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Background:
Systematic Review

The Association Between Non-Syndromic Tooth Agenesis and MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD Gene Mutations: A Systematic Review

by
Fotios Bakouros-Kouroupakis
*,
Ioannis Tsolianos
and
Eleni Kotsiomiti
Department of Prosthodontics, School of Dentistry, Faculty of Health Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
*
Author to whom correspondence should be addressed.
Prosthesis 2025, 7(6), 142; https://doi.org/10.3390/prosthesis7060142
Submission received: 8 May 2025 / Revised: 23 October 2025 / Accepted: 26 October 2025 / Published: 5 November 2025
(This article belongs to the Section Prosthodontics)
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Abstract

Background: Tooth development or odontogenesis is a complicated, multi-staged process, regulated by a plethora of genes. Disruptions during the early stages of odontogenesis may cause the complete absence of one or more teeth, known as tooth agenesis (TA). Except for PAX9, alterations in MSX1, AXIN2, WNT10A, and EDA/EDAR/EDARADD have gathered an increasing amount of interest. Objectives: This systematic review aims to investigate whether non-syndromic tooth agenesis (NSTA) is associated with MSX1, AXIN2, WNT10A, and EDA/EDAR/EDARADD mutations and to list the related phenotypic patterns of these alterations with regard to missing teeth. Methods: MEDLINE, Scopus, and Web of Science were the three selected databases. Duplicates were removed using Mendeley, and the records were assessed via the Rayyan platform. The Newcastle–Ottawa Scale was used to evaluate the quality of the evidence. Results: Fifteen case–control studies were eligible for this systematic review. The MSX1 gene was examined in most studies, whereas second premolars and lateral incisors were the most commonly missing teeth among TA cases. In total, 61.29% to 84.9% of the cases included one or two absent teeth. Conclusions: Due to the considerable heterogeneity in reporting results across the included studies, along with the high risk of bias present in most of them, it was not feasible to conduct a meta-analysis of the data. Nonetheless, the findings suggest that the NSTA phenotypes linked to the studied genes are similar to those associated with other forms of TA and share a common pattern of missing teeth. Future research should adopt a more standardized approach in presenting findings by adhering to established terminology and definitions and by utilizing common cut-off points to categorize results.

1. Introduction

The process of teeth development during embryonic growth, referred to as odontogenesis, is regarded as a fundamental pillar of organogenesis [1]. It is based on reciprocal interactions between two embryonic tissue types, ectoderm and mesenchyme [2,3]. Tooth development begins with the thickening of the epithelium in the regions that will become the future maxilla and mandible [2,4]. Further immersion of dental epithelial thickening into the underlying mesenchyme leads to the bud, cap, and bell stages of odontogenesis [1,4,5]. Cell differentiation of the epithelium and mesenchyme forms ameloblasts and odontoblasts, respectively [1,4]; these create the hard tissues of the crown, enamel, and dentine. The complex multi-step process of odontogenesis is regulated by various genes [1,4]. Homeobox genes seem to play a pivotal role during odontogenesis [6], and four main signaling pathways (BMP, FGF, WNT, and SHH) and their receptors are of crucial importance as well [1,3,4].
Complications during the initial stages of tooth development may cause the congenital absence of one or more teeth [7,8]. This disorder is called tooth agenesis (TA) and is one of the most common dental anomalies [9,10], with its prevalence varying according to sex and ethnicity [11]. Based on the number of missing teeth, TA is classified as hypodontia (less than six missing teeth, excluding third molars), oligodontia (six or more missing teeth, excluding third molars), or anodontia (all teeth missing) [9,12]. TA is presented either as part of a syndrome (syndromic) or as an individual trait (non-syndromic tooth agenesis—NSTA) [10]. It may appear bilaterally or unilaterally [13] and may affect not only permanent but also, more rarely, deciduous teeth [14].
Third molars excluded, the most frequently missing teeth are the lateral incisors and second premolars [15,16,17,18], and several theories have been proposed to interpret this pattern [19]. Severe TA can significantly impact oral function, aesthetics, nutrition, and psychological well-being, in addition to disrupting normal craniofacial development. Therefore, it requires continuous treatment with targeted interventions from a multidisciplinary team of dental and medical professionals [13,20].
The prosthodontic management of children and adolescents with missing teeth constitutes a challenging task, especially in cases of severe TA. Intraoral changes, as well as ongoing craniofacial growth, should be taken into account when planning and monitoring prosthodontic interventions [11,21]. Furthermore, TA cases often involve other dental abnormalities, such as teeth with atypical shapes or reduced sizes, which can complicate treatment planning [22,23]. Removable prostheses, typically mucosa-borne acrylic partial dentures, are generally regarded as the preferred treatment option for children and adolescents, as they serve as interim appliances until the growth is complete and permanent prosthodontic options can be realized [24,25].
The etiology of TA is mainly attributed to genetic and environmental factors [7], and mutations of specific genes have been identified in many cases [26]. In NSTA, mutations in PAX9, MSX1, AXIN2, WNT10A, and EDA/EDAR/EDARADD appear to be responsible for the majority of the cases [9,27]. These genes play various roles during the early stages of odontogenesis, such as transcription factors (PAX9; MSX1) [28,29], regulators of the Wnt signaling pathway (AXIN2; WNT10A) [6,14,30], or members of the EDA pathway (EDA-ligand, EDAR-receptor, and EDARADD-adaptor protein) [31,32]. The combined (synergistic or antagonistic) action of these molecules and their corresponding pathways could possibly explain the considerable heterogeneity regarding phenotype patterns of NSTA [10,18,33].
According to the existing literature, PAX9 appears to be the most prevalent gene linked to NSTA [28,34,35]. More than 50 PAX9 mutations have been associated with TA and impairments in specific gene loci, resulting in varying severity and phenotype [28,34]. However, regarding the rest of the genes that have been studied in connection with NSTA, the scientific evidence has not yet been systematically reviewed.
The purpose of this systematic review was to explore the relationships between mutations in the MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD genes and NSTA, with a particular focus on the phenotypic aspects. Specifically, we aimed to determine whether alterations in these genes are linked to distinct patterns of agenesis, differing from those associated with PAX9 mutations or syndrome-related TA.

2. Materials and Methods

2.1. Protocol Registration

The protocol of this systematic review was developed in accordance with the latest version of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement [36] and has been uploaded to the PROSPERO database for the prospective registration of systematic reviews and meta-analyses (CRD42023430408).

2.2. Eligibility Criteria

Studies were eligible for this systematic review under the following prerequisites:
  • Case–control study design;
  • English language;
  • Two study arms: participants with diagnosed NSTA and healthy controls;
  • Outcome of interest: prevalence of gene mutations (MSX1, AXIN2, WNT10A, EDA/EDAR/EDARADD) in both study groups.
The diagnosis of TA had to be verified by radiographs and/or clinical examination, while gