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Copyright of Wissen Kompakt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Objectives: Damage-regulated autophagy modulator (DRAM) 1 is a p53 target gene with possible involvement in oral inflammation and infection. This study sought to examine the presence and regulation of DRAM1 in periodontal diseases.Material and methods: In vitro, human periodontal ligament fibroblasts were exposed to interleukin (IL)-1β and Fusobacterium nucleatum for up to 2 days. The DRAM1 synthesis and its regulation were analyzed by real-time PCR, immunocytochemistry, and ELISA. Expressions of other autophagy-associated genes were also studied by real-time PCR. In vivo, synthesis of DRAM1 in gingival biopsies from rats and patients with and without periodontal disease was examined by real-time PCR and immunohistochemistry. For statistics, ANOVA and post-hoc tests were applied (p < 0.05).Results: In vitro, DRAM1 was significantly upregulated by IL-1β and F. nucleatum over 2 days and a wide range of concentrations. Additionally, increased DRAM1 protein levels in response to both stimulants were observed. Autophagy-associated genes ATG3, BAK1, HDAC6, and IRGM were also upregulated under inflammatory or infectious conditions. In vivo, the DRAM1 gene expression was significantly enhanced in rat gingival biopsies with induced periodontitis as compared to control. Significantly increased DRAM1 levels were also detected in human gingival biopsies from sites of periodontitis as compared to healthy sites.Conclusion: Our data provide novel evidence that DRAM1 is increased under inflammatory and infectious conditions in periodontal cells and tissues, suggesting a pivotal role of DRAM1 in oral inflammation and infection.Clinical relevance: DRAM1 might be a promising target in future diagnostic and treatment strategies for periodontitis. [ABSTRACT FROM AUTHOR]

Copyright of Wissen Kompakt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: Different studies suggest that inflammation as well as hypoxia leads to an increase of p53 protein levels. However, the implication of p53 during oral inflammatory processes is still unknown. The aim of this study was therefore to investigate the effect of hypoxia and inflammation on p53 regulation in human periodontium in vitro and in vivo. Materials and methods: Under hypoxic and normoxic conditions, human primary periodontal ligament (PDL) fibroblasts ( n = 9) were stimulated with lipopolysaccharides (LPS) from Porphyromonas gingivalis ( P.g.), a periodontal pathogenic bacterium. After different time points, cell viability was tested; p53 gene expression, protein synthesis, and activation were measured using quantitative RT-PCR, immunoblotting, and immunofluorescence. Moreover, healthy and inflamed periodontal tissues were obtained from 12 donors to analyze p53 protein in oral inflammatory diseases by immunohistochemistry. Results: LPS- P.g. and hypoxia initially induced a significant upregulation of p53 mRNA expression and p53 protein levels. Nuclear translocation of p53 after inflammatory stimulation supported these findings. Hypoxia first enhanced p53 levels, but after 24 h of incubation, protein levels decreased, which was accompanied by an improvement of PDL cell viability. Immunohistochemistry revealed an elevation of p53 immunoreactivity in accordance to the progression of periodontal inflammation. Conclusions: Our data indicate that p53 plays a pivotal role in PDL cell homeostasis and seems to be upregulated in oral inflammatory diseases. Clinical relevance: Upregulation of p53 may promote the destruction of periodontal integrity. A possible relationship with carcinogenesis may be discussed. [ABSTRACT FROM AUTHOR]

Background: Antimicrobial peptides (AMPs), such as human beta-defensin-2 (hBD-2) and the CC-chemokine ligand 20 (CCL20), exhibit direct microbicidal effects and mediator-like activity. It was hypothesized that wounding induces the expression of AMPs and pro-inflammatory mediators and that endogenous mediators, such as insulin-like growth factor-1 (IGF-1) and transforming growth factor-alpha (TGF-alpha), modulate this induced expression. Material and methods: Monolayers of gingival epithelial cells (GECs) and gingival fibroblast (HGFs) from three different donors were wounded using the scratch assay (in vitro wounding) in the presence (test group) or absence (control group) of IGF-1 and TGF-alpha. In vitro wound closure was monitored over time (0, 6, 24, 48, 72 h), and wound areas were microscopically analyzed (Axio-Vision® Software, Zeiss). Gene expression analysis of the GAPDH, hBD-2, CCL20, interleukin-1 beta (IL-1 beta), and interleukin-8 (IL-8) was performed by qPCR. Results: In comparison to control cells, IGF-1 and TGF-alpha significantly enhanced in vitro wound closure ( P < 0.05). In GECs, IGF-1 induced the gene expression of IL-1 beta and IL-8 when compared to control cells ( P < 0.05). In HGFs, wounding per se induced the messenger RNA of hBD-2, CCL20, and IL-1 beta, whereas IGF-1 and TGF-alpha reversed this effect ( P < 0.05). Conclusion: In gingival cells, the gene expression of AMPs was altered by injury, and endogenous growth factors further influenced the expression profiles, but with high interindividual differences. [ABSTRACT FROM AUTHOR]

