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DVL3 regulates tooth initiation, root formation, and craniofacial patterning through canonical and non-canonical WNT signalling. The objective of this study was to investigate the dental and craniofacial phenotypes associated with rare or novel DVL3 variants in Thai and Turkish patients. It aimed to broaden the understanding of the clinical spectrum of DVL3-related conditions, particularly their role in odontogenesis and craniofacial development. We evaluated 11 patients from Thai and Turkish cohorts with confirmed DVL3 variants through clinical, radiographic, and whole-exome and Sanger sequencing. All patients exhibited variable dental anomalies, including root malformations, oral exostoses, and mesiodens. Unlike the broader craniofacial and skeletal manifestations seen in syndromic Robinow syndrome, these cohorts demonstrated a dental-predominant phenotype, indicating a possible genotype-phenotype distinction. These findings highlight the role of canonical-noncanonical WNT signalling dysregulation in odontogenesis and dentoalveolar development. Rare or novel DVL3 variants can manifest primarily as complex dental anomalies with or without syndromic features. Early recognition and genetic evaluation of such cases are essential for accurate diagnosis, clinical management, and counselling. This study provides novel insights into the role of DVL3 in tooth and craniofacial development, with implications for future research and interdisciplinary care.

DOI： 10.1016/j.identj.2025.104019

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OBJECTIVE: Kinesin Family Member 7 (KIF7) regulates ciliary integrity. Cilia-mediated sonic hedgehog signalling regulates tooth number, position, and morphology. The objective of the study was to investigate whether KIF7 variants could contribute to the formation of supernumerary teeth. METHODS: Whole-exome sequencing was performed on 153 individuals from 130 families with isolated supernumerary tooth types. Immunohistochemistry of Kif7 expression during early odontogenesis was performed in mouse embryos. Mutant KIF7 protein models were generated. RESULTS: We identified 4 rare missense variants (c.160C>T;p.His54Tyr, c.175G>A;p.Val59Met, c.1964C>G;p.Pro655Arg, and c.2551C>T;p.Arg851Cys), 1 novel missense variant (c.1882 G>A;p.Glu628Lys), and 1 insertion variant (c.1893_1894insGAGGAG;p.Glu630_Glu631dup) in the KIF7 gene in patients with various orodental presentations: 5 individuals from 4 families with mesiodens, 1 proband with a supernumerary molar, and 1 proband with a compound odontoma. The p.His54Tyr and p.Val59Met variants, located in the motor domain of the KIF7 protein, are predicted to disrupt its interaction with tubulin, resulting in abnormal localisation of KIF7 in cilia. The Arg851Cys variant in the coiled-coil region and the Glu628Lys, Glu630_Glu631dup, and Pro655Arg variants in the region of unknown structure are predicted to disrupt charge balance. CONCLUSION: This is the first report demonstrating that KIF7 variants may be contributing factors to supernumerary tooth phenotypes.

DOI： 10.1016/j.identj.2025.100928

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Biallelic variants in the PEX1 and PEX6 genes are implicated in Heimler syndrome, which is characterized by amelogenesis imperfecta, sensorineural hearing loss, retinitis pigmentosa, and nail defects. The objective of this study is to find the genetic variant and to analyze the teeth of a patient with Heimler syndrome. Clinical and radiographic examination and whole exome sequencing were performed on a Heimler syndrome patient and his parents. Scanning electron microscopy and micro-computed tomography were performed on a tooth. Immunohistochemical study of Pex1 was performed. Mutant protein models were made. The authors report an 18-year-old male with Heimler syndrome who carried a compound heterozygous (c.2966T>C; p.Ile989Thr and c.2097_2098insT; p.Ile700TyrfsTer42) mutation in the PEX1 gene. Clinical manifestations included amelogenesis imperfecta of the posterior permanent teeth, mild sensorineural hearing loss, retinitis pigmentosa, and leukonychia. SEM showed enamel and dentin dysmineralization. The newly findings include arachnodactyly, tooth agenesis, microdontia, root maldevelopment, and failure of tooth eruption. The p.Ile700TyrfsTer42 variant is predicted to produce a non-viable protein. The p.Ile989Thr variant is predicted to disrupt its interaction with PEX6. A patient with Heimler syndrome may have arachnodactyly, tooth agenesis, microdontia, delayed dental development, root maldevelopment, enamel and dentin dysmineralization, and failure of tooth eruption.

