Dental Malocclusion
Dental malocclusion refers to the misalignment of teeth and/or an improper relationship between the upper and lower dental arches when the jaws close. This common condition can manifest in various forms, including crowding, spacing, overbites, underbites, and crossbites, affecting the overall bite and function of the oral cavity.
The biological basis of dental malocclusion is complex, involving a combination of genetic, epigenetic, and environmental factors that influence tooth development and craniofacial growth[1]. Research indicates that structural dental anomalies, such as tooth agenesis (missing teeth), enamel hypoplasia (defective enamel formation), and tooth impaction, often co-occur and can contribute to the development of malocclusion, suggesting underlying shared genetic etiologies [1]. These developmental processes, when disrupted, can lead to deviations in tooth position and jaw alignment.
Clinically, malocclusion can lead to a range of oral health problems. These may include difficulties with chewing, speech impediments, and increased wear on tooth surfaces. More severe consequences can involve delayed eruption or impaction of teeth, temporomandibular joint (TMJ) pain and dysfunction, and periodontal disease due to excessive or improper occlusal forces[1]. Furthermore, crowded or misaligned teeth can be more challenging to clean effectively, increasing susceptibility to dental caries (cavities) due to structural defects or areas where food debris and bacteria can accumulate[1].
Beyond the clinical implications, dental malocclusion also carries significant social importance. The aesthetic impact of misaligned teeth can affect an individual’s self-esteem, confidence, and social interactions. Addressing malocclusion often involves orthodontic treatment, which can improve both oral function and facial aesthetics, thereby enhancing an individual’s quality of life.
Limitations
Section titled “Limitations”Understanding the genetic and environmental factors contributing to dental malocclusion is complex, and current research faces several inherent limitations that impact the interpretation and generalizability of findings. These limitations span methodological challenges, phenotypic definition, and the intricate interplay of genetic and environmental influences.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Genetic studies of complex traits like dental malocclusion are often constrained by statistical power, which is directly related to sample size. Many studies, particularly early genome-wide association studies (GWAS), may have insufficient sample sizes to detect genetic variants with small effect sizes, which are characteristic of complex multifactorial conditions[2]. This limitation can lead to an inflation of reported effect sizes for initially identified associations and contributes to difficulties in replicating findings across different cohorts. Furthermore, the complex genetic architecture of dental traits, involving numerous genes with subtle contributions, necessitates very large cohorts to achieve the statistical power required for robust identification of associated genetic loci [2]. The absence of consistent genetic association signals in some dental traits underscores the challenges in overcoming these statistical hurdles [2].
Phenotypic Heterogeneity and Generalizability Across Populations
Section titled “Phenotypic Heterogeneity and Generalizability Across Populations”A significant challenge in studying dental malocclusion lies in its phenotypic heterogeneity and the consistency of its measurement. Malocclusion encompasses a wide range of conditions, and variations in diagnostic criteria, classification systems, and measurement approaches across different studies can introduce variability and make meta-analyses or direct comparisons difficult[2]. This “trade-off between phenotypic refinement and obtaining valid phenotype data in sufficiently large cohorts” highlights a persistent issue in dental research [2]. Moreover, the generalizability of genetic findings is often limited by the ancestral composition of study populations. While some recent research has included multi-ethnic cohorts [1], many foundational genetic studies have predominantly focused on populations of European ancestry [2]. This can restrict the applicability of findings to other ancestral groups, potentially missing population-specific genetic variants or gene-environment interactions that contribute to malocclusion in diverse populations.
