YouTube as an information source for bleeding gums: A quantitative and qualitative analysis.

Gum bleeding is a common dental problem, and numerous patients seek health-related information on this topic online. The YouTube website is a popular resource for people searching for medical information. To our knowledge, no recent study has evaluated content related to bleeding gums on YouTube™. Therefore, this study aimed to conduct a quantitative and qualitative analysis of YouTube videos related to bleeding gums. A search was performed on YouTube using the keyword "bleeding gums" from Google Trends. Of the first 200 results, 107 videos met the inclusion criteria. The descriptive statistics for the videos included the time since upload, the video length, and the number of likes, views, comments, subscribers, and viewing rates. The global quality score (GQS), usefulness score, and DISCERN were used to evaluate the video quality. Statistical analysis was performed using the Kruskal-Wallis test, Mann-Whitney test, and Spearman correlation analysis. The majority (n = 69, 64.48%) of the videos observed were uploaded by hospitals/clinics and dentists/specialists. The highest coverage was for symptoms (95.33%). Only 14.02% of the videos were classified as "good". The average video length of the videos rated as "good" was significantly longer than the other groups (p <0.05), and the average viewing rate of the videos rated as "poor" (63,943.68%) was substantially higher than the other groups (p <0.05). YouTube videos on bleeding gums were of moderate quality, but their content was incomplete and unreliable. Incorrect and inadequate content can significantly influence patients' attitudes and medical decisions. Effort needs to be expended by dental professionals, organizations, and the YouTube platform to ensure that YouTube can serve as a reliable source of information on bleeding gums.

Dental Bleaching with Phthalocyanine Photosensitizers: Effects on Dentin Color and Collagen Content.

With the increasing demand for tooth bleaching in esthetic dentistry, its safety has been the focus of a comprehensive body of literature. In this context, the aim of the present study was to evaluate the application effects of pentalysine ß-carbonylphthalocyanine zinc (ZnPc(Lys)5)-mediated photodynamic therapy in dentin bleaching and its effects on dentin collagen. We first established a new and reproducible tooth staining model using dentin blocks stained by Orange II and then bleached with ZnPc(Lys)5 (25 µM) and hydrogen peroxide (10% or 30%). Data were analyzed with one- and two-way ANOVA and a significance level of p < 0.05. ZnPc(Lys)5 effectively bleached the dentin samples to an extent comparable to hydrogen peroxide at either 10% or 30% concentrations. Further studies on the dentin morphology, chemical element distribution, and protein constituents, using an electron microscope, energy dispersive spectroscopy, X-ray photoelectron spectroscopy, and SDS-PAGE, demonstrated that treatment with the photosensitizer preserved the dentin structure and, at the same time, the major organic component, collagen type I. For comparison, hydrogen peroxide (10% or 30%) treatment significantly degraded the collagen protein. This work indicated that the photosensitizer exerts potent bleaching effects on dentin staining; importantly, does not damage dentin and its collagen content; and opens up a new strategy to further explore various photosensitizers for the bleaching of both tooth enamel and dentin.

Expanding the applications of photodynamic therapy-tooth bleaching.

OBJECTIVES: The current tooth bleaching materials are associated with adverse effect. Photodynamic method based on a novel photosensitizer alone, without combining with peroxides, is evaluated for tooth bleaching application. MATERIALS AND METHODS: Teeth samples were randomly divided into 3 groups with different treatment schemes, including negative control group (group A, physiological saline), experimental group (group B, ZnPc(Lys)5), and the positive control group (group C, hydrogen peroxide). Tooth color, surface microhardness, and roughness were determined at baseline, right after the first and second phase of bleaching, as well as 1 week and 1 month post-bleaching. Four samples in each group was randomly selected to evaluate the changes in surface morphology using the scanning electron microscope. RESULTS: The color change values (ΔE) in group B (7.10 ± 1.03) and C (12.22 ± 2.35) were significantly higher than that in group A (0.93 ± 0.30, P < 0.05). Additionally, surface microhardness and roughness were significantly affected in group C, but not in the group A and B. Furthermore, the scanning electron microscope images showed no adverse effect of enamel in the group A and B while the group C demonstrated corrosive changes. CONCLUSIONS: ZnPc(Lys)5 had a satisfactory bleaching effect and is promising to be a new type of tooth bleaching agent. CLINICAL RELEVANCE: The current tooth bleaching materials give a satisfactory clinical outcome and long-term stability, but associated with some adverse reactions. Photosenstizer ZnPc(Lys)5 eliminated the main side effects observed in hydrogen peroxide-based agents on the enamel, and also had a satisfactory bleaching effect and provide a novel selective bleaching scheme for clinical use.

Osteogenic and angiogenic profiles of the palatal process of the maxilla and the palatal process of the palatine bone.

