Regulation of bone biology by prostaglandin endoperoxide H synthases (PGHS): A rose by any other name…

Li, Li; Pettit, Allison R.; Gregory, Laura S.; Forwood, Mark R.

doi:10.1016/j.cytogfr.2006.01.005

Cited by 33 publications

(27 citation statements)

References 116 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In general, bone formation and bone resorption occur simultaneously in equilibrium, and they are regulated by systemic hormones (such as vitamin D and parathyroid hormone) [48,49], bone-derived local factors including prostaglandins [48], proinflammatory cytokines [48][49][50], nitric oxide [51] and the function of immune cells [52]. Among the prostaglandin E 2 (PGE 2 ) produced by osteoblastic lineage [53] is a potent local factor stimulating bone resorption both in vivo [54] and in vitro [54,55] in response to the catabolic effects of vitamin D, parathyroid hormone and cytokines [56,57]. In vitro studies [58][59][60] show that effects of PGE 2 on bone formation are biphasic and concentration dependent.…”

Section: Discussionmentioning

confidence: 99%

Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model☆☆☆

Shen

Yeh

Cao

et al. 2010

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model☆☆☆

Shen

Yeh

Cao

et al. 2010

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

“…COX-1 and COX-2 are the rate limiting enzymes involved in the conversion of arachidonic acid into prostaglandins. PGE 2 , primarily produced by COX-2 during inflammation, has numerous roles in bone biology. PGE 2 is a potent stimulator of osteoclastogenesis, and COX-2 and PGE 2 are required for the response to many hormonal and cytokine mediators of bone resorption.…”

mentioning

confidence: 99%

“…PGE 2 is a potent stimulator of osteoclastogenesis, and COX-2 and PGE 2 are required for the response to many hormonal and cytokine mediators of bone resorption. 2 COX-2 and PGE 2 are also important mediators of mechanotransduction, bone formation and bone adaptation to loading. 3 There is convincing evidence that selective COX-2 inhibitors and non-selective NSAIDs compromise the healing of complete fractures.…”

mentioning

confidence: 99%

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Kidd

Cowling

et al. 2012

Journal Orthopaedic Research

View full text Add to dashboard Cite

Anti-inflammatory drugs are widely used to manage pain associated with stress fractures (SFxs), but little is known about their effects on healing of those injuries. We hypothesized that selective and non-selective anti-inflammatory treatments would retard the healing of SFx in the rat ulna. SFxs were created by cyclic loading of the ulna in Wistar rats. Ulnae were harvested 2, 4 or 6 weeks following loading. Rats were treated with non-selective NSAID, ibuprofen (30 mg/kg/day); selective COX-2 inhibition, [5,5-dimethyl-3-3 (3 fluorophenyl)-4-(4 methylsulfonal) phenyl-2 (5H)-furanone] (DFU) (2.0 mg/kg/day); or the novel c5a anatagonist PMX53 (10 mg/kg/ day, 4 and 6 weeks only); with appropriate vehicle as control. Quantitative histomorphometric measurements of SFx healing were undertaken. Treatment with the selective COX-2 inhibitor, DFU, reduced the area of resorption along the fracture line at 2 weeks, without affecting bone formation at later stages. Treatment with the non-selective, NSAID, ibuprofen decreased both bone resorption and bone formation so that there was significantly reduced length and area of remodeling and lamellar bone formation within the remodeling unit at 6 weeks after fracture. The C5a receptor antagonist PMX53 had no effect on SFx healing at 4 or 6 weeks after loading, suggesting that PMX53 would not delay SFx healing. Both selective COX-2 inhibitors and non-selective NSAIDs have the potential to compromise SFx healing, and should be used with caution when SFx is diagnosed or suspected. ß

show abstract

“…Monocytes and Mfs are known producers of OSM (Zarling et al, 1986), a cytokine that has been shown to increase osteogenic differentiation and mineralization both in vitro and in vivo (Nicolaidou et al, 2012;Walker et al, 2010). PGE 2 has been reported to have many important roles in bone including osteoclast and osteoblast formation and function, bone mechanotransduction and repair (Kawaguchi et al, 1995;Li et al, 2006). It has been demonstrated that in bone fracture sites infiltrating Mfs have elevated expression of COX2 and that this is required for bone repair (Xie et al, 2008).…”

Section: Macrophages and Bonementioning

confidence: 96%

Immune cells and bone: coupling goes both ways

Horwood¹

2013

Immunological Investigations

View full text Add to dashboard Cite

There is a mounting body of research describing how cells of the immune system direct bone cell function whilst bone cells are involved in the generation and retention of immune cells and their precursors. Recent works into regulation of the haemopoietic stem cell niche have firmly implicated osteoblasts and osteoclasts. On the other hand, virtually all of the mature immune cells have been described to influence bone formation in vitro and in vivo. This review will summarize the latest developments and discuss the importance of the coupling of bone formation to resorption when considering the contributions from cells of the immune system.

show abstract

Regulation of bone biology by prostaglandin endoperoxide H synthases (PGHS): A rose by any other name…

Cited by 33 publications

References 116 publications

Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model☆☆☆

Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model☆☆☆

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Immune cells and bone: coupling goes both ways

Contact Info

Product

Resources

About