Evolving concepts of heredity and genetics in orthodontics

Abstract

The field of genetics emerged from the study of heredity early in the 20th century. Since that time, genetics has progressed through a series of defined eras based on a number of major conceptual and technical advances. Orthodontics also progressed through a series of conceptual stages over the past 100 years based in part on the ongoing and often circular debate about the relative importance of heredity (nature) and the local environment (nurture) in the etiology and treatment of malocclusion and dentofacial deformities. During the past 20 years, significant advancements in understanding the genomic basis of craniofacial development and the gene variants associated with dentofacial deformities have resulted in a convergence of the principles and concepts in genetics and in orthodontics that will lead to significant advancement of orthodontic treatments. Fundamental concepts from genetics and applied translational research in orthodontics provide a foundation for a new emphasis on precision orthodontics, which will establish a modern genomic basis for major improvements in the treatment of malocclusion and dentofacial deformities as well as many other areas of concern to orthodontists through the assessment of gene variants on a patient-by-patient basis.

Malocclusion in children and adolescents with Down syndrome: A systematic review and meta‐analysis

“…Malocclusion is associated with factors, emerging from genetic, environmental, behavioural, and illness issues. 29 Several factors reported in the literature are related to the higher prevalence of malocclusion among DS individuals. Anterior crossbite and Angle Class III malocclusion are prevalent occlusal traits among DS children/adolescents.…”

Implications of Vertebrate Craniodental Evo‐Devo for Human Oral Health

“…Understanding human pathology informs studies of human Evo‐Devo and vice versa. Much like the false dichotomy of deeming research either fundamental or medical (Firestein, ) is “the futility of…the debate over heredity versus environment” (McKeever, ), which are yin and yang (Carlson, ) in the etiology of craniodental disorders. Interaction between the intrinsic/prior (genetic) and the extrinsic/proximate (epigenetic, functional) is imperative for healthy craniodental development and growth (Moss, ) (Fig.…”

“…This epiphenomic model may also be a useful template for oral health clinicians who wish to integrate patient phenotype with genotype (Carlson, 2015) and, perhaps, with behavior into a personalized treatment plan (Moreno Uribe and Miller, 2015). Evidence-based behavioral therapies for TMDs have already become mainstream (Carlson, 2007;Scrivani et al, 2008): there is compelling evidence to implement behavior-based approaches to mitigate impaction and malocclusion, especially if implemented soon after weaning when kids start chewing solid foods (Campbell-Malone et al, 2011;Ungar et al, 2012).…”

Altering calcium and phosphorus levels in utero affects adult mouse mandibular morphology

“…The aetiology of skeletal malocclusion is yet unclear. In the 19th century, skeletal malocclusions were theorized to be caused by dietary deficiencies, endocrine malfunction or mental degeneracy rather than genetic transmission . However, the relationship between genetics and skeletal malocclusion began to gain popularity since the 1960s, which ultimately resulted in the identification of several candidate genes that play a role in the aetiology of Class II and Class III malocclusion.…”

“…In the 19th century, skeletal malocclusions were theorized to be caused by dietary deficiencies, endocrine malfunction or mental degeneracy rather than genetic transmission . However, the relationship between genetics and skeletal malocclusion began to gain popularity since the 1960s, which ultimately resulted in the identification of several candidate genes that play a role in the aetiology of Class II and Class III malocclusion. For example, collagen type 1A ( COLIAI ), cartilage matrix protein matrilin‐1 ( MATN1 ) and fibroblast growth factor 2 ( FGFR2 ) were associated with increased risk of Class III malocclusion, whereas T‐Box 5 ( TBX5 ) was associated with decreased risk .…”