Publications by authors named "Hideto Imura"

16 Publications

  • Page 1 of 1

Case of feeding disorder due to lymphangioma of the tongue: Importance in developing countries.

Congenit Anom (Kyoto) 2021 Feb 1. Epub 2021 Feb 1.

Cleft Lip and Palate Center, Aichi Gakuin University Dental Hospital, Nagoya, Japan.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/cga.12410DOI Listing
February 2021

SPECC1L regulates palate development downstream of IRF6.

Hum Mol Genet 2020 03;29(5):845-858

Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA.

SPECC1L mutations have been identified in patients with rare atypical orofacial clefts and with syndromic cleft lip and/or palate (CL/P). These mutations cluster in the second coiled-coil and calponin homology domains of SPECC1L and severely affect the ability of SPECC1L to associate with microtubules. We previously showed that gene-trap knockout of Specc1l in mouse results in early embryonic lethality. We now present a truncation mutant mouse allele, Specc1lΔC510, that results in perinatal lethality. Specc1lΔC510/ΔC510 homozygotes showed abnormal palate rugae but did not show cleft palate. However, when crossed with a gene-trap allele, Specc1lcGT/ΔC510 compound heterozygotes showed a palate elevation delay with incompletely penetrant cleft palate. Specc1lcGT/ΔC510 embryos exhibit transient oral epithelial adhesions at E13.5, which may delay shelf elevation. Consistent with oral adhesions, we show periderm layer abnormalities, including ectopic apical expression of adherens junction markers, similar to Irf6 hypomorphic mutants and Arhgap29 heterozygotes. Indeed, SPECC1L expression is drastically reduced in Irf6 mutant palatal shelves. Finally, we wanted to determine if SPECC1L deficiency also contributed to non-syndromic (ns) CL/P. We sequenced 62 Caucasian, 89 Filipino, 90 Ethiopian, 90 Nigerian and 95 Japanese patients with nsCL/P and identified three rare coding variants (p.Ala86Thr, p.Met91Iso and p.Arg546Gln) in six individuals. These variants reside outside of SPECC1L coiled-coil domains and result in milder functional defects than variants associated with syndromic clefting. Together, our data indicate that palate elevation is sensitive to deficiency of SPECC1L dosage and function and that SPECC1L cytoskeletal protein functions downstream of IRF6 in palatogenesis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/hmg/ddaa002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104672PMC
March 2020

Rat Palatine Fissure: A Suitable Experimental Model for Evaluating Bone Regeneration.

Tissue Eng Part C Methods 2019 09 11;25(9):513-522. Epub 2019 Sep 11.

Department of Oral Anatomy, Aichi Gakuin University School of Dentistry, Nagoya, Japan.

Impact Statement: The rat palatine fissure is anatomically similar to human alveolar cleft. In this study, we examined potential bone repair by an autologous bone implant and beta-tricalcium phosphate (β-TCP) using rat palatine fissure as a model. Autologous bone chips or β-TCP granules were implanted into the rat palatine fissure. Our model demonstrated that higher bone volume and bone mineral density were achieved with autologous bone graft than with β-TCP. We have provided the first demonstration of the suitability of the rat palatine fissure as the implant site to simulate the transplantation of bone graft materials into human alveolar cleft.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/ten.TEC.2019.0143DOI Listing
September 2019

Patients with SATB2-associated syndrome exhibiting multiple odontomas.

Am J Med Genet A 2018 12 21;176(12):2614-2622. Epub 2018 Dec 21.

