Evaluating Morphology of the Pterygomaxillary Junction and Its Association With the Orbit in Different Facial Skeletal Relationships.

PURPOSE: The etiology for blindness after Le Fort I osteotomy is poorly understood. The authors propose that a study of the morphology and anatomical relationship of the pterygomaxillary junction to orbital vital structures may be crucial for understanding the possible etiology. MATERIALS AND METHODS: This retrospective observational study involved analysis of data procured from computed tomography scans of individuals who were categorized into 4 groups based on their skeletal characteristics: skeletal Class I, II, and III and cleft lip and palate (CLP). The outcome variables included i) the height, width, and thickness of the pterygomaxillary junction (PTMJ) which represent its morphology and ii) distance of the PTMJ to the superior orbital fissure and optic canal, to demonstrate its proximity to orbital vital structures. Primary outcome measures were to i) compare variance of the outcome variables across groups, ii) determine association between PTMJ morphology and its proximity to the orbit, and iii) determine association between skeletal morphology and the outcome variables. Data were analyzed using descriptive and inferential statistics to study variance and association. RESULTS: Forty patients (80 sides) were divided into 4 groups. The CLP group demonstrated maximum height and thickness of the PTMJ, whereas the Class II group demonstrated the minimum (P < .001 and P = .001, respectively). The CLP group demonstrated the closest proximity of the PTMJ to orbital vital structures (P < .001), with Class II being the farthest (P < .001). There was a weak positive correlation between the PTMJ height and its thickness and width, whereas a moderate negative correlation was seen between the PTMJ height and its distance from the optic canal and superior orbital fissures (P < .001). CONCLUSIONS: Morphology of the PTMJ varies with facial skeletal relationship and also influences the relationship of the PTMJ with the orbital vital structures. This may be critical in understanding the pathophysiology of blindness after Le Fort I osteotomies.

Three-Dimensional Geometric Morphometry of Facial Soft Tissue Changes After Bilateral Sagittal Split Ramus Osteotomy.

ABSTRACT: This study aimed to evaluate the performance of geometric morphometry (GM) to assess the changes in facial soft tissue after orthognathic surgery. Subjects were 27 patients (skeletal class III) who underwent bilateral sagittal split ramus osteotomy and 27 volunteers as a control group. Computed tomography images of each patient were obtained before surgery (T0) and 6 months after surgery (T1). Computed tomography images of 27 volunteers (skeletal class I) were also obtained as a control group. Using a three-dimensional (3D) modeling software, 3D models were created and exported to a 3D surface analyzing software for geometric morphometry and principal component (PC) analysis. Significant differences in facial soft tissue were found in the first and second of 15 PC. The first PC represented variation in the lower facial height, and the second PC represented variation in the anterior-posterior position of the chin. Comparing the pre- and post-operative images, they illustrated that lower facial height was decreased, and the chin and lower lip moved posteriorly. Geometric morphometry showed to be a successful tool to isolate surgery-related changes from interindividual morphological variations.

Bone morphogenetic protein induces bone invasion of melanoma by epithelial-mesenchymal transition via the Smad1/5 signaling pathway.

Oral malignant melanoma, which frequently invades the hard palate or maxillary bone, is extremely rare and has a poor prognosis. Bone morphogenetic protein (BMP) is abundantly expressed in bone matrix and is highly expressed in malignant melanoma, inducing an aggressive phenotype. We examined the role of BMP signaling in the acquisition of an aggressive phenotype in melanoma cells in vitro and in vivo. In five cases, immunohistochemistry indicated the phosphorylation of Smad1/5 (p-Smad1/5) in the nuclei of melanoma cells. In the B16 mouse and A2058 human melanoma cell lines, BMP2, BMP4, or BMP7 induces morphological changes accompanied by the downregulation of E-cadherin, and the upregulation of N-cadherin and Snail, markers of epithelial-mesenchymal transition (EMT). BMP2 also stimulates cell invasion by increasing matrix metalloproteinase activity in B16 cells. These effects were canceled by the addition of LDN193189, a specific inhibitor of Smad1/5 signaling. In vivo, the injection of B16 cells expressing constitutively activated ALK3 enhanced zygoma destruction in comparison to empty B16 cells by increasing osteoclast numbers. These results suggest that the activation of BMP signaling induces EMT, thus driving the acquisition of an aggressive phenotype in malignant melanoma.