DOI： 10.1016/j.identj.2025.04.002

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OBJECTIVE: Natal teeth are teeth that are present at birth. Multiple natal teeth are extremely rare. The objective of this study was to find the molecular aetiology of a unique dental phenotype including natal teeth, tooth agenesis, and root maldevelopment in a 5-generation family. METHODS: Oral and radiographic examination, linkage analysis, whole genome sequencing, and an immunohistochemical study of Kdf1 during tooth development in the mouse embryo were performed. A protein model was generated. RESULTS: We report a 5-generation family in which multiple natal teeth, oligodontia, and root maldevelopment manifested with autosomal dominant inheritance. Linkage analysis and whole genome sequencing revealed a novel pathogenic variant c.845T>G; p.Ile282Ser, which cosegregated in 9 affected and 10 unaffected family members. This amino acid Ile282 is highly conserved and is important for the stabilization of a small helical fragment. This stabilization is lost in the Ile282Ser mutant, resulting in disruption of the interaction of KDF1 with its partner proteins, including IKKA, which are important for epidermal proliferation and differentiation and subsequent tooth development. CONCLUSIONS: Our study demonstrates for the first time that natal teeth, tooth agenesis, and root maldevelopment are caused by a KDF1 variant. Our study highlights the important role of KDF1 in tooth formation and eruption.

DOI： 10.1016/j.identj.2025.100860

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BACKGROUND: Genomes are constantly exposed to a myriad of DNA-damaging agents. Robust DNA repair mechanisms protect DNA by removing or tolerating damage. However, it remains unclear whether these mechanisms are required for organogenesis. RESULTS: Multiple epithelial layers are essential for skin function, including body protection. The epidermis is initiated as a single layer and then stratifies in utero. Stratification did not occur in mice with epithelial conditional deletion of the DNA repair molecule Reptin (Reptinfl/fl;K14Cre). DNA damage was observed in the mutant epidermis but not in the wild-type epidermis. The mutant epidermis also showed reduced cell proliferation and upregulated p53 expression. Stratification was restored when p53 was deleted in the Reptin mutant mice by generating Reptin and p53 double mutant mice (Reptinfl/fl;K14Cre;p53-/-). CONCLUSION: In the wild-type epidermis, DNA is likely damaged at the initiation of embryonic stratification and promptly repaired by DNA repair mechanisms involving Reptin.

DOI： 10.1002/dvdy.70046

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Dysfunction of primary cilia leads to genetic disorder, ciliopathies, which shows various malformations in many vital organs such as brain. Multiple tongue deformities including cleft, hamartoma, and ankyloglossia are also seen in ciliopathies, which yield difficulties in fundamental functions such as mastication and vocalization. Here, we found these tongue anomalies in mice with mutation of ciliary protein. Abnormal cranial neural crest-derived cells (CNCC) failed to evoke Hh signal for differentiation of mesoderm-derived cells into myoblasts, which resulted in abnormal differentiation of mesoderm-derived cells into adipocytes. The ectopic adipose subsequently arrested tongue swelling formation. Ankyloglossia was caused by aberrant cell migration due to lack of non-canonical Wnt signaling. In addition to ciliopathies, these tongue anomalies are often observed as non-familial condition in human. We found that these tongue deformities could be reproduced in wild-type mice by simple mechanical manipulations to disturb cellular processes which were disrupted in mutant mice. Our results provide hints for possible future treatment in ciliopathies.

DOI： 10.7554/eLife.85042

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Congenital insensitivity to pain is a rare human condition in which affected individuals do not experience pain throughout their lives. This study aimed to identify the molecular etiology of congenital insensitivity to pain in two Thai patients. Clinical, radiographic, histopathologic, immunohistochemical, and molecular studies were performed. Patients were found to have congenital insensitivity to pain, self-mutilation, acro-osteolysis, cornea scars, reduced temperature sensation, tooth agenesis, root maldevelopment, and underdeveloped maxilla and mandible. The skin biopsies revealed fewer axons, decreased vimentin expression, and absent neurofilament expression, indicating lack of dermal nerves. Whole exome and Sanger sequencing identified a rare homozygous variant c.4039C>T; p.Arg1347Cys in the plakin domain of Plec, a cytolinker protein. This p.Arg1347Cys variant is in the spectrin repeat 9 region of the plakin domain, a region not previously found to harbor pathogenic missense variants in other plectinopathies. The substitution with a cysteine is expected to decrease the stability of the spectrin repeat 9 unit of the plakin domain. Whole mount in situ hybridization and an immunohistochemical study suggested that Plec is important for the development of maxilla and mandible, cornea, and distal phalanges. Additionally, the presence of dental anomalies in these patients further supports the potential involvement of Plec in tooth development. This is the first report showing the association between the Plec variant and congenital insensitivity to pain in humans.

