Skeletal Site-specific Effects of Zoledronate on in vivo Bone Remodeling and in vitro BMSCs Osteogenic Activity

Gong, Xue; Yu, Wanlu; Zhao, Hang; Su, Jian; Sheng, Quan Z.

doi:10.1038/srep36129

Cited by 56 publications

(43 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent work by Gong et al showed that, following tooth extraction, zoledronic acid prevents bone resorption by osteoclasts by downregulating the RANKL/OPG ratio and RANKL/RANK/OPG pathway and inhibits osteoblast mineralization by downregulating Wnt-3a and the canonical Wnt/β-catenin pathway ( Gong et al, 2017 ). Jacobs et al also reported that mechanical forces in combination with BPs affect the OPG/RANKL system, osteoclastogenesis and bone apposition factors.…”

Section: Mechanical Traumamentioning

confidence: 99%

Bisphosphonate-related osteonecrosis of the jaw: a mechanobiology perspective

2018

View full text Add to dashboard Cite

Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is a dramatic disintegration of the jaw that affects patients treated with bisphosphonates (BPs) for diseases characterized by bone loss. These diseases are often metastasizing cancers (like multiple myeloma, breast cancer and prostate cancer (Aragon-Ching et al., 2009)) as well as osteoporosis. BRONJ is incompletely understood, although it is believed to arise from a defect in bone remodeling—the intricate process by which sensory osteocytes signal to osteoclasts and osteoblasts to resorb and form bone in response to stimuli. Further, tooth extraction and infection have been overwhelmingly linked to BRONJ (Ikebe, 2013). Because bone cells are highly networked, the importance of multicellular interactions and mechanotransduction during the onset of these risk factors cannot be overstated. As such, this perspective addresses current research on the effects of BPs, mechanical load and inflammation on bone remodeling and on development of BRONJ. Our investigation has led us to conclude that improved in vitro systems capable of adequately recapitulating multicellular communication and incorporating effects of osteocyte mechanosensing on bone resorption and formation are needed to elucidate the mechanism(s) by which BRONJ ensues.

show abstract

Section: Mechanical Traumamentioning

confidence: 99%

Bisphosphonate-related osteonecrosis of the jaw: a mechanobiology perspective

2018

View full text Add to dashboard Cite

show abstract

“… 27 – 31 The tissues investigated were bone, oral mucosa, periodontium, and blood vessel supply. 23 , 24 , 32 – 43 The studies differed in the type of BP used as well as the route of application. 25 , 44 – 49 Only 2 studies analyzed non-N-BPs (clodronate at 20 mg/kg and etidronate at 5 mg/kg); the remaining 44 trials used N-BPs with zoledronate (0.01–0.6 mg/kg) being the most commonly used (30 studies), followed by alendronate (0.01–1 mg/kg) (14 studies), pamidronate (0.01–3 mg/kg) (5 studies), and ibandronate (0.003–0.3 mg/kg) and risedronate (0.1–1 mg/kg) (1 study each).…”

Section: Resultsmentioning

confidence: 99%

Pathogenesis of medication-related osteonecrosis of the jaw: a comparative study of in vivo and in vitro trials

et al. 2018

View full text Add to dashboard Cite

ObjectiveThis study was performed to determine whether the results of prevailing in vivo and in vitro studies offer a reliable model for investigation of medication-related osteonecrosis of the jaw (MRONJ).MethodsEmbase, Medline, and the Cochrane Library were searched for articles published from September 2003 to June 2017 involving experimental approaches to the pathogenesis of MRONJ. In vivo and in vitro trials were analyzed with respect to the scientific question, study design, methodology, and results.ResultsOf 139 studies, 87, 46, and 6 conducted in vivo, in vitro, and both in vivo and in vitro experiments, respectively. Rats, mice, dogs, minipigs, sheep, and rabbits were the preferred animal models used. Osteoblasts, osteoclasts, fibroblasts, keratinocytes, macrophages, and human umbilical vein endothelial cells were the preferred cell types. Zoledronate, alendronate, ibandronate, and risedronate were the most frequent bisphosphonates used. MRONJ was most reliably induced in minipigs because of the close relationship with human bone physiology. In vitro studies showed that reduced viability, growth, and migration of cells in the bone and soft tissues were causative for MRONJ. Other than exposed jawbone after tooth extraction, no reliable cofactors were found.ConclusionThe minipig is the most suitable animal model for MRONJ.

show abstract

“…The potential applications of BMSCs in tissue engineering, particularly of bone tissue, have attracted much attention in recent years. A thorough understanding of the molecular mechanisms associated with osteogenesis is essential to maintaining osteogenic capacity and realizing the therapeutic potential of BMSCs [15][16][17]. A number of critical signaling pathways, including Wnt, TGF-β/BMP, and Hedgehog, are involved in regulating the lineage commitment of MSCs [18][19][20].…”

Section: Discussionmentioning

confidence: 99%

The lncRNA MCF2L-AS1 controls osteogenic differentiation by regulating miR-33a

Chen

Wang

2020

Cell Cycle

View full text Add to dashboard Cite

Bone homeostasis is maintained by balanced osteoblast-mediated tissue production and osteoclastmediated tissue destruction, and is disrupted in pathological conditions such as osteoporosis. The mechanisms underlying osteogenic differentiation of bone marrow mesenchymal stem cells, which is critical to bone homeostasis, are not completely clear, despite extensively studies. Long noncoding RNAs (lncRNAs) have recently emerged as novel therapeutic targets in various diseases. However, the expression pattern and biological function of lncRNAs in osteogenic differentiation remain unclear. In this study, we aimed to determine the role of lncRNAs in osteogenic differentiation of human bone marrow mesenchymal stem cells. We found high lncRNA MCF2L-AS1 expression in human bone marrow mesenchymal stem cells, and used bioinformatics analysis to analyze its function. MCF2L-AS1 knockdown induced inhibition of osteoblast differentiation. Silencing of MCF2L-AS1 increased the expression of miR-33a and subsequently inhibited Runx2 expression at the post-transcriptional level. Moreover, MCF2L-AS1 directly interacted with miR-33a, and downregulation of miR-33a efficiently reversed the suppression of Runx2 induced by MCF2L-AS1 short hairpin RNA (shRNA). Thus, MCF2L-AS1 positively regulated the expression of Runx2 by sponging miR-33a, and promoted osteogenic differentiation in BMSCs. Our results indicated that the lncRNA MCF2L-AS1 plays a critical role in the osteogenic differentiation of BMSCs, and targeting lncRNA MCF2L-AS1 could be a promising strategy to promote osteogenic differentiation.

show abstract

Skeletal Site-specific Effects of Zoledronate on in vivo Bone Remodeling and in vitro BMSCs Osteogenic Activity

Cited by 56 publications

References 44 publications

Bisphosphonate-related osteonecrosis of the jaw: a mechanobiology perspective

Bisphosphonate-related osteonecrosis of the jaw: a mechanobiology perspective

Pathogenesis of medication-related osteonecrosis of the jaw: a comparative study of in vivo and in vitro trials

The lncRNA MCF2L-AS1 controls osteogenic differentiation by regulating miR-33a

Contact Info

Product

Resources

About