Bone, Inflammation, and Inflammatory Bowel Disease

Agrawal, Manasi; Arora, Shitij; Li, Jianjun; Rahmani, Rabin; Sun, Li; Steinlauf, Adam F.; Mechanick, Jeffrey I.; Zaidi, Mone

doi:10.1007/s11914-011-0077-9

Cited by 62 publications

(42 citation statements)

References 59 publications

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“…multiple positive and negative receptors, the effect of IgGs varies among the different subtypes and the effect of monomeric and polymeric IgG also differs, it has been difficult to elucidate the molecular basis of IgG regulation of osteoclastogenesis despite the wealth of in vitro and in vivo observations of the involvement of FcgRs in bone metabolism 6,7,14,[6][7][8][9][10][11][12][13][14][15][16][17][18]28,29 . This study affords a detailed picture of the regulation of osteoclastogenesis by the IgG-FcgR system, in which both ligands and receptors are differentially regulated under physiological and pathological conditions, providing clear evidence for the IC-mediated regulation of bone metabolism.…”

Section: Discussionmentioning

confidence: 99%

“…It is well documented that enhanced bone resorption is associated with the activation of the immune system observed in autoimmune or inflammatory diseases, such as rheumatoid arthritis (RA) 11 , systemic lupus erythematosus (SLE) 12 and inflammatory bowel disease 13 . The role of FcgRs has been explored in arthritis models [14][15][16][17][18] ; however, it has been difficult to observe their direct effects on bone metabolism due to their central contribution to the onset of autoimmune disease and inflammation.…”

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confidence: 99%

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Immune complexes regulate bone metabolism through FcRγ signalling

et al. 2015

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Autoantibody production and immune complex (IC) formation are frequently observed in autoimmune diseases associated with bone loss. However, it has been poorly understood whether ICs regulate bone metabolism directly. Here we show that the level of osteoclastogenesis is determined by the strength of FcRg signalling, which is dependent on the relative expression of positive and negative FcgRs (FcgRI/III/IV and IIB, respectively) as well as the availability of their ligands, ICs. Under physiological conditions, unexpectedly, FcgRIII inhibits osteoclastogenesis by depriving other osteoclastogenic Ig-like receptors of FcRg. Fcgr2b À / À mice lose bone upon the onset of a hypergammaglobulinemia or the administration of IgG1 ICs, which act mainly through FcgRIII. The IgG2 IC activates osteoclastogenesis by binding to FcgRI and FcgRIV, which is induced under inflammatory conditions. These results demonstrate a link between the adaptive immunity and bone, suggesting a regulatory role for ICs in bone resorption in general, and not only in inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Immune complexes regulate bone metabolism through FcRγ signalling

et al. 2015

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“…Bones are targets of inflammation, with inflammatory cytokines promoting bone resorption which results in systemic bone loss (30). A clear example of an infl ammatory entity and a bone detrimental effect is infl ammatory bowel disease (IBD) (33). Patients with IBD demonstrate elevated levels of IL-6, TNF α and IL1β, all of which are associated with osteoclastic activity through the activation of p38 mitogen-activated protein kinase (MAPK) pathways (33,34).…”

Section: Note: the Numerical Values Shown In The Table Represent Meanmentioning

confidence: 99%

“…A clear example of an infl ammatory entity and a bone detrimental effect is infl ammatory bowel disease (IBD) (33). Patients with IBD demonstrate elevated levels of IL-6, TNF α and IL1β, all of which are associated with osteoclastic activity through the activation of p38 mitogen-activated protein kinase (MAPK) pathways (33,34). Our previous study on older Mexico City children had shown elevated concentrations of TNF α and IL1β (5), thus a osteoclastic synergistic action is likely to be taking place as the children grow up in their polluted environment.…”

Section: Note: the Numerical Values Shown In The Table Represent Meanmentioning

confidence: 99%

Exposure to Urban Air Pollution and Bone Health in Clinically Healthy Six-year-old Children

Calderón‐Garcidueñas

Mora-Tiscareño

Franco-Lira

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Air pollution induces systemic infl ammation, as well as respiratory, myocardial and brain infl ammation in children. Peak bone mass is infl uenced by environmental factors. We tested the hypothesis that six-yearolds with lifetime exposures to urban air pollution will have alterations in infl ammatory markers and bone mineral density (BMD) as opposed to low-polluted city residents when matched for BMI, breast feeding history, skin phototype, age, sex and socioeconomic status. This pilot study included 20 children from Mexico City (MC) (6.17 years ± 0.63 years) and 15 controls (6.27 years ± 0.76 years). We performed full paediatric examinations, a history of outdoor exposures, seven-day dietary recalls, serum infl ammatory markers and dual-energy X-ray absorptiometry (DXA). Children in MC had signifi cantly higher concentrations of IL-6 (p=0.001), marked reductions in total blood neutrophils (p= 0.0002) and an increase in monocytes (p=0.005). MC children also had an insuffi cient Vitamin D intake and spent less time outdoors than controls (p<0.001) in an environment characterized by decreased UV light, with ozone and fi ne particulates concentrations above standard values. There were no signifi cant differences between the cohorts in DXA Z scores. The impact of systemic infl ammation, vitamin D insuffi ciency, air pollution, urban violence and poverty may have long-term bone detrimental outcomes in exposed paediatric populations as they grow older, increasing the risk of low bone mass and osteoporosis. The selection of reference populations for DXA must take into account air pollution exposures.

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“…In patients with inflammatory bowel disease bone loss is an early systemic process and occurs even before clinical disease manifests (14), and in COPD patients the prevalence of osteoporosis is high (15). In periodontitis, which is one of the most common chronic disorders in humans, both local and systemic bone loss has been described (16).…”

Section: Bone and Inflammationmentioning

confidence: 99%

Sclerostin: A Novel Player Regulating Bone Mass in Inflammation?

Albisetti

Giarratana

Viganò³

et al. 2013

Eur J Inflamm

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Inflammation is a common albeit overlooked cause of local and systemic bone loss which results from an imbalance between bone formation and bone resorption. The Wnt pathway, which plays an essential role in the regulation of bone turnover, has been proposed as a potential molecular link between inflammation and inflammatory bone loss. We here recapitulate present knowledge about sclerostin, a Wnt pathway inhibitor, and bone damage in inflammation. A better understanding of sclerostin action and regulation might help in designing an effective treatment strategy in inflammatory bone loss.

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Bone, Inflammation, and Inflammatory Bowel Disease

Cited by 62 publications

References 59 publications

Immune complexes regulate bone metabolism through FcRγ signalling

Immune complexes regulate bone metabolism through FcRγ signalling

Exposure to Urban Air Pollution and Bone Health in Clinically Healthy Six-year-old Children

Sclerostin: A Novel Player Regulating Bone Mass in Inflammation?

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