DOI： 10.3390/ijms25126358

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KCTD1 plays crucial roles in regulating both the SHH and WNT/β-catenin signaling pathways, which are essential for tooth development. The objective of this study was to investigate if genetic variants in KCTD1 might also be associated with isolated dental anomalies. We clinically and radiographically investigated 362 patients affected with isolated dental anomalies. Whole exome sequencing identified two unrelated families with rare (p.Arg241Gln) or novel (p.Pro243Ser) variants in KCTD1. The variants segregated with the dental anomalies in all nine patients from the two families. Clinical findings of the patients included taurodontism, unseparated roots, long roots, tooth agenesis, a supernumerary tooth, torus palatinus, and torus mandibularis. The role of Kctd1 in root development is supported by our immunohistochemical study showing high expression of Kctd1 in Hertwig epithelial root sheath. The KCTD1 variants in our patients are the first variants found to be located in the C-terminal domain, which might disrupt protein-protein interactions and/or SUMOylation and subsequently result in aberrant WNT-SHH-BMP signaling and isolated dental anomalies. Functional studies on the p.Arg241Gln variant are consistent with an impact on β-catenin levels and canonical WNT signaling. This is the first report of the association of KCTD1 variants and isolated dental anomalies.

DOI： 10.3390/ijms25105179

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OBJECTIVES: To identify the molecular etiology of distinct dental anomalies found in eight Thai patients and explore the mutational effects on cellular functions. MATERIALS AND METHODS: Clinical and radiographic examinations were performed for eight patients. Whole exome sequencing, mutant protein modelling, qPCR, western blot analysis, scratch assays, immunofluorescence, confocal analysis, in situ hybridization, and scanning electron micrography of teeth were done. RESULTS: All patients had molars with multiple supernumerary cusps, single-cusped premolars, and a reduction in root number. Mutation analysis highlighted a heterozygous c.865A>G; p.Ile289Val mutation in CACNA1S in the patients. CACNA1S is a component of the slowly inactivating L-type voltage-dependent calcium channel. Mutant protein modeling suggested that the mutation might allow leakage of Ca2+ or other cations, or a tightening, to restrict calcium flow. Immunohistochemistry analysis showed expression of Cacna1s in the developing murine tooth epithelium during stages of crown and root morphogenesis. In cell culture, the mutation resulted in abnormal cell migration of transfected CHO cells compared to wildtype CACNA1S, with changes to the cytoskeleton and markers of focal adhesion. CONCLUSIONS: The malformations observed in our patients suggest a role for calcium signaling in organization of both cusps and roots, affecting cell dynamics within the dental epithelium.

DOI： 10.1111/odi.14551

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Chronic obstructive pulmonary disease (COPD) was previously known as chronic bronchitis and emphysema. It has various main symptoms, such as dyspnea, chronic cough, and sputum, and is often accompanied by dysphagia. Although many published clinical reports have described COPD-related dysphagia, the physiological mechanisms underlying swallowing changes due to COPD remain unclear. Therefore, we analyzed how COPD affects the swallowing reflex using COPD model rats. We performed an electrophysiological study of respiration and swallowing using COPD model induced by intratracheal administration of porcine pancreatic elastase and lipopolysaccharide in Sprague-Dawley male rats. To identify the respiration and swallowing responses, electromyographic activity was recorded from the diaphragm, digastric (Dig), and thyrohyoid (TH) muscles. We confirmed COPD using micro-computed tomography analysis and hematoxylin and eosin staining of the lungs. The duty cycle was defined as the ratio of the inspiration duration to the total respiratory duration. In COPD model rats, the duty cycle was significantly higher than that in control rats. The frequency of the swallowing reflex evoked by electrical stimulation of the superior laryngeal nerve during the inspiration phase was higher in COPD model rats than in control rats. Furthermore, long-term COPD altered Dig and TH muscle activity without pathological muscle change. Our results suggest that COPD increases the frequency of swallowing initiation during the inspiration phase. Furthermore, long-term COPD affects swallowing-related muscle activity without pathological muscle changes. These physiological changes may increase the risk of developing dysphagia. Further studies are necessary to clarify the mechanisms contributing to the functional changes in respiration and swallowing in COPD.

