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Research on Bone Cells in Health and Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 May 2024 | Viewed by 4227

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Dr. David Gyori

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Guest Editor

Department of Physiology, Semmelweis University, 1015 Budapest, Hungary
Interests: osteoclast; bone metastasis; tumor biology; immunology

Special Issue Information

Dear Colleagues,

Bone homeostasis is maintained by the dynamic interaction between bone cells, including osteoclasts, osteoblasts and osteocytes. Osteoblast-mediated bone formation and osteoclast-mediated bone resorption are tightly coupled by the extensive cellular network formed by osteocytes. However, under pathological conditions, the fine-tuned balance between bone formation and resorption is altered, such as in osteoporosis, autoimmune disease-associated inflammatory bone loss, periodontitis and tumor-induced osteolysis. For instance, inflammatory lymphocytes and osteotropic tumor cells can produce several growth factors and differentiation inducers, which promote the development and function of osteoclasts directly or indirectly via osteoblasts and osteocytes. Therefore, the development of novel strategies for the treatment of bone diseases is urgently needed, which requires a better understanding of the molecular and cellular mechanisms underlying bone formation and resorption during the process of bone remodeling.

This Special Issue entitled “Research on Bone Cells in Health and Disease” welcomes original research articles and timely reviews on the cellular and molecular mechanisms underlying bone formation and resorption, with a special focus on the activation of osteoclasts, osteoblasts and osteocytes in pathological conditions, such as osteoporosis, inflammatory and tumor-induced bone loss.

Dr. David Gyori
Guest Editor

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Keywords

osteoclasts
osteoblasts
osteocytes
osteoporosis
bone tumors
periodontitis
rheumatoid arthritis
bone remodeling

Published Papers (5 papers)

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Research

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16 pages, 3218 KiB

Open AccessArticle

Leukocytes within Autologous Blood Concentrates Have No Impact on the Growth and Proliferation of Human Primary Osteoblasts: An In Vitro Study

by Carlos Fernando Mourão, Eva Dohle, Büşra Bayrak, Anne Winter, Robert Sader and Shahram Ghanaati

Int. J. Mol. Sci. 2024, 25(8), 4542; https://doi.org/10.3390/ijms25084542 - 21 Apr 2024

Viewed by 383

Abstract

Platelet-rich fibrin (PRF) is a widely used autologous blood concentrate in regenerative medicine. This study aimed to characterize the cellular composition and distribution of different PRF matrices generated by high (710 g) and low (44 g) relative centrifugal forces (RCFs) and to analyze their bioactivity on human primary osteoblasts (pOBs). PRF was separated into upper layer (UL) and buffy coat (BC) fractions, and their cellular contents were assessed using histological and immunohistochemical staining. The release of platelet-derived growth factor (PDGF) and transforming growth factor (TGF-β) was quantified using an ELISA. Indirect PRF treatment on pOBs was performed to evaluate cell viability and morphology. A histological analysis revealed higher quantities of leukocytes and platelets in the low-RCF PRF. TGF-β release was significantly higher in the low-RCF PRF compared to the high-RCF PRF. All PRF fractions promoted pOB proliferation regardless of the centrifugation protocol used. The low-RCF PRF showed higher TGF-β levels than the high-RCF PRF. These findings contribute to understanding the cellular mechanisms of PRF and provide insights into optimizing PRF protocols for bone regeneration, advancing regenerative medicine, and improving patient outcomes. Full article

(This article belongs to the Special Issue Research on Bone Cells in Health and Disease)

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17 pages, 9458 KiB

Open AccessArticle

Eldecalcitol Induces Minimodeling-Based Bone Formation and Inhibits Sclerostin Synthesis Preferentially in the Epiphyses Rather than the Metaphyses of the Long Bones in Rats

by Tomoka Hasegawa, Tomomaya Yamamoto, Hiromi Hongo, Tsuneyuki Yamamoto, Mai Haraguchi-Kitakamae, Hotaka Ishizu, Tomohiro Shimizu, Hitoshi Saito, Sadaoki Sakai, Kenji Yogo, Yoshihiro Matsumoto and Norio Amizuka

Int. J. Mol. Sci. 2024, 25(8), 4257; https://doi.org/10.3390/ijms25084257 - 11 Apr 2024

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Abstract

This study aimed to examine minimodeling-based bone formation between the epiphyses and metaphyses of the long bones of eldecalcitol (ELD)-administered ovariectomized rats. Sixteen-week-old female rats were divided into four groups: sham-operated rats receiving vehicle (Sham group), ovariectomized (OVX) rats receiving vehicle (Vehicle group), or ELDs (30 or 90 ng/kg BW, respectively; ELD30 and ELD90 groups). ELD administration increased bone volume and trabecular thickness, reducing the number of osteoclasts in both the epiphyses and metaphyses of OVX rats. The Sham and Vehicle groups exhibited mainly remodeling-based bone formation in both regions. The epiphyses of the ELD groups showed a significantly higher frequency of minimodeling-based bone formation than remodeling-based bone formation. In contrast, the metaphyses exhibited significantly more minimodeling-based bone formation in the ELD90 group compared with the ELD30 group. However, there was no significant difference between minimodeling-based bone formation and remodeling-based bone formation in the ELD90 group. While the minimodeling-induced new bone contained few sclerostin-immunoreactive osteocytes, the underlying pre-existing bone harbored many. The percentage of sclerostin-positive osteocytes was significantly reduced in the minimodeling-induced bone in the epiphyses but not in the metaphyses of the ELD groups. Thus, it seems likely that ELD could induce minimodeling-based bone formation in the epiphyses rather than in the metaphyses, and that ELD-driven minimodeling may be associated with the inhibition of sclerostin synthesis. Full article

