Comparative analysis of collagen membranes for the treatment of implant dehiscence defects

Guided bone regeneration (GBR) evolved from the concept of guided tissue regeneration (GTR) and has been used for reconstructing sites with bone deficiencies associated with dental implants. For GBR, the use of absorbable collagen membranes has been increasing, but, at present, scientific information on the use of collagen membranes for GBR is limited. This study was aimed to clinically and histomorphometrically compare two collagen membranes, Bio-Gide ® and BioMend Extend TM , for the treatment of implant dehiscence defects in eight mongrel dogs. Implant dehiscence defects were surgically created in edentulous ridges, followed by the placement of three endosseous implants bilaterally in the mandible. Each implant dehiscence defect was randomly assigned to one of three treatment groups: (1) control (no membrane), (2) porcine dermis collagen barrier (Bio-Gide) or (3) bovine tendon collagen barrier (BioMend Extend). Dogs were sacrificed at 4 and 16 weeks (four dogs each) after treatment. Histomorphometric analysis included percentage linear bone fill (LF), new bone-to-implant contact (BIC) and area of new bone fill (BF). The results of the study revealed no significant differences among groups for any parameter at 4 weeks. However, at 16 weeks, more LF, BIC, and BF were noted in the membrane-treated groups than controls. BioMend Extend-treated defects demonstrated significantly greater BIC than control ( P  < 0.05) at this time point. BIC at 16 weeks was significantly greater than 4-week BIC ( P  < 0.05). Membrane exposure occurred in 9 out of 15 sites examined, resulting in significantly less LF and BIC than the sites without membrane exposure ( P  < 0.05). The results of this study indicate that: (1) GBR treatment with collagen membranes may significantly enhance bone regeneration, manifested at late stage (16 weeks) of healing; and (2) space maintenance and membrane coverage were the two most important factors affecting GBR using bioabsorbable collagen membranes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72252/1/j.1600-0501.2003.140111.x.pd

Circadian Rhythm and Cartilage Extracellular Matrix Genes in Osseointegration: A Genome-Wide Screening of Implant Failure by Vitamin D Deficiency

Successful dental and orthopedic implants require the establishment of an intimate association with bone tissue; however, the mechanistic explanation of how biological systems accomplish osseointegration is still incomplete. We sought to identify critical gene networks involved in osseointegration by exploring the implant failure model under vitamin D deficiency.Adult male Sprague-Dawley rats were exposed to control or vitamin D-deficient diet prior to the osteotomy surgery in the femur bone and the placement of T-shaped Ti4Al6V implant. Two weeks after the osteotomy and implant placement, tissue formed at the osteotomy site or in the hollow chamber of T-shaped implant was harvested and total RNA was evaluated by whole genome microarray analyses.Two-way ANOVA of microarray data identified 103 genes that were significantly (>2 fold) modulated by the implant placement and vitamin D deficiency. Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses assigned the highest z-score to the circadian rhythm pathway including neuronal PAS domain 2 (NPAS2), and period homolog 2 (Per2). NPAS2 and Aryl hydrocarbon receptor nuclear translocator-like (ARNTL/Bmal 1) were upregulated around implant and diminished by vitamin D deficiency, whereas the expression pattern of Per2 was complementary. Hierarchical cluster analysis further revealed that NPAS2 was in a group predominantly composed of cartilage extracellular matrix (ECM) genes. Whereas the expression of bone ECM genes around implant was not significantly affected by vitamin D deficiency, cartilage ECM genes were modulated by the presence of the implant and vitamin D status. In a proof-of-concept in vitro study, the expression of cartilage type II and X collagens was found upregulated when mouse mesenchymal stem cells were cultured on implant disk with 1,25D supplementation.This study suggests that the circadian rhythm system and cartilage extracellular matrix may be involved in the establishment of osseointegration under vitamin D regulation

The Neuronal and Peripheral Expressed Membrane-Bound UNC93A Respond to Nutrient Availability in Mice

Many transporters such as the solute carriers belonging to the Major facilitator superfamily Pfam clan are orphans in that their tissue and cellular localization as well as substrate profile and function are still unknown. Here we have characterized the putative solute carrier UNC93A. We aimed to investigate the expression profile on both protein and mRNA level of UNC93A in mouse since it has not been clarified. UNC93A staining was found in cortex, hippocampus and cerebellum. It was found to be expressed in many neurons, but not all, with staining located in close proximity to the plasma membrane. Furthermore, we aimed to extend the starvation data available for Unc93a in hypothalamic cell cultures from mouse. We investigated the Unc93a alterations with focus on amino acid deprivation in embryonic cortex cells from mice as well as 24 h starvation in adult male mice and compared it to recently studied putative and known solute carriers. Unc93a expression was found both in the brain and peripheral organs, in low to moderate levels in the adult mice and was affected by amino acid deprivation in embryonic cortex cultures and starvation in in vivo samples. In conclusion, the membrane-bound UNC93A is expressed in both the brain and peripheral tissues and responds to nutrient availability in mice

The gene expression of the neuronal protein, SLC38A9, changes in mouse brain after in vivo starvation and high-fat diet.

