Effects of a Cannabinoid Receptor 2 Selective Antagonist on the Inflammatory Reaction to Titanium Particles <i>In Vivo</i> and <i>In Vitro</i>

Zhou, Feng; Lu, Jiajie; Zhu, Xuesong; Mao, Haiqing; Yang, Huilin; Geng, Dechun; Xu, Yaozeng

doi:10.1177/147323001003800616

Cited by 12 publications

(21 citation statements)

References 32 publications

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“…However, Bzb may inhibit inflammatory response at both of the two stages without disturbing the basal secretion of these cytokines. The secretion profiles of TNF-α and IL-1 reported here are consistent with some reports [28], but they differ from those of Zhou et al [29] who found that the elevated secretion of TNF-α can continue up to day 14 after Ti injection. Different physical characteristics of the particles and different drug interventions may account for these differences.…”

Section: Discussionsupporting

confidence: 75%

Therapeutic Potential of the Proteasome Inhibitor Bortezomib on Titanium Particle-Induced Inflammation in a Murine Model

et al. 2011

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Wear particle-induced aseptic loosening has been recognized as a harmful inflammatory process that jeopardizes the longevity of total joint replacement. The proteasome controls the activation of NF-κB and subsequent inflammatory mediators, such as TNF-α and IL-1β; thus, we investigated whether proteasome inhibition can ameliorate wear particle-induced inflammation in a murine model. A total of 48 BALB/C mice were divided into four groups. Titanium (Ti) particles were injected into the established air pouches of all mice (except negative controls) to provoke inflammation, and then 0.1 or 0.5 mg/kg of Bortezomib (Bzb, a proteasome inhibitor) was administered to ameliorate the inflammation response, while air pouches without Bzb administration were used as loading controls. The air pouches were harvested 2 or 7 days after Bzb injection for molecular and histological analyses. Inflammation responses in the air pouch tissues of Bzb treatment groups are lower than those in the Ti-stimulated group, and this occurs in a dose-dependent manner. Bzb can significantly attenuate the severity of Ti-induced inflammation in air pouches.

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Section: Discussionsupporting

confidence: 75%

Therapeutic Potential of the Proteasome Inhibitor Bortezomib on Titanium Particle-Induced Inflammation in a Murine Model

et al. 2011

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“…Small particles are easily phagocytosed, but they cannot be digested. Phagocytes in the tissue around the implant site engulf wear particles, which results in activated cells that secrete high levels of inflammatory cytokines such as TNF-a and IL-1b, both of which promote osteoclastogenesis and, eventually, contribute to the osteolytic process [32,33]. In a macrophage depletion mouse model TNF-a and IL-1b expression was significantly reduced, as was the number of TRAP + cells in pouch tissues [34].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of luteolin on titanium particle-induced osteolysis in a mouse model

et al. 2012

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“…Some cytokine inhibitors have been investigated using in vitro and in vivo animal models. Potential treatments include the following.AM630 is a selective inhibitor of cannabinoid receptor 2 that inhibits IL-1 β and TNF- α [69]. …”

Section: Therapy Of Aseptic Loosening By Regulation Of the Innate mentioning

confidence: 99%

The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines

Landgraeber

Jäger

Jacobs

et al. 2014

Mediators of Inflammation

140

112

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All of the over 1 million total joint replacements implanted in the US each year are expected to eventually fail after 15–25 years of use, due to slow progressive subtle inflammation at the bone implant interface. This inflammatory disease state is caused by implant debris acting, primarily, on innate immune cells, that is, macrophages. This slow progressive pathological bone loss or “aseptic loosening” is a potentially life-threatening condition due to the serious complications in older people (>75 yrs) of total joint replacement revision surgery. In some people implant debris (particles and ions from metals) can influence the adaptive immune system as well, giving rise to the concept of metal sensitivity. However, a consensus of studies agrees that the dominant form of this response is due to innate reactivity by macrophages to implant debris where both danger (DAMP) and pathogen (PAMP) signalling elicit cytokine-based inflammatory responses. This paper discusses implant debris induced release of the cytokines and chemokines due to activation of the innate (and the adaptive) immune system and the subsequent formation of osteolysis. Different mechanisms of implant-debris reactivity related to the innate immune system are detailed, for example, danger signalling (e.g., IL-1β, IL-18, IL-33, etc.), toll-like receptor activation (e.g., IL-6, TNF-α, etc.), apoptosis (e.g., caspases 3–9), bone catabolism (e.g., TRAP5b), and hypoxia responses (Hif1-α). Cytokine-based clinical and basic science studies are in progress to provide diagnosis and therapeutic intervention strategies.

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Effects of a Cannabinoid Receptor 2 Selective Antagonist on the Inflammatory Reaction to Titanium Particles In Vivo and In Vitro

Cited by 12 publications

References 32 publications

Therapeutic Potential of the Proteasome Inhibitor Bortezomib on Titanium Particle-Induced Inflammation in a Murine Model

Therapeutic Potential of the Proteasome Inhibitor Bortezomib on Titanium Particle-Induced Inflammation in a Murine Model

Inhibitory effects of luteolin on titanium particle-induced osteolysis in a mouse model

The Pathology of Orthopedic Implant Failure Is Mediated by Innate Immune System Cytokines

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