Osteoporosis: Over-active Osteoclasts https://greenmedinfo.com/taxonomy/term/6154/all en An active component in propolis, caffeic acid phenethyl ester, suppresses osteoclastogenesis. https://greenmedinfo.com/article/active-component-propolis-caffeic-acid-phenethyl-ester-suppresses-osteoclastog PMID:  Int Immunopharmacol.2009 Jun;9(6):774-80. Epub 2009 Mar 12. PMID: 19285574 Abstract Title:  Caffeic acid phenethyl ester inhibits osteoclastogenesis by suppressing NF kappaB and downregulating NFATc1 and c-Fos. Abstract:   Osteoclasts are multinuclear cells of myeloid lineage responsible for bone resorption. The anti-inflammatory property of caffeic acid phenethyl ester (CAPE), an active component of the propolis of honeybee hives, has been revealed. Since the regulatory mechanism of differentiation and activation of osteoclasts shares many well-known signaling pathways with that of inflammation, we investigated whether CAPE has any effect on osteoclastogenesis. CAPE potently suppressed osteoclastogenesis in cultures of bone marrow-derived precursor cells with the osteoclast differentiation factor, receptor activator of nuclear factor kappaB ligand (RANKL). While the RANKL-stimulated activation of the ERK, JNK, and p38 MAPK signaling pathways was not affected, the DNA binding and transcription activity of NF kappaB were reduced by CAPE treatment. In addition, CAPE blocked the induction of NFATc1 and c-Fos following RANKL stimulation. Forced expression of c-Fos could reverse the inhibitory effect of CAPE on osteoclastogenesis. Finally, CAPE significantly inhibited the RANKL-induced osteoclast formation in mouse calvariae in vivo. We propose that CAPE might be useful as a therapeutic agent for treatment of bone destructive diseases. https://greenmedinfo.com/article/active-component-propolis-caffeic-acid-phenethyl-ester-suppresses-osteoclastog#comments Bee Propolis Bone Destructive Diseases: Over-Active Osteoclasts Osteoporosis: Over-active Osteoclasts Osteoclastogenesis Suppression Animal Study Sat, 18 Jul 2009 02:57:37 +0000 greenmedinfo 45720 at https://greenmedinfo.com Horsetail extracts have the ability to modulate osteoclastogenesis in vitro. https://greenmedinfo.com/article/horsetail-extracts-have-ability-modulate-osteoclastogenesis-vitro PMID:  Cell Prolif. 2012 Dec ;45(6):566-76. PMID: 23106302 Abstract Title:  Inhibition of human in vitro osteoclastogenesis by Equisetum arvense. Abstract:  OBJECTIVES: Equisetum arvense has long been used in traditional medicines to treat different disorders, including bone pathologies. In this study a hydromethanolic extract of E. arvense was assessed for its effects on human osteoclastogenesis.MATERIALS AND METHODS: Osteoclast precursors were maintained in non-stimulated and stimulated (presence of M-CSF and RANKL) conditions, or in co-cultures with osteoblasts. Cell cultures were treated with 0.00016-0.5 mg/ml of a hydromethanolic E. arvense extract.RESULTS: The extract did not affect spontaneous osteoclastogenesis. In osteoclast precursors committed to osteoclastogenesis (stimulated or co-cultured with osteoblasts), E. arvense caused dose-dependent inhibitory effect that became statistically significant at concentrations≥0.004 mg/ml. This was observed using different osteoclast differentiation and activation markers. Cell response was associated with changes in relative contribution of MEK and NFkB signalling pathways, as well as PGE2 production. As there were differences in the response of osteoclast precursorsmaintained in the presence of inductive factors, or co-cultured with osteoblastic cells, it seems that E. arvense extract had the ability to modulate osteoclastogenesis, either by acting directly on osteoclast precursor cells, and/or via osteoblasts.CONCLUSIONS: Equisetum appeared to have a negative