Inhibition of titanium-particle-induced inflammatory osteolysis after local administration of dopamine and suppression of osteoclastogenesis via D2-like receptor signaling pathway

Yang, Huilin; Xu, Yaozeng; Zhu, Mo; Gu, Ye; Wen, Zhang; Shao, Hu; Wang, Yijun; Ping, Zichuan; Hu, Xuanyang; Wang, Liangliang; Geng, Dechun

doi:10.1016/j.biomaterials.2015.11.046

Cited by 75 publications

(77 citation statements)

References 38 publications

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“…The present study has demonstrated that strontium significantly increased bone volume and reduced osteolysis, which is consistent with previous studies13. These findings gave rise to the question as to the mechanism of strontium action in the prevention of wear-debris-induced osteolysis.…”

Section: Discussionsupporting

confidence: 93%

“…Infiltration of multinucleated osteoclast in model and peri-prosthesis tissue has been well defined, and our previous work confirmed that Ti particles significantly increased osteoclastogenesis in vivo and in vitro 891213. Therapeutic strategy targeting osteoclast formation significant inhibits particle-associated bone resorption1013. Therefore, we considered whether the protective effects of strontium were mediated by the inhibition of osteoclast formation and osteoclatic bone resorption.…”

Section: Discussionmentioning

confidence: 94%

“…After establishing that SrRan reduced mature osteoclast numbers in osteolytic sites stimulated with Ti particles, and our previous studies have demonstrated that RANKL is critical in mediating wear-debris induced osteoclastogenesis7913, we want to determine whether SrRan could modify the expression of RANKL in calvaria of particle-stimulated mice. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Briefly, there are three important events in wear particle-induced-osteolysis, including chronic inflammation, osteoclast formation, and osteoclastic bone resorption5678910111213. Particles worn from prosthesis are easily phagocytized by the peri-prosthetic phagocytes in the tissue4.…”

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confidence: 99%

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Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Zhu

Tao

et al. 2016

Sci Rep

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Wear-particle-induced chronic inflammation and osteoclastogenesis have been identified as critical factors of aseptic loosening. Although strontium is known to be involved in osteoclast differentiation, its effect on particle-induced inflammatory osteolysis remains unclear. In this study, we investigate the potential impact and underling mechanism of strontium on particle-induced osteoclast activation and chronic inflammation in vivo and in vitro. As expected, strontium significantly inhibited titanium particle-induced inflammatory infiltration and prevented bone loss in a murine calvarial osteolysis model. Interestingly, the number of mature osteoclasts decreased after treatment with strontium in vivo, suggesting osteoclast formation might be inhibited by strontium. Additionally, low receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor-α, interleukin-1β, interleukin-6 and p65 immunochemistry staining were observed in strontium-treatment groups. In vitro, strontium obviously decreased osteoclast formation, osteoclastogenesis-related gene expression, osteoclastic bone resorption and pro-inflammatory cytokine expression in bone-marrow-derived macrophages in a dose-dependent manner. Furthermore, we demonstrated that strontium impaired osteoclastogenesis by blocking RANKL-induced activation of NF-κB pathway. In conclusion, our study demonstrated that strontium can significantly inhibit particle-induced osteoclast activation and inflammatory bone loss by disturbing the NF-κB pathway, and is an effective therapeutic agent for the treatment of wear particle-induced aseptic loosening.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Zhu

Tao

et al. 2016

Sci Rep

Self Cite

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“…Furthermore several laboratories have reported evidence of dopaminergic and serotonergic receptor gene expression in primary osteoblast and osteoclast cells as well as MC3T3 cells which differentiate into osteoblasts 26,[40][41][42] . Dopamine is present in marrow and inhibits osteoclastogenesis and osteoblastogenesis in both primary human osteoclasts and mouse primary osteoclasts and osteoblasts 26,41,43 . Furthermore, the effect of dopamine to inhibit osteoclastogenesis in murine cells was antagonized by the dopamine antagonist, risperidone, further confirming a direct effect of dopamine and AA medications on bone biology 26 .…”

Section: Elucidating Underlying Mechanisms: Direct Effectsmentioning

confidence: 99%

Elucidating the Mechanism(s) Underlying Antipsychotic- and Antidepressant-Mediated Fractures

Houseknecht

Bouchard

Black

2017

J Mental Health & Clin Psychology

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Mood spectrum disorders and medications used to treat these disorders, such as atypical antipsychotic drugs (AA), are associated with metabolic and endocrine side effects including obesity, dyslipidemia, hyperglycemia and increased risk of fractures. Antidepressant medications, including selective serotonin reuptake inhibitors (SSRI), have also been reported to increase fracture risk in some patients. The pharmacology underlying the increased risk of fractures is currently unknown. Possible mechanisms include alternations in dopaminergic and/or serotonergic signaling pathways. As these medications distribute to the bone marrow as well as to the brain, it is possible that drug-induced fractures are due to both centrally mediated effects as well as direct effects on bone turnover. Given the growing patient population that is prescribed these medications for both on- and off-label indications, understanding the level of risk and the mechanisms underlying drug-induced fractures is important for informing both prescribing and patient monitoring practices.

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tBHQ Suppresses Osteoclastic Resorption in Xenogeneic‐Treated Dentin Matrix‐Based Scaffolds

Sun

et al. 2017

Adv Healthcare Materials

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Extracellularmatrix (ECM)-based scaffolds are important for their potential therapeutic application. Treated dentin matrix (TDM), a kind of ECM, seeded with allogeneic dental follicle stem cells (TDM/aDFC) provides a suitable inductive microenvironment for tooth root regeneration. Considering the limited sources, xenogeneic TDM (xTDM) is a possible alternative to allogeneic TDM; however, xTDM-based scaffold presents severe osteolysis and resorption lacunae causing regenerated tooth root failure. Immune response-induced excessive osteoclastogenesis plays a critical role in xenogeneic scaffold osteolysis and resorption. The impact of antioxidant, tert-butylhydroquinone (tBHQ), on xTDM/aDFCs-induced osteoclastogenesis and osteoclastic resorption in vivo and in vitro are investigated. tBHQ upregulates heme oxygenase-1 release and downregulates high mobility group box 1 mRNA expression. mRNA expression of other osteoclast-related genes including nuclear factor-kappa Bp65, receptor activator of nuclear factor kappa-B, nuclear factor of activated T-cells cytoplasmic 1, cathepsin K, and integrin β3, also decreases significantly. Furthermore, tBHQ-treated xTDM/aDFCs scaffolds implanted into rhesus macaques show reduced osteolysis and osteoclastic resorption by microcomputed tomography and tartrate-resistant acid phosphatase staining. tBHQ-induced suppression of xTDM/aDFC-induced osteoclastogenesis and osteoclastic resorption presents a new strategy for the regeneration of biological tooth root and could be applied to the regeneration of other complex tissues and organs.

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Inhibition of titanium-particle-induced inflammatory osteolysis after local administration of dopamine and suppression of osteoclastogenesis via D2-like receptor signaling pathway

Cited by 75 publications

References 38 publications

Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Elucidating the Mechanism(s) Underlying Antipsychotic- and Antidepressant-Mediated Fractures

tBHQ Suppresses Osteoclastic Resorption in Xenogeneic‐Treated Dentin Matrix‐Based Scaffolds

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