Enhanced junctional epithelial permeability in TRPV4-deficient mice.

BACKGROUND AND OBJECTIVE: As the interface between the oral cavity and the teeth, the junctional epithelial barrier is critical for gingival defense. The junctional epithelium is subject to mechanical stresses from biting force or external insults such as bacterial attacks, but little is known about the effects of mechanical stimuli on epithelial functions. Transient receptor potential vanilloid 4 (TRPV4) functions as a mechanosensitive nonselective cation channel. In the present study, based on marked expression of TRPV4 in the mouse junctional epithelium, we aimed to clarify the putative links between TRPV4 and junctional complexes in the junctional epithelium. METHODS AND RESULTS: Histological observations revealed that the junctional epithelium in TRPV4-deficient (TRPV4-/- ) mice had wider intercellular spaces than that in wild-type (TRPV4+/+ ) mice. Exogenous tracer penetration in the junctional epithelium was greater in TRPV4-/- mice than in TRPV4+/+ mice, and immunoreactivity for adherens junction proteins was suppressed in TRPV4-/- mice compared with TRPV4+/+ mice. Analysis of a mouse periodontitis model showed greater bone volume loss in TRPV4-/- mice compared with TRPV4+/+ mice, indicating that an epithelial barrier deficiency in TRPV4-/- mice may be associated with periodontal complications. CONCLUSION: The present findings identify a crucial role for TRPV4 in the formation of adherens junctions in the junctional epithelium, which could regulate its permeability. TRPV4 may be a candidate pharmacological target to combat periodontal diseases.

Identifying Differences Between a Straight Face and a Posed Smile Using the Homologous Modeling Technique and the Principal Component Analysis.

Recently, a homologous modeling method was developed to simulate 3D human body forms, which can visualize principal component analysis (PCA) results and facilitate its detailed comparison with results of previous method. Herein, we aimed to construct a homologous model of the face to identify differences between a straight face and a posed smile. Thirty-eight volunteers (19 males and 19 females, 38 straight faces and 38 posed smiles) with no medical history associated with a posed smile were enrolled. Three-dimensional images were constructed using the Homologous Body Modeling software and the HBM-Rugle; 9 landmarks were identified on the 3D-model surfaces. The template model automatically fitted into an individually scanned point cloud of the face by minimizing external and internal energy functions. Faces were analyzed using PCA; differences between straight faces and posed smiles were analyzed using paired t tests. Contribution of the most important principal component was 23.8%; 8 principal components explained >75% of the total variance. A significant difference between a straight face and a posed smile was observed in the second and the fourth principal components. The second principal component images revealed differences between a straight face and a posed smile and changes around the chin area with regard to length, shape, and anteroposterior position. Such changes were inclusive of individual differences. However, the fourth principal component image only revealed differences between a straight face and a posed smile; observed differences included simultaneous shortening of upper and lower eyelid length, evaluation of the nasal ala ase, swelling of the cheek area, and elevation of the mouth angle. Although these results were clinically apparent, we believe that this article is the first to statistically verify the same.Consequently, the homologous model technique and PCA are useful for evaluation of the facial soft-tissue changes.

Targeting ID2 expression triggers a more differentiated phenotype and reduces aggressiveness in human salivary gland cancer cells.

Inhibitors of DNA-binding (ID) proteins are negative regulators of basic helix-loop-helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. We previously determined that ID1 was highly expressed in aggressive salivary gland cancer (SGC) cells in culture. Here, we show that ID2 is also expressed in aggressive SGC cells. ID2 knockdown triggers important changes in cell behavior, that is, it significantly reduces the expression of N-cadherin, vimentin and Snail, induces E-cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. Moreover, ID2 knockdown almost completely suppresses invasion and the expression of matrix metalloproteinase 9. In conclusion, ID2 expression maintains an aggressive phenotype in SGC cells, and ID2 repression triggers a reduction in cell aggressiveness. ID2 therefore represents a potential therapeutic target during SGC progression. ID proteins are negative regulators of basic helix-loop-helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. ID2 knockdown triggers important changes in cell behavior, that is, it significantly reduces the expression of N-cadherin, vimentin and Snail, induces E-cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. ID2 therefore represents a potential therapeutic target during SGC progression.

Efficient regulation of branching morphogenesis via fibroblast growth factor receptor 2c in early-stage embryonic mouse salivary glands.

Salivary gland (SG) defects have a wide range of health implications, including xerostomia, bacterial infections, and oral health issues. Branching morphogenesis is critical for SG development. A clear understanding of the mechanisms underlying this process will accelerate SG regeneration studies. Fibroblast growth factor receptor 2 (FGFR2) interacts with multiple fibroblast growth factors (FGFs), which promote development. FGFR2 consists of two isoforms, FGFR2b and FGFR2c. FGFR2b is critical for SG development, but little is known about the expression and function of FGFR2c. We investigated the expression of all FGFR family members in fetal SGs between embryonic day 12.5 (E12.5) and E18.5. Based on RT-PCR, we observed an increase in the expression of not only Fgfr2b, but also Fgfr2c in early-stage embryonic mouse SGs, suggesting that FGFR2c is related to SG development. The branch number decreased in response to exogenous FGF2 stimulation, and this effect was suppressed by a mouse anti-FGFR2c neutralizing antibody (NA) and siRNA targeting FGFR2c, whereas FGFR2b signaling was not inhibited. Moreover, the expression of marker genes related to EMT was induced by FGF2, and this expression was suppressed by the NA. These results suggested that branching morphogenesis in SGs is regulated by FGFR2c, in addition to FGFR2b. Interestingly, FGFR2c signaling also led to increased fgf10 expression, and this increase was suppressed by the NA. FGFR2c signaling regulates branching morphogenesis through the activation of FGFR2b signaling via increased FGF10 autocrine. These results provide new insight into the mechanisms by which crosstalk between FGFR2b and FGFR2c results in efficient branching morphogenesis.

Primary wound closure after tooth extraction for prevention of medication-related osteonecrosis of the jaw in patients under denosumab.

OBJECTIVES: Some recent reports have indicated that local infection causes osteonecrosis of the jaw and described that tooth extraction may not be a direct cause of developing medication-related osteonecrosis of the jaw (MRONJ) in patients receiving antiresorptive medications. Tooth extraction and elimination of the source of infection are expected to reduce the risk of developing MRONJ. However, there is no data regarding prevention for developing osteonecrosis of the jaw in patients receiving denosumab. Therefore, the aim of this study was to investigate the outcome of tooth extractions with proper wound closure in patients receiving denosumab. PATIENTS AND METHODS: Forty teeth in 19 patients treated with denosumab therapy were extracted under preoperative intravenous antibiotics. Patients who had already developed MRONJ in the extraction sites or who had a history of radiation therapy were excluded. During surgery, bone edges were smoothed and all wounds were closed using the double-layered technique. RESULTS: Thirty-seven extraction sites (92.5 %) in 17 out of 19 patients (89.5 %) were healed. However, three extraction sites in two patients had complications; one patient had exposed bone and developed MRONJ (stage 1) and the other developed a mucosa fistula. Additional surgical procedures were performed and all wounds were completely healed. CONCLUSIONS: Tooth extractions in patients receiving denosumab can be performed in an appropriate manner and result in good outcomes. CLINICAL RELEVANCE: This study indicated that tooth extraction with proper wound closure to avoid secondary infection may be effective for the prevention of MRONJ even in high-risk patients.

Involvement of the T-box transcription factor Brachyury in early-stage embryonic mouse salivary gland.

