Protective effects of COX-2 inhibitor on titanium-particle-induced inflammatory osteolysis via the down-regulation of RANK/RANKL

Geng, Dechun; Mao, Haiqing; Wang, Junhua; Zhu, Xuesong; Huang, Can; Chen, Liang; Yang, Huilin; Xu, Yaozeng

doi:10.1016/j.actbio.2011.05.007

Cited by 22 publications

(22 citation statements)

References 38 publications

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“…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.…”

Section: Discussionsupporting

confidence: 53%

“…Recent studies have showed that RANKL is overexpressed in tissues adjacent to failure implant8. Therapeutic methods which down-regulated RANKL expression have been shown to effectively inhibits particle-stimulated osteoclastic bone resorption913. Using the murine calvarial model, we observed that RANKL expression significantly increased in particle-stimulated mice when compared with the sham group.…”

Section: Discussionmentioning

confidence: 80%

“…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.…”

mentioning

confidence: 99%

“…Particles worn from prosthesis are easily phagocytized by the peri-prosthetic phagocytes in the tissue4. Engulfing these wear particles, phagocytes can be activated and secrete amount of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-65791112. These factors mediate fibroblasts and osteoblasts secreting high levels of receptor activator of nuclear factor-κB (RANK) ligand (RANKL)1415.…”

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

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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: 53%

Section: Discussionmentioning

confidence: 80%

Section: Resultsmentioning

confidence: 99%

mentioning

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

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Adherence to gastroprotection during cyclooxygenase 2 inhibitor treatment and the risk of upper gastrointestinal tract events: A population‐based study

Valkhoff¹,

Soest²,

Mazzaglia

et al. 2012

Arthritis & Rheumatism

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Objective. Guidelines recommend coprescription of gastroprotective agents (GPAs) in patients receiving cyclooxygenase 2 inhibitors (coxibs) who are at high risk of upper gastrointestinal (UGI) tract complications (i.e., patients with a previous complicated ulcer or with multiple risk factors). Suboptimal GPA adherence has been shown to diminish the gastroprotective effect during use of nonselective nonsteroidal antiinflammatory drugs, but little is known about the effect of GPA adherence during coxib treatment. We undertook this study to determine the association between GPA adherence and UGI tract events among patients receiving coxibs.Methods. Using primary care data from 3 databases, we conducted a case-control study in a cohort of patients age >50 years who were newly starting treatment with coxibs and concomitantly taking GPAs. Patients who had a UGI tract event (bleeding or symptomatic ulcer) were matched to event-free controls for age, sex, database, and calendar date. Coxib treatment intervals were defined as consecutive coxib prescriptions with intervening gaps not exceeding the duration of the previous coxib prescription. Adherence to GPAs was calculated as the proportion of days of coxib treatment covered by a GPA prescription. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated using conditional logistic regression analysis.Results. The coxib plus GPA-treated cohort consisted of 14,416 coxib-treated patients who received GPAs for at least 1 day, yielding 16,442 coxib treatment intervals in which a GPA was coprescribed. Most patients were treated with coxibs for <30 days. Seventyfour patients had a UGI tract event during or shortly after a coxib treatment interval in which a GPA was coprescribed, with an incidence rate of 11.9 (95% CI Study results were presented in part by Drs. Valkhoff and

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Positive modulation of osteogenesis‐ and osteoclastogenesis‐related gene expression with strontium‐containing microstructured Ti implants in rabbit cancellous bone

Park

Kim

Jang

et al. 2012

J Biomedical Materials Res

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This study investigated the in vivo osteoblast and osteoclast gene expression in the peri-implant bone tissue of the strontium (Sr)-incorporated microstructured Ti implants (SLA/Sr) in order to evaluate whether local Sr delivery to the implant surface as in the form of SrTiO(3) also exerts original bone healing enhancement effect of Sr that take place through the dual modes of action of a stimulation of osteogenesis and an inhibition of osteoclastogenesis. The in vivo mRNA expression of osteoblast- and osteoclast-related genes in the peri-implant bone and removal torque forces of the SLA/Sr implants were compared with a chemically modified super-hydrophilic SLA implants (SLActive®) in rabbit cancellous bone after 2 weeks of implantation. There was no significant difference in the removal torque values between the two groups. Both the torque-tested SLA/Sr and SLActive implants exhibited a considerable quantity of bone attached to the surface. Real-time PCR analysis revealed notably increased mRNA expression of osteoblast genes (Runx2, osterix and osteocalcin) in the peri-implant bone of the SLA/Sr implants compared with the SLActive implants (p < 0.05), whereas osteoclast phenotype gene (TRAP) expression was markedly decreased in the SLA/Sr implant (p < 0.05). The results at the molecular level suggest that local Sr delivery as in the form of the Sr-incorporated Ti oxide layer favors early osseointegration of microrough Ti implants via a positive modulation of bone healing, that is, a promotion of osteoblast differentiation and suppression of osteoclastogenesis, in the bone-implant interface of cancellous bone.

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Protective effects of COX-2 inhibitor on titanium-particle-induced inflammatory osteolysis via the down-regulation of RANK/RANKL

Cited by 22 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

Adherence to gastroprotection during cyclooxygenase 2 inhibitor treatment and the risk of upper gastrointestinal tract events: A population‐based study

Positive modulation of osteogenesis‐ and osteoclastogenesis‐related gene expression with strontium‐containing microstructured Ti implants in rabbit cancellous bone

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