Environmental Confounders and Unexplained Heritability
Section titled “Environmental Confounders and Unexplained Heritability”The development of dental malocclusion is significantly influenced by a complex interplay of genetic, epigenetic, and environmental factors[3]. Current genetic studies often struggle to adequately capture and account for the full spectrum of environmental exposures and their intricate interactions with genetic predispositions. Factors such as diet, oral hygiene practices, and early childhood habits can act as significant confounders or modifiers of genetic effects, making it challenging to isolate purely genetic contributions. This incomplete accounting for gene-environment interactions contributes to the phenomenon of “missing heritability,” where common genetic variants identified by GWAS explain only a fraction of the estimated total heritability for complex traits[2]. The remaining knowledge gaps suggest that a substantial portion of the genetic etiology of malocclusion may involve rare variants, structural genomic variations, or epigenetic modifications that are not routinely captured or fully understood by current research methodologies.
Variants
Section titled “Variants”The intricate development of teeth and craniofacial structures is influenced by a complex interplay of genetic and environmental factors, with specific genetic variants potentially contributing to conditions like dental malocclusion. Genome-wide association studies (GWAS) have identified numerous genetic loci associated with various dental traits, including caries and structural anomalies, underscoring the genetic basis of oral health[3]. Malocclusion, characterized by misaligned teeth or jaws, can arise from developmental disruptions that affect tooth eruption, jaw growth, and overall oral architecture.
The GRK3gene, which encodes G protein-coupled receptor kinase 3, plays a critical role in regulating cellular signaling pathways. GRK3 is a member of the GRK family, responsible for phosphorylating activated G protein-coupled receptors (GPCRs), thereby desensitizing them and regulating the duration and intensity of cellular responses. These signaling pathways are fundamental to various physiological processes, including bone metabolism, cell differentiation, and tissue development. While the specific impact of the variantrs371297519 on GRK3 function or malocclusion is not directly detailed in specific studies, alterations in such a regulatory gene could potentially affect the precise signaling required for normal craniofacial and dental formation. Disruptions in these pathways during development could contribute to structural dental anomalies and, consequently, to the development of malocclusion [3].
Similarly, the NSUN6 gene encodes NOP2/Sun RNA methyltransferase family member 6, an enzyme involved in modifying RNA molecules, particularly through methylation. RNA methylation is a crucial epigenetic mechanism that influences RNA stability, translation efficiency, and overall gene expression. Precise control of gene expression is essential for the ordered processes of cell growth, differentiation, and tissue patterning during embryonic development, including the formation of teeth and jawbones. The variant rs76147210 within NSUN6could theoretically alter the enzyme’s activity or expression, leading to aberrant RNA modification patterns. Such changes could impair the accurate synthesis of proteins vital for dental and craniofacial development, potentially resulting in structural defects that contribute to dental malocclusion. Genetic factors are recognized as key contributors to dental anomalies, which can manifest as malocclusion[3].
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs371297519 | GRK3 | dental malocclusion |
| rs76147210 | NSUN6 | dental malocclusion |
Classification, Definition, and Terminology
Section titled “Classification, Definition, and Terminology”Defining Structural Dental Anomalies and Their Relevance
Section titled “Defining Structural Dental Anomalies and Their Relevance”The provided research primarily focuses on “structural dental anomalies,” which are defined as deviations in the normal development, number, size, shape, or eruption of teeth[3]. These anomalies are significant in oral health, as they can directly impact the alignment of teeth and the relationship between the dental arches, thereby influencing mastication, speech, aesthetics, and overall dental function. Precise definitions for these conditions are crucial for establishing diagnostic criteria and developing conceptual frameworks for studying complex dental traits that often underpin broader occlusal issues. For instance, conditions such as tooth agenesis, characterized by the congenital absence of one or more teeth, or supernumerary teeth, which involve the presence of extra teeth, represent fundamental deviations from typical dental architecture [3].
Classification and Subtypes of Dental Anomalies
Section titled “Classification and Subtypes of Dental Anomalies”The classification of structural dental anomalies involves categorizing distinct deviations observed in the dentition, which can contribute to malocclusion. Key subtypes identified in studies include hypoplasia, supernumerary teeth, tooth agenesis, enamel hypoplasia, and impaction [3]. Hypoplasia refers to the incomplete development of an organ or tissue, which, in dental terms, often relates to enamel or dentin. Supernumerary teeth are additional teeth beyond the normal complement, while tooth agenesis describes the congenital absence of one or more teeth [3]. Impaction specifically refers to a tooth that has not erupted into its functional position within the expected developmental window [3]. These categorical distinctions are fundamental to nosological systems, allowing for the differential diagnosis and targeted study of each specific anomaly.