Department of Human Genetics, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Special AT-rich sequence-binding protein 2 (SATB2)-associated syndrome (SAS) is characterized by alterations of SATB2. Its clinical features include intellectual disability and craniofacial abnormalities, such as cleft palate, dysmorphic features, and dental abnormalities. Here, we describe three previously undiagnosed, unrelated patients with SAS who exhibited dental abnormalities, including multiple odontomas. Although isolated odontomas are common, multiple odontomas are rare. Individuals in families 1 and 3 underwent whole-exome sequencing. Patient 2 and parents underwent targeted amplicon sequencing. On the basis of the hg19/GRCh37 reference and the RefSeq mRNA NM_001172517, respective heterozygous mutations were found and validated in Patients 1, 2, and 3: a splice-site mutation (chr2:g.200137396C > T, c.1741-1G > A), a nonsense mutation (chr2:g.200213750G > A, c.847C > T, p.R283*), and a frame-shift mutations (chr2:g.200188589_200188590del, c.1478_1479del, p.Q493Rfs*19). All mutations occurred de novo. The mutations in Patients 1 and 3 were novel; the mutation in Patient 2 has been described previously. Tooth mesenchymal cells derived from Patient 2 showed diminished SATB2 expression. Multiple odontomas were evident in the patients in this report; however, this has not been recognized previously as a SAS-associated phenotype. We propose that multiple odontomas be considered as an occasional manifestation of SAS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/ajmg.a.40670DOI Listing
December 2018

Cleft palate formation after palatal fusion occurs due to the rupture of epithelial basement membranes.

J Craniomaxillofac Surg 2018 Dec 20;46(12):2027-2031. Epub 2018 Sep 20.

Division of Research and Treatment for Oral and Maxillofacial Congenital Anomalies, School of Dentistry, Aichi-Gakuin University, Japan.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces cleft palate and hydronephrosis in the mouse embryo. Cleft palate occurs due to failure in palatal grow, but the underlying mechanisms are unclear. We investigated the mechanisms of cleft palate development in TCDD-exposed mouse embryos. We administered olive oil (control group) or TCDD diluted in olive oil (40 μg/kg) via gastric tubes to pregnant mice on gestational day (GD) 12. Embryos of control and TCDD-exposed groups were removed from pregnant mice on GD 14 and GD 15, respectively. One mouse embryo from the control group had anteroposterior palatal fusion. Palatal fusion was observed in three TCDD-exposed mouse embryos. Palates of TCDD-exposed mice fused from the interior to the middle of the palates, while the palates were separated in the posterior region. The middle of the embryonic palatal shelves in TCDD-exposed animals was narrow and split at the fusional position. At this position, palatal and blood cells were dispersed from the palatal tissue and the epithelium was split, with a discontinuous basement membrane. The results suggest that decreased intercellular adhesion or insufficient tissue strength of the palatal shelves may be involved in the development of cleft palate following palatal fusion.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jcms.2018.09.016DOI Listing
December 2018

Association of MEOX2 polymorphism with nonsyndromic cleft palate only in a Vietnamese population.

Congenit Anom (Kyoto) 2018 Jul 28;58(4):124-129. Epub 2017 Nov 28.

Division of Research and Treatment for Oral Maxillofacial Congenital Anomalies, Aichi Gakuin University, Nagoya, Japan.

To evaluate the association between the single nucleotide polymorphism (SNP) rs227493 in the MEOX2 gene and nonsyndromic cleft palate only, this research was conducted as a case-control study by comparing a nonsyndromic cleft palate only group with an independent, healthy, and unaffected control group who were both examined by specialists. Based on clinical examination and medical records, we analyzed a total of 570 DNA samples, including 277 cases and 293 controls, which were extracted from dry blood spot samples collected from both the Odonto and Maxillofacial Hospital in Ho Chi Minh City and Nguyen Dinh Chieu Hospital in Ben Tre province, respectively. The standard procedures of genotyping the specific SNP (rs2237493) for MEOX2 were performed on a StepOne Realtime PCR system with TaqMan SNP Genotyping Assays. Significant statistical differences were observed in allelic frequencies (allele T and allele G) between the non-syndromic cleft palate only and control groups in female subjects, with an allelic odds ratio of 1.455 (95% confidence interval: 1.026-2.064) and P < 0.05. These study findings suggest that nonsyndromic isolated cleft palate might be influenced by variation of MEOX2, especially SNP rs2237493 in Vietnamese females.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/cga.12259DOI Listing
July 2018

Homeobox family Hoxc localization during murine palate formation.