The mouse submandibular gland (SMG) is important organ for embryonic development, and branching morphogenesis is regulated by many molecules containing transcription factors. Real-time reverse transcriptase polymerase chain reaction revealed that the expression of Brachyury increased in the SMG and peaked between E12.5-E13.5, concomitant with the early stage of branching morphogenesis. The expression of Brachyury in SMG rudiments between E12.5-E13.5 was confirmed by western blotting. In addition, fibronectin and Btbd7 (regulated by fibronectin), which are both essential for cleft formation, were expressed strongly during the same period. The Sox2 and Wnt3a, which regulate cell growth, were also expressed strongly during E12.5-E13.5. On the other hand, cleft formation and branching morphogenesis was suppressed by knockdown of Brachyury gene, suggesting that Brachyury plays a central role in regulating cell growth and cleft formation in early-stage embryonic mouse salivary gland development.

Acceleration of bone development and regeneration through the Wnt/ß-catenin signaling pathway in mice heterozygously deficient for GSK-3ß.

Glycogen synthase kinase (GSK)-3ß plays an important role in osteoblastogenesis by regulating the Wnt/ß-catenin signaling pathway. Therefore, we investigated whether GSK-3ß deficiency affects bone development and regeneration using mice heterozygously deficient for GSK-3ß (GSK-3ß(+/-)). The amounts of ß-catenin, c-Myc, cyclin D1, and runt-related transcription factor-2 (Runx2) in the bone marrow cells of GSK-3ß(+/-) mice were significantly increased compared with those of wild-type mice, indicating that Wnt/ß-catenin signals were enhanced in GSK-3ß(+/-) mice. Microcomputed tomography of the distal femoral metaphyses demonstrated that the volumes of both the cortical and trabecular bones were increased in GSK-3ß(+/-) mice compared with those in wild-type mice. Subsequently, to investigate the effect of GSK-3ß deficiency on bone regeneration, we established a partial bone defect in the femur and observed new bone at 14 days after surgery. The volume and mineral density of the new bone were significantly higher in GSK-3ß(+/-) mice than those in wild-type mice. These results suggest that bone formation and regeneration in vivo are accelerated by inhibition of GSK-3ß, probably through activation of the Wnt/ß-catenin signaling pathway.

Does skeletal surgery for asymmetric mandibular prognathism influence the soft tissue contour and thickness?

PURPOSE: The purpose of the present study was to investigate whether asymmetric mandibular prognathism accompanies a fundamental difference in soft tissue thickness and whether asymmetric mandibular setback surgery would influence the contour and thickness of the soft tissue of the chin. MATERIALS AND METHODS: The present retrospective study included skeletal class III patients with significant mandibular chin deviation greater than 6 mm at the pogonion, who had undergone cone-beam computed tomography before and 6 months after surgery during a 2-year period. The predictor variables were timing (pre- and postoperatively) and side (asymmetric vs contralateral). The outcome measures were the hard and soft tissue contours and soft tissue thickness of the chin at the infradentale, B-point, and pogonion level evaluated with reformatted computed tomography images. The study variables were statistically compared using regression model and correlation analysis. RESULTS: The present study consisted of 20 patients (10 males and 10 females; average age 20.2 years; range, 18 to 25). Preoperatively, the chin deviation side showed a more prominent hard and soft tissue outline but had a thinner soft tissue thickness, which camouflaged the hard tissue asymmetry. After surgery, the hard and soft tissue outline was greatly improved, and the soft tissue thickness had become nearly symmetric. Most of the soft tissue thickness changes correlated negatively with the hard tissue changes. CONCLUSIONS: Asymmetric mandibular prognathism accompanied the 3-dimensional soft tissue contour and thickness asymmetry. Because the soft tissue responds favorably after skeletal surgery, the correction of 3-dimensional asymmetry of bone should be emphasized in patients with asymmetric mandibular prognathism.

Regulated interaction of protein phosphatase 1 and protein phosphatase 2A with phospholipase C-related but catalytically inactive protein.

Protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A) are major members of the protein serine/threonine phosphatase families. We have identified PP1 and PP2A as interacting partners of PRIP (phospholipase C-related but catalytically inactive protein), a protein isolated in our laboratory. We first investigated the interaction of PRIP with two phosphatases, using purified recombinant proteins. PRIP immobilized on beads pulled down the catalytic subunits of both PP1 and PP2A, indicating that the interactions were in a direct manner, and the binding of PP1 and the binding of PP2A to PRIP were mutually exclusive. Site-directed mutagenesis experiments revealed that the binding sites for PP1 and PP2A on PRIP were not identical, but similar. Phosphorylation of PRIP by protein kinase A (PKA) resulted in the weakened binding of PP1, but not PP2A. Rather, the dissociation of PP1 from PRIP by phosphorylation accompanied the strengthened binding of PP2A in in vitro experiments. This regulation of binding of PP1 and PP2A to PRIP by PKA-dependent phosphorylation was also observed in living cells treated with forskolin or isoproterenol. These results suggested that PRIP directly interacts with the catalytic subunits of two distinct phosphatases in a mutually exclusive manner and the interactions are regulated by phosphorylation, thus functioning as a scaffold to regulate the activities and subcellular localizations of both PP1 and PP2A in phospho-dependent cellular signaling.

Transfection of hypoxia-inducible factor-1 decoy oligodeoxynucleotides suppresses expression of vascular endothelial growth factor in oral squamous cell carcinoma cells.

Vasculature development is thought to be an important aspect in the growth and metastasis of solid tumors. Among the many angiogenic factors produced by tumor cells, vascular endothelial growth factor (VEGF) is considered to play a key role in angiogenic processes. VEGF synthesis is modulated by hypoxia-inducible factor-1 (HIF-1) function within the hypoxic microenvironment of growing cancer tissue. To inhibit HIF-1 activation, oligodeoxynucleotides (ODNs) were synthesized and transferred with either the consensus sequence for HIF-1 binding or a mutated form of this sequence. If we could transfer a large number of ODNs into the cancer cell nucleus, activated HIF-1 might bind to the ODNs, resulting in inhibition of hypoxia-induced VEGF synthesis. We transferred these ODNs into cultured oral squamous cell carcinoma cells (SAS cells) using the hemagglutinating virus of Japan (HVJ)-liposome method. Hypoxia-mediated expression of VEGF by cancer cells was suppressed by transfection of HIF-1 decoy ODNs, but not by mutated HIF-1 decoy ODNs. HIF-1 decoy ODN transfection also inhibited VEGF protein synthesis. These results suggest that transfection with HIF-1 decoy ODNs is effective for regulating tumor growth by reducing VEGF.

The effect of simple heat treatment on apatite formation on grit-blasted/acid-etched dental Ti implants already in clinical use.

Grit-blasted/acid-etched titanium dental implants have a moderately roughened surface that is suitable for cell adhesion and exhibits faster osseointegration. However, the roughened surface does not always maintain stable fixation over a long period. In this study, a simple heat treatment at 600°C was performed on a commercially available dental Ti implant with grit-blasting/acid-etching, and its effect on mineralization capacity was assessed by examining apatite formation in a simulated body fluid (SBF). The as-purchased implant displayed a moderately roughened surface at the micrometer scale. Its surface was composed of titanium hydride accompanied by a small amount of alumina particles derived from the grit-blasting. Heat treatment transformed the titanium hydride into rutile without evidently changing the surface morphology. The immersion in SBF revealed that apatite formed on the heated implant at 7 days. Furthermore, apatite formed on the Ti rod surface within 1 day when the metal was subjected to acid and heat treatment without blasting. These indicate that apatite formation was conferred on the commercially available dental implant by simple heat treatment, although its induction period was slightly affected by alumina particles remaining on the implant surface. The heat-treated implant should achieve stronger and more stable bone bonding due to its apatite formation.

Evaluation of pterygomaxillary anatomy using computed tomography: are there any structural variations in cleft patients?

