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

Bar‐Shavit, Zvi

doi:10.1002/jcb.21702

Cited by 63 publications

(88 citation statements)

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“…26) In healthy individuals, the process of osteoclastogenesis and bone resorption is maintained at subtle levels to allow a regulated rate of bone remodeling. 1) However, various pathophysiological stimuli or aberrant signaling can cause an unregulated increase in bone loss.…”

Section: Discussionmentioning

confidence: 99%

Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

Deepak

Kasonga

Kruger

et al. 2016

Biological & Pharmaceutical Bulletin

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Bone is a dynamic tissue that undergoes continuous remodeling coupled with the action of osteoblasts and osteoclasts. Osteoclast activity is elevated during osteoporosis and periodontitis resulting in excessive loss of trabecular and alveolar bone. Osteoclasts are formed in an inflammatory response to cytokine production receptor activator of nuclear factor-kappaB (NF-κB) ligand (RANKL) and bacterial challenge lipopolysaccharide (LPS). Carvacrol, a monoterpenic phenol present in Origanum vulgare and Thymus vulgaris, is a natural compound with known medicinal properties. We investigated the effects of carvacrol Key words osteoclast; osteoporosis; periodontitis; receptor activator of nuclear factor-κB ligand (RANKL); lipopolysaccharide (LPS) Bone homeostasis is tightly coupled to the bone-forming activity of osteoblasts and bone-resorbing activity of osteoclasts.1) Osteoclasts are multi-nucleated cells that arise from hematopoietic progenitors of monocyte/macrophage lineage and specialize in bone resorption.2) Bone-loss related diseases such as osteoporosis and periodontitis are associated with increased osteoclast formation and elevated osteoclast activity. [3][4][5] Binding of receptor activator of nuclear factor-κB ligand (RANKL) to its receptor RANK in osteoclast precursors triggers trimerization of the receptor and subsequent activation of downstream signaling pathways that includes inhibitor of kappaB (IκB)-a/b kinase (IKK), nuclear factor kappa-B (NF-κB), mitogen-activated protein kinases (MAPKs)-p38, extracellular-signal-regulated kinase (ERK) and c-Jun Nterminal kinase (JNK).6) Activation of these pathways leads to the formation of tartrate resistant acid phosphatase-positive (TRAP+) osteoclasts and bone resorption.Development of apical periodontitis is associated with the presence of microorganisms in the root canal system. 7) Gramnegative bacteria are the most common causative agents in endodontic infections. 8) Bacterial death causes release of lipopolysaccharide (LPS) in the necrotic pulp and dental wall of periapically affected teeth. 9) LPS elicits alveolar bone loss during periodontitis. 10) LPS stimulates the secretion of cytokines by osteoclast precursors such as monocytes and macrophages, resulting in osteoclast formation and bone resorption in vitro and in vivo.11) Earlier studies have also shown that injection of LPS into mouse gingiva induces alveolar bone resorption. 12)

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Section: Discussionmentioning

confidence: 99%

Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

Deepak

Kasonga

Kruger

et al. 2016

Biological & Pharmaceutical Bulletin

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“…2A; refs. [33][34][35]. To establish whether the observed loss of ACP5/TRAP expression may be due to loss of precursors, we performed immunohistochemistry on OS sections for CD68, a specific marker for cells of the monocyte/macrophage lineage (36).…”

Section: Acp5/trap Expression Is Reduced In Os Biopsies and Further Rmentioning

confidence: 99%

Loss of Osteoclasts Contributes to Development of Osteosarcoma Pulmonary Metastases

et al. 2010

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We conducted a transcriptomic screen of osteosarcoma (OS) biopsies and found that expression of osteoclast-specific tartrate-resistant acid phosphatase 5 (ACP5/TRAP) is significantly downregulated in OS compared with nonmalignant bone (P < 0.0001). Moreover, lesions from OS patients with pulmonary metastases had 2-fold less ACP5/TRAP expression (P < 0.018) than lesions from patients without metastases. In addition, we found a direct correlation (P = 0.0166) between ACP5/TRAP expression and time to metastasis. Therefore, we examined whether metastasis-competent (MC) OS cells could induce loss of ACP5 + osteoclasts and contribute to metastasis. We found that MC OS cell lines can inhibit osteoclastogenesis in vitro and in vivo. In addition, osteoclasts can inhibit the migration of MC OS cells in vitro. Finally, ablation of osteoclasts with zoledronic acid increases the number of metastatic lung lesions in an orthotopic OS model, whereas fulvestrant treatment increases osteoclast numbers and reduces metastatic lesions. These data indicate that the metastatic potential of OS is determined early in tumor development and that loss of osteoclasts in the primary lesion enhances OS metastasis.

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“…During cell maturation, mononuclear precursor cells fuse to generate multinucleated osteoclasts. This multinucleation process is necessarily required for osteoclastic maturation to undergo efficient bone resorption (7,8). In reorganizing genetic networks during osteoclastogenesis, diverse transcription factors play pivotal roles, and among them, nuclear factor of activated T-cells calcineurin-dependent 1 (NFATc1) is the necessary and sufficient transcription factor (9,10).…”

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confidence: 99%

JMJD5, a Jumonji C (JmjC) Domain-containing Protein, Negatively Regulates Osteoclastogenesis by Facilitating NFATc1 Protein Degradation

Youn

Yokoyama

Fujiyama‐Nakamura

et al. 2012

Journal of Biological Chemistry

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

Abstract: The article to which this erratum refers was published in J Cell Biochem (2007) 102: 1130–1139. © 2007 Wiley‐Liss, Inc.

Cited by 63 publications

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Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

Loss of Osteoclasts Contributes to Development of Osteosarcoma Pulmonary Metastases

JMJD5, a Jumonji C (JmjC) Domain-containing Protein, Negatively Regulates Osteoclastogenesis by Facilitating NFATc1 Protein Degradation

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