A potential therapeutic approach to overload-induced bone loss around implant: Parathyroid hormone (PTH)

Zeng, Xin; He, Huaqiang; Zhang, Liang; Wu, Yingying; Wang, Yanying; Gong, Ping

doi:10.1016/j.mehy.2011.06.016

Cited by 11 publications

(8 citation statements)

References 47 publications

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“…These methods have improved conditions in patients with non-union or delayed healing defects but still, face substantial challenges. For example, metal implants are standard tools to provide appropriate mechanical support; but they lack inherent biological functions to fully replace the lost bone [ [6] , [7] , [8] ]. Allogeneic/xenogeneic grafts may solve the insufficiency of autologous bone for transplantation, yet they risk immunogenic rejection and other medical and ethical issues [ [9] , [10] , [11] ].…”

Section: Introduction: Modulating But Not Resisting Macrophages At mentioning

confidence: 99%

Modulating macrophage activities to promote endogenous bone regeneration: Biological mechanisms and engineering approaches

Niu

Wang

Shi

et al. 2021

Bioactive Materials

112

123

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A coordinated interaction between osteogenesis and osteoimmune microenvironment is essential for successful bone healing. In particular, macrophages play a central regulatory role in all stages of bone repair. Depending on the signals they sense, these highly plastic cells can mediate the host immune response against the exterior signals of molecular stimuli and implanted scaffolds, to exert regenerative potency to a varying extent. In this article, we first encapsulate the immunomodulatory functions of macrophages during bone regeneration into three aspects, as sweeper, mediator and instructor. We introduce the phagocytic role of macrophages in different bone healing periods (‘sweeper’) and overview a variety of paracrine cytokines released by macrophages either mediating cell mobilisation, vascularisation and matrix remodelling (‘mediator’), or directly driving the osteogenic differentiation of bone progenitors and bone repair (‘instructor’). Then, we systematically classify and discuss the emerging engineering strategies to recruit, activate and modulate the phenotype transition of macrophages, to exploit the power of endogenous macrophages to enhance the performance of engineered bone tissue.

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Section: Introduction: Modulating But Not Resisting Macrophages At mentioning

confidence: 99%

Modulating macrophage activities to promote endogenous bone regeneration: Biological mechanisms and engineering approaches

Niu

Wang

Shi

et al. 2021

Bioactive Materials

112

123

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“…14 Particularly, clinical trials assessing alveolar bone indicated that PTH has a synergistic function in bone regeneration against severe periodontitis. 34 We hypothesized that PTH impedes the pathophysiological processes reducing DM-induced HBMSCs. ALP represents a valuable osteogenic marker mainly expressed early during mineralization.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 MAPK signaling

et al. 2020

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Diabetes mellitus (DM)-induced glucolipotoxicity is a factor strongly contributing to alveolar bone deficiency. Parathyroid hormone (PTH) has been identified as a main systemic mediator to balance physiological calcium in bone. This study aimed to uncover PTH's potential role in ameliorating the osteogenic capacity of human bone marrow mesenchymal stem cells (HBMSCs) against glucolipotoxicity. Optimal PTH concentrations and high glucose and palmitic acid (GP) were administered to cells, followed by alkaline phosphatase (ALP) staining and ALP activity assay. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Immunoblot were carried out for assessing mRNA and protein amounts, respectively. Cell counting kit-8 (CCK-8) and flow cytometry were performed for quantitating cell proliferation. Osteogenesis and oxidative stress were determined, and the involvement of mitogen-activated protein kinase (MAPK) signaling was further verified. About 1-50 mmol/ml GP significantly inhibited the osteogenic differentiation of HBMSCs. 10 −9 mol/L PTH was found to be the optimal concentration for HBMSC induction.

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“…[27] Therefore, PTH was modified into various biological small active peptides, such as PTH (1–31), PTH (1–34), and PTH (1–38). [12] PTH is the major regulator of calcium and phosphorus metabolism and skeletal metabolism, [28] the action of which is mediated through PTH receptor. PTH is a G-protein-coupled plasma membrane receptor expressed in osteoblasts but not in osteoclasts in bone tissue.…”

Section: Discussionmentioning

confidence: 99%

“…PTH, an 84-amino acid peptide, is an endocrine hormone secreted by parathyroid glands; [12] this peptide performs important functions in calcium regulation and bone remodeling. [13] In addition, PTH is receiving increasing attention over the recent years in the field of bone repair because of its various biological activities in inducing bone formation both orthotopically and ectopically in the body.…”

Section: Introductionmentioning

confidence: 99%

Dose-dependence of PTH-related peptide-1 on the osteogenic induction of MC3T3-E1 cells in vitro

Wang

Yang

et al. 2017

Medicine

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Parathyroid hormone (PTH), an 84-amino acid peptide, is an endocrine hormone that is secreted by parathyroid glands. PTH performs important functions in calcium regulation and bone remodeling. The PTH (1–34) named teriparatide, a 34-amino acid peptide derived from the N-terminus of PTH, conserves most of the functions of PTH, specifically the osteogenic capability. However, teriparatide is only used by injection and exhibits short duration. In addition, this PTH could not thoroughly expose active sites. In this study, a novel PTH-related peptide (designated PTHrP-1) derived from the N-terminus of PTH was added into the complete medium at different concentrations of PTHrP-1 (0, 50, 100, and 200 ng/mL) to induce the MC3T3-E1 cells. PTHrP-1 was detected by high-performance liquid chromatography and matrix-assisted laser desorption/ionization–time-of-flight mass spectroscopy. Cell morphology, cell proliferation, alkaline phosphatase (ALP), and ALP activity, osteocalcin concentration, and collagen type I (Col-I), osteopontin (OPN), and osteocalcin (OCN) mRNA expression by RT-PCR and protein expression by western blotting were observed and detected. The purity of the PTHrP-1 was 95.14%, and the PTHrP-1 can induce MC3T3-E1 cells into osteoblasts, thus improving ALP activity and OCN concentration, and increasing Col-I, OPN, and OCN mRNA expression and protein expression in MC3T3-E1 cell cultures. The PTHrP-1 proved to be an ideal active peptide. In addition, the osteogenic ability of PTHrP-1 at 200 and 100 ng/mL concentrations was not significantly different but significantly higher than 50 and 0 ng/mL groups. Results indicate that PTHrP-1 is a kind of active peptides that exhibits good biocompatibility with MC3T3-E1 cells and could improve cell proliferation and osteogenic differentiation. Moreover, PTHrP-1, at the preferable concentration of 100 ng/mL, could effectively promote MC3T3-E1 cells into osteoblasts.

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A potential therapeutic approach to overload-induced bone loss around implant: Parathyroid hormone (PTH)

Cited by 11 publications

References 47 publications

Modulating macrophage activities to promote endogenous bone regeneration: Biological mechanisms and engineering approaches

Modulating macrophage activities to promote endogenous bone regeneration: Biological mechanisms and engineering approaches

Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 MAPK signaling

Dose-dependence of PTH-related peptide-1 on the osteogenic induction of MC3T3-E1 cells in vitro

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