Congenit Anom (Kyoto) 2016 Jul;56(4):172-9

Osaka Medical College, Takatsuki, Osaka, Japan.

Homeobox genes play important roles in craniofacial morphogenesis. However, the characteristics of the transcription factor Hoxc during palate formation remain unclear. We examined the immunolocalization patterns of Hoxc5, Hoxc4, and Hoxc6 in palatogenesis of cleft palate (Eh/Eh) mice. On the other hand, mutations in the FGF/FGFR pathway are exclusively associated with syndromic forms of cleft palate. We also examined the immunolocalization of Fgfr1 and Erk1/2 to clarify their relationships with Hoxc in palatogenesis. Some palatal epithelial cells showed Hoxc5 labeling, while almost no labeling of mesenchymal cells was observed in +/+ mice. As palate formation progressed in +/+ mice, Hoxc5, Hoxc4, and Hoxc6 were observed in medial epithelial seam cells. Hoxc5 and Hoxc6 were detected in the oral epithelium. The palatal mesenchyme also showed intense staining for Fgfr1 and Erk1/2 with progression of palate formation. In contrast, the palatal shelves of Eh/Eh mice exhibited impaired horizontal growth and failed to fuse, resulting in a cleft. Hoxc5 was observed in a few epithelial cells and diffusely in the mesenchyme of Eh/Eh palatal shelves. No or little labeling of Fgfr1 and Erk1/2 was detected in the cleft palate of Eh/Eh mice. These findings suggest that Hoxc genes are involved in palatogenesis. Furthermore, there may be the differences in the localization pattern between Hoxc5, Hoxc4, and Hoxc6. Additionally, Hoxc distribution in palatal cells during palate development may be correlated with FGF signaling. (228/250 words) © 2016 Japanese Teratology Society.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/cga.12153DOI Listing
July 2016

Diagnostic/genetic sreening - approach for genetic diagnoses and prevention of cleft lip and/or palate.

Chin J Dent Res 2013 ;16(2):95-100

The treatment, research and volunteer work for cleft lip and/or palate (CL/P) has been led for over 30 years by our team. Within this period, more than 4,000 cases of CL/P were treated and at the same time, and approximately 400 papers were published as the first or partner researcher in Nature Genetics, New England Journal of Medicine and others. In addition, with $20 million that was donated from companies and laypeople, and the grant from the Japanese government, CL/P centres in many countries and in Japan, the oral and craniofacial congenital anomaly gene bank in our CL/P centre was established by our leadership. In the bank there are genes from approximately more than 8,000 cases. The genes were mapped with Professor Jeffery Murray of Iowa University in the United States, the findings about genetic syndromes such as Van der Woude Syndrome and basal cell nevus syndrome were applied in clinical settings. The genetic counselling section that specialises in the oral and maxillofacial field was established by our effort for the first time in Japan. In this review, our clinical experience and approach for genetic diagnoses and prevention of cleft lip and/or palate will be discussed.
View Article and Find Full Text PDF

Download full-text PDF

Source
March 2014

Replication of genome wide association identified candidate genes confirm the role of common and rare variants in PAX7 and VAX1 in the etiology of nonsyndromic CL(P).

Am J Med Genet A 2013 May 5;161A(5):965-72. Epub 2013 Mar 5.

Department of Pediatrics, University of Iowa, Iowa City, IA 52242-1181, USA.