(This article belongs to the Special Issue Research on Bone Cells in Health and Disease)

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15 pages, 2677 KiB

Open AccessArticle

Ethanol Extract of Radix Asteris Suppresses Osteoclast Differentiation and Alleviates Osteoporosis

by Sung-Ju Lee, Hyun Yang, Seong Cheol Kim, Dong Ryun Gu, Jin Ah Ryuk, Seon-A Jang and Hyunil Ha

Int. J. Mol. Sci. 2023, 24(22), 16526; https://doi.org/10.3390/ijms242216526 - 20 Nov 2023

Viewed by 919

Abstract

Radix Asteris, the root of Aster tataricus L. f., is historically significant in East Asian medicine for treating respiratory conditions. Yet, its implications on bone health remain uncharted. This research investigated the impact of an aqueous ethanol extract of Radix Asteris (EERA) on osteoclast differentiation and its prospective contribution to osteoporosis management. We discerned that EERA retards osteoclast differentiation by inhibiting receptor activator of nuclear factor kappa-B ligand (RANKL) expression and obstructing RANKL-induced osteoclastogenesis. EERA markedly suppressed RANKL-induced expression of NFATc1, a pivotal osteoclastogenic factor, via modulating early RANK signaling. EERA’s therapeutic potential was underscored by its defense against trabecular bone degradation and its counteraction to increased body and perigonadal fat in ovariectomized mice, mirroring postmenopausal physiological changes. In the phytochemical analysis of EERA, we identified several constituents recognized for their roles in regulating bone and fat metabolism. Collectively, our findings emphasize the potential of EERA in osteoclast differentiation modulation and in the management of osteoporosis and associated metabolic changes following estrogen depletion, suggesting its suitability as an alternative therapeutic strategy for postmenopausal osteoporosis intertwined with metabolic imbalances. Full article

(This article belongs to the Special Issue Research on Bone Cells in Health and Disease)

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Review

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16 pages, 1430 KiB

Open AccessReview

Local Effects of Steroid Hormones within the Bone Microenvironment

by Luca F. Sandor, Reka Ragacs and David S. Gyori

Int. J. Mol. Sci. 2023, 24(24), 17482; https://doi.org/10.3390/ijms242417482 - 14 Dec 2023

Viewed by 941

Abstract

Steroid hormone production via the adrenal cortex, gonads, and placenta (so-called glandular steroidogenesis) is responsible for the endocrine control of the body’s homeostasis and is organized by a feedback regulatory mechanism based on the hypothalamus–pituitary–steroidogenic gland axis. On the other hand, recently discovered extraglandular steroidogenesis occurring locally in different tissues is instead linked to paracrine or autocrine signaling, and it is independent of the control by the hypothalamus and pituitary glands. Bone cells, such as bone-forming osteoblasts, osteoblast-derived osteocytes, and bone-resorbing osteoclasts, respond to steroid hormones produced by both glandular and extraglandular steroidogenesis. Recently, new techniques to identify steroid hormones, as well as synthetic steroids and steroidogenesis inhibitors, have been introduced, which greatly empowered steroid hormone research. Based on recent literature and new advances in the field, here we review the local role of steroid hormones in regulating bone homeostasis and skeletal lesion formation. The novel idea of extraglandular steroidogenesis occurring within the skeletal system raises the possibility of the development of new therapies for the treatment of bone diseases. Full article

(This article belongs to the Special Issue Research on Bone Cells in Health and Disease)

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13 pages, 574 KiB

Open AccessReview

Extracellular Signal-Regulated Kinases Play Essential but Contrasting Roles in Osteoclast Differentiation

by Chaekyun Kim

Int. J. Mol. Sci. 2023, 24(20), 15342; https://doi.org/10.3390/ijms242015342 - 19 Oct 2023

Cited by 1 | Viewed by 977

Abstract

Bone homeostasis is regulated by the balanced actions of osteoblasts that form the bone and osteoclasts (OCs) that resorb the bone. Bone-resorbing OCs are differentiated from hematopoietic monocyte/macrophage lineage cells, whereas osteoblasts are derived from mesenchymal progenitors. OC differentiation is induced by two key cytokines, macrophage colony-stimulating factor (M-CSF), a factor essential for the proliferation and survival of the OCs, and receptor activator of nuclear factor kappa-B ligand (RANKL), a factor for responsible for the differentiation of the OCs. Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), p38, and c-Jun N-terminal kinases, play an essential role in regulating the proliferation, differentiation, and function of OCs. ERKs have been known to play a critical role in the differentiation and activation of OCs. In most cases, ERKs positively regulate OC differentiation and function. However, several reports present conflicting conclusions. Interestingly, the inhibition of OC differentiation by ERK1/2 is observed only in OCs differentiated from RAW 264.7 cells. Therefore, in this review, we summarize the current understanding of the conflicting actions of ERK1/2 in OC differentiation. Full article

(This article belongs to the Special Issue Research on Bone Cells in Health and Disease)

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