The osteoclast: A multinucleated, hematopoietic‐origin, bone‐resorbing osteoimmune cell

Bar‐Shavit, Zvi

doi:10.1002/jcb.21553

Cited by 237 publications

(122 citation statements)

References 55 publications

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Section: Differentiation Of Osteoclastsmentioning

confidence: 99%

“…As the exclusive osteoresorptive cells, osteoclasts are directly responsible for physiological bone resorption and pathological bone destruction [18,19]. They arise from myeloid hematopoietic progenitor cells of the monocyte/macrophage lineage through a series of differentiation stages that generate large multinucleated, tartrate-resistant acid phosphatase (TRAP)-positive mature cells [20,21].…”

Section: Differentiation Of Osteoclastsmentioning

confidence: 99%

“…Given their central role in the osteolytic processes, osteoclast lineage cells (including OCPs) have become a focus of studies investigating inflammatory osteoresorption [1,4,5,8,9,13,18,19].…”

Section: Characterization Of Osteoclast Progenitorsmentioning

confidence: 99%

“…Osteoclasts create bone erosions by resorbing periarticular and subchondral bone over a period of months to years, although an individual osteoclast life span is much shorter (2 to 4 weeks) [10,18,19,26]. Thus, mature osteoclasts must be constantly renewed by OCPs in order to sustain pathological bone resorption [8,9,24].…”

Section: Characterization Of Osteoclast Progenitorsmentioning

confidence: 99%

“…They arise from myeloid hematopoietic progenitor cells of the monocyte/macrophage lineage through a series of differentiation stages that generate large multinucleated, tartrate-resistant acid phosphatase (TRAP)-positive mature cells [20,21]. Abnormally enhanced osteoclast formation and activity accelerate pathogenesis of arthritis and other diseases characterized by inflammatory osteolysis, causing bone loss that inevitably results in pain, deformity, osteopenia and structural changes [2,3,5, 18,19].Osteoclast differentiation is physiologically triggered by RANKL/RANK binding, in the presence of macrophage colony stimulating factor (M-CSF/CSF-1) [22][23][24], and these essential osteoclastogenic molecules are abundantly expressed in inflammatory conditions such as arthritis and periodontitis [3,8]. RANKL, expressed on osteoblasts and hypertrophying chondrocytes, as well as on activated T lymphocytes, is up-regulated by pro-resorptive hormones, cytokines and inflammatory mediators, including vitamin D 3 , parathyroid hormone, prostaglandin E 2 (PGE 2 ), IL-1, 7,8].…”

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confidence: 99%

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Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Šućur

Katavić

Kelava

et al. 2014

International Orthopaedics (SICOT)

