Effects of mechanical forces on osteogenesis and osteoclastogenesis in human periodontal ligament fibroblasts

Li, M; Zhang, C; Yang, Yan

doi:10.1302/2046-3758.81.bjr-2018-0060.r1

Cited by 54 publications

(64 citation statements)

References 55 publications

(174 reference statements)

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“… 4 , 5 They are involved in a variety of biological processes through their regulatory function in mechanisms of post-transcriptional gene expression ( Table I ). 6 - 10 Cell and animal studies have demonstrated that miRNAs are altered during muscle cell proliferation, differentiation, apoptosis, and regeneration. 2 , 3 , 6 In recent years, miRNAs have emerged as regulators of skeletal muscle function and aberrant expression of miRNAs is thought to be associated with the progression of muscle atrophy in various diseases.…”

Section: Introductionmentioning

confidence: 99%

Role of microRNA in muscle regeneration and diseases related to muscle dysfunction in atrophy, cachexia, osteoporosis, and osteoarthritis

Brzeszczyńska

Brzeszczyński

Hamilton

et al. 2020

Bone & Joint Research

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MicroRNAs (miRNAs) are a class of small non-coding RNAs that have emerged as potential predictive, prognostic, and therapeutic biomarkers, relevant to many pathophysiological conditions including limb immobilization, osteoarthritis, sarcopenia, and cachexia. Impaired musculoskeletal homeostasis leads to distinct muscle atrophies. Understanding miRNA involvement in the molecular mechanisms underpinning conditions such as muscle wasting may be critical to developing new strategies to improve patient management. MicroRNAs are powerful post-transcriptional regulators of gene expression in muscle and, importantly, are also detectable in the circulation. MicroRNAs are established modulators of muscle satellite stem cell activation, proliferation, and differentiation, however, there have been limited human studies that investigate miRNAs in muscle wasting. This narrative review summarizes the current knowledge as to the role of miRNAs in the skeletal muscle differentiation and atrophy, synthesizing the findings of published data. Cite this article: Bone Joint Res 2020;9(11):798–807.

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Section: Introductionmentioning

confidence: 99%

Role of microRNA in muscle regeneration and diseases related to muscle dysfunction in atrophy, cachexia, osteoporosis, and osteoarthritis

Brzeszczyńska

Brzeszczyński

Hamilton

et al. 2020

Bone & Joint Research

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“…Mechanically activated PdL cells therefore release crucial factors that modulate the initiated local inflammation together with differentiation programs of diverse cells regulating alveolar bone remodeling processes 8,9 . Among PdL cells, PdL fibroblasts show many osteoblast-like properties, as they express osteogenic markers like alkaline phosphatase and form mineralized nodules in vitro 10–12 . Furthermore, they also have important roles in osteoclastogenesis 12,13 and are therefore a suitable cell culture system to study mechanical-induced changes in vitro 14 .…”

Section: Introductionmentioning

confidence: 99%

“…Among PdL cells, PdL fibroblasts show many osteoblast-like properties, as they express osteogenic markers like alkaline phosphatase and form mineralized nodules in vitro 10–12 . Furthermore, they also have important roles in osteoclastogenesis 12,13 and are therefore a suitable cell culture system to study mechanical-induced changes in vitro 14 .…”

Section: Introductionmentioning

confidence: 99%

Mechanically-induced GDF15 Secretion by Periodontal Ligament Fibroblasts Regulates Osteogenic Transcription

Symmank

Zimmermann²,

Goldschmitt³

et al. 2019

Sci Rep

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The alveolar bone provides structural support against compressive and tensile forces generated during mastication as well as during orthodontic treatment. To avoid abnormal alveolar bone resorption and tooth loss, a balanced bone turnover by bone-degrading osteoclasts and bone-generating osteoblasts is of great relevance. Unlike its contradictory role in regulating osteoclast and osteoblast cell differentiation, the TGF-β/BMP-family member GDF15 is well known for its important functions in the regulation of cell metabolism, as well as cell fate and survival in response to cellular stress. Here, we provide first evidence for a potential role of GDF15 in translating mechanical stimuli into cellular changes in immature osteoblasts. We detected enhanced levels of GDF15 in vivo in periodontal ligament cells after the simulation of tooth movement in rat model system as well as in vitro in mechanically stressed human periodontal ligament fibroblasts. Moreover, mechanical stimulation enhanced GDF15 secretion by periodontal ligament cells and the stimulation of human primary osteoblast with GDF15 in vitro resulted in an increased transcription of osteogenic marker genes like RUNX2 , osteocalcin ( OCN) and alkaline phosphatase ( ALP) . Together, the present data emphasize for the first time a potential function of GDF15 in regulating differentiation programs of immature osteoblasts according to mechanical stimulation.

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“…Although it is well accepted that the cementoblasts lining the root surface play an important role in preventing root resorption during orthodontic tooth movement, the causes and predisposing factors for orthodontically induced root resorption are not fully understood [11]. Several studies have confirmed the destructive effect of leptin on periodontal fibroblasts [6,[12][13][14]. Here, it has been shown that higher leptin levels are associated with an upregulation of somatostatin receptor 2, indicating a potential mechanism how adipokines could contribute to periodontal destruction through their proinflammatory characteristics [14].…”

Section: Introductionmentioning

confidence: 99%

Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment

et al. 2020

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Objectives Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown. Material and methods OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression of ObR, Runx-2, Osteocalcin, Rank-L, Sost, Caspase 3, 8, and 9 were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated. Results In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression. Conclusions Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a proinflammatory and pro-apoptotic effect. Clinical relevance Our findings indicate that leptin exacerbates the physiological effect of compressive forces on cementoblasts promoting the release of PGE2 and increases the rate of cell apoptosis, and thus, increased levels of leptin may influence the inflammatory response during orthodontically induced tooth movement.

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Effects of mechanical forces on osteogenesis and osteoclastogenesis in human periodontal ligament fibroblasts

Cited by 54 publications

References 55 publications

Role of microRNA in muscle regeneration and diseases related to muscle dysfunction in atrophy, cachexia, osteoporosis, and osteoarthritis

Role of microRNA in muscle regeneration and diseases related to muscle dysfunction in atrophy, cachexia, osteoporosis, and osteoarthritis

Mechanically-induced GDF15 Secretion by Periodontal Ligament Fibroblasts Regulates Osteogenic Transcription

Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment

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