A review of the biological response to ionic dissolution products from bioactive glasses and glass-ceramics

Review of bioactive glass: from Hench to hybrids.

Bioactive glass and glass-ceramics are used in bone repair applications and are being developed for tissue engineering applications. Bioactive glasses/Bioglass are very attractive materials for producing scaffolds devoted to bone regeneration due to their versatile properties, which can be properly designed depending on their composition. An important feature of bioactive glasses, which enables them to work for applications in bone tissue engineering, is their ability to enhance revascularization, osteoblast adhesion, enzyme activity and differentiation of mesenchymal stem cells as well as osteoprogenitor cells. An extensive amount of research work has been carried out to develop silicate, borate/borosilicate bioactive glasses and phosphate glasses. Along with this, some metallic glasses have also been investigated for biomedical and technological applications in tissue engineering. Many trace elements have also been incorporated in the glass network to obtain the desired properties, which have beneficial effects on bone remodeling and/or associated angiogenesis. The motivation of this review is to provide an overview of the general requirements, composition, structure-property relationship with hydroxyapatite formation and future perspectives of bioglasses.Attention has also been given to developments of metallic glasses and doped bioglasses along with the techniques used for their fabrication.

A review of bioactive glasses: Their structure, properties, fabrication and apatite formation

Background Activation of the group 2 innate lymphoid cell (ILC2) population leads to production of the classical type 2 cytokines, thus promoting type 2 immunity. Chemoattractant receptor-homologous molecule expressed on T H2 cells (CRTH2), a receptor for prostaglandin D2 (PGD2), is expressed by human ILC2s. However, the function of CRTH2 in these cells is unclear. Objectives We sought to determine the role of PGD2 and CRTH2 in human ILC2s and compare it with that of the established ILC2 activators IL-25 and IL-33. Methods The effects of PGD 2, IL-25, and IL-33 on the cell migration, cytokine production, gene regulation, and receptor expression of ILC2s were measured with chemotaxis, ELISA, Luminex, flow cytometry, quantitative RT-PCR, and QuantiGene assays. The effects of PGD2 under physiologic conditions were evaluated by using the supernatant from activated mast cells. Results PGD2 binding to CRTH2 induced ILC2 migration and production of type 2 cytokines and many other cytokines. ILC2 activation through CRTH2 also upregulated the expression of IL-33 and IL-25 receptor subunits (ST2 and IL-17RA). The effects of PGD 2 on ILC2s could be mimicked by the supernatant from activated human mast cells and inhibited by a CRTH2 antagonist. Conclusions PGD2 is an important and potent activator of ILC2s through CRTH2 mediating strong proallergic inflammatory responses. Through IgE-mediated mast cell degranulation, these innate cells can also contribute to adaptive type 2 immunity; thus CRTH2 bridges the innate and adaptive pathways in human ILC2s. © 2013 American Academy of Allergy, Asthma & Immunology.

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Prostaglandin D2 activates group 2 innate lymphoid cells through chemoattractant receptor-homologous molecule expressed on TH2 cells

This article provides an overview on the application of metallic ions in the fields of regenerative medicine and tissue engineering, focusing on their therapeutic applications and the need to design strategies for controlling the release of loaded ions from biomaterial scaffolds. A detailed summary of relevant metallic ions with potential use in tissue engineering approaches is presented. Remaining challenges in the field and directions for future research efforts with focus on the key variables needed to be taken into account when considering the controlled release of metallic ions in tissue engineering therapeutics are also highlighted.

https://royalsocietypublishing.org/doi/pdf/10.1098/rsif.2011.0611

Metallic ions as therapeutic agents in tissue engineering scaffolds: an overview of their biological applications and strategies for new developments.

