Peripheral Blood Mononuclear Cells Spontaneous Osteoclastogenesis: Mechanisms Driving the Process and Clinical Relevance in Skeletal Disease

Salamanna, Francesca; Maglio, Melania; Borsari, Veronica; Giavaresi, Gianluca; Aldini, N. Nicoli; Fini, Milena

doi:10.1002/jcp.25134

Cited by 18 publications

(13 citation statements)

References 32 publications

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“…Osteoclastogenesis also requires the presence of macrophage colony‐stimulating factor (M‐CSF), which is released by OB as well and acts on OC through its receptor, colony‐stimulating factor 1 receptor (CSFR). The RANK/RANKL/OPG and M‐CSF/CSFR regulatory axes couple OB and OC activity, thereby controlling the balance between bone formation and resorption (Salamanna et al , ).…”

Section: Effects Of Relaxin On Bonementioning

confidence: 99%

Relaxin and insulin‐like peptide 3 in the musculoskeletal system: from bench to bedside

Ferlin

Toni

Sandri

et al. 2016

British J Pharmacology

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Section: Effects Of Relaxin On Bonementioning

confidence: 99%

Relaxin and insulin‐like peptide 3 in the musculoskeletal system: from bench to bedside

Ferlin

Toni

Sandri

et al. 2016

British J Pharmacology

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“…Osteoclasts derive from cells of the monocyte/macrophage lineage (2–4) present in bone marrow (5), but also present in peripheral blood (6). Osteoclasts play a key role in diseases that are associated with increased bone loss (7). Such diseases include common diseases such as the rheumatic diseases, osteoporosis, periodontitis, cancers that metastasize to bone and Crohn's disease.…”

Section: Introductionmentioning

confidence: 99%

What Are the Peripheral Blood Determinants for Increased Osteoclast Formation in the Various Inflammatory Diseases Associated With Bone Loss?

et al. 2019

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Local priming of osteoclast precursors (OCp) has long been considered the main and obvious pathway that takes place in the human body, where local bone lining cells and RANKL-expressing osteocytes may facilitate the differentiation of OCp. However, priming of OCp away from bone, such as in inflammatory tissues, as revealed in peripheral blood, may represent a second pathway, particularly relevant in individuals who suffer from systemic bone loss such as prevalent in inflammatory diseases. In this review, we used a systematic approach to review the literature on osteoclast formation in peripheral blood in patients with inflammatory diseases associated with bone loss. Only studies that compared inflammatory (bone) disease with healthy controls in the same study were included. Using this core collection, it becomes clear that experimental osteoclastogenesis using peripheral blood from patients with bone loss diseases in prevalent diseases such as rheumatoid arthritis, osteoporosis, periodontitis, and cancer-related osteopenia unequivocally point toward an intrinsically increased osteoclast formation and activation. In particular, such increased osteoclastogenesis already takes place without the addition of the classical osteoclastogenesis cytokines M-CSF and RANKL in vitro. We show that T-cells and monocytes as OCp are the minimal demands for such unstimulated osteoclast formation. In search for common and disease-specific denominators of the diseases with inflammation-driven bone loss, we demonstrate that altered T-cell activity and a different composition—such as the CD14+CD16+ vs. CD14+CD16– monocytes—and priming of OCp with increased M-CSF, RANKL, and TNF- α levels in peripheral blood play a role in increased osteoclast formation and activity. Future research will likely uncover the barcodes of the OCp in the various inflammatory diseases associated with bone loss.

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“…Different pathologies can accelerate bone loss by impacting the processes of bone formation by osteoblasts and bone resorption by osteoclasts (OCL). Under many different pathological bone conditions, the primary driver of bone loss is increased osteoclastic bone resorption that is oftentimes mediated by immune signaling ( 12 , 13 ).…”

Section: Introductionmentioning

confidence: 99%

Microbiota Reconstitution Does Not Cause Bone Loss in Germ-Free Mice

Quach

Collins

Parameswaran

et al. 2018

mSphere

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The microbiota has been shown to be an important regulator of health and development. With regard to its effect on bone health, a previous study has suggested that gut microbes negatively impact bone density. However, we show here that this is not generalizable to all microbial communities and mouse strain backgrounds. Our results demonstrate that colonization of mice, both outbred and inbred strains, did not have a major impact on bone health. The identification of microbial communities that do not negatively impact bone health may provide a foundation for future investigations that seek to identify microbes that are either beneficial or detrimental to bone metabolism.

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Peripheral Blood Mononuclear Cells Spontaneous Osteoclastogenesis: Mechanisms Driving the Process and Clinical Relevance in Skeletal Disease

Cited by 18 publications

References 32 publications

Relaxin and insulin‐like peptide 3 in the musculoskeletal system: from bench to bedside

Relaxin and insulin‐like peptide 3 in the musculoskeletal system: from bench to bedside

What Are the Peripheral Blood Determinants for Increased Osteoclast Formation in the Various Inflammatory Diseases Associated With Bone Loss?

Microbiota Reconstitution Does Not Cause Bone Loss in Germ-Free Mice

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