Mechanisms of TNF-α– and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis

Ritchlin, Christopher T.; Haas-Smith, Sally A.; Li, Ping; Hicks, David G.; Schwarz, Edward M.

doi:10.1172/jci16069

Cited by 354 publications

(380 citation statements)

References 54 publications

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“…Although it is beyond the scope of the present study to assess the relationship between the inflammatory milieu and tissue remodeling in SpA, since that would require prospective and longitudinal data in larger cohorts, our analysis of PsA is of particular interest in this context. Whereas tissue destruction is modest in SpA as compared with RA, PsA can display both extensive destructive features and marked signs of repair (53). If the differing structural phenotype between RA and SpA is mainly due to differences in the local inflammatory milieu, one may expect this inflammatory milieu to also be different in PsA.…”

Section: Discussionmentioning

confidence: 99%

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Vandooren¹,

Noordenbos²,

Ambarus³

et al. 2009

Arthritis & Rheumatism

154

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Objective. Peripheral spondylarthritis (SpA) is characterized by macrophages that express CD163, a marker of alternative activation (M2). The purpose of this study was to assess whether this differential infiltration with macrophage subsets was associated with a different local inflammatory milieu in SpA as compared with rheumatoid arthritis (RA).Methods Conclusion. The local inflammatory milieu is clearly different in SpA as compared with RA peripheral arthritis. Synovitis in SpA, including that in PsA, is characterized by a selective decrease in M1-derived proinflammatory mediators, such as TNF␣ and IL-1␤.

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Section: Discussionmentioning

confidence: 99%

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Vandooren¹,

Noordenbos²,

Ambarus³

et al. 2009

Arthritis & Rheumatism

154

View full text Add to dashboard Cite

show abstract

“…17 It further functions to direct homing, migration, and fusion of the precursor cells to mature bone-resorbing osteoclasts. 49 Moreover, TNF-␣ induction of Smurf-mediated degradation of Runx2 leads to the inhibition of osteoblast activity in restoring bone. 50 In this study, alveolar bone loss in LPS-treated rats was largely reduced by the MAO inhibitor phenelzine in association with strongly reduced ROS (H 2 O 2 ) and TNF-␣ expression in the junctional epithelium.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Ekuni

Firth

Nayer

et al. 2009

The American Journal of Pathology

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Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. Junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >4-fold.

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“…Among diverse inflammatory mediators that can induce vascular permeability, it is well known that NO and PGE 2 are major factors involved in the pathogenesis of many inflammation-associated diseases [13,37]. They are also known mediators of pain induction and perception [16,34].…”

mentioning

confidence: 99%

Anti-Inflammatory Effects of an Ethanol Extract of Angelica gigas in a Carrageenan-Air Pouch Inflammation Model

Shin¹,

Jeon²,

Park³

et al. 2009

Exp. Anim.

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Anti-inflammatory effects of an ethanol extract of Angelica gigas (EAG; 50, 160, or 500 mg/kg) were investigated in a carrageenan-induced air pouch inflammation model. Injection of 1 ml of carrageenan (1%) into mouse air pouches markedly increased the exudate volume and exudate albumin concentration, which were significantly attenuated by oral pretreatment with EAG. EAG also markedly reduced carrageenan-induced infiltrations of neutrophils, monocytes, and lymphocytes, but did not influence eosinophils or basophils. Carrageenan dramatically increased levels of tumor necrosis factor-a and interleukin-6, which might be derived from the infiltrated cells. It also elevated nitric oxide, and slightly increased prostaglandin E 2 . EAG pretreatment significantly lowered tumor necrosis factor-a and nitric oxide, but did not alter interleukin-6 or prostaglandin E 2 levels. These results indicate that EAG attenuates some inflammatory responses by blocking the tumor necrosis factor-a-nitric oxide pathway, and that EAG could be a promising anti-inflammatory drug candidate for inflammatory diseases.

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Mechanisms of TNF-α– and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis

Cited by 354 publications

References 54 publications

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Anti-Inflammatory Effects of an Ethanol Extract of Angelica gigas in a Carrageenan-Air Pouch Inflammation Model

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