Osteoporosis, Inflammation and Ageing

Ginaldi, Lia; Mengoli, Lucia Paola; Martinis, Massimo De

doi:10.1007/978-1-4020-9063-9_64

Cited by 87 publications

(122 citation statements)

References 131 publications

(30 reference statements)

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“…Indeed, elevated plasma concentrations of IL-6, IL-1␤, and TNF-␣ have been described in elderly populations and were postulated as predictive markers of functional disability, frailty and mortality (Bruunsgaard et al, 2003;Ershler and Keller, 2000;O'Mahony et al, 1998) and it has been suggested that chronic inflammation supports the development and progression of age-related diseases, such as osteoporosis, neurodegeneration and atherosclerosis (Gao and Hong, 2008;Ginaldi et al, 2005;Libby, 2002). Subclinical inflammation may be caused by chronic stimulation of the innate immune system by degradation products and/or by the partial inability of the aged immune system to eliminate certain pathogens (Weinberger et al, 2009), this inflammatory status may slowly damage one or several organs, especially when unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together with the onset of age-related chronic diseases (reviewed by Cevenini et al, 2010 andVasto et al, 2007).…”

Section: Inflamm-ageing and T Lymphocytesmentioning

confidence: 99%

B cells and immunosenescence: A focus on IgG+IgD−CD27− (DN) B cells in aged humans

Bulati¹,

Buffa²,

Candore³

et al. 2011

Ageing Research Reviews

101

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a b s t r a c tImmunosenescence contributes to the decreased ability of the elderly to control infectious diseases, which is also reflected in their generally poor response to new antigens and vaccination. It is known that the T cell branch of the immune system is impaired in the elderly mainly due to expansion of memory/effector cells that renders the immune system less able to respond to new antigens. B lymphocytes are also impaired in the elderly in terms of their response to new antigens. In this paper we review recent work on B cell immunosenescence focusing our attention on memory B cells and a subset of memory B cells (namely IgG + IgD − CD27 − ) that we have demonstrated is increased in healthy elderly.

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Section: Inflamm-ageing and T Lymphocytesmentioning

confidence: 99%

B cells and immunosenescence: A focus on IgG+IgD−CD27− (DN) B cells in aged humans

Bulati¹,

Buffa²,

Candore³

et al. 2011

Ageing Research Reviews

101

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“…Senescent cells also secrete many cytokines which, due to their diverse function, could have multiple consequences on the ageing of tissues and the development/progression of disease (Ginaldi et al 2005;Payne 2006;Salvioli et al 2006;Sue and Griffin 2006;Libby 2006). These secreted proteins may not just impact on local tissue but also tissues found throughout the organism.…”

Section: Biological Impact Of the Senescent Phenotypementioning

confidence: 99%

Cellular senescence, ageing and disease

Burton

2008

AGE

118

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Cellular senescence is the irreversible growth arrest of individual mitotic cells, which as a consequence display a radically altered phenotype that is thought to impair tissue function and predispose tissues to disease development and/or progression as they gradually accumulate. However, in the past, research into mechanisms of ageing has commonly been researched and treated separately from disease development. This may partly be due to the lack of understanding concerning mechanisms of ageing and the difficulty in implementing what was known into models of disease development. Only in the last 10 years, with increasing knowledge of the senescent phenotype and the ability to detect senescent cells in human tissues, have biologists been able to investigate the relationship between cellular senescence and disease. This review therefore brings together and discusses recent findings which suggest that cellular senescence does contribute to ageing and the development/ progression of disease.

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“…Nuclear factor kappa B (NF-κ B) receptor activator (RANK), receptor activator of NF-κ B ligand (RANKL), and osteoprotegerin (OPG) play a role in the pathogenesis of osteoporosis (Ginaldi et al 2005;Kearnes et al 2008). OPG, a soluble protein produced by osteoblasts, is a decoy receptor that can bind to RANKL, which is also produced by osteoblasts.…”

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confidence: 99%