Diagnostic Approaches and Measurement Criteria
Section titled “Diagnostic Approaches and Measurement Criteria”The diagnostic criteria for structural dental anomalies rely on comprehensive clinical assessment. Dental examinations, including in-person assessments and detailed intraoral photographs, serve as primary measurement approaches to identify and characterize these conditions [3]. While specific biomarkers for these anomalies are not detailed in the provided context, the operational definitions involve visual inspection and morphological assessment. Research criteria often involve careful recording of the presence or absence of specific anomalies, contributing to a categorical approach in studies [4]. For instance, the presence of certain anomalies like supernumerary teeth or impaction can be quantified for research purposes, providing a basis for understanding their prevalence and genetic associations [3].
Signs and Symptoms
Section titled “Signs and Symptoms”Clinical Presentation and Associated Oral Health Issues
Section titled “Clinical Presentation and Associated Oral Health Issues”Dental malocclusion is recognized clinically as a serious problem that can significantly affect oral health[3]. Typical signs of malocclusion can include delayed eruption of teeth, the presence of impacted teeth, and general dental crowding within the arch [3]. These observable patterns represent key clinical phenotypes associated with the condition and indicate deviations from normal occlusal relationships.
Beyond structural signs, malocclusion can manifest through common symptoms such as temporomandibular joint pain and dysfunction[3]. It can also lead to secondary oral health issues, including periodontal disease, which may result from excessive occlusal forces, and an increased susceptibility to dental caries, particularly when crowding or structural defects compromise oral hygiene[3]. The diagnostic significance of these symptoms lies in identifying the broader impact of malocclusion on patient well-being and dental integrity, highlighting the need for comprehensive assessment and potential intervention.
Phenotypic Diversity and Contributing Dental Anomalies
Section titled “Phenotypic Diversity and Contributing Dental Anomalies”The presentation of dental malocclusion exhibits considerable phenotypic diversity, often arising as a consequence of various structural dental anomalies during tooth development[3]. These contributing anomalies include tooth agenesis, enamel hypoplasia, impaction, rotation, supernumerary teeth, and tooth displacement [3]. The variability in malocclusion phenotypes is therefore closely tied to the specific type and severity of these underlying developmental defects, influencing the overall clinical presentation.
Assessment methods for understanding malocclusion thus involve identifying and characterizing these structural dental anomalies, which can serve as objective measures of contributing factors [3]. The diagnostic value of this approach is enhanced by recognizing that these dental defects frequently co-occur in the same patient, suggesting complex interplay and potentially shared genetic etiologies [3]. This comprehensive evaluation of associated anomalies is crucial for a complete understanding of malocclusion’s presentation and for guiding appropriate clinical management.
Causes of Dental Malocclusion
Section titled “Causes of Dental Malocclusion”Dental malocclusion, characterized by the misalignment of teeth and jaws, is a complex trait influenced by a variety of interacting factors. Its etiology is multifactorial, encompassing genetic predispositions, developmental processes, environmental exposures, and the presence of other dental anomalies.
Genetic Predisposition
Section titled “Genetic Predisposition”An individual’s genetic makeup plays a significant role in determining susceptibility to dental malocclusion. Research indicates a substantial genetic component, with studies supporting the heritability of malocclusion[5]. This genetic influence can manifest through inherited variants that affect the size and shape of the jaws, the number and size of teeth, and the patterns of tooth eruption. The genetic architecture of malocclusion often involves polygenic risk, where multiple genes interact rather than a single gene dictating the outcome. Advanced sequencing technologies, such as genome-wide association studies (GWAS), are being employed to identify specific genetic loci and variants associated with structural dental anomalies that are direct precursors to malocclusion[1]. Furthermore, some genetic variants are recognized to contribute to multiple different dental anomalies, suggesting a shared genetic etiology for various craniofacial and dental defects that ultimately lead to malocclusion.
