Molecular Changes in Dental Mesenchyme During Tooth Development

Congenital missing permanent second molar is an extremely rare condition. Non syndromic mandibular second molar agenesis associated with other anomalies has occasionally been reported in literature, but isolated sporadic cases are rarely observed. Number of interactions between genetic and environmental factors during the process of tooth development might be the causative etiology for agenesis. This report presents an isolated case of hypodontia with absence of bilateral mandibular second molar agenesis in a healthy 18 year old female patient is presented and literature review on prevalence of most missing teeth with incidence of missing second molar in various regions of the world and in various regions of Indian continent is presented. No such case has been reported in Indian literature so far.

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Dental Development in Children After Chemotherapy

Revista de Chimie ◽

10.37358/rc.17.6.5681 ◽

2017 ◽

Vol 68 (6) ◽

pp. 1397-1400

Author(s):

Cristina Bica ◽

Mihaela Chincesan ◽

Daniela Esian ◽

Krisztina Martha ◽

Valentin Ion ◽

...

Keyword(s):

Acute Lymphoblastic Leukemia ◽

Tooth Development ◽

Lymphoblastic Leukemia ◽

Treatment Method ◽

Paediatric Oncology ◽

Structural Defects ◽

Dental Development ◽

Cytostatic Agents ◽

Dental Abnormalities ◽

Tooth Buds

Chemotherapy, as a treatment method in paediatric oncology, coincides with the physiological process of tooth development. The interference between cytostatic agents and the cycle of the cells with specialised functions in the formation and mineralisation of dental structures leads to the appearance of abnormalities in the development of the tooth buds, structural defects and disorderly eruption. We have looked into the distribution of developmental tooth disorders in a group of children suffering from malignant ailments. The study reveals a high occurrence of microdontia and agenesis of premolars among children diagnosed with high-risk acute lymphoblastic leukemia at the age between 1 and 6, as well as tooth eruption disturbances in 70% of the children. The nature and the severity of dental abnormalities depend on the type of cytostatic medication, the dosage and the frequency of therapeutic cycles, the age of the child at the beginning of the oncological therapy, as well as on the stage of the odontogenesis.

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Lif Deficiency Leads to Iron Transportation Dysfunction in Ameloblasts

Journal of Dental Research ◽

10.1177/00220345211011986 ◽

2021 ◽

pp. 002203452110119

Author(s):

L. Fan ◽

Y.J. Ou ◽

Y.X. Zhu ◽

Y.D. Liang ◽

Y. Zhou ◽

...

Keyword(s):

Tooth Development ◽

Iron Status ◽

Acid Resistance ◽

Blue Staining ◽

Maturation Stage ◽

Wild Type ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway ◽

Stem Cell Pluripotency ◽

Underlying Mechanisms

Leukemia inhibitory factor (LIF), a member of the interleukin 6 family of cytokines, is involved in skeletal metabolism, blastocyst implantation, and stem cell pluripotency maintenance. However, the role of LIF in tooth development needs to be elucidated. The aim of the present study was to investigate the effect of Lif deficiency on tooth development and to elucidate the functions of Lif during tooth development and the underlying mechanisms. First, it was found that the incisors of Lif-knockout mice had a much whiter color than those of wild-type mice. Although there were no structural abnormalities or defective mineralization according to scanning electronic microscopy and computed tomography analysis, 3-dimensional images showed that the length of incisors was shorter in Lif−/− mice. Microhardness and acid resistance assays showed that the hardness and acid resistance of the enamel surface of Lif−/− mice were decreased compared to those of wild-type mice. In Lif−/− mice, whose general iron status was comparable to that of the control mice, the iron content of the incisors was significantly reduced, as confirmed by energy-dispersive X-ray spectroscopy (EDS) and Prussian blue staining. Histological staining showed that the cell length of maturation-stage ameloblasts was shorter in Lif−/− mice. Likewise, decreased expression of Tfrc and Slc40a1, both of which are crucial proteins for iron transportation, was observed in Lif−/− mice and Lif-knockdown ameloblast lineage cell lines, according to quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot. Moreover, the upregulation of Tfrc and Slc40a1 induced by Lif stimulation was blocked by Stattic, a signal transducer and activator of transcription 3 (Stat3) signaling inhibitor. These results suggest that Lif deficiency inhibits iron transportation in the maturation-stage ameloblasts, and Lif modulates expression of Tfrc and Slc40a1 through the Stat3 signaling pathway during enamel development.

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Anti–USAG-1 therapy for tooth regeneration through enhanced BMP signaling

Science Advances ◽

10.1126/sciadv.abf1798 ◽

2021 ◽

Vol 7 (7) ◽

pp. eabf1798

Author(s):

A. Murashima-Suginami ◽

H. Kiso ◽

Y. Tokita ◽

E. Mihara ◽

Y. Nambu ◽

...

Keyword(s):

Tooth Development ◽

Bmp Signaling ◽

Tooth Agenesis ◽

Tooth Regeneration ◽

Missing Teeth ◽

Morphogenetic Protein ◽

Genetic Abnormalities ◽

Direct Binding ◽

Tooth Germs ◽

Lipoprotein Receptor Related Protein

Uterine sensitization–associated gene-1 (USAG-1) deficiency leads to enhanced bone morphogenetic protein (BMP) signaling, leading to supernumerary teeth formation. Furthermore, antibodies interfering with binding of USAG-1 to BMP, but not lipoprotein receptor–related protein 5/6 (LRP5/6), accelerate tooth development. Since USAG-1 inhibits Wnt and BMP signals, the essential factors for tooth development, via direct binding to BMP and Wnt coreceptor LRP5/6, we hypothesized that USAG-1 plays key regulatory roles in suppressing tooth development. However, the involvement of USAG-1 in various types of congenital tooth agenesis remains unknown. Here, we show that blocking USAG-1 function through USAG-1 knockout or anti–USAG-1 antibody administration relieves congenital tooth agenesis caused by various genetic abnormalities in mice. Our results demonstrate that USAG-1 controls the number of teeth by inhibiting development of potential tooth germs in wild-type or mutant mice missing teeth. Anti–USAG-1 antibody administration is, therefore, a promising approach for tooth regeneration therapy.

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