Primary failure of eruption: Clinical and genetic findings in the mixed dentition

Grippaudo, Cristina; Cafiero, Concetta; D'Apolito, Isabella; Ricci, Beatrice; Frazier‐Bowers, Sylvia A.

doi:10.2319/062717-430.1

Cited by 31 publications

(34 citation statements)

References 16 publications

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“…Even though human and mice PFE shares the similar phenotypes, the difference in genetic conditions should be considered. While in human PFE is caused by loss‐of‐function mutations in PTHR1 gene (Decker et al, ; Frazier‐Bowers et al, , ; Grippaudo et al, ; Jelani et al, ; Risom et al, ; Roth et al, ; Yamaguchi et al, ), mouse PFE is caused by the artificial genetic manipulation in which PPR is specifically deleted in a population of PTHrP‐expressing mesenchymal progenitors of the dental follicle (Takahashi et al, ). Therefore, the actual mechanism underlying human PFE might be different from that of mouse PFE.…”

Section: Discussionmentioning

confidence: 99%

“…Loss-of-function mutations in Parathyroid hormone receptor 1 (PTHR1, also known as PTH/PTHrP receptor, PPR) are associated with PFE in humans (Decker et al, 2008;Frazier-Bowers et al, 2014;Frazier-Bowers, Simmons, Wright, Proffit, & Ackerman, 2010;Grippaudo, Cafiero, D'Apolito, Ricci, & Frazier-Bowers, 2018;Jelani et al, 2016;Risom et al, 2013;Roth et al, 2014;Yamaguchi et al, 2011). PTHR1 is a G protein-coupled receptor that binds to parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) in an equivalent affinity (Dean, Vilardaga, Potts, & Gardella, 2008;Jüppner et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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A three‐dimensional analysis of primary failure of eruption in humans and mice

et al. 2019

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Objectives Primary failure of eruption (PFE) is a genetic disorder exhibiting the cessation of tooth eruption. Loss‐of‐function mutations in parathyroid hormone (PTH)/parathyroid hormone‐related peptide (PTHrP) receptor (PTH/PTHrP receptor, PPR) were reported as the underlying cause of this disorder in humans. We showed in a PFE mouse model that PTHrP‐PPR signaling is responsible for normal dental follicle cell differentiation and tooth eruption. However, the mechanism underlying the eruption defect in PFE remains undefined. In this descriptive study, we aim to chronologically observe tooth eruption and root formation of mouse PFE molars through 3D microCT analyses. Setting and Sample Population Two individuals with PFE were recruited at Showa University. A mouse PFE model was generated by deleting PPR specifically in PTHrP‐expressing dental follicle and divided into three groups, PPRfl/fl;R26RtdTomato/+(Control), PTHrP‐creER;PPRfl/+;R26RtdTomato/+(cHet), and PTHrP‐creER;PRRfl/fl;R26RtdTomato/+(cKO). Materials and Methods Images from human PFE subjects were acquired by CBCT. All groups of mouse samples were studied at postnatal days 14, 25, 91, and 182 after a tamoxifen pulse at P3, and superimposition of 3D microCT images among three groups was rendered. Results Mouse and human PFE molars exhibited a similar presentation in the 3D CT analyses. The quantitative analysis in mice demonstrated a statistically significant decrease in the eruption height of cKO first and second molars compared to other groups after postnatal day 25. Additionally, cKO molars demonstrated significantly shortened roots with dilacerations associated with the reduced interradicular bone height. Conclusions Mouse PFE molars erupt at a much slower rate compared to normal molars, associated with shortened and dilacerated roots and defective interradicular bones.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A three‐dimensional analysis of primary failure of eruption in humans and mice

et al. 2019

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“…Becker [ 13 ] cites a number of unusual anomalies associated with the failure of permanent molars to erupt: dentigerous cyst (increased intracystic pressure), ankylosis (usually subjective), invasive cervical root resorption, hooked or dilacerated root (cause or effect?) [ 4 ], primary failure of eruption (affects all teeth posterior to most anteriorly affected tooth) [ [27] , [28] , [29] ], pre-eruptive intracoronal resorption, and root encirclement of the inferior alveolar nerve. In regards to a molar not erupting due to ankylosis, Becker [ 13 ] states “ankylosis of an impacted tooth is often very casually determined on the empirical basis that the tooth has not responded to extrusive orthodontic forces…it is an entirely outcome-oriented, fall back designation.…”

Section: Etiologic Factorsmentioning

confidence: 99%

The management of mesially inclined/impacted mandibular permanent second molars

Turley

2020

Journal of the World Federation of Orthodontists

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Mesially impacted mandibular second molars are a common occurrence in orthodontic practices, especially those using the lingual arch or lip bumper for alleviating anterior crowding. Horizontally impacted second molars, on the other hand, occur so infrequently that most practitioners have limited experience in treating such a patient. Because of this there is little consensus on the management of these cases. As opposed to vertically impacted molars that may be associated with ankylosis or other factors preventing eruption, the mesially angulated, horizontally impacted mandibular second molar usually has eruption potential, because its impaction is more commonly due to lack of space and/or abnormal eruption path. Hence, orthodontic uprighting shows the most promise and can commonly be done without extracting the third molar or surgically exposing the impacted second molar. Modern clinicians have at their disposal a myriad of biomechanical choices that can be used to successfully reposition these teeth and enable finishing with an optimal occlusion.

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“…If the first permanent molar is involved, extraction should be planned to allow mesial drifting of the second permanent molar. However, if the second permanent molar is similarly affected, then it undermines a conservative extraction plan [62].…”

Section: Clinical Manifestations Include Unilateral or Bilateralmentioning

confidence: 99%

Developmental Dental Anomalies of Primary and Permanent Dentition

Puranik¹

2019

OAJDS

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Development of the primary and permanent dentition is a highly regulated process in humans. A cascade of signaling pathways occur in a spatio-temporal manner resulting in the development and eruption of the human dentition. Any developmental aberrations in shape, size, number, and position can lead to deviations from normal development of teeth. This chapter discusses each developmental dental anomaly in both dentitions with special emphasis on causative factors at local, systemic, environmental or genetic levels. A review of findings, clinical implications and treatment options is provided for each anomaly. Dentists should be aware of these developmental dental anomalies due to the possible associations with systemic conditions or pathologies.

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Primary failure of eruption: Clinical and genetic findings in the mixed dentition

Abstract: Novel mutations were reported in the PTH1R gene that included PFE-affected primary molars, thus providing the basis for using a genetic diagnostic tool for early diagnosis leading to proper management.

Cited by 31 publications

References 16 publications

A three‐dimensional analysis of primary failure of eruption in humans and mice

A three‐dimensional analysis of primary failure of eruption in humans and mice

The management of mesially inclined/impacted mandibular permanent second molars

Developmental Dental Anomalies of Primary and Permanent Dentition

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