Developmental and Epigenetic Influences
Section titled “Developmental and Epigenetic Influences”The intricate process of tooth and craniofacial development during early life is crucial for establishing proper occlusion, and any disturbances during this period can contribute to malocclusion. Structural dental anomalies, which are often direct causes of malocclusion, are presumed to arise from complex interactions between genetic, epigenetic, and environmental factors during tooth development [1]. Epigenetic mechanisms, including DNA methylation and histone modifications, are key regulators of gene expression without altering the underlying DNA sequence. These epigenetic changes can be influenced by early life experiences and environmental exposures, thereby modulating the developmental pathways of teeth and jaws, and potentially impacting tooth number, size, shape, and eruption timing, which in turn affect occlusal relationships.
Environmental and Lifestyle Factors
Section titled “Environmental and Lifestyle Factors”Environmental factors, alongside genetic predispositions, are important contributors to the development of dental anomalies and malocclusion. Lifestyle choices, dietary habits, and various exposures throughout an individual’s life can influence oral health and developmental trajectories. For example, while widely recognized as contributors to dental caries, factors such as high sugar consumption, poor oral hygiene, and lower socioeconomic status[6] can indirectly affect occlusal relationships by impacting tooth integrity, leading to premature tooth loss, or altering the developmental environment of the oral cavity. Crucially, malocclusion often results from an intricate interplay between genetic predispositions and environmental triggers. Genetic susceptibilities can be modulated by environmental factors during critical developmental windows, potentially exacerbating or mitigating the expression of malocclusion [1]. This gene-environment interaction underscores the multifactorial nature of malocclusion’s etiology.
Structural Dental Anomalies and Other Contributing Factors
Section titled “Structural Dental Anomalies and Other Contributing Factors”Structural dental anomalies represent direct and significant causes of malocclusion. Conditions such as tooth agenesis (the congenital absence of teeth), enamel hypoplasia, tooth impaction (failure of teeth to erupt), and tooth rotation are developmental defects that can severely disrupt the normal alignment and occlusion of teeth [1]. These anomalies can lead to a range of clinical problems, including delayed eruption, further impaction, and direct malocclusion due to improper spacing, crowding, or misalignment. The tendency for various dental defects to co-occur in the same patient suggests a shared underlying etiology, which further complicates the presentation and treatment of malocclusion [1]. While not extensively detailed in the provided studies for malocclusion, broader health considerations such as certain comorbidities, effects of medications on bone or tooth development, and age-related changes in jaw structure could also influence the onset or progression of malocclusion.
Biological Background of Dental Malocclusion
Section titled “Biological Background of Dental Malocclusion”Dental malocclusion refers to the improper alignment of teeth and jaws, a condition that can arise from a complex interplay of biological factors. These factors span from molecular and cellular processes governing early development to genetic predispositions and their pathophysiological consequences. Understanding the biological underpinnings of malocclusion is crucial for its prevention and treatment.
Craniofacial Development and Tooth Maturation
Section titled “Craniofacial Development and Tooth Maturation”Dental development is a highly intricate biological process that commences in the eighth week of gestation with the formation of primary teeth and continues postnatally, culminating in the maturation of permanent teeth around 18 to 25 years of age [7]. The formation, eruption, and emergence of tooth structures are intertwined events, integral to overall human tooth maturation. Disruptions during any of these stages, such as delayed dental development, can lead to inadequate dental occlusion, resulting in functional problems like mastication difficulties, speech impediments, and aesthetic concerns [7].