Hard palate consists anteriorly of the palatal process of the maxilla (ppmx) and posteriorly of the palatal process of the palatine (ppp). Currently, palatal osteogenesis is receiving increasing attention. This is the first study to provide an overview of the osteogenesis process of the mouse hard palate. We found that the period in which avascular mesenchymal condensation becomes a vascularized bone structure corresponds to embryonic day (E) 14.5 to E16.5 in the hard palate. The ppmx and ppp differ remarkably in morphology and molecular respects during osteogenesis. Osteoclasts in the ppmx and ppp are heterogeneous. There was a multinucleated giant osteoclast on the bone surface at the lateral-nasal side of the ppmx, while osteoclasts in the ppp were more abundant and adjacent to blood vessels but were smaller and had fewer nuclei. In addition, bone remodeling in the hard palate was asymmetric and exclusively occurred on the nasal side of the hard palate at E18.5. During angiogenesis, CD31-positive endothelial cells were initially localized in the surrounding of palatal mesenchymal condensation and then invaded the condensation in a sprouting fashion. At the transcriptome level, we found 78 differentially expressed genes related to osteogenesis and angiogenesis between the ppmx and ppp. Fifty-five related genes were up/downregulated from E14.5 to E16.5. Here, we described the morphogenesis and the heterogeneity in the osteogenic and angiogenic genes profiles of the ppmx and ppp, which are significant for subsequent studies of normal and abnormal subjects.

Defining the critical period of hedgehog pathway inhibitor-induced cranial base dysplasia in mice.

BACKGROUND: The hedgehog signaling pathway is critical for developmental patterning of the limb, craniofacial and axial skeleton. Disruption of this pathway in mice leads to a series of structural malformations, but the exact role and critical period of the Hh pathway in the early development of the cranial base have been rarely described. RESULTS: Embryos exposed to vismodegib from E7.5, E9.5, and E10.5 had a higher percentage of cranial base fenestra. The peak incidence of hypoplasia in sphenoid winglets and severe craniosynostosis in cranial base synchondroses was observed when vismodegib was administered between E9.5 and E10.5. Cranial base craniosynostosis results from accelerating terminal differentiation of chondrocytes and premature osteogenesis. CONCLUSIONS: We define the critical periods for the induction of cranial base deformity by vismodegib administration at a meticulous temporal resolution. Our findings suggest that the Hh pathway may play a vital role in the early development of the cranial base. This research also establishes a novel and easy-to-establish mouse model of synostosis in the cranial base using a commercially available pathway-selective inhibitor.

Leptin Overexpression in Bone Marrow Stromal Cells Promotes Periodontal Regeneration in a Rat Model of Osteoporosis.

BACKGROUND: Osteoporosis is associated with widespread periodontitis and impaired periodontal healing. However, there is a lack of information about the outcomes of regenerative approaches under the influence of osteoporosis. This study investigates the effect of leptin (LEP) overexpression on the regenerative potential of bone marrow stromal cells (BMSCs) in an osteoporotic rat periodontal fenestration defect model. METHODS: Rat BMSCs were transfected with adenoviruses harboring the human (h)LEP gene. Cell proliferation and osteogenic differentiation were evaluated. A ß-tricalcium phosphate scaffold seeded with transfected cells was implanted into nude mice to investigate ectopic osteogenesis and into an osteoporotic rat defect to study periodontal regeneration. Regenerated periodontal and bone-like tissues were analyzed by histologic methods. RESULTS: hLEP overexpression induced osteogenic differentiation of BMSCs as evidenced by the upregulation of osteogenesis-related genes such as Runt-related transcription factor 2, alkaline phosphatase (ALP), and collagen Type I, as well as increased ALP activity and enhanced mineralization. Mice implanted with hLEP-BMSC-containing scaffolds showed more extensive formation of bone-like tissue than those in other groups. Periodontal defects were also filled to a greater degree when treated with hLEP-BMSCs and contained cementum and a well-organized periodontal ligament after 10 and 28 days. CONCLUSION: hLEP overexpression in BMSCs can stimulate periodontal regeneration in osteoporotic conditions and might be a promising strategy for periodontal regeneration in patients with osteoporosis.

Dental pulp stem cells express tendon markers under mechanical loading and are a potential cell source for tissue engineering of tendon-like tissue.

Postnatal mesenchymal stem cells have the capacity to differentiate into multiple cell lineages. This study explored the possibility of dental pulp stem cells (DPSCs) for potential application in tendon tissue engineering. The expression of tendon-related markers such as scleraxis, tenascin-C, tenomodulin, eye absent homologue 2, collagens I and VI was detected in dental pulp tissue. Interestingly, under mechanical stimulation, these tendon-related markers were significantly enhanced when DPSCs were seeded in aligned polyglycolic acid (PGA) fibre scaffolds. Furthermore, mature tendon-like tissue was formed after transplantation of DPSC-PGA constructs under mechanical loading conditions in a mouse model. This study demonstrates that DPSCs could be a potential stem cell source for tissue engineering of tendon-like tissue.

