Serum OPG and RANKL levels before and after intravenous bisphosphonate treatment in Paget's disease of bone

Martini, Giuseppe; Gennari, Luigi; Merlotti, Daniela; Salvadori, Stefania; Franci, Maria Beatrice; Campagna, S.; Avanzati, Annalisa; Paola, Vincenzo De; Valleggi, F.; Nuti, Ranuccio

doi:10.1016/j.bone.2006.08.003

Cited by 70 publications

(57 citation statements)

References 52 publications

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“…OPG levels are consistently increased in patients with PDB compared with controls (405)(406)(407). This lends support to the concept of increased OPG circulating in conditions of elevated turnover potentially as a protective mechanism, although the relationship between OPG levels and bone turnover in unaffected individuals is less clear as discussed earlier.…”

Section: Paget's Disease Of Bonesupporting

confidence: 52%

“…The primary mechanism of action of bisphosphonates is to inhibit bone resorption by impairing key metabolic pathways of osteoclasts, although some in vitro cell studies and animal studies suggest potential effects on osteoblasts (408 -411). OPG levels in PDB have been reported to increase modestly after treatment with pamidronate (406) and risedronate (407) and to decrease after treatment with tiludronate (405). These differing results may be due to differences in the mechanism of action of amino bisphosphonates compared with non-amino bisphosphonates on osteoclasts and osteoblasts, or due to differences in study populations.…”

Section: Paget's Disease Of Bonementioning

confidence: 45%

“…This lends support to the concept of increased OPG circulating in conditions of elevated turnover potentially as a protective mechanism, although the relationship between OPG levels and bone turnover in unaffected individuals is less clear as discussed earlier. RANKL levels are elevated in PDB in some studies (406) but not in others (407). The response of OPG and RANKL levels in PDB to treatment with bisphosphonates has also been investigated.…”

Section: Paget's Disease Of Bonementioning

confidence: 99%

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Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

2007

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Osteoclasts and osteoblasts dictate skeletal mass, structure, and strength via their respective roles in resorbing and forming bone. Bone remodeling is a spatially coordinated lifelong process whereby old bone is removed by osteoclasts and replaced by bone-forming osteoblasts. The refilling of resorption cavities is incomplete in many pathological states, which leads to a net loss of bone mass with each remodeling cycle. Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling, which leads to accelerated bone loss and increased risk of fracture. Bone resorption is dependent on a cytokine known as RANKL (receptor activator of nuclear factor B ligand), a TNF family member that is essential for osteoclast formation, activity, and survival in normal and pathological states of bone remodeling. The catabolic effects of RANKL are prevented by osteoprotegerin (OPG), a TNF receptor family member that binds RANKL and thereby prevents activation of its single cognate receptor called RANK. Osteoclast activity is likely to depend, at least in part, on the relative balance of RANKL and OPG. Studies in numerous animal models of bone disease show that RANKL inhibition leads to marked suppression of bone resorption and increases in cortical and cancellous bone volume, density, and strength. RANKL inhibitors also prevent focal bone loss that occurs in animal models of rheumatoid arthritis and bone metastasis. Clinical trials are exploring the effects of denosumab, a fully human anti-RANKL antibody, on bone loss in patients with osteoporosis, bone metastasis, myeloma, and rheumatoid arthritis. (Endocrine Reviews 29: 2008)

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Section: Paget's Disease Of Bonesupporting

confidence: 52%

Section: Paget's Disease Of Bonementioning

confidence: 45%

Section: Paget's Disease Of Bonementioning

confidence: 99%

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Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

2007

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“…OPG and RANKL secreted by osteoblasts act as remodeling regulator proteins 34) , and normal remodeling occurs when the optimal balance between these proteins is maintained. OPG and RANKL are also used as markers of bone repair 35) .…”

mentioning

confidence: 99%

Jawbone Changes in Sodium Zoledronic Acid- and Dexamethasone-Treated Rats

Tezuka

Tanaka

2016

J. Hard Tissue Biology.

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Previous studies have evaluated bisphosphonate-related osteonecrosis of the jaw (ONJ) after tooth extraction with concurrent administration of bisphosphonate zoledronic acid (ZOL) and steroids. However, details of jawbone changes after administration of ZOL and steroids without tooth extraction remain unclear. In this study, we administered ZOL and dexamethasone (DEX) in rats and compared changes in the jawbone with and without tooth extraction. The right maxillary first molar (M 1 ) was extracted from 8-week-old rats treated with ZOL, ZOL+DEX or DEX. The right maxillary M 1 region as the extraction sample and the left maxillary M 1 region as the non-extraction sample were compared with macroscopic, radiological, histologic and immunohistochemical examinations. In the extraction samples, we detected incomplete mucosal closure macroscopically and found ONJ on histological examination. In addition, immunohistochemical and threedimensional analysis of trabecular bone structure showed inhibition of remodeling and angiogenesis in the extraction samples. In the non-extraction samples, we observed inhibition of remodeling, reduced activity of osteoclasts and osteoblasts and suppression of angiogenesis. These findings demonstrate that ONJ can develop under the mucosa with ZOL and DEX treatment, even without invasive procedures. The data suggest that ZOL and DEX can induce ONJ in rats under both invasive and noninvasive conditions because ZOL suppresses osteoclast activity and DEX inhibits remodeling by suppressing osteoblast activity. The results also suggest that surgical stress, such as tooth extraction or bacterial infection, might lead to more severe bisphosphonaterelated ONJ.

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“…No presente estudo, observamos a ausência de expressão da proteína RANKL no osso alveolar da porção oclusal da cripta nos animais tratados com alendronato, o que justifica o reduzido número de osteoclastos ativados e corrobora com os resultados descritos na literatura. Esta diminuição pode estar relacionada a danos ocorridos no folículo dentário subjacente devido ao contato das (Martini et al, 2007). A análise de osteoclastos obtidos da medula óssea de seres humanos que utilizam alendronato in vitro demonstra diminuição da osteoclastogênese e da expressão de RANKL pelas células estromais (Eslami et al, 2011), o que reforça a hipótese levantada pelos resultados obtidos no presente estudo.…”

Section: Western Blottingunclassified

Estudo da osteoclastogênese e da remodelação óssea durante a formação e erupção de molares de ratos tratados com bisfosfonatos.

Corrêa¹

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Serum OPG and RANKL levels before and after intravenous bisphosphonate treatment in Paget's disease of bone

Cited by 70 publications

References 52 publications

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

Jawbone Changes in Sodium Zoledronic Acid- and Dexamethasone-Treated Rats

Estudo da osteoclastogênese e da remodelação óssea durante a formação e erupção de molares de ratos tratados com bisfosfonatos.

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