinreb et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of cyclo-oxigenase-2 activity does not abolish the anabolic effect of prostaglandin E2 in vivo or in vitro

Weinreb

Kelner²,

Keila³

2002

Journal of Endocrinology

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It was previously reported that the expression of cyclooxigenase-2 (COX-2) is induced by prostaglandin E 2 (PGE 2 ) in vitro in an osteogenic cell line and organ culture, suggesting an autoamplification mechanism. In this study, we first tested whether this phenomenon also occurs in bone tissue in vivo and found that a single anabolic dose of PGE 2 (5 mg/kg) induced (between 30 and 120 min) in rat tibiae, an increase in the mRNA level of COX-2 (2·5-to 9-fold) but not that of COX-1. Secondly, to test whether COX-2 activity in generating endogenous prostaglandins (PGs) is required for the in vivo anabolic properties of PGE 2 , young male rats were injected daily with either vehicle (8% ethanol) or 5 mg/kg PGE 2 for 21 days. PGE 2 -injected rats received, 45 min prior to PGE 2 , either dimethyl sulphoxide (as vehicle) or one of two doses of NS-398, a selective COX-2 inhibitor: a low dose (3 mg/kg) or a high dose (10 mg/kg). PGE 2 increased bone formation (measured as cancellous mineralizing surface, mineral apposition rate and bone formation rate) and bone mass (measured as cancellous bone area and surface and cortical width). None of these increases was suppressed by pre-administration of NS-398. In contrast, the high dose of NS-398 effectively suppressed an increase in rat hind-paw volume induced by a local carrageenan injection. Furthermore, since COX-2 inactivation may affect PG receptor expression, we found that preadministration of NS-398 did not abolish the induction in EP 4 receptor mRNA levels, caused by PGE 2 in rat bone tissue. For in vitro testing, rat femoral bone marrow stromal cell cultures were initiated and were incubated in the absence or presence of PGE 2 at 100 nM (as an inducer) and with increasing concentrations of NS-398 (10 8 M to 10 5 M) for 21 days, after which time mineralized (Von-Kossa positive) nodules were counted. PGE 2 increased nodule formation as previously reported; however, NS-398 reduced nodule formation in both control and PGE 2 -treated cultures to the same extent. We conclude that while the level of COX-2 mRNA is increased in vivo by administration of PGE 2 , inhibition of its activity (i.e. generation of endogenous PGs) does not abolish the anabolic effect of PGE 2 .

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“…Motion in the fracture site and PGs (mainly PGE2) stimulate differentiation of the osteoprogenitor cells and fibrocartilaginous callus growth (Cohen 1956, Jee et al 1987, Shih and Norrdin 1986. Bone remodeling does not commence until the late phase of callus formation (Frost 1973).…”

mentioning

confidence: 99%

“…After pin stabilization of rabbit fractures, an increased release of PGs of the E and F series was found in bone and muscle when compared with controls (Dekel et al 1981 ). PGs stimulate bone formation by preosteoblast cell differentiation, osteoblast proliferation, and collagen synthesis (Jee et al 1987, Chyun and Raisz 1984, Rodan andRodan 1985, Shih andNorrdin 1986).…”

mentioning

confidence: 99%

Release of prostaglandins from bone and muscle after femoral osteotomy in rats

Wittenberg

1991

Acta Orthopaedica Scandinavica

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The role of bone cells in increasing metaphyseal hard tissue in rapidly growing rats treated with prostaglandin E2

Cited by 124 publications

References 31 publications

Neurogenic heterotopic ossification in spinal cord injury

Neurogenic heterotopic ossification in spinal cord injury

Inhibition of cyclo-oxigenase-2 activity does not abolish the anabolic effect of prostaglandin E2 in vivo or in vitro

Release of prostaglandins from bone and muscle after femoral osteotomy in rats

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