Tooth size patterns in patients with hypodontia and supernumerary teeth

Brook, A.H.; Griffin, Rebecca; Smith, Richard N.; Townsend, Grant; Kaur, Gurpreet; Davis, G. R.; Fearne, Janice M.

doi:10.1016/j.archoralbio.2008.05.016

Cited by 64 publications

(69 citation statements)

References 18 publications

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“…Bailit (1975) suggested a polygenic model and agreed with Brook in his hypothesised model; both suggested that tooth agenesis illustrates the quasi continuous trait. [55,62,63,64] According to both, the variable expression of tooth agenesis reports especially in monozygotic twins, supports the hypothesis of this model . [61][62][63][64][65][66] …”

Section: Multi Factorial Model Of Dental Anomalies Of Tooth Number Ansupporting

confidence: 60%

“…[38,39] This multifactorial etiology can include environmental factors as well, since a combination of environmental and genetic factors might contribute to the occurrence of dental agenesis These include infection, trauma and drugs, as well as genes associated with about 120 syndromes, such as cleft lip, cleft palate or both, ectodermal dysplasia and Down, Rieger and Book syndromes A possible general explanation is that except in hereditary cases, Congenitally missing teeth has greater occurrence likelihood when the dental germ is developing after the surrounding tissues have closed the space needed for the tooth development. [37,64] Other investigations demonstrated that delays in tooth development and reductions in tooth size correlate with advanced Congenitally missing teeth. Both of these might accord with the terminal reduction theory.…”

Section: Discussionmentioning

confidence: 99%

“…It is progressive, occurring over a long period, yet with critical stages. [1,37,64]The series of interactions involving multiple genetic signalling pathways are also influenced by extracellular factors. Interactions, gradients and spatial field effects of multiple genes, epigenetic and environmental factors all influence the development of individual teeth, groups of teeth and the dentition as a whole.…”

Section: Discussionmentioning

confidence: 99%

“…Related to the action of a number of the developmental regulatory genes active in odontogenesis, in different tissues, mutations can result in syndromes of which dental anomalies are part. [1,37,64] Disruption of the antagonistic balance between developmental regulatory genes, acting as activators or inhibitors can result in dental anomalies. There are critical stages in the development of the individual tooth germs and, if progression fails, the germ will not develop further or undergoes apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…They also need to collate findings at each level and exploit the accurate definition of both human and murine phenotypes now possible. [1,37,64] Clinicians could be assisted by knowing the Congenitally missing teeth risk factors and its pattern of occurrence. As a general rule, if only a few teeth are missing, the absent tooth would be the most distal tooth of any given type.…”

Section: Discussionmentioning

confidence: 99%

See 4 more Smart Citations

Tooth Agenesis; Aetiological Factors

Azzaldeen¹,

Watted²,

Mai³

et al. 2017

IOSR JDMS

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Section: Multi Factorial Model Of Dental Anomalies Of Tooth Number Ansupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Tooth Agenesis; Aetiological Factors

Azzaldeen¹,

Watted²,

Mai³

et al. 2017

IOSR JDMS

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Tooth Agenesis

Luder¹,

Mitsiadis²

2012

Encyclopedia of Life Sciences

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Tooth agenesis denotes a condition where teeth are missing due to a developmental failure. According to severity, this malformation can be subdivided into hypodontia, oligodontia and anodontia. With a frequency of 20–30%, tooth agenesis is the most prevalent dental dysplasia, but not all teeth are equally affected. Familial occurrence and concordance in twins indicate potential genetic causes. Thus far, mutations could be identified for the genes MSX1 , PAX9 and AXIN2 . All result in oligodontia. It is assumed that the defects cause haploinsufficiency, reducing the functional gene products below a critical level, which is required for normal odontogenesis. Both hypodontia and oligodontia can occur as an isolated dental malformation or in combination with defects in other organs, for example the skin and its appendages. Such syndromes can result from genetic defects affecting MSX1 and the EDA signalling pathway. In the case of isolated hypodontia, associations have been found with sequence variants of several genes. Key Concepts: Tooth agenesis is a dental malformation in which teeth are missing, because they fail to develop. Tooth agenesis in humans allows inferences to be drawn regarding the control of odontogenesis, when phenotypes and genotypes are related to experimental findings obtained from mice. Mutations in human genes regulating early stages of tooth formation cause agenesis of multiple teeth, that is, oligodontia. Defects of genes important for early odontogenesis probably result in haploinsufficiency and lead to a disruption of dental development, because the quantity of functional gene products is reduced below a critical level required for normal tooth formation. Not all teeth are equally susceptible to a reduction in odontogenic potential. Tooth agenesis can occur in a syndromic form, that is, in combination with defects in other organs and tissue, for example the skin and its appendages. DNA sequence variants, which have less severe consequences for gene products are also likely to contribute to mild forms of tooth agenesis, where only a few teeth are congenitally absent.

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