Malocclusion often stems from anomalies in the proper formation and positioning of teeth within the oral cavity or the development of the surrounding craniofacial bones. Structural dental anomalies, including tooth agenesis (missing teeth), enamel hypoplasia (defective enamel), tooth impaction, and rotation, are presumed to result from complex interactions between genetic, epigenetic, and environmental factors during tooth development [3]. These dental defects frequently co-occur in the same individual, suggesting a potential shared genetic etiology that influences the overall development of dental structures [3].
Genetic and Epigenetic Regulation of Orofacial Structures
Section titled “Genetic and Epigenetic Regulation of Orofacial Structures”Genetic mechanisms are fundamental in determining the precise development and arrangement of teeth and jaws, with research indicating a significant heritable component for malocclusion [5]. Specific gene functions are essential for orchestrating the complex sequence of events required for proper tooth formation, eruption, and the growth of the alveolar bone and jaw structures. Genetic variants can influence the timing and morphology of dental development, contributing to conditions such as tooth agenesis, variations in tooth size, or abnormal tooth shape[3].
The precise control of dental maturation relies on intricate regulatory elements and gene expression patterns. Key gene families, including Fibroblast Growth Factors (FGF), Wingless-related integration site (WNT), and Bone Morphogenetic Proteins (BMP), have been associated with dental development, primarily identified through studies in animal models[7]. Additionally, epigenetic modifications, which alter gene activity without changing the underlying DNA sequence, interact with both genetic and environmental factors to modulate tooth development. These complex regulatory networks collectively govern the cellular processes that form the craniofacial complex, ultimately influencing the stability and proper alignment of the dentition.
Molecular Signaling and Cellular Functions in Dental Development
Section titled “Molecular Signaling and Cellular Functions in Dental Development”The intricate formation of dental and craniofacial structures is orchestrated by a network of molecular and cellular pathways. Signaling pathways, involving critical biomolecules such as specific proteins, enzymes, receptors, and hormones, guide essential cellular functions like differentiation, proliferation, and migration during odontogenesis (tooth formation) and osteogenesis (bone formation). For example, the FGF, WNT, and BMP families represent crucial signaling molecules that direct the formation of tooth structures and the surrounding bone, acting through their respective receptors to initiate intracellular cascades[7].
Transcription factors, as key regulatory proteins, play a pivotal role by binding to specific DNA sequences to activate or repress the transcription of genes vital for dental development. Disruptions in these regulatory networks, or in the function of critical structural components and metabolic processes, can lead to developmental anomalies that manifest as malocclusion. The proper functioning and coordination of these cellular processes and the biomolecules involved are paramount for establishing a normal occlusion and preventing structural deviations that contribute to malocclusion.
Pathophysiological Consequences and Interconnections
Section titled “Pathophysiological Consequences and Interconnections”Malocclusion, arising from disrupted developmental processes, can lead to a range of pathophysiological issues beyond simply misaligned teeth. It can contribute to temporomandibular joint pain and dysfunction, often due to imbalanced occlusal forces and improper jaw mechanics[3]. Furthermore, the presence of excessive occlusal force resulting from malocclusion can predispose individuals to periodontal disease, a condition affecting the supporting structures of the teeth[3].
The presence of malocclusion, particularly when associated with defects in tooth structure or dental crowding, can also increase an individual’s susceptibility to dental caries[3]. These interconnections highlight how structural anomalies can disrupt oral homeostasis, create environments conducive to other oral health problems, and negatively impact an individual’s overall oral health quality of life [1].
Evolutionary Aspects
Section titled “Evolutionary Aspects”Genetic Architecture and Developmental Canalization
Section titled “Genetic Architecture and Developmental Canalization”Dental malocclusion, a complex trait, exhibits a notable genetic component, underscored by its documented heritability[8]. The manifestation of malocclusion results from intricate interactions among genetic, epigenetic, and environmental factors throughout the critical stages of tooth development [1]. This multifactorial etiology implies that numerous genes, potentially acting through pleiotropic effects, influence the nuanced development of craniofacial structures and tooth positioning that define occlusal relationships. The frequent co-occurrence of various structural dental anomalies, many of which contribute to malocclusion, further suggests shared underlying genetic pathways, where a single genetic variant might impact multiple developmental outcomes [1]. Such deep developmental interdependencies can impose evolutionary constraints, meaning that selective pressures acting on one aspect of craniofacial development may indirectly affect other traits, potentially contributing to the persistence of malocclusion as a byproduct of otherwise adaptive developmental programs.