DOI： 10.3389/fphys.2024.1445336

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DOI： 10.1111/odi.14162

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Other Link： https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20K10092/

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BACKGROUND: Enamel knots and Hertwig epithelial root sheath (HERS) regulate the growth and folding of the dental epithelium, which subsequently determines the final form of tooth crown and roots. We would like to investigate the genetic etiology of seven patients affected with unique clinical manifestations, including multiple supernumerary cusps, single prominent premolars, and single-rooted molars. METHODS: Oral and radiographic examination and whole-exome or Sanger sequencing were performed in seven patients. Immunohistochemical study during early tooth development in mice was performed. RESULTS: A heterozygous variant (c. 865A>G; p.Ile289Val) in CACNA1S was identified in all the patients, but not in an unaffected family member and control. Immunohistochemical study showed high expression of Cacna1s in the secondary enamel knot. CONCLUSIONS: This CACNA1S variant seemed to cause impaired dental epithelial folding; too much folding in the molars and less folding in the premolars; and delayed folding (invagination) of HERS, which resulted in single-rooted molars or taurodontism. Our observation suggests that the mutation in CACNA1S might disrupt calcium influx, resulting in impaired dental epithelium folding, and subsequent abnormal crown and root morphology.

DOI： 10.3390/diagnostics13050895

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OBJECTIVE: Our objective was to investigate the molecular etiology of osteogenesis imperfecta type VIII and dental anomalies in 4 siblings of a Karen tribe family. MATERIALS AND METHODS: Four patients and their unaffected parents were studied by clinical and radiographic examination. In situ hybridization of P3h1 during early murine tooth development, whole-exome sequencing, and Sanger direct sequencing were performed. RESULTS: A novel homozygous missense P3H1 mutation (NM_001243246.1; c.2141A>G; NP_001230175.1; p.Lys714Arg) was identified in all patients. Their unaffected parents were heterozygous for the mutation. The mutation is hypothesized to belong to isoform c of P3H1. Mutations in P3H1 are associated with autosomal recessive osteogenesis imperfecta type VIII. Hypodontia, a mesiodens, and single-rooted permanent second molars found in our patients have never been reported in patients with P3H1 mutations. Single-rooted second permanent molars or failure to form multiple roots implies effects of the P3H1 mutation on root development. CONCLUSIONS: We report a novel P3H1 mutation as the underlying cause of osteogenesis imperfecta type VIII with dental anomalies. Our study suggests that isoform c of P3H1 is also a functional isoform of P3H1. We report, for the first time, to our knowledge, the association of P3H1 mutation and osteogenesis imperfecta type VIII with dental anomalies.

DOI： 10.1016/j.oooo.2021.01.023

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DOI： 10.1111/joa.13328

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BACKGROUND: Juberg-Hayward syndrome (JHS; MIM 216100) is a rare autosomal recessive malformation syndrome, characterized by cleft lip/palate, microcephaly, ptosis, short stature, hypoplasia or aplasia of thumbs, and dislocation of radial head and fusion of humerus and radius leading to elbow restriction. OBJECTIVE: To report for the first time the molecular aetiology of JHS. PATIENT AND METHODS: Clinical and radiographic examination, whole exome sequencing, Sanger sequencing, mutant protein model construction, and in situ hybridization of Esco2 expression in mouse embryos were performed. RESULTS: Clinical findings of the patient consisted of repaired cleft lip/palate, microcephaly, ptosis, short stature, delayed bone age, hypoplastic fingers and thumbs, clinodactyly of the fifth fingers, and humeroradial synostosis leading to elbow restriction. Intelligence is normal. Whole exome sequencing of the whole family showed a novel homozygous base substitution c.1654C>T in ESCO2 of the proband. The sister was homozygous for the wildtype variant. Parents were heterozygous for the mutation. The mutation is predicted to cause premature stop codon p.Arg552Ter. Mutations in ESCO2, a gene involved in cohesin complex formation, are known to cause Roberts/SC phocomelia syndrome. Roberts/SC phocomelia syndrome and JHS share similar clinical findings, including autosomal recessive inheritance, short stature, cleft lip/palate, severe upper limb anomalies, and hypoplastic digits. Esco2 expression during the early development of lip, palate, eyelid, digits, upper limb, and lower limb and truncated protein model are consistent with the defect. CONCLUSIONS: Our study showed that Roberts/SC phocomelia syndrome and JHS are allelic and distinct entities. This is the first report demonstrating that mutation in ESCO2 causes JHS, a cohesinopathy.

