Репозиторий Университета

© 2020 Bone age is used widely by pediatricians to assess the skeletal maturity of a child and predict growth potential. This entails measuring the size of secondary ossification centers (SOCs), which develop with age in the ends of long bones, which are initially cartilaginous. However, little is presently known about the developmental biology, evolution and functional role of these skeletal elements. Here, we summarize the knowledge currently available in this area and discuss potential primary functions of the SOC.

© 2020 Bone age is used widely by pediatricians to assess the skeletal maturity of a child and predict growth potential. This entails measuring the size of secondary ossification centers (SOCs), which develop with age in the ends of long bones, which are initially cartilaginous. However, little is presently known about the developmental biology, evolution and functional role of these skeletal elements. Here, we summarize the knowledge currently available in this area and discuss potential primary functions of the SOC.

© 2020 Bone age is used widely by pediatricians to assess the skeletal maturity of a child and predict growth potential. This entails measuring the size of secondary ossification centers (SOCs), which develop with age in the ends of long bones, which are initially cartilaginous. However, little is presently known about the developmental biology, evolution and functional role of these skeletal elements. Here, we summarize the knowledge currently available in this area and discuss potential primary functions of the SOC.

© 2019 The authors. Estrogens may affect bone growth locally or systemically via the known estrogen receptors ESR1, ESR2 and G protein-coupled estrogen receptor 1 (GPER1). Mouse and human growth plate chondrocytes have been demonstrated to express GPER1 and ablation of this receptor increased bone length in mice. Therefore, GPER1 is an attractive target for therapeutic modulation of bone growth, which has never been explored. To investigate the effects of activated GPER1 on the growth plate, we locally exposed mouse metatarsal bones to different concentrations of the selective GPER1 agonist G1 for 14 days ex vivo. The results showed that none of the concentrations of G1 had any direct effect on metatarsal bone growth when compared to control. To evaluate if GPER1 stimulation may systemically modulate bone growth, ovariectomized C57BL/6 mice were treated with G1 or β-estradiol (E2). Similarly, G1 did not influence tibia and femur growth in treated mice. As expected, E2 treatment suppressed bone growth in vivo. We conclude that ligand stimulation of GPER1 does not influence bone growth in mice.

© 2018 by the authors. Licensee MDPI, Basel, Switzerland. Articular hyaline cartilage is extensively hydrated, but it is neither innervated nor vascularized, and its low cell density allows only extremely limited self-renewal. Most clinical and research efforts currently focus on the restoration of cartilage damaged in connection with osteoarthritis or trauma. Here, we discuss current clinical approaches for repairing cartilage, as well as research approaches which are currently developing, and those under translation into clinical practice. We also describe potential future directions in this area, including tissue engineering based on scaffolding and/or stem cells as well as a combination of gene and cell therapy. Particular focus is placed on cell-based approaches and the potential of recently characterized chondro-progenitors; progress with induced pluripotent stem cells is also discussed. In this context, we also consider the ability of different types of stem cell to restore hyaline cartilage and the importance of mimicking the environment in vivo during cell expansion and differentiation into mature chondrocytes.

© 2018 Astro Ltd. Lasers offer new possibilities in the treatment of such widespread diseases as osteoarthritis, with both direct and indirect effects on cell metabolism. Cyclic hydrostatic pressure is one of the main natural stimuli of cartilage chondrocytes. The present work shows that hydrostatic stimulation with magnitudes of up to 20 MPa can be realized locally through infrared impact on the neighboring media of chondrocytes. We compare indirect (thermomechanical, λ = 1560 nm) and direct (photo-modulation, λ1 = 1560 nm, λ2 = 670 nm) laser effects on the synthetic activity of chondrocytes in cultures within a 1 min exposure time limit, to study separately the photo-modulation and thermomechanical components of laser impact. The chondrocyte activity was monitored by immunohistochemical analysis in normoxic and hypoxic conditions. Collagen II and proteoglycan accumulation increased significantly (up to 70%) after a pulsed thermomechanical laser impact. Thermomechanical laser irradiation showed the more pronounced stimulation in both normoxic and hypoxic conditions, while the effect of photo-modulation was inhibited by oxygen concentration increase. Theoretical calculations of the laser-induced temperature and stress fields show that the spreading of the stress field with a maximum at 19.2 MPa is approximately three times greater than that of appreciable (>1 °C) heating. Thus, thermomechanical infrared stimulation of chondrocytes can be a perspective method for the restoration of hyaline-type cartilage.

© 2018 The Authors There are several pitfalls associated with research based on transgenic mice. Here, we describe our interpretation and analysis of mTORC1 activation in growth plate chondrocytes and compare these to a recent publication (Yan et al., Nature Communications 2016, 7:11151). Both laboratories employed TSC1-floxed mice crossed with collagen type 2-driven Cre (Col2-Cre), but drew substantially different conclusions. It was reported that activation of mechanistic target of rapamycin complex 1 (mTORC1) via Tsc1 ablation promotes the hypertrophy of growth plate chondrocytes, whereas we observe only disorganization in the resting zone, with no effect on chondrocyte hypertrophy or proliferation. Here, we present our data and discuss the differences in comparison to the earlier phenotypic characterization of TSC1 ablation in cartilage. Importantly, we detect Col2-Cre activity in non-cartilaginous tissues (including the brain) and discuss it in relation to other studies reporting non-cartilaginous expression of collagen alpha(1) II. Altogether, we conclude that mouse phenotypes following genetic ablation using Col2-Cre should be interpreted with care. We also conclude that activation of mTORC1 by TSC1 ablation in postnatal chondrocytes with inducible Col2-Cre (Col2-CreERt) leads to disorganization of the resting zone but causes no changes in chondrocyte proliferation or differentiation.

© 2018, Media Sphera Publishing Group. All rights reserved. Pectus excavatum (PE) and pectus carinatum (PC) in children are the most common congenital deformities that cause complications in the thoracic organs; however, the role of chondrocytes and cartilage canals in the pathogenesis of these conditions remains unexplored. Objective — to investigate qualitative and quantitative changes of cartilage lacunae and canals in the costal cartilages in children with PE and PC compared to those with normal chests. Subject and methods. Costal cartilages were investigated in 10 children with normal chests (a control group), in 12 children with PE, and in 12 children with PC. Tissue fragments were fixed in 10% neutral formalin and embedded in compacted paraffin. Sections were stained with hematoxylin and eosin. Slides were examined by light microscopy. Cartilage lacunae, hyper-and hypolacunar zones, and cartilage canals were morphometrically examined, followed by statistical data analysis. Results. There was a significant decrease in the number of cartilage lacunae and in the frequency of hyperlacunar zones and an increase in that of hypolacunar zones in the PE and PC groups. There were no significant differences in these parameters between the PE and PC groups; however, there was a tendency to the smallest number of cartilage lacunae and canals in the PC group and that to the preponderance of empty lacunae in the PE group. Only the PC group showed also negative correlations between the proportions of empty lacunae and the age of children. Conclusion. The pathogenesis of PE and PC in children is related to the impaired trophism of costal cartilages due to the smaller number of cartilage channels containing vessels and lacunae with chondrocytes. The development of PE and PC is associated with specific costal cartilage morphological changes that suggest that PE and PC are different manifestations of the same disease, namely connective tissue dysplasia.