The vacuolar ATPase (V-ATPase) is a multisubunit enzyme that couples ATP hydrolysis to proton pumping across membranes. Recently, there is increasing evidence that V-ATPase may contribute to the pathogenesis of bone resorption disorders due to it is predominantly expressed in osteoclasts also function in bone resorption making it a good candidate in a therapeutic target for osteoporosis. Osteoclasts are capable of generating an acidic microenvironment necessary for bone resorption by utilizing V-ATPases to pump protons into the resorption lacuna. In addition, it has been shown that therapeutic interventions have been proposed that specifically target inhibition of the osteoclast proton pump. Modulation of osteoclastic V-ATPase activity has been considered to be a suitable therapy for the treatment of osteoporosis. All theses findings suggest that V-ATPase have important biological effects in bone resorption that might be a promising therapeutic target for osteoporosis. In this review, we will briefly discuss the biological features of osteoporosis and summarize recent advances on the role of V-ATPase in the pathogenesis and treatment of osteoporosis.

The vacuolar ATPase in bone cells: a potential therapeutic target in osteoporosis

The role of interleukin-17 in mediating joint destruction in rheumatoid arthritis

The aim of this study was to examine whether drugs such as amiloride that block acid sensing ion channels (ASICs) could attenuate articular cartilage destruction in adjuvant-induced arthritis (AA). Articular chondrocytes were isolated from the normal rats, and intracellular calcium ([Ca2+]i) was analyzed with laser scanning confocal microscopy. The cell injury was analyzed with lactate dehydrogenase release assay and electron microscopy. Amiloride or phosphate buffered saline was administered daily to AA rats for 1 week from the time of arthritis onset. Morphology of the articular cartilage was examined by hematoxylin and eosin staining, and Mankin score was calculated. The expression level of type II collagen (COII) and aggrecan mRNA and proteins in the articular cartilage was evaluated by real-time PCR and Western blotting, respectively. The rapid decrease in extracellular pH (6.0) induced a conspicuous increase in [Ca2+]i in the articular chondrocytes. Amiloride reduced this increase in [Ca2+]i, and inhibited acid-induced articular chondrocyte injury. Amiloride significantly decreased Mankin scores in the articular cartilage in AA rats. COII and aggrecan mRNA and protein expression in the articular cartilage was significantly increased by amiloride. These findings represent some experimental evidence of a potential role for ASICs in the pathogenesis of articular cartilage destruction in rheumatoid arthritis.

Inhibition of acid-sensing ion channels in articular chondrocytes by amiloride attenuates articular cartilage destruction in rats with adjuvant arthritis

Regulatory T cells as a potent target for controlling bone loss.

Interleukin-21 (IL-21) is a new member of the type I cytokine superfamily, which binds to a composite receptor that consists of a private receptor (IL-21R) and the common cytokine receptor γ chain. Recently, increasing evidence has shown that IL-21 contributes to the pathogenesis of chronic inflammatory and autoimmune diseases because of its pro-inflammatory and immune-mediated properties. IL-21 induced T-cell activation and pro-inflammatory cytokine secretion in rheumatoid arthritis (RA). IL-21R RNA transcripts were found in synovial tissue samples of patients with RA. In addition, blockade of the IL-21/IL-21R pathway ameliorated disease in animal models of RA and significantly inhibited inflammatory cytokine production in vitro. Moreover, IL-21R deficiency in the K/BxN mouse model of inflammatory arthritis was sufficient to block arthritis initiation completely. All theses findings suggest that IL-21 has important biological effects in autoimmunity that might be a promising therapeutic target for RA. In this review, we discuss the biological features of IL-21 and summarize recent advances in the role of IL-21 in the pathogenesis and treatment of RA.

Jian-Ping Li

Papers

The vacuolar ATPase in bone cells: a potential therapeutic target in osteoporosis

The role of interleukin-17 in mediating joint destruction in rheumatoid arthritis

Inhibition of acid-sensing ion channels in articular chondrocytes by amiloride attenuates articular cartilage destruction in rats with adjuvant arthritis

Regulatory T cells as a potent target for controlling bone loss.

Targeting interleukin-21 in rheumatoid arthritis.