DOI： 10.1093/ejo/cjaa023

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DOI： 10.1111/odi.13384

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DOI： 10.1111/joa.13096

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DOI： 10.1016/j.gep.2019.119062

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Mandibular prognathism is characterized by a prognathic or prominent mandible. The objective of this study was to find the gene responsible for mandibular prognathism. Whole exome sequencing analysis of a Thai family (family 1) identified the ADAMTSL1 c.176C>A variant as the potential defect. We cross-checked our exome data of 215 people for rare variants in ADAMTSL1 and found that the c.670C>G variant was associated with mandibular prognathism in families 2 and 4. Mutation analysis of ADAMTSL1 in 79 unrelated patients revealed the c.670C>G variant was also found in family 3. We hypothesize that mutations in ADAMTSL1 cause failure to cleave aggrecan in the condylar cartilage, and that leads to overgrowth of the mandible. Adamtsl1 is strongly expressed in the condensed mesenchymal cells of the mouse condyle, but not at the cartilage of the long bones. This explains why the patients with ADAMTSL1 mutations had abnormal mandibles but normal long bones. This is the first report that mutations in ADAMTSL1 are responsible for the pathogenesis of mandibular prognathism.

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The tongue is a critical organ, involved in functions such as speaking, swallowing, mastication, and degustation. Although Sox genes are known to play critical roles in many biological processes, including organogenesis, the expression of the Sox family members during tongue development remains unclear. We therefore performed a comparative in situ hybridization analysis of 17 Sox genes (Sox1-14, 17, 18, and 21) during murine tongue development. Sox2, 4, 6, 8, 9, 10, 11, 12, and 21 were found to be expressed in the tongue epithelium, whereas Sox2, 4-6, 8-11, 13, and 21 showed expression in the mesenchyme of the developing tongue. Expression of Sox1, 4, 6, 8-12, and 21 were observed in the developing tongue muscle. Sox5 and 13 showed expression only at E12, while Sox1 expression was observed only on E18. Sox6, 8, 9, and 12 showed expression at several stages. Although the expression of Sox2, 4, 10, 11, and 21 was detected during all the four stages of tongue development, their expression patterns differed among the stages. We thus identified a dynamic spatiotemporal expression pattern of the Sox genes during murine tongue development. To understand whether Sox genes are involved in the development of other craniofacial organs through similar roles to those in tongue development, we also examined the expression of Sox genes in eyelid primordia, which also contain epithelium, mesenchyme, and muscle. However, expression patterns and timing of Sox genes differed between tongue and eyelid development. Sox genes are thus related to organogenesis through different functions in each craniofacial organ.

DOI： 10.1155/2018/1601363

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The Japanese government and communities have designed and tried many programs to develop and propagate dietary education ; of these, school-lunch programs are thought to be one of the most useful tools. The first aim of the present observational study was to clarify the different effects of Japanese staple foods such as noodles, boiled rice, and breads on masticatory parameters with regard to school-lunch intake. The next aim was to discuss the school-lunch menus, with reference to the above observational results and the replies submitted to a questionnaire by the general public.In the observational study, the subjects included six elementary school children aged 11 to 12years, who were recorded on videotape eating the six kinds of school-lunches. The school-lunches consisted of three kinds of staple foods with two different side menus. The masticatory parameters were calculated based on the recorded videotapes, and the differences among the school-lunches were statistically analyzed. The questionnaire survey roughly consisted of four categories on the schoollunch, and 170 adult cooperators submitted their replies.The observational study revealed that the staple foods included in the school-lunches had little effect on the masticatory parameters. According to the results of the questionnaire, more than 80% ofthe general public would like to have rice included in the menus three to five times per week, and approximately 65% expected the other menus two to four times per month.Since four of the present menus consisted of noodles and breads which presented a poor balance of nutrients, it was therefore indicated that the school-lunches should be primarily composed of boiled rice. More than half of the general public, however, sometimes hopes for menus other than the rice menus. From a masticatory perspective, there were few differences among the six menus. It may therefore be taken into consideration that menus with noodles or breads should be served a few times a month for school-lunches.

DOI： 10.11411/jspd.48.3_388

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DOI： 10.11411/pdj.20.22

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2010&ichushi_jid=J00999&link_issn=&doc_id=20110118400002&doc_link_id=%2Fdj2ngtdt%2F2010%2F004002%2F002%2F0125-0130%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fdj2ngtdt%2F2010%2F004002%2F002%2F0125-0130%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

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