New Insights Into Osteoclast Biology

McDonald, Michelle M.; Kim, Albert Sungsoo; Mulholland, Bridie S; Rauner, Martina

doi:10.1002/jbm4.10539

Cited by 61 publications

(39 citation statements)

References 115 publications

(247 reference statements)

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“…Osteoporosis is by far the most frequent metabolic bone disease and associated with a significant social and economic burden; it is regarded as a gender specific heterogeneous disorder that results from an imbalance of bone remodeling, i.e., the coupled processes of bone formation and bone resorption ( Figure 1 ). For a detailed description of bone biology, bone remodeling and its regulation, the reader is referred to previous publications [ 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. In this narrative review, we delineated the pathophysiology of osteoporosis in RA from different perspectives.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Systemic Osteoporosis in Rheumatoid Arthritis

Pietschmann

Butylina

Kerschan‐Schindl

et al. 2022

IJMS

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Rheumatoid arthritis (RA), an autoimmune disease, is characterized by the presence of symmetric polyarthritis predominantly of the small joints that leads to severe cartilage and bone destruction. Based on animal and human data, the pathophysiology of osteoporosis, a frequent comorbidity in conjunction with RA, was delineated. Autoimmune inflammatory processes, which lead to a systemic upregulation of inflammatory and osteoclastogenic cytokines, the production of autoantibodies, and Th cell senescence with a presumed disability to control the systemic immune system’s and osteoclastogenic status, may play important roles in the pathophysiology of osteoporosis in RA. Consequently, osteoclast activity increases, osteoblast function decreases and bone metabolic and mechanical properties deteriorate. Although a number of disease-modifying drugs to treat joint inflammation are available, data on the ability of these drugs to prevent fragility fractures are limited. Thus, specific treatment of osteoporosis should be considered in patients with RA and an associated increased risk of fragility fractures.

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Section: Introductionmentioning

confidence: 99%

Mechanisms of Systemic Osteoporosis in Rheumatoid Arthritis

Pietschmann

Butylina

Kerschan‐Schindl

et al. 2022

IJMS

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“…The NF-κB pathway is the key pathway regulating osteoclast differentiation, which affects the differentiation of osteoclasts and bone resorption via regulating NFATc1 (Kim and Kim, 2016;Ono and Nakashima, 2018). Osteoclasts are distinctive cells for bone resorption and are derived from hematopoietic progenitor cells (McDonald et al, 2021). Osteoclast precursor cells showed and upregulated c-Fos and NFATc1 expression under RANKL stimulation, finally differentiated into mature osteoclasts (Grigoriadis et al, 1994;Ikeda et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Isoliensinine Suppresses Osteoclast Formation Through NF-κB Signaling Pathways and Relieves Ovariectomy-Induced Bone Loss

Liu

Huang

et al. 2022

Front. Pharmacol.

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Osteoporosis is among the major contributors of pathologic fracture in postmenopausal women, which is caused by the bone metabolic disorder owing to the over-activation of osteoclasts. Inhibition of osteoclast differentiation and maturation has become a mainstream research interest in the prevention of osteoporosis. Isoliensinine (Iso) is a dibenzyl isoquinoline alkaloid with antioxidant, anti-inflammatory, and anti-cancer activities. However, whether it can be used as a potential treatment for osteoporosis remains undiscovered. Here, we investigated whether Iso might suppress the differentiation of osteoclasts in vitro and in vivo to play an anti-osteoporosis role. Our results showed that Iso inhibits the formation of mature multinuclear osteoclasts induced by RANKL, the bone resorption, and the osteoclast-specific genes expression by blocking the nuclear translocation of NF-κB p65, and the effect was in a dosage-dependent way. Furthermore, we investigated the therapeutic effect of Iso on osteoporosis in ovariectomized (OVX) mice. We found that Iso attenuated bone loss in the OVX mice and significantly promoted BS, Conn. DN, Tb.Th, TB.N, and BV/TV Index. All in all, Iso showed a prominent effect of osteoclast inhibition, with great promise for treating osteoporosis.

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“…Osteoclasts, which are derived from hematopoietic stem cells, are capable of bone resorption. Under normal conditions, osteoblasts and osteoclasts are in relative balance in vivo to regulate osteogenesis and development (McDonald et al, 2021). When a bone defect occurs, the balance of osteoblasts and osteoclasts is disrupted.…”

Section: Osteoblastsmentioning

confidence: 99%

Engineered bone cement trigger bone defect regeneration

Xia

Wang

et al. 2022

Front. Mater.

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Bone defects, which can be caused by factors such as trauma, tumor, or osteomyelitis, are clinically common. They lessen the weight a bone is able to bear and cause severe pain to the patient. Although bone transplantation is the gold standard for treating bone defects, it is not suitable for all patients due to its poor availability, risk of spreading disease, and possibility of requiring a secondary surgery. Bone cement as a filler for bone defects can fill any shape of bone defect, and can quickly solidify when injected, providing mechanical strength sufficient for supporting the normal physiological activities of the bone. However, traditional bone cement lacks the ability to induce bone regeneration. Recently, various methods for enhancing the bone regeneration ability of bone cement have been developed, such as adding bone morphogenetic proteins, mesenchymal stem cells, and inorganic substances to bone cement. These methods not only ensure the original biological properties of the bone cement, but also improve the bone cement in terms of its mechanical strength and ability to induce bone regeneration. The aim of this review is to overview the process of bone regeneration, introduce improved bone cement formulations designed to promote bone regeneration, and discuss the clinical application of bone cement and its possibilities for future improvement.

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New Insights Into Osteoclast Biology

Abstract: This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process which may lead to differences between this version and the Version of Record. Please cite this article as

Cited by 61 publications

References 115 publications

Mechanisms of Systemic Osteoporosis in Rheumatoid Arthritis

Mechanisms of Systemic Osteoporosis in Rheumatoid Arthritis

Isoliensinine Suppresses Osteoclast Formation Through NF-κB Signaling Pathways and Relieves Ovariectomy-Induced Bone Loss

Engineered bone cement trigger bone defect regeneration

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