We have used various techniques such as X-ray diffraction, Fourier transform infrared spectroscopy as well as dielectric measurements with a 4 GHz Microwave resonator to investigate the structure of uniaxially drawn α-polyamide 6 films. The influence of uniaxial drawing on several parameters such as degree of crystallinity, orientation and size of crystallites, permittivity and anisotropy was studied as a function of the drawing ratio. The main axis (b-axis) of the polyamide 6 nano-crystals is aligned in the direction of drawing, while the hydrogen bonds (a-axis) are oriented transverse to the drawing direction. Increasing the drawing ratio yields a higher crystallinity, a better orientation of the crystallites, and a stronger dielectric anisotropy of the films. The good agreement of the results demonstrates that all the three experimental techniques are well suited to characterize the microstructure of polyamide films. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Wissen Kompakt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study examined the histological changes and possible effects of intermittent parathyroid hormone (PTH) (1-34) treatment during the early and late phase of periodontal repair in a rat model of tooth root resorption. In a total of 70 animals, which either received intermittent PTH(1-34) systemically or sham injections for up to 70 days after discontinuation of an orthodontic force, histological characteristics were correlated to time-dependent distinct expression patterns of osteoprotegerin and receptor activator of nuclear factor kappaB ligand by PDL cells in the former compression and tension side of tooth movement by means of immunohistochemistry and histomorphometrical analysis. The balance of these key regulators of bone remodeling was demonstrated to be shifted in favor of hard tissue repair by intermittent PTH administration, which was demonstrated to exert anabolic effects in several cell culture and animal experiments as well as in humans, in the late phase of repair. These data indicate a role for PDL cells as potent regulators of periodontal repair by modifying the local microenvironment and point to the anabolic potential of an intermittent PTH administration to support these reparative processes. [ABSTRACT FROM AUTHOR]

We have investigated the influence of drawing on orientation, crystallinity, and structural properties of polyamide 6 films using X-ray diffraction. The samples were uniaxially and biaxially stretched resulting in the formation of monoclinic crystallites (α-form) in the size range of 8–10 nm. Depending on the drawing ratio, a degree of crystallinity of up to 60% is obtained. The average orientation of the crystallite axes was evaluated using the pole figure technique. The b*-axis, which corresponds to the chain direction of the polyamide molecules, lies in the film plane and shows a preferred orientation upon drawing. For uniaxial drawing, b* aligns with the drawing direction. For biaxially drawn films, which were prepared using the sequential stretching method, the second drawing determines the orientation of b*, at least at the center of the films. At the sides, b* is located between the two drawing directions reflecting the inhomogeneous distribution of mechanical stress during stretching. [ABSTRACT FROM AUTHOR]

Copyright of Oral & Maxillofacial Surgery is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Periodontal ligament (PDL) cells exhibit several osteoblastic traits and are parathyroid hormone (PTH)-responsive providing evidence for a role of these cells in dental hard-tissue repair. To examine the hypothesis that PDL cells respond to PTH stimulation with changes in proliferation and apoptotic signaling through independent but convergent signaling pathways, PDL cells were cultured from human bicuspids obtained from six patients. PDL cells at different states of maturation were challenged with PTH(1–34) intermittently for 0, 1, or 24 h/cycle or exposed continuously. Specific inhibitors to protein kinases A and C (PKA, PKC) and the mitogen-activated protein kinase cascade (MAPK) were employed. At harvest, the cell number, BrdU incorporation, and DNA fragmentation were determined by means of cell counting and immunoassays. Intermittent PTH(1–34) caused a significant increase in cell number in confluent cells as opposed to a reduction in pre-confluent cells. In confluent cells, the effect resulted from a significant increase in proliferation, whereas DNA fragmentation was reduced when PTH(1–34) was administered for 1 h/cycle but increased after PTH(1–34) for 24 h/cycle. Inhibition of PKC inhibited PTH(1–34)-induced proliferation but enhanced apoptosis. Inhibition of PKA enhanced proliferation and DNA fragmentation. Similar results were obtained in less mature cells, although, in the presence of the PKA inhibitor, the PTH(1–34)-induced changes were more pronounced than in confluent cells. In the presence of the MAPK inhibitor, all of the parameters examined were reduced significantly in both maturation states. Thus, PTH(1–34) mediates proliferative and apoptotic signaling in human PDL cells in a maturation-state-dependent manner via PKC-dependent and PKA-dependent pathways. [ABSTRACT FROM AUTHOR]

