Ai Mei Chou

Purpose To systematically evaluate the diagnostic efficacy of intraoral radiographs and evidence supporting the indications for taking of intraoral radiographs in children in the following five clinical categories: caries, pathological conditions (including acute odontogenic infections and periodontal disease), dental/developmental anomalies, dental trauma, and enhancement of comfort/technique for taking radiographs in children. This was carried out to facilitate the updating of existing European Academy of Paediatric Dentistry (EAPD) guidelines on dental radiography in pediatric dentistry. Methods A systematic electronic literature search was conducted on Cochrane Library (1992–24 July 2018), MEDLINE (PubMed, 1946–24 July 2018), EMBASE (Embase.com, 1974–24 July 2018) and Scopus (pre-1970–24 July 2018). Hand search of handbooks and grey literature search was also performed. Study screening and study inclusions were agreed upon by three authors. Data extraction, and methodological quality and risk of bias assessment were carried out in duplicate for each of the included studies. Results A total of 9581 papers were identified. Following the primary and secondary assessment process, 36 papers were included in the final analysis. The included studies were further categorized into five main clinical categories for analysis: caries, pathological conditions, dental/developmental anomalies, dental trauma and comfort/technique-related studies. Only one paper was found to be of good quality and at low risk of bias; while, 9 papers were found of be at moderate risk of bias and 26 papers were at high risk of bias. Meta-analysis was not possible for any of the aforementioned clinical situations, and only a narrative synthesis was done. Conclusion There is insufficient high-quality evidence for the use of intraoral radiographs in pediatric dentistry and current guidelines are based largely on expert opinion. There is a clear need for well-conducted and standardized studies regarding the use of intraoral radiography in pediatric dentistry.

The insulin receptor substrate of 53 kDa, IRSp53, is an adaptor protein that works with activated GTPases, Cdc42 and Rac, to modulate actin dynamics and generate membrane protrusions in response to cell signaling. Adult mice that lack IRSp53 fail to regulate synaptic plasticity and exhibit hippocampus-associated learning deficiencies. Here, we show that 60% of IRSp53 null embryos die at mid to late gestation, indicating a vital IRSp53 function in embryonic development. We find that IRSp53 KO embryos displayed pleiotropic phenotypes such as developmental delay, oligodactyly and subcutaneous edema, and died of severely impaired cardiac and placental development. We further show that double knockout of IRSp53 and its closest family member, IRTKS, resulted in exacerbated placental abnormalities, particularly in spongiotrophoblast differentiation and development, giving rise to complete embryonic lethality. Hence, our findings demonstrate a hitherto under-appreciated IRSp53 function in embryonic development, and further establish an essential genetic interaction between IRSp53 and IRTKS in placental formation.

Rif induces dorsal filopodia but the signaling pathway responsible for this has not been identified. We show here that Rif interacts with the I-BAR family protein IRTKS (also known as BAIAP2L1) through its I-BAR domain. Rif also interacts with Pinkbar (also known as BAIAP2L2) in N1E-115 mouse neuroblastoma cells. IRTKS and Rif induce dorsal membrane ruffles and filopodia. Dominant-negative Rif inhibits the formation of IRTKS-induced morphological structures, and Rif activity is blocked in IRTKS-knockout (KO) cells. To further define the Rif–IRTKS signaling pathway, we identify Eps8 and WAVE2 (also known as WASF2) as IRTKS interactors. We find that Eps8 regulates the size and number of dorsal filopodia and membrane ruffles downstream of Rif–IRTKS signaling, whereas WAVE2 modulates dorsal membrane ruffling. Furthermore, our data suggests that Tir, a protein essential for enterohemorrhagic Escherichia coli infection, might compete for Rif for interaction with the I-BAR domain of IRTKS. Based on this evidence, we propose a model in which Rho family GTPases use the I-BAR proteins, IRSp53 (also known as BAIAP2), IRTKS and Pinkbar, as a central mechanism to modulate cell morphology.