Following recent genome wide association studies (GWAS), significant genetic associations have been identified for several genes with nonsyndromic cleft lip with or without cleft palate (CL(P)). To replicate two of these GWAS signals, we investigated the role of common and rare variants in the PAX7 and VAX1 genes. TaqMan genotyping was carried out for SNPs in VAX1 and PAX7 and transmission disequilibrium test (TDT) was performed to test for linkage and association in each population. Direct sequencing in and around the PAX7 and VAX1 genes in 1,326 individuals of European and Asian ancestry was done. The TDT analysis showed strong associations with markers in VAX1 (rs7078160, P = 2.7E-06 and rs475202, P = 0.0002) in a combined sample of Mongolian and Japanese CL(P) case-parent triads. Analyses using parent-of-origin effects showed significant excess transmission of the minor allele from both parents with the effect in the mothers (P = 6.5E-05, OR (transmission) = 1.91) more striking than in the fathers (P = 0.004, OR (transmission) = 1.67) for VAX1 marker rs7078160 in the combined Mongolian and Japanese samples when all cleft types were combined. The rs6659735 trinucleotide marker in PAX7 was significantly associated with all the US cleft groups combined (P = 0.007 in all clefts and P = 0.02 in CL(P)). Eight rare missense mutations found in PAX7 and two rare missense mutations in VAX1. Our study replicated previous GWAS findings for markers in VAX1 in the Asian population, and identified rare variants in PAX7 and VAX1 that may contribute to the etiology of CL(P). Determining the role of rare variants clearly warrants further investigation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/ajmg.a.35749DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634899PMC
May 2013

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin suggests abnormal palate development after palatal fusion.

Congenit Anom (Kyoto) 2010 Jun 11;50(2):77-84. Epub 2010 Feb 11.

Division of Research and Treatment for Oral and Maxillofacial Congenital Anomalies, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.

Mouse embryos exposed to 2,3,7,8-tetrachloridedibenzo-p-dioxin (TCDD) develop cleft palates and hydronephrosis. Cleft palates occur after TCDD exposure due to contact and/or fusion failure. We investigated whether cleft palate can be induced by dissociation of the palatine process after fusion. Pregnant mice on gestational day (GD) 12 were randomly divided into two groups: one group was administered through gastric tubes one dose of olive oil (control group) and the other group was administered one dose of TCDD diluted with olive oil, both at a dose of 40 microg/kg body weight. Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 13-18) and the palatal form was observed using a stereoscopic microscope. In TCDD-exposed embryos, palatal fusion was observed on GD 14, 15 and 16 and the incidence of cleft palate was 100% on GD 18. Fusion rates were 17.5 +/- 15.2% and 12.4 +/- 11.8% on GD 15 and 16, respectively. Some palates from the TCDD-exposed mouse embryos showed clearly developed cleft palate after fusion of the lateral palatine processes during palatal formation. A mass of cells, which were chiefly epithelial in the fused palates was observed in the TCDD-exposed mouse embryos. A decrease in E-cadherin expression was observed in this mass of cells, indicating its involvement in the development of cleft palate.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1741-4520.2010.00271.xDOI Listing
June 2010

Osteomyelitis of the mandible secondary to infantile osteopetrosis: a case report.

Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009 Jun;107(6):e25-9

Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutic Sciences, Okayama, Japan.

A case of infantile malignant osteopetrosis with refractory mandibular osteomyelitis is reported. A female child was diagnosed with osteopetrosis at 2 years 8 months of age, and was scheduled to receive a bone marrow transplantation (BMT) in a pediatric department at 3 years 11 months of age. Her lower incisors were extracted at a dental clinic, after which she had recurring abscesses with progressive severity. She was referred to our department to control local infections before the BMT and was diagnosed with chronic mandibular osteomyelitis caused by osteopetrosis. Sequestrotomy and curettage were performed under general anesthesia. After surgery, daily saline irrigation was continued and osteomyelitis was well controlled. An uneventful BMT was performed, although it was refused and failed. A second BMT was planned, but during chemotherapy, cellulitis occurred after a recurrence of osteomyelitis caused by a newly erupted tooth. The local infection was controlled, but pneumonia recurred. She ultimately died of respiratory failure at 5 years of age.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.tripleo.2009.02.015DOI Listing
June 2009

Bone formation in a rat calvarial defect model after transplanting autogenous bone marrow with beta-tricalcium phosphate.