Haemostatic and aseptic effects and intricate cut geometry are beneficial aspects of non-contact laser osteotomy. Collateral thermal damage, however, has severely limited the use of conventional lasers. The purpose of this study was to test the side effects on bone after cutting it with short CO2 laser pulses and simultaneous application of a fine air–water spray. The 10.6 μm CO2 laser emitted 80-μs pulses of 46 mJ energy, f=100 Hz, focused to a spot diameter of 130 ìm. Scan rate amounted to 40 mm/s. To approximate live conditions 10 samples of cortical bone and 10 rib segments were prepared immediately after sacrificing of pigs. A reference cut with a bandsaw and three laser cuts with an increasing number of beam passes (4, 16, 64) were performed on each sample. Half of the samples were decalcified in EDTA. The others were embedded in plastic to cut non-decalcified sections. The laser incisions were not accompanied by carbonisation. The incisions with slightly convergent walls were 150 ìm wide. The depths of the cavities increased with the number of the beam passes from approximately 0.5 mm (4 passes) to 3 mm (64 passes). At the border of the incisions two narrow zones of damage were noted: an amorphous intensively stained zone of 1–3 μm width and a wider, also sharply demarcated but faintly stained zone of 7–10 μm. A broader zone of about 50 μm was characterised by empty lacunae and osteocyte damage. These effects were not predictable; intact osteocytes were also observed near to the cut surface. Polarised light microscopy showed no alterations in the inorganic structure of the bone at the cut borders. The histological results indicated only minimal damage to bone ablated at the specified parameters. The described laser procedure might have advantages over mechanical instruments. [ABSTRACT FROM AUTHOR]

Osteoblasts and osteoclasts are involved in bone formation and resorption. RANK and RANKL [receptor activator of nuclear factor kappaB (ligand)], two cytokine-like proteins of the tumor necrosis factor superfamily, are localized on these bone cells and are crucial for the regulation of osteoclastic cell differentiation from hematopoietic precursors and also for the upregulation of mature osteoclasts mediated by cell-to-cell contact and a subsequent cascade of diverse intracellular signaling processes in the osteoclasts. It was the aim of this study to examine the sites of expression of RANKL and RANK in the corresponding cells of human dental hard and periodontal tissues using immunohistochemical light microscopical methods on tissue sections of 15 paraffin-embedded human deciduous teeth undergoing root resorption. We detected granular cytoplasmic RANKL-immunoreactivity in odontoblasts, pulp fibroblasts, periodontal ligament fibroblasts, and in single odontoclasts, the latter finding suggesting an autocrine/paracrine role. RANK-positive cells were identified as multinucleated odontoclasts localized near the dentine surface in resorption lacunae or as mononucleated precursors. These findings indicate that human dental cells express key mediators of hard tissue resorption and, though the RANK/RANKL-system may not be the sole regulator of tooth root resorption, these factors could at least contribute to this complex process under both physiological and pathological conditions. [ABSTRACT FROM AUTHOR]

Copyright of Mund-, Kiefer- und Gesichtschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Immunohistochemical methods were used to study the effects of botulinum toxin A on the concentration of acetylcholinesterase in the submandibular gland of the rat. The toxin was injected into the glands of healthy adult female Wistar rats and immunohistochemistry performed on the excised organs. Morphometric measurements were also carried out to study changes of cell morphology after local applications of botulinum toxin A. Compared with untreated glands or glands injected with saline there was a decrease of acetylcholinesterase in the glands treated with botulinum toxin. As the cholinergic pathway of the autonomic nervous system plays an important role in eliciting secretion from the salivary glands, inhibition of secretion by local application of botulinum toxin could be considered a therapeutic option for the treatment of various diseases affecting salivary gland function. [ABSTRACT FROM AUTHOR]

Copyright of Surgical & Radiologic Anatomy is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The role of extracellular matrix molecules in ontogenetic differentiation processes is a matter of increasing interest. In cartilage development, type II collagen is suspected of promoting chondrogenic differentiation, since its expression has been demonstrated in a range of precartilaginous tissues of vertebrate species. Up to now, no studies supplying a coherent description of type II collagen expression in the skeletogenesis of human embryos including early embryonic stages have been published. In this work, we examine the temporal and spatial distribution of type II collagen mRNA during vertebral column development in human embryos from 4 to 12 weeks of gestation using non-radioactive in situ hybridization. The onset of gene expression was demonstrable in the 5th week in precartilaginous mesenchymal cells and in notochordal cells. Additionally, we found a weaker hybridization signal in the mesenchymal precursors of the intervertbral discs. In the anlagen of the axial skeleton, type II collagen expression decreased during osteogenic reconstruction in the 11th/12th week, whereas expression continued in the notochordal remnants of the future nuclei pulposi. The results suggest a relatively late occurrence of type II collagen in human vertebral development compared with other vertebrate species. The distribution of gene expression is concordant with a possible role of this molecule in promoting differentiation of mesenchymal cells into chondrocytes. The mechanism of this influence remains to be established. [ABSTRACT FROM AUTHOR]

