Increased bone fracture prevalence in postmenopausal women suffering from pollen-allergy

Ferencz, Viktória; Mészáros, Szilvia; Csupor, Emőke; Tóth, Edit; Bors, Katalin; Falus, András; Horváth, Csaba

doi:10.1007/s00198-005-0011-z

Cited by 20 publications

(16 citation statements)

References 37 publications

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“…In a study investigating whether pollen-allergy can affect bone mass and fractures in postmenopausal women, it was shown that H1R antagonists may compensate for the negative effect of allergy on bone fracture risk. 36 The use of an H1-antihistamine/mast cell stabilizer in a patient with systemic mastocytosis and extensive skeletal involvement, including elevated parameters of bone resorption, improved the bone parameters. 37 We confirmed that osteoblasts also express H1R and H2R 14,15 and showed that in primary osteoblasts their expression varied with the differentiation stage.…”

Section: Discussionmentioning

confidence: 99%

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Duplan

Baroukh

et al. 2009

The American Journal of Pathology

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In addition to the numerous roles of histamine in both the immune and nervous systems, previous studies have suggested that this bioamine might also be involved in bone metabolism. Following our observations of impaired bone resorption in ovariectomized rats after histamine receptor antagonist treatment, we focused in this study on osteoclasts and osteoclast precursors. We looked for a direct action of histamine on these cells using both in vivo and in vitro approaches. In vivo, we triggered a remodeling sequence in rat mandibular bone and treated the animals with either histamine or histamine receptor antagonists. Histamine was shown to increase the number of osteoclasts and osteoclast precursors whereas antagonists of histamine receptor-1 and -2 decreased both osteoclast recruitment and resorption. In vitro, spleen cells from histamine-deficient mice were treated with receptor activator for nuclear factor kappa B ligand and macrophage colony stimulating factor, giving rise to both reduced numbers of osteoclasts and decreased resorption on dentin slices. Histamine enhanced resorption in these cultures in a dose-dependent manner. In addition, we identified osteoclast precursors as a source of histamine. In contrast, histamine increased the receptor activator for nuclear factor kappa B ligand/osteoprotegerin ratio in primary osteoblasts that did not secrete histamine. We observed a differential expression of histamine receptor-1 and -2 mRNAs in both primary osteoclasts and osteoblasts, confirming their functional roles with selective antagonists. Thus, histamine acts directly on osteoclasts, osteoclast precursors, and osteoblasts, promoting osteoclastogenesis through autocrine/paracrine mechanisms.

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Section: Discussionmentioning

confidence: 99%

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Duplan

Baroukh

et al. 2009

The American Journal of Pathology

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“…There are several possible mechanisms. First, pollen allergy has in itself been linked to fracture risk [44], perhaps mediated through the effects of mast-cell-derived histamine. Second, side effects of pseudoephedrine include tremor and insomnia, which could increase the occurrence of falls.…”

Section: Discussionmentioning

confidence: 99%

Mapping the prescriptiome to fractures in men—a national analysis of prescription history and fracture risk

Abrahamsen

Brixen

2008

Osteoporos Int

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“…Interestingly, obese patients are prone to developing allergic complications. 121,158 Mast-cell effector functions…”

Section: The Complement Systemmentioning

confidence: 99%

Mast cells in human and experimental cardiometabolic diseases

2015

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Mast cells, like many other types of inflammatory cell, perform pleiotropic roles in cardiometabolic diseases such as atherosclerosis, abdominal aortic aneurysms, obesity, and diabetes mellitus, as well as complications associated with these diseases. Low numbers of mast cells are present in the heart, aorta, and adipose tissue of healthy humans, but patients with cardiometabolic diseases and animals with experimentally-induced cardiometabolic pathologies have high numbers of mast cells with increased activity in the affected tissues. Mediators released by the activated mast cells, such as chemokines, cytokines, growth factors, heparin, histamine, and proteases, not only function as biomarkers of cardiometabolic diseases, but might also directly contribute to the pathogenesis of such diseases. Mast-cell mediators impede the functions of vascular cells, the integrity of the extracellular matrix, and the activity of other inflammatory cells, thereby contributing to the pathobiology of the conditions at multiple levels. In mouse models, mast-cell activation aggravates the progression of various cardiometabolic pathologies, whereas a genetic deficiency or pharmacological stabilization of mast cells, or depletion or inhibition of specific mast-cell mediators, tends to delay the progression of such conditions. Pharmacological inhibition of mast-cell activation or their targeted effector functions offers potential novel therapeutic strategies for patients with cardiometabolic disorders.

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Increased bone fracture prevalence in postmenopausal women suffering from pollen-allergy

Cited by 20 publications

References 37 publications

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Mapping the prescriptiome to fractures in men—a national analysis of prescription history and fracture risk

Mast cells in human and experimental cardiometabolic diseases

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