SLC38A9 is characterized as a lysosomal component of the amino acid sensing Ragulator-RAG GTPase complex, controlling the mechanistic target of rapamycin complex 1 (mTORC1). Here, immunohistochemistry was used to map SLC38A9 in mouse brain and staining was detected throughout the brain, in cortex, hypothalamus, thalamus, hippocampus, brainstem and cerebellum. More specifically, immunostaining was found in areas known to be involved in amino acid sensing and signaling pathways e.g. piriform cortex and hypothalamus. SLC38A9 immunoreactivity co-localized with both GABAergic and glutamatergic neurons, but not with astrocytes. SLC38A9 play a key role in the mTORC1 pathway, and therefore we performed in vivo starvation and high-fat diet studies, to measure gene expression alterations in specific brain tissues and in larger brain regions. Following starvation, Slc38a9 was upregulated in brainstem and cortex, and in anterior parts of the brain (Bregma 3.2 to -2.1mm). After high-fat diet, Slc38a9 was specifically upregulated in hypothalamus, while overall downregulation was noticed throughout the brain (Bregma 3.2 to -8.6mm)

Thermomechanical stability and integrability of an embedded ceramic antenna with an integrated sensor element for wireless reading in harsh environments

This paper reports on the design, manufacturing and evaluation of a small, wirelessly powered and read resonating antenna circuit with an integrated pressure sensor. The work aims at developing miniature devices suitable for harsh environments, where high temperature prevents the use of conventional, silicon-based microdevices. Here, the device is made of alumina with platinum as conducting material. Ceramic green tapes were structured using high-precision milling, metallized using screen printing, and subsequently laminated to form stacks before they were sintered. The device’s frequency shift as a function of temperature was studied up to 900°C. The contributions to the shift both from the thermomechanical deformation of the device at large, and from the integrated and, so far, self-pressurized sensor were sorted out. A total frequency shift of 3200 ppm was observed for the pressure sensor for heating over the whole range. Negligible levels of thermally induced radius of curvature were observed. With three-point bending, a frequency shift of 180 ppm was possible to induce with a curvature of radius of 220 m at a 10 N load. The results indicate that a robust pressure sensor node, which can register pressure changes of a few bars at 900°C and wirelessly transmit the signal, is viable

Putative Membrane-Bound Transporters MFSD14A and MFSD14B Are Neuronal and Affected by Nutrient Availability

Characterization of orphan transporters is of importance due to their involvement in cellular homeostasis but also in pharmacokinetics and pharmacodynamics. The tissue and cellular localization, as well as function, is still unknown for many of the solute carriers belonging to the major facilitator superfamily (MFS) Pfam clan. Here, we have characterized two putative novel transporters MFSD14A (HIAT1) and MFSD14B (HIATL1) in the mouse central nervous system and found protein staining throughout the adult mouse brain. Both transporters localized to neurons and MFSD14A co-localized with the Golgi marker Giantin in primary embryonic cortex cultures, while MFSD14B staining co-localized with an endoplasmic retention marker, KDEL. Based on phylogenetic clustering analyses, we predict both to have organic substrate profiles, and possible involvement in energy homeostasis. Therefore, we monitored gene regulation changes in mouse embryonic primary cultures after amino acid starvations and found both transporters to be upregulated after 3 h of starvation. Interestingly, in mice subjected to 24 h of food starvation, both transporters were downregulated in the hypothalamus, while Mfsdl4a was also downregulated in the brainstem. In addition, in mice fed a high fat diet (HFD), upregulation of both transporters was seen in the striatum. Both MFSD14A and MFSD14B were intracellular neuronal membrane bound proteins, expressed in the Golgi and Endoplasmic reticulum, affected by both starvation and HFD to varying degree in the mouse brain

<i>Slc38a9</i> gene expression in mouse brain following starvation and high-fat diet.

<p>Relative <i>Slc38a9</i> mRNA expression ±SD are plotted and compared with controls (Unpaired t-tests, significance adjusted for multiple testing, *p≤0.049375, **p≤0.009975, ***p≤0.001, n represents technical replicates). (a) Control group (white bars), Starved group (light grey bars), n = 6 for both groups and all tissue tested, except n = 5 for starved group in cerebellum, Brainstem (p = 0.0442), Cerebellum (p = 0.4865), Cortex (p = 0.0055), Hypothalamus (p = 0.9803). (b) Control group (white bars), High fat diet group (dark grey bars), n = 6 for both groups and all tissue tested, Brainstem (p = 0.9111), Cerebellum (p = 0.6745), Cortex (p = 0.5967), Hypothalamus (p = 0.0014). (c) Control group (white bars, (region I, II, III and VI, n = 2, region IV, V and VII, n = 3), Starved group (light grey bars, (n = 3 for all regions except for regions I and VII were n = 2)). (I (p = 0.0310), II (p = 0.0297), III (p = 0.0009), IV (p = 0.0159), V (p = 0.0743), VI (p = 0.6162) and VII (p = 0.8486)). (d) Control group (white bars, (region I, II, III and VI, n = 2, region IV, V and VII, n = 3)), High-fat diet group (dark grey bars, (n = 3 for all brain regions except for region V, n = 2)). (p = 0.0016), II (p = 0.0007), III (p<0.0001), IV (p = 0.0006), V (p = 0.0266), VI (p = 0.0124) and VII (p = 0.0151). (e) Representation of the mouse brain displaying the brain regions I-VII, with corresponding Bregma numbers (mm).</p