Osteocyte Mechanobiology

Uda, Yutaka; Azab, Ehab; Sun, Ningyuan; Shi, Chao; Pajevic, Paola Divieti

doi:10.1007/s11914-017-0373-0

Cited by 162 publications

(141 citation statements)

References 63 publications

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“…OCs are key regulators of the bone modeling process, and several studies have shown that CD4 + T cells are closely related to the differentiation of OCs by secreting RANKL (Uda, Azab, Sun, Shi, & Pajevic, ; Walsh & Choi, ). We investigated the possible interaction between activated T cells and miR‐21.…”

Section: Resultsmentioning

confidence: 99%

“…Both in vivo and in vitro experiments further showed decreased RANKL expression in miR‐21 −/− mice, thereby inducing severe imbalance in the RANKL/OPG ratio, indicating that miR‐21 promoted tooth movement through RANKL/OPG. While RANKL is known to be synthesized by neutrophils, monocytes, dendritic cells, and especially osteoblasts and active T cells (Hu et al, ; Neve, Corrado, & Cantatore, ; Uda et al, ), how miR‐21 mediates RANKL expression remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐21 promotes orthodontic tooth movement by modulating the RANKL/OPG balance in T cells

Lin

et al. 2019

Oral Diseases

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Objectives The present study was designed to investigate the effects of microRNA‐21 (miR‐21) on orthodontic tooth movement. Methods The orthodontic tooth movement model was established in C57BL/6 and miR‐21−/− mice with or without implantation of activated T cells. Histological and histomorphometrical analyses were performed by hematoxylin–eosin staining. Tartrate‐resistant acid phosphate staining was used to analyze the osteoclast numbers during tooth movement. Enzyme‐linked immunosorbent assay, reverse transcription polymerase chain reaction, and immunohistochemistry analysis were used to examine the expression of RANKL and OPG. Results In miR‐21−/− mice, the distance of tooth movement was retarded, the osteoclast number was decreased, and serum RANKL expression was strongly reduced. MiR‐21 promoted the secretion of RANKL from activated T cells. Furthermore, activated T cells could partially rescue the decreased orthodontic tooth movement distance in miR‐21−/− mice. MiR‐21 was shown to promote orthodontic tooth movement by modulating the RANKL/OPG balance in T cells. Conclusions The impact of miR‐21 on tooth movement was better elucidated, furthering our understanding of its role and clinical applications in orthodontics.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐21 promotes orthodontic tooth movement by modulating the RANKL/OPG balance in T cells

Lin

et al. 2019

Oral Diseases

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“…; Uda et al . ). Part of the reason for this lies in the fact that the cartilage is not easily visualised; its thickness is inferred from the gap between the ends of the bone (the joint space) on a plain radiograph.…”

Section: Articular Cartilage Is Adapted To Withstand Mechanical Stressmentioning

confidence: 97%

Mechanoadaptation: articular cartilage through thick and thin

Vincent

Wann

2018

The Journal of Physiology

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The articular cartilage is exquisitely sensitive to mechanical load. Its structure is largely defined by the mechanical environment and destruction in osteoarthritis is the pathophysiological consequence of abnormal mechanics. It is often overlooked that disuse of joints causes profound loss of volume in the articular cartilage, a clinical observation first described in polio patients and stroke victims. Through the 1980s, the results of studies exploiting experimental joint immobilisation supported this. Importantly, this substantial body of work was also the first to describe metabolic changes that resulted in decreased synthesis of matrix molecules, especially sulfated proteoglycans. The molecular mechanisms that underlie disuse atrophy are poorly understood despite the identification of multiple mechanosensing mechanisms in cartilage. Moreover, there has been a tendency to equate cartilage loss with osteoarthritic degeneration. Here, we review the historic literature and clarify the structural, metabolic and clinical features that clearly distinguish cartilage loss due to disuse atrophy and those due to osteoarthritis. We speculate on the molecular sensing pathways in cartilage that may be responsible for cartilage mechanoadaptation.

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“…It is now widely believed that osteocytes play key roles in the regulation of bone remodeling and in the mediation of bone mechanotransduction, although the mechanisms are currently incompletely defined. [1][2][3][4][5][6][7][8][9][10] Elucidating these mechanisms will advance the progress of bone biology research and help define new targets for the treatment of metabolic bone diseases.…”

Section: Introductionmentioning

confidence: 99%

Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice

et al. 2020

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Our recent studies demonstrate that the focal adhesion protein Kindlin-2 is critical for chondrogenesis and early skeletal development. Here, we show that deleting Kindlin-2 from osteoblasts using the 2.3-kb mouse Col1a1-Cre transgene minimally impacts bone mass in mice, but deleting Kindlin-2 using the 10-kb mouse Dmp1-Cre transgene, which targets osteocytes and mature osteoblasts, results in striking osteopenia in mice. Kindlin-2 loss reduces the osteoblastic population but increases the osteoclastic and adipocytic populations in the bone microenvironment. Kindlin-2 loss upregulates sclerostin in osteocytes, downregulates β-catenin in osteoblasts, and inhibits osteoblast formation and differentiation in vitro and in vivo. Upregulation of β-catenin in the mutant cells reverses the osteopenia induced by Kindlin-2 deficiency. Kindlin-2 loss additionally increases the expression of RANKL in osteocytes and increases osteoclast formation and bone resorption. Kindlin-2 deletion in osteocytes promotes osteoclast formation in osteocyte/bone marrow monocyte cocultures, which is significantly blocked by an anti-RANKLneutralizing antibody. Finally, Kindlin-2 loss increases osteocyte apoptosis and impairs osteocyte spreading and dendrite formation. Thus, we demonstrate an important role of Kindlin-2 in the regulation of bone homeostasis and provide a potential target for the treatment of metabolic bone diseases.Bone Research (2020) 8:2; https://doi.

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Osteocyte Mechanobiology

Cited by 162 publications

References 63 publications

MicroRNA‐21 promotes orthodontic tooth movement by modulating the RANKL/OPG balance in T cells

MicroRNA‐21 promotes orthodontic tooth movement by modulating the RANKL/OPG balance in T cells

Mechanoadaptation: articular cartilage through thick and thin

Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice

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