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The inflammatory milieu favors recruitment and activation of osteoclasts, and leads to bone destruction as a serious complication associated with arthritis and with other inflammatory processes.The frequency and activity of osteoclast progenitors (OCPs) correspond to arthritis severity, and may be used to monitor disease progression and bone resorption, indicating the need for detailed characterization of the discrete OCP subpopulations. Collectively, current studies suggest that the most potent murine bone marrow OCP population can be identified among lymphoid negative population within the immature myeloid lineage cells, as B220 -CD3 -CD11b -/lo CD115 + CD117 + CX3CR1 + and possibly also Ter119 -CD11c -CD135 lo Ly6C + RANK -. In the peripheral blood OCP population bears the monocytoid phenotype B220 -CD3 -NK1.1 -CD11b + Ly-6C hi CD115 + CX3CR1 + , presumably expressing RANK in committed OCPs. Much less is known about human OCPs and their regulation in arthritis, but the circulating OCP subset is, most probably, comprised among the lymphoid negative population (CD3 -CD19 -CD56 -), within immature monocyte subset (CD11b + CD14 + CD16 -), expressing receptors for M-CSF and RANKL (CD115 + RANK + ). Our preliminary data confirmed positive association between the proportion of peripheral blood OCPs, defined as CD3 -CD19 -CD56 -CD11b + CD14 + , and the disease activity score (DAS28) in the follow-up samples from patient with psoriatic arthritis receiving anti-TNF therapy. In addition, we reviewed cytokines and chemokines which, directly or indirectly, activate OCPs and enhance their differentiation potential, thus mediating osteoresorption.Control of the activity and migratory behavior of OCPs as well as the identification of crucial bone/joint chemotactic mediators represent promising therapeutic targets in arthritis.Keyword: osteoclast progenitors, arthritis, inflammation, cytokines, chemokines, osteoresorption 3 Inflammation induced bone lossBone is a highly dynamic tissue important for its mechanical and metabolic functions, and characterized by rapid response to numerous physical, endocrine and paracrine stimuli in physiological and pathological conditions. Among others signals, osteoresorptive mediators (such as interleukin (IL)-1, IL-6, IL-15, IL-17, IL, 21, IL-33, tumor necrosis factor (TNF)-α and receptor activator of nuclear factor-κB ligand (RANKL), CCL2, CXCL12) produced by inflammatory/immune cells create conditions that promote maturation and function of osteoclasts [1][2][3][4]. Bone resorption and osteolysis are the prominent features and causes of substantial morbidity in inflammatory processes associated with arthritis as well as with localized bacterial infections of bone and adjacent tissues, peri-prosthetic loosening, vasculitis, connective tissue diseases, chronic viral infections and inflammatory bowel diseases [5][6][7][8]. Bone resorption in arthritisInflammatory arthritides comprise a heterogeneous group of joint disorders that are characterized by chronic inflammatory response as we...

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Section: Differentiation Of Osteoclastsmentioning

confidence: 99%

Section: Differentiation Of Osteoclastsmentioning

confidence: 99%

Section: Characterization Of Osteoclast Progenitorsmentioning

confidence: 99%

Section: Characterization Of Osteoclast Progenitorsmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Šućur

Katavić

Kelava

et al. 2014

International Orthopaedics (SICOT)

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Herb‐Derived Phytochemicals for Dental Implant Applications

Varadarajan,

Muthusamy,

Nambirajan

et al. 2023

Pharmacological Studies in Natural Oral Care

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Bioinspired Collagen Scaffolds in Cranial Bone Regeneration: From Bedside to Bench

Lee

Volpicelli

2017

Adv Healthcare Materials

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Calvarial defects are common reconstructive dilemmas secondary to a variety of etiologies including traumatic brain injury, cerebrovascular disease, oncologic resection, and congenital anomalies. Reconstruction of the calvarium is generally undertaken for the purposes of cerebral protection, contour restoration for psychosocial well-being, and normalization of neurological dysfunction frequently found in patients with massive cranial defects. Current methods for reconstruction using autologous grafts, allogeneic grafts, or allo-plastic materials have significant drawbacks that are unique to each material. The combination of wide medical relevance and the need for a better clinical solution render defects of the cranial skeleton an ideal target for development of regenerative strategies focused on calvarial bone. With the improved understanding of the instructive properties of tissue-specific extracellular matrices and the advent of precise nanoscale modulation in materials science, strategies in regenerative medicine have shifted in paradigm. Previously considered to be simple carriers of stem cells and growth factors, increasing evidence exists for differential materials directing lineage specific differentiation of progenitor cells and tissue regeneration. In this work, we review the clinical challenges for calvarial reconstruction, the anatomy and physiology of bone, and extracellular matrix-inspired, collagen-based materials that have been tested for in vivo cranial defect healing.

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The osteoclast: A multinucleated, hematopoietic‐origin, bone‐resorbing osteoimmune cell

Cited by 237 publications

References 55 publications

Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Herb‐Derived Phytochemicals for Dental Implant Applications

Bioinspired Collagen Scaffolds in Cranial Bone Regeneration: From Bedside to Bench

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