Selection Pressures and Adaptive Trade-offs
Section titled “Selection Pressures and Adaptive Trade-offs”Historically, the severity of dental malocclusion would have been subject to natural selection due to its direct implications for individual fitness. Severe forms of malocclusion can lead to a spectrum of clinical challenges, including delayed tooth eruption, impaction, temporomandibular joint dysfunction, and an increased risk of periodontal disease stemming from excessive occlusal forces[1]. Furthermore, malocclusion can heighten susceptibility to dental caries, particularly due to structural defects or tooth crowding, which would have represented a significant health burden in ancestral environments[1]. These adverse health outcomes signify fitness costs that would have historically favored individuals with optimal occlusion, enhancing masticatory efficiency and reducing disease vulnerability. However, the contemporary prevalence of malocclusion in human populations may suggest a relaxation of these strong negative selective pressures, possibly influenced by shifts in diet and advancements in dental care, or it could reflect adaptive trade-offs where genetic variants contributing to mild malocclusion offer compensatory benefits in other craniofacial or developmental contexts.
Population Dynamics and Geographic Variation
Section titled “Population Dynamics and Geographic Variation”The evolutionary history of human populations, shaped by forces such as genetic drift and migration, has profoundly influenced the observed variability in malocclusion traits across diverse ethnic groups. Differences in allele frequencies, often arising from events like founder effects or population bottlenecks, can lead to distinct patterns and prevalences of dental and craniofacial characteristics within isolated populations. For example, research into the variability and patterning of permanent tooth size across various human ethnic groups highlights the genetic and historical divergence in dental morphology[9]. Moreover, historical human migrations and subsequent admixture events between previously separated populations have introduced novel genetic combinations, thereby enriching the overall genetic landscape of dental traits. These population-specific genetic backgrounds, coupled with diverse environmental exposures, contribute to the intricate geographic spread and differential expression of malocclusion phenotypes observed worldwide.
Frequently Asked Questions About Dental Malocclusion
Section titled “Frequently Asked Questions About Dental Malocclusion”These questions address the most important and specific aspects of dental malocclusion based on current genetic research.
1. My family has crooked teeth; will my kids automatically get them?
Section titled “1. My family has crooked teeth; will my kids automatically get them?”Not automatically, but your children do have a higher genetic predisposition. Dental malocclusion often runs in families because craniofacial growth and tooth development are strongly influenced by inherited genetic factors. However, environmental factors like early childhood habits also play a role, so it’s not a guarantee they will inherit the exact same condition.
2. Why do I get so many cavities even though I brush well?
Section titled “2. Why do I get so many cavities even though I brush well?”Malocclusion can make your teeth harder to clean effectively, even with good brushing habits. Misaligned or crowded teeth create areas where food debris and bacteria can accumulate, increasing your susceptibility to dental caries. Some structural dental anomalies that contribute to malocclusion, like enamel defects, can also make teeth more prone to cavities, suggesting a shared genetic link.
3. Does having misaligned teeth actually impact my social life?
Section titled “3. Does having misaligned teeth actually impact my social life?”Yes, it absolutely can. Beyond the functional issues, the aesthetic impact of misaligned teeth can significantly affect your self-esteem, confidence, and how you interact socially. Addressing malocclusion often improves both oral function and facial aesthetics, which can enhance your overall quality of life.
4. Why do I have trouble chewing certain foods with my bite?
Section titled “4. Why do I have trouble chewing certain foods with my bite?”Your malocclusion, or misaligned bite, can definitely make chewing difficult. An improper relationship between your upper and lower dental arches means your teeth aren’t meeting correctly, leading to inefficient chewing and potential discomfort with certain foods. This can also cause increased wear on specific tooth surfaces.