PURPOSE: Structural characteristics of the pterygomaxillary region in patients with cleft lip and palate (CLP) have not been fully investigated. This study aimed to evaluate the regional anatomy of the pterygomaxillary junction of patients with CLP using computed tomography. MATERIALS AND METHODS: The pterygomaxillary structures of patients with unilateral or bilateral CLP were compared with those of a control group using axial computed tomography. The thickness and width of the pterygoid plate, the distance from the greater palatine foramen to the lateral pterygomaxillary junction, the lateral and medial pterygoid plate lengths, and the maxillary posterior transverse width were investigated with axial computed tomography just beneath the level of the inferior nasal concha and approximately 3 to 5 mm above the nasal floor. The difference between the cleft and noncleft sides or the right and left sides of each group and the measurement differences between the groups were statistically compared. RESULTS: The study group was composed of 14 patients with unilateral CLP and 6 with bilateral CLP, and the control group were 20 age- and gender-matched patients with skeletal Class III without CLP. Patients with unilateral CLP and those with bilateral CLP were statistically equivalent for all radiographic variables. In patients with CLP, the width of the pterygomaxillary region and the greater palatine foramen region were on average 1.5 to 1.8 mm larger than in control patients (P < .05). Lateral pterygoid plate length and maxillary posterior transverse width were similar in the 2 groups. However, the patients with CLP showed a 2.3-mm shorter medial pterygoid length (P < .05). CONCLUSION: Patients with CLP had larger and thicker pterygomaxillary dimensions, and the results imply that careful attention to pterygomaxillary anatomy is needed in patients with CLP undergoing Le Fort I surgery.

Characteristics of craniofacial morphology and factors affecting them in patients with isolated cleft palate.

BACKGROUND: Myriad maxillo-mandibular occlusal relationships are observed in patients with isolated cleft palate (ICP), unlike in patients with other cleft types, such as cleft lip and palate. OBJECTIVES: This study aimed to categorise the characteristics of craniofacial morphology in patients with ICP, and investigate the clinical factors affecting these categorised morphological characteristics. METHODS: Thirty-six girls with ICP (age (mean ± SD): 5.36 ± 0.36 years) underwent cephalometric measurement. Their craniofacial morphology was categorised using cluster analysis. Profilograms were created and superimposed onto the standard Japanese profilograms to visualise the morphological characteristics of each group (cluster). The mean values and variations in the linear and angular measurements of each group were compared with the Japanese standards and statistically analysed using Dunnett's test after the analysis of variance. Fisher's exact test was used to analyse the differences between the cleft types (cleft in the hard and/or soft palate) and skills of the operating surgeons in the groups. RESULTS: Cluster analysis of craniofacial morphologies in patients with ICP resulted in the formation of three categories: the first cluster exhibited a relatively harmonious anteroposterior relationship between the maxilla and the mandible (22.2%); the second cluster exhibited crossbite owing to a significantly smaller maxilla (33.3%); and the third cluster exhibited a smaller mandible with posterior rotation showing skeletal class II malocclusion (44.4%). Differences in cleft types and surgeons were not associated with the distribution of patients in each cluster. CONCLUSIONS: Patients with ICP exhibited characteristic morphological patterns, such as bimaxillary retrusion or severe mandibular retrusion, besides the anterior crossbite frequently found in patients with cleft lip and palate . Understanding the typical morphological characteristics could enable better diagnostic categorisation of patients with ICP, which may eventually improve orthodontic treatment planning.

Masticatory muscle function affects the pathological conditions of dentofacial deformities.

The causes of dentofacial deformities include various known syndromes, genetics, environmental and neuromuscular factors, trauma, and tumors. Above all, the functional effects of muscles are important, and deformation of the mandible is often associated with a mechanical imbalance of the masticatory muscles. With the vertical position of the face, weakness of the sling of the masseter muscle and medial pterygoid muscle causes dilatation of the mandibular angle. In patients with a deep bite, excessive function of the masticatory muscles is reported. Myosin heavy chain　(MyHC) properties also affect jawbone morphology. In short-face patients, the proportion of type II fibers, which are fast muscles, is high. The proportions of muscle fiber types are genetically determined but can be altered by postnatal environmental factors. Orthognathic surgery may results in the transition of MyHC to type II (fast) fibers, but excessive stretching enhances the release of inflammatory mediators and causes a shift toward a greater proportion of slow muscle fibers. This feature can be related to postoperative relapse. Bones and muscles are in close crosstalk, and it may be possible to use biochemical approaches as well as biomechanical considerations for the treatment of jaw deformities.