effect on human osteoclastogenesis, which is in line with its putative beneficial role in pathophysiological conditions associated with increased osteoclastic activity, and might suggest potential utility for treatment with bone regeneration strategies. https://greenmedinfo.com/article/horsetail-extracts-have-ability-modulate-osteoclastogenesis-vitro#comments Horsetail Osteoporosis: Over-active Osteoclasts Plant Extracts In Vitro Study Fri, 22 Jan 2016 04:11:01 +0000 greenmedinfo 123357 at https://greenmedinfo.com Rosiglitazone may increase the risk of bone fracture by increasing osteoclast (bone-dissolving cells) generation. https://greenmedinfo.com/article/rosiglitazone-may-increase-risk-bone-fracture-increasing-osteoclast-bone-disso PMID:  Cell Metab. 2010 Jun 9;11(6):503-16. PMID: 20519122 Abstract Title:  PGC1beta mediates PPARgamma activation of osteoclastogenesis and rosiglitazone-induced bone loss. Abstract:  Long-term usage of rosiglitazone, a synthetic PPARgamma agonist, increases fracture rates among diabetic patients. PPARgamma suppresses osteoblastogenesis while activating osteoclastogenesis, suggesting that rosiglitazone decreases bone formation while sustaining or increasing bone resorption. Using mouse models with genetically altered PPARgamma, PGC1beta, or ERRalpha, here we show that PGC1beta is required for the resorption-enhancing effects of rosiglitazone. PPARgamma activation indirectly induces PGC1beta expression by downregulating beta-catenin and derepressing c-jun. PGC1beta, in turn, functions as a PPARgamma coactivator to stimulate osteoclast differentiation. Complementarily, PPARgamma also induces ERRalpha expression, which coordinates with PGC1beta to enhance mitochondrial biogenesis and osteoclast function. ERRalpha knockout mice exhibit osteoclast defects, revealing ERRalpha as an important regulator of osteoclastogenesis. Strikingly, PGC1beta deletion in osteoclasts confers complete resistance to rosiglitazone-induced bone loss. These findings identify PGC1beta as an essential mediator for the PPARgamma stimulation of osteoclastogenesis by targeting both PPARgamma itself and ERRalpha, thus activating two distinct transcriptional programs. https://greenmedinfo.com/article/rosiglitazone-may-increase-risk-bone-fracture-increasing-osteoclast-bone-disso#comments Osteoporosis Osteoporosis: Over-active Osteoclasts Rosiglitazone (trade name Avandia) Animal Study Sat, 06 Nov 2010 15:34:17 +0000 greenmedinfo 58431 at https://greenmedinfo.com Sulforaphane inhibits osteoclastogenesis by inhibiting nuclear factor-kappaB. https://greenmedinfo.com/article/sulforaphane-inhibits-osteoclastogenesis-inhibiting-nuclear-factor-kappab PMID:  Mol Cells. 2005 Dec 31;20(3):364-70. PMID: 16404151 Abstract Title:  Sulforaphane inhibits osteoclastogenesis by inhibiting nuclear factor-kappaB. Abstract:  We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-kB ligand (RANKL) in osteoclast (OC) precursors. Sulforaphane, an aliphatic isothiocyanate, is a known cancer chemo-preventative agent with anti-oxidative properties. Nuclear factor-kB (NF-kB) is a critical transcription factor in RANKL-induced osteoclastogenesis, and electrophoretic mobility shift assays (EMSAs) and assay of NF-kB-mediated secreted alkaline phosphatase (SEAP) revealed that sulforaphane selectively inhibited NF-kappaB activation induced by RANKL. Inhibition may involve interaction of sulforaphane with thiol groups, since it was prevented by reducing agents. https://greenmedinfo.com/article/sulforaphane-inhibits-osteoclastogenesis-inhibiting-nuclear-factor-kappab#comments Bone Destructive Diseases: Over-Active Osteoclasts Osteoporosis: Over-active Osteoclasts Sulforaphane NF-kappaB Inhibitor In Vitro Study Wed, 27 Oct 2010 02:36:53 +0000 greenmedinfo 58112 at https://greenmedinfo.com