The paraxial mesenchyme in seven human embryos aged between Carnegie stages 12 and 17 was studied by lectin histochemistry with the lectins AIA, Con A, GSA II, LFA, LTA, PNA, RCA I, SBA, SNA, WGA. The paraxial mesenchyme was found to be segmented into sclerotomes by intersegmental vessels and from late stage 12 by intrasclerotomal clefts dividing each sclerotome into a cranial and caudal half. The lectins Con A, GSA II, LFA, LTA, SBA and SNA did not react at all in the paraxial mesenchyme. Staining for AIA, PNA, RCA I and WGA was found in the developing sclerotomes. However, no differences in the staining pattern between the two sclerotomal halves could be seen. It was striking that in contrast to the chick embryo no differences in binding for PNA between the cranial and caudal sclerotomal parts was observed. These findings reveal that PNA-binding sites do not play the same functional role in segmented axonal outgrowth and neural crest immigration into cranial sclerotomal halves in the human embryo, as found in chick embryonic development. Beginning with the stage 16-embryo, the already condensed caudal sclerotomal halves express Con A-, RCA- and PNA-binding sites. The staining for PNA in particular marked the differentiation of chondrogenous structures developing in this half. From the late stage 12 or stage 13, the walls of intersegmental and other vessels showed binding sites for AIA, PNA, RCA I, SNA and WGA. [ABSTRACT FROM AUTHOR]

Paraffin sections from vertebral columns of ten human embryos and fetuses ranging from stage 16 to the 12th week were stained with the FITC-coupled lectins PNA, RCA I, Con A and WGA in order to investigate changes in carbohydrate-binding sites during vertebral development. PNA revealed a specific binding site in the vertebral body blastema in the precartilaginous stage of development. Beginning with the 25-mm CRL embryo, PNA-binding sites occurred in the developing fibrous annulus and the inner zone of the intervertebral discs. The first binding sites for RCA I were seen in the extracellular matrix of vertebral bodies during the cartilaginous stage of vertebral development. During early ossification of the vertebrae, staining for RCA I-binding sites in the cytoplasm of the chondrocytes and the area around the future cartilaginous end-plates was observed. Con A bound to the chondrocyte cytoplasm, and also very strongly to notochordal cells in all developmental stages examined. WGA-binding sites appeared simultaneously with cartilage formation. Connective tissue components, e.g. ligaments, were diffusely stained by WGA. Also this lectin showed an affinity for vertebral body chondrocytes. We discuss the biochemical aspects of these lectin-binding sites, and their possible roles in the differentiation process of the human vertebral column. The results of this first lectin histochemical study on human vertebral development are compared with related results in other species. [ABSTRACT FROM AUTHOR]

In the present work we compared the appearance of carbohydrate binding sites for mannose, maltose, sialic acid and N-acetyl-glucosamine in the 11 to 13-day-old mouse embryo with the appearance of BSA and lectin binding sites. The carbohydrate-binding sites were localized with FITC-coupled neoglycoproteins, synthesized by chemical glycosylation of bovine serum albumin (BSA). These localizations were compared with binding of the FITC-labelled unglycosylated BSA. Furthermore the localizations of neoglycoprotein and BSA binding sites were correlated with binding of the FITC-labelled lectins WGA, RCA I and Con A. Initial appearance of neoglycoprotein binding sites occurred in the lens capsule of the 13 day old mouse embryo. Binding sites for the unglycosylated BSA appeared earlier, i.e. already in the 12-day-old embryo, in the basement membranes of the choroid plexus and the lung bud and lectin binding sites were seen in these structures in the 11-day-old embryo. The staining of the basement membrane and the lens capsule for BSA binding sites in the 12-and 13-day-old embryos correspond to WGA binding to these membranes. From these results we concluded that 1) specific carbohydrates which are probably involved in embryonic development appear much earlier in the embryo than the endogenous lectins which are able to react with these carbohydrates and 2) BSA is a protein which like WGA probably binds N-acetylglucosamine or sialic acid moieties. [ABSTRACT FROM AUTHOR]