Acta Histochem 2010 May 29;112(3):270-7. Epub 2009 Apr 29.

Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Medical and Dental School, 2-5-1 Shikata, Okayama-city 7008525, Japan.

In the present study, we evaluated the osteogenic potential of an autogenous bone marrow graft combined with beta-tricalcium phosphate (beta-TCP) in a rat calvarial bone defect model. The bone marrow harvested from the tibia of 7-week-old rats was grafted autogenously in a calvarial defect together with beta-TCP (=BTG group, n=16) or without beta-TCP (=BG group, n=16). Groups of animals were also treated with beta-TCP alone (=TG group, n=16) and control animals (n=8) received no graft implanted into the defect. We then observed the process of bone formation by histology, enzyme histochemistry and immunohistochemistry. Five days after grafting, in the BTG and BG groups, cell proliferation and osteogenic differentiation were observed. From 5 to 10 days after surgery, active Runx2, osteopontin (OPN), and TRAP- positive cells appeared in the BTG and BG groups. New bone formation started in the defect in both the BTG and BG groups. At 30 days after grafting, the BTG group showed new bone development and replacement of beta-TCP to fill the bone defect. New bone formation in the BTG group was significantly greater than in the BG group (P<0.01). The TG group showed no marked bone formation in the defect. The combination graft of bone marrow with beta-TCP showed marked bone formation in rat calvarial defects. Our results indicate that the combination grafts of bone marrow with beta-TCP may be an effective technique for repairing bone defects Beta-TCPgraft (TG) group.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.acthis.2009.01.003DOI Listing
May 2010

Morphological and immunohistochemical studies on cleft palates induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice.

Congenit Anom (Kyoto) 2008 Jun;48(2):68-73

Cleft Lip and Palate Center, Aichi Gakuin University, Nagoya, Japan.

Morphological and immunohistological examinations were performed to reveal the mechanisms of cleft palate induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). ICR strain mice 8-10 weeks of age were used in the study. TCDD was administered in olive oil on gestation day (GD) 12.5 with gastric tubes at 40 microg/kg. From GD 13.5 to 16.5, palates were examined by scanning electron microscopy (SEM), hematoxyline-eosin (HE) staining, and immunohistochemical staining of FGFR1/2, TGF-beta3, MSX1 and LHX8. In the control group, both of the palatal shelves began elevating on GD 14.0 and finished within 6 h. After the elevation, all of the shelves had completely fused with each other on GD 14.5. In the TCDD-treated group, palatal shelves elevated 1 day later than in the control group. However, all palates had elevated by GD 15.0. After the elevation, the shelves contacted each other and fused; however, they were separated on GD16.0. HE staining showed that medial edge epithelium (MEE) was thinner in the TCDD group than in the control group. MEE observed under a high magnification (x2500) exhibited filopodia-like filaments and the cells were bulged in the control group. In contrast, in the TCDD group, no filaments were observed and the cells were flat with unclear boundaries. Immunohistologically, there were no characteristic findings except for FGFR1. FGFR1 was not expressed in the TCDD group after the fusion phase (GD 14.5). TCDD induces many morphological and molecular changes to MEE cells and causes cleft palates.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1741-4520.2008.00181.xDOI Listing
June 2008

Relationships between nasalance scores and nasopharyngeal shapes in cleft palate patients.

J Craniomaxillofac Surg 2008 Jan 28;36(1):11-4. Epub 2008 Jan 28.

Department of Oral and Maxillofacial Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8525, Japan.

Objectives: The aim of the present study is to clarify the relationship between nasalance scores and nasopharyngeal shapes obtained by lateral cephalograms.