Increased osteogenesis in osteoporotic bone marrow stromal cells by overexpression of leptin.

Osteoporosis leads to increased bone fractures and net bone loss, in part because of the dysfunction of bone marrow stromal cells (BMSCs). Leptin is an adipokine that plays important roles in many biological processes, including the regulation of the actions of mesenchymal stem cells. Our aim is to investigate the osteogenic effects of leptin in osteoporotic BMSCs in vitro and in vivo. The leptin gene was transferred into BMSCs isolated from osteoporotic rats by using recombinant adenoviruses. Once the gene and protein expression of leptin had been confirmed, MTT assays were performed; leptin overexpression was confirmed not to affect the viability of osteoporotic BMSCs. However, alkaline phosphatase (ALP) activity measurements, Alizarin red staining and analyses by quantitative real-time reverse transcription with the polymerase chain reaction revealed that leptin upregulated ALP activity, mineral deposition and the mRNA levels of runt-related transcription factor 2, ALP and collagen type І. Lastly, the effects of leptin on osteogenic differentiation were assessed in vivo. Cells transfected with leptin exhibited increased osteogenic differentiation and enhanced formation of bone-like structures. This study thus reveals, for the first time, that the overexpression of leptin in osteoporotic BMSCs (1) enhances their capacity to differentiate into osteoblasts and to form bone-like tissue and (2) might be a useful skeletal regenerative therapy in osteoporotic patients.

Augmented BMPRIA-mediated BMP signaling in cranial neural crest lineage leads to cleft palate formation and delayed tooth differentiation.

The importance of BMP receptor Ia (BMPRIa) mediated signaling in the development of craniofacial organs, including the tooth and palate, has been well illuminated in several mouse models of loss of function, and by its mutations associated with juvenile polyposis syndrome and facial defects in humans. In this study, we took a gain-of-function approach to further address the role of BMPR-IA-mediated signaling in the mesenchymal compartment during tooth and palate development. We generated transgenic mice expressing a constitutively active form of BmprIa (caBmprIa) in cranial neural crest (CNC) cells that contributes to the dental and palatal mesenchyme. Mice bearing enhanced BMPRIa-mediated signaling in CNC cells exhibit complete cleft palate and delayed odontogenic differentiation. We showed that the cleft palate defect in the transgenic animals is attributed to an altered cell proliferation rate in the anterior palatal mesenchyme and to the delayed palatal elevation in the posterior portion associated with ectopic cartilage formation. Despite enhanced activity of BMP signaling in the dental mesenchyme, tooth development and patterning in transgenic mice appeared normal except delayed odontogenic differentiation. These data support the hypothesis that a finely tuned level of BMPRIa-mediated signaling is essential for normal palate and tooth development.

Functional redundancy between human SHOX and mouse Shox2 genes in the regulation of sinoatrial node formation and pacemaking function.

The homeodomain transcription factor Shox2 plays a crucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nkx2.5, as demonstrated by failed differentiation of SAN in Shox2 null mice. The SHOX (short stature homeobox) gene family consists of two closely related members, SHOX and SHOX2 in humans, but a SHOX ortholog does not exist in the mouse genome. These two genes exhibit overlapping and distinct expression patterns in many developing organs but whether they share functional redundancy is not known. In this study, we set to investigate possible functional redundancy between SHOX and SHOX2 in vitro and in vivo. We first showed that human SHOX and SHOX2 and mouse Shox2 possess similar transcriptional repressive activities in cell cultures, particularly the repressive effects on the Nkx2.5 promoter activity. We further created an SHOX/Shox2 knock-in mouse line (replacement of Shox2 with SHOX, referred as Shox2(KI/KI)). Mice carrying the hypomorphic Shox2(KI+Neo/KI+Neo) allele exhibit bradycardia and arrhythmia and die a few days after birth. However, mice carrying the Shox2(KI/KI) allele grow to adulthood. Physiological, histological, and molecular analyses demonstrate a fully developed SAN and normal pacemaking function in Shox2(KI/KI) mice. Our results demonstrate a functional redundancy between human SHOX and mouse Shox2 in the regulation of SAN formation and pacemaking function in addition to several other organs. The SHOX/Shox2 dose appears to be critical for normal pacemaking function.

Wnt5a regulates growth, patterning, and odontoblast differentiation of developing mouse tooth.

Wnt/ß-catenin signaling is essential for tooth development beyond the bud stage, but little is known about the role of non-canonical Wnt signaling in odontogenesis. Here we compared the expression of Wnt5a, a representative of noncanonical Wnts, with that of Ror2, the Wnt5a receptor for non-canonical signaling, in the developing tooth, and analyzed tooth phenotype in Wnt5a mutants. Wnt5a-deficient mice exhibit retarded tooth development beginning from E16.5, leading to the formation of smaller and abnormally patterned teeth with a delayed odontoblast differentiation at birth. These defects are associated with upregulated Axin2 and Shh expression in the dental epithelium and reduced levels of cell proliferation in the dental epithelium and mesenchyme. Retarded tooth development and defective odontoblast differentiation were also observed in Ror2 mutant mice. Our results suggest that Wnt5a regulates growth, patterning, and odontoblast differentiation during odontogenesis, at least partially by modulating Wnt/ß-catenin canonical signaling.

BmprIa is required in mesenchymal tissue and has limited redundant function with BmprIb in tooth and palate development.

The BMP signaling plays a pivotal role in the development of craniofacial organs, including the tooth and palate. BmprIa and BmprIb encode two type I BMP receptors that are primarily responsible for BMP signaling transduction. We investigated mesenchymal tissue-specific requirement of BmprIa and its functional redundancy with BmprIb during the development of mouse tooth and palate. BmprIa and BmprIb exhibit partially overlapping and distinct expression patterns in the developing tooth and palatal shelf. Neural crest-specific inactivation of BmprIa leads to formation of an unusual type of anterior clefting of the secondary palate, an arrest of tooth development at the bud/early cap stages, and severe hypoplasia of the mandible. Defective tooth and palate development is accompanied by the down-regulation of BMP-responsive genes and reduced cell proliferation levels in the palatal and dental mesenchyme. To determine if BmprIb could substitute for BmprIa during tooth and palate development, we expressed a constitutively active form of BmprIb (caBmprIb) in the neural crest cells in which BmprIa was simultaneously inactivated. We found that substitution of BmprIa by caBmprIb in neural rest cells rescues the development of molars and maxillary incisor, but the rescued teeth exhibit a delayed odontoblast and ameloblast differentiation. In contrast, caBmprIb fails to rescue the palatal and mandibular defects including the lack of lower incisors. Our results demonstrate an essential role for BmprIa in the mesenchymal component and a limited functional redundancy between BmprIa and BmprIb in a tissue-specific manner during tooth and palate development.

Application of autologous periosteal cells for the regeneration of class III furcation defects in Beagle dogs.

The aim of this study was to evaluate the healing of class III furcation defects following transplantation of autogenous periosteal cells combined with beta-tricalcium phosphate (beta-TCP). Periosteal cells obtained from Beagle dogs' periosteum explant cultures, were inoculated onto the surface of beta-TCP. Class III furcation defects were created in the mandibular premolars. Three experimental groups were used to test the defects' healing: group A, beta-TCP seeded with periosteal cells were transplanted into the defects; group B, beta-TCP alone was used for defect filling; and group C, the defect was without filling materials. Twelve weeks post surgery, the tissue samples were collected for histology, immunohistology and X-ray examination. It was found that both the length of newly formed periodontal ligament and the area of newly formed alveolar bone in group A, were significantly increased compared with both group B and C. Furthermore, both the proportion of newly formed periodontal ligament and newly formed alveolar bone in group A were much higher than those of group B and C. The quantity of cementum and its percentage in the defects (group A) were also significantly higher than those of group C. These results indicate that autogenous periosteal cells combined with beta-TCP application can improve periodontal tissue regeneration in class III furcation defects.

Effects of DMEM and RPMI 1640 on the biological behavior of dog periosteum-derived cells.

Periosteum-derived cells (PDCs) are being extensively studied as potential tissue engineering seed cells and have demonstrated tremendous promise to date. There is convincing evidence that culture medium could modulate the biological behavior of cultured cells. In this study, we investigate the effects of DMEM (low glucose) and RPMI 1640 on cell growth and cell differentiation of PDCs in vitro. PDCs isolated from Beagle dogs were maintained in DMEM and RPMI 1640, respectively. Then, the cell migration rate of periosteum tissues was analyzed. PDCs of the third passage were harvested for the study of proliferation and osteogenic activity. Proliferation was detected by MTT assay. Alkaline phosphatase activity and mineralized nodules were measured to investigate osteogenic differentiation. Our data demonstrated that DMEM induced alkaline phosphatase activity and strongly stimulated matrix mineralization in cell culture, while similar cell migration rates and proliferation behaviors were observed in the two culture conditions. Interestingly, the osteogenic differentiation of PDCs could be enhanced in DMEM compared with that in RPMI 1640. Thus, it can be ascertained that DMEM may serve as a suitable culture condition allowing osteogenic differentiation of dog PDCs.