Transducer of Cdc42-dependent actin assembly (Toca-1) consists of an F-BAR domain, a Cdc42 binding site and an SH3 domain. Toca-1 interacts with N-WASP, an activator of actin nucleation that binds Cdc42. Cdc42 may play an important role in regulating Toca-1 and N-WASP functions. We report here that the cellular expression of Toca-1 and N-WASP induces membrane tubulation and the formation of motile vesicles. Marker and uptake analysis suggests that the tubules and vesicles are associated with clathrin-mediated endocytosis. Forster resonance energy transfer (FRET) and Fluorescence Lifetime Imaging Microscopy (FLIM) analysis shows that Cdc42, N-WASP and Toca-1 form a trimer complex on the membrane tubules and vesicles and that Cdc42 interaction with N-WASP is critical for complex formation. Modulation of Cdc42 interaction with Toca-1 and/or N-WASP affects membrane tubulation, vesicle formation and vesicle motility. Thus Cdc42 may influence endocytic membrane trafficking by regulating the formation and activity of the Toca-1/N-WASP complex.

This paper reports on a 2-phase study of a novel membrane-scaffold graft construct, its ability to support periodontal ligament fibroblast (PDLF) and alveolar osteoblast (AO) growth in vitro, and its use for tissue engineering a PDL-AO interface in vivo. Human PDLFs were seeded onto perforated poly(epsilon-caprolactone) membranes (n=30) at 78,000 cells/cm2; human AOs were seeded on poly(epsilon-caprolactone) scaffolds (n=30) with fibrin glue at 625,000 cells/cm3. Cell attachment, morphology, viability, and metabolic activity were monitored for 3 weeks in vitro. Subsequently, cell-seeded membrane-scaffold constructs (experimental group, n=9) and nonseeded constructs (control group, n=4) assembled with fibrin glue were implanted subcutaneously into 7 athymic mice for 4 weeks. PDLFs formed confluent layers on membranes, whereas AOs produced mineralized matrices within scaffolds upon osteoinduction in vitro. Well-vascularized tissue formation was observed after implantation. Integration at the membrane-scaffold interface was enhanced in the experimental group. Type I collagen, type III collagen, fibronectin, and vitronectin were found adjacent to membranes and within constructs. Bone sialoprotein expression and bone formation were undetectable. Membrane perforation and scaffold porosity facilitated tissue integration and vascularization at the construct-recipient site. However, the interaction between PDLF and AO could have interfered with osteogenesis at the interface of soft and mineralizing tissues. Both matrices supported PDLF and AO attachment and proliferation in vitro. The membrane-scaffold construct facilitated tissue growth and vascularization while providing strength and form in vivo.

This study investigated the human alveolar osteoblasts (AOs) proliferation and extracellular matrix formation at seeding density of 0.05, 0.1, 0.2, 0.4, and 0.8 million (M) per 3 × 4 × 4 mm³ on medical grade polycaprolactone‐tricalcium phosphate (mPCL‐TCP) scaffolds designed for bone regeneration. Over 80–90% of the initial seeded cells were retained in the scaffolds after 24 h. AOs bridged over pores at density of 0.2M/scaffold and below, but formed cell balls at density of 0.4M/scaffold and above. At seeding density of 0.2M and below, cell proliferation increased with time having DNA content peaked to 1600 ng/scaffold at day 21 and 28, respectively, whereas at 0.4 and 0.8M, the corresponding DNA content decreased to 1600 ng in 28 days. At day 7, higher alkaline phosphatase (ALP) activity and higher osteocalcin (OCN) secretion were detected at 0.2M/scaffold and below. After 28 days, multilayered cell‐sheet formation and collagen fibers were observed at all densities. ALP and OCN in matrix and mineral nodules were found mainly at the border of AOs‐scaffold construct. These findings demonstrated that the density of 0.2M and below per 3 × 4 × 4 mm³ scaffold resulted in better cell proliferation and extracellular matrix synthesis, potentially resulting in better mineralized tissue formation. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006