|Year : 2015 | Volume
| Issue : 4 | Page : 147-148
Genetics and its relation to pediatric dentistry
Sara Mohamed Hamid
Department of Pediatric Dentistry, University of Al-Neelain, Khartoum, Sudan
|Date of Web Publication||17-Feb-2016|
Dr. Sara Mohamed Hamid
Department of Pediatric Dentistry, University of Al-Neelain, Khartoum
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Hamid SM. Genetics and its relation to pediatric dentistry. J Dent Res Rev 2015;2:147-8
The successful completion of the Human Genome Project in 2000 led to the development of new tools for human genetic studies. These tools have been widely applied to many human traits of complex etiology, including orofacial clefts (OFCs) and dental caries, which are both of interest for pediatric oral health. Genome-wide association (GWA) studies of OFCs have been remarkably successful compared with other human complex traits, with about 13 genes showing a statistically significant association. Some of them have been extensively replicated and are estimated to account for about 55% of OFC case. GWA studies are only the first step as they represent population-level statistical results but cannot reveal which genes/loci are etiologic in any particular individual or family.  Studies of the common lymphoid progenitor (CLP) phenotype in twins indicate that monozygous twins have a 35% concordance rate, whereas dizygous twins show <5% concordance; however, despite many extensive investigations, no simple pattern of inheritance has been demonstrated. This has led to proposals for a variety of genetic modes of inheritance for CLP, including dominance, recessiveness, and gender linkage, and has led ultimately to the documentation of modifying conditions that may be present, such as incomplete penetrance and variable gene expressivity. There are three important reasons for the failure to resolve the question of a hereditary basis for clefts: (1) Some clefts are of a nongenetic origin and should not be included in a genetic analysis (such cases are seldom recognized and are difficult to prove), (2) individuals who have increased genetic liability for having a child with CLP often fail to be recognized, but because they do not have CLP themselves, they cannot be identified with certainty, and (3) CLP, although sometimes appearing to be relatively simple in origin, is undoubtedly a complex of diseases with different etiologies lumped together because of clinical disease resemblance (they all show clefting).
Dental caries is the most common disease of childhood and is due to a combination of genetic and environmental/behavioral factors. Early evidence of a genetic component comes from animal models and human studies, with particularly strong evidence from studies of twins reared apart. The caries phenotype is traditionally expressed as the number of decayed, missing, or filled surfaces or teeth in the mouth. Dental caries results from a chronic imbalance between multiple risk and protective factors.  These factors include (1) environmental factors, such as diet, oral hygiene, fluoride exposure, and level of cariogenic bacteria and (2) host factors, such as salivary flow, salivary buffering capacity, position of teeth in the arch, surface characteristics of tooth enamel, and depth of occlusal fissures on posterior teeth.  While much is known about the causes of dental caries, in general, the development of caries in very early life is less well understood.
Although there is clear evidence that dental caries is a multifactorial, infectious disease, with many contributory environmental factors, there is strong evidence for a genetic component in the etiology of this disease. This may explain that some individuals appear to be more susceptible to caries while others are extremely resistant, irrespective of the environmental risk factors to which they are exposed, so both genetics, environmental determinants should be considered in any study of dental caries.
A genetic susceptibility to caries has been proposed based on twin studies investigating the heritability (i.e. proportion of variation due to genes) of dental caries in children have clearly supported the critical role of genetics in tooth decay. This has been supported by studies in both humans and animals.  More recent studies estimated the heritability for caries as ranging from 45-64%, with primary dentition caries showing higher heritability than permanent dentition.  Heritability studies alone are not sufficient to demonstrate a genetic component in caries because shared behavior and other environmental factors can contribute to the covariance between relatives and mimic genetic correlation. The major candidate gene categories studied to date include enamel formation genes, immune response genes, genes related to saliva, genes related to taste, and others. 
In summary, the tools of the Human Genome Project combined with detailed phenotype studies are applied to disorders of pediatric oral health impact. The results from combining these complementary types of studies hold great promise in bringing etiologic clarity to OFCs and caries, thereby leading to improved translational avenues.
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