5. Is my jaw pain linked to my crooked bite?
Section titled “5. Is my jaw pain linked to my crooked bite?”Yes, there’s a strong possibility your jaw pain is related. Malocclusion can lead to excessive or improper occlusal forces, which can contribute to temporomandibular joint (TMJ) pain and dysfunction. Correcting your bite can often alleviate these issues by distributing forces more evenly across your teeth and jaw.
6. Why do some people have perfect teeth without braces?
Section titled “6. Why do some people have perfect teeth without braces?”Some people naturally develop well-aligned teeth and jaws due to a favorable combination of genetic and environmental factors. Their genes likely guide optimal craniofacial growth and tooth eruption patterns, leading to a balanced bite. While genetics play a significant role, the absence of detrimental environmental influences also contributes to their perfect smile.
7. Can my child’s early habits make their teeth crooked?
Section titled “7. Can my child’s early habits make their teeth crooked?”Yes, early childhood habits can significantly influence your child’s dental development and contribute to malocclusion. While genetics lay a foundation for craniofacial growth, environmental factors like thumb-sucking, prolonged pacifier use, or tongue thrusting can modify jaw development and tooth position. Addressing these habits early can be beneficial.
8. Why did some of my teeth get stuck and never fully come in?
Section titled “8. Why did some of my teeth get stuck and never fully come in?”This condition, known as tooth impaction, often has underlying genetic causes. Structural dental anomalies like impaction are known to co-occur with malocclusion, suggesting shared genetic etiologies that disrupt normal tooth development and eruption pathways. It’s not uncommon for these developmental processes to be genetically influenced.
9. Does my bite affect how I speak clearly?
Section titled “9. Does my bite affect how I speak clearly?”Yes, your bite can definitely affect your speech clarity. An improper relationship between your upper and lower teeth, or malocclusion, can lead to speech impediments because the tongue, lips, and teeth need to coordinate precisely to form sounds. Correcting your bite can often improve your articulation.
10. Does my ethnic background affect my risk for a bad bite?
Section titled “10. Does my ethnic background affect my risk for a bad bite?”Yes, your ethnic background can influence your risk for certain types of malocclusion. While many genetic studies have focused on populations of European ancestry, research in multi-ethnic cohorts shows that different ancestral groups can have varying genetic predispositions and specific gene-environment interactions that contribute to dental traits. This means genetic risk factors can differ across populations.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Alotaibi, R. N., et al. “Genome-Wide Association Study (GWAS) of dental caries in diverse populations.”BMC Oral Health, 2021, PMID: 34311721.
[2] Shungin, Dmitry, et al. “Genome-wide analysis of dental caries and periodontitis combining clinical and self-reported data.”Nature Communications, vol. 10, no. 1, 2019, p. 2841.
[3] Alotaibi RN. “Multivariate GWAS of Structural Dental Anomalies and Dental Caries in a Multi-Ethnic Cohort.”Front Dent Med, 2022.
[4] Shaffer JR. “Genome-wide association scan for childhood caries implicates novel genes.” J Dent Res, 2011.
[5] Mossey, P. A. “The heritability of malocclusion: part 2. The influence of genetics in malocclusion.”
[6] Haworth S. “Consortium genome-wide meta-analysis for childhood dental caries traits.”Hum Mol Genet, 2018.
[7] Grgic, O., et al. “Novel Genetic Determinants of Dental Maturation in Children.” Journal of Dental Research, vol. 102, no. 3, 2023, PMID: 36437532.
[8] Mossey, P. A. “The heritability of malocclusion: part 2. The influence of genetics in malocclusion.” British Journal of Orthodontics, vol. 26, no. 2, 1999, pp. 103–10.
[9] Brook, A. H., et al. “Variability and patterning in permanent tooth size of four human ethnic groups.”Archives of Oral Biology, 2009.