Regulation of NF-kB Signalling Through the PR55ß-RelA Interaction in Osteoblasts.

BACKGROUND/AIM: Nuclear factor kappa B (NF-kB) signalling including the RelA subunit is activated upon fibroblast growth factor (FGF) stimulation. A clear understanding of the mechanisms underlying this action will provide insights into molecular targeting therapy. Furthermore, protein phosphatase 2A (PP2A) is involved in RelA dephosphorylation, but little is known about the underlying mechanism. MATERIALS AND METHODS: Because the regulatory subunits of PP2A drive NF-kB signalling via RelA, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in MC3T3-E1 cells. We examined weather FGF2 interacts with NF-kB using immunocytochemistry (IC), immunoprecipitation (IP), and pull-down assay (PD) using recombinant proteins. RESULTS: PR55ß expression was increased, whereas activated RelA was dephosphorylated upon FGF2 stimulation. Further, the interaction of PR55ß with RelA was confirmed by IC, IP, and PD. CONCLUSION: FGF2-induced PR55ß directly interacts with RelA and regulates NF-kB signalling.

Effects of acidic calcium phosphate concentration on setting reaction and tissue response to ß-tricalcium phosphate granular cement.

Beta-tricalcium phosphate granular cement (ß-TCP GC), consisting of ß-TCP granules and an acidic calcium phosphate (Ca-P) solution, shows promise in the reconstruction of bone defects as it sets to form interconnected porous structures, that is, ß-TCP granules are bridged with dicalcium phosphate dihydrate (DCPD) crystals. In this study, the effects of acidic Ca-P solution concentration (0-600 mmol/L) on the setting reaction and tissue response to ß-TCP GC were investigated. The ß-TCP GC set upon mixing with its liquid phase, based on the formation of DCPD crystals, which bridged ß-TCP granules to one another. Diametral tensile strength of the set ß-TCP GC was relatively the same, at ∼0.6 MPa, when the Ca-P concentration was 20-600 mmol/L. Due to the setting ability, reconstruction of the rat's calvarial bone defect using ß-TCP GC with 20, 200, and 600 mmol/L Ca-P solution was much easier compared to that with ß-TCP granules without setting ability. Four weeks after the reconstruction, the amount of new bone was the same, ∼17% in both ß-TCP GC and ß-TCP granules groups. Cellular response to ß-TCP granules and ß-TCP GC using the 20 mmol/L acidic Ca-P solution was almost the same. However, ß-TCP GC using the 200 and 600 mmol/L acidic Ca-P solution showed a more severe inflammatory reaction. It is concluded, therefore, that ß-TCP GC, using the 20 mmol/L acidic Ca-P solution, is recommended as this concentration allows surgical techniques to be performed easily and provides good mechanical strength, and the similar cellular response to ß-TCP granules. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 108B:22-29, 2020.

Lower Lip Cancer Managed by Reconstruction with a Double Abbe Flap - A Case Report.

Although the incidence of lower lip cancer is not high in Japan, its treatment requires an approach that considers both esthetics and function. When surgical resection is required, the method used for reconstruction varies depending on the affected part. Despite various studies proposing different types of algorithms, no single method is considered the best. If the loss of half or more of the lip is predicted, a free flap may need to be considered, depending on the case. Here, we report a case involving a 78-year-old edentulous woman with lower lip cancer whose resection area involved approximately 70% of the red and white portions of the lower lip. Fortunately, no resection was required at the commissure. We accordingly performed reconstruction with a double Abbe flap in accordance with a detailed treatment plan. The patient was extremely satisfied with the esthetic and functional outcomes of the surgery.