Patients: Eight patients who underwent a Wardill-Kilner push-back palatoplasty were included in this study. Perceptual judgment by a speech pathologist indicated that these patients had no hypernasality and no nasal emission at blowing. As normal controls, 33 non-cleft individuals, 4 boys and 10 girls aged 6 years old and 5 boys and 14 girls aged 7 years old, were investigated.

Methods: Lateral cephalograms at rest were taken for both groups. For the cleft (palate) patients, lateral cephalograms at phonation /a/ and blowing were analyzed and nasometries were also performed using a kitsutsuki passage.

Results And Conclusion: There was no significant difference in the velar length, the pharyngeal depth, the ratio of the velar length to the pharyngeal depth and the velar angle between the cleft patients and the non-cleft individuals. Multiple regression analyses indicated that standardized regression coefficients of ratios for the velar length to the pharyngeal depth and the velar ascent at blowing had higher nasalance scores for sentences 1 and 3, which had high coefficients of determination, respectively.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jcms.2007.07.009DOI Listing
January 2008

Dialectal and gender differences in nasalance scores in a Japanese population.

J Craniomaxillofac Surg 2008 Jan 7;36(1):8-10. Epub 2007 Nov 7.

Department of Oral and Maxillofacial Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata-cho, Okayama, 700-8525, Japan.

Objectives: The aim of the present study was to determine whether there are dialectal and gender-related differences in nasalance scores for normal Japanese speakers.

Materials: Sixty-eight volunteers consisting of 31 males (age 23.8+/-2.0) and 37 females (age 23.2+/-2.5) were included in this study. They had no diseases affecting speech, and lived in the same region until high school from birth. According to geography, they were divided into four regional groups: Chugoku region, Kinki region, Shikoku region, and other regions.

Methods: A kitsutsuki passage, which consisted of Japanese non-nasal consonants and vowels, and the Japanese vowels /a/, /i/, /u/, /e/ and /o/, were read three times, and the mean nasalance scores were then obtained with a Nasometer II 6400. The scores of males and females were compared statistically by means of a Student's t-test. The differences among the three regions, Chugoku, Kinki and Shikoku region, were also investigated by means of a one-way analysis of variance (ANOVA).

Results And Conclusion: For all sentences and vowels, the nasalance scores were significantly different between males and females. The one-way ANOVA showed that there were no significant differences among the three regions in both males and females.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jcms.2007.07.008DOI Listing
January 2008

Cleft lip and palate in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin: a morphological in vivo study.

Congenit Anom (Kyoto) 2006 Mar;46(1):21-5

Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

It is well-known that TCDD (2,3,7,8, tetrachloridedibenzo-p-dioxin) induces cleft palates (CPs) in pregnant C57BL mice. However, it is unclear if TCDD is a possible teratogen for cleft lip. We examined maxillofacial malformations including cleft lip in three animal strains: A/J mice, C57BL/6J mice and ICR mice. The A/J mouse develops cleft lip and palate spontaneously at a 5-10% rate. TCDD was administered in olive oil on gestation day (GD) 12.5 with gastric tubes at 10 microg/kg, 20 microg/kg, or 40 microg/kg to examine the dose-response, and on a single day from GD 8.5-14.5 to examine the timing effects of TCDD administration on lip and palate formation. Furthermore, the palatal shelf movements during GD 8.5-14.5 were observed with a stereoscopic microscope. All embryos had cleft palates when the TCDD was administered just before palatogenesis (GD11.5-GD12.5). With respect to the TCDD effects, there were large differences among the strains. In the A/J mice, the difference between a lethal dose and a dose that could induce a cleft palate was close. Cleft lips were not induced, even when the TCDD was given just before labiogenesis. Morphologically, both palatal shelves contacted perfectly along their lengths, but separated and formed cleft palates. In conclusion, TCDD is a strong inducer of cleft palates, and interferes with the fusion phase of the secondary palate, but has no effect on the lip.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1741-4520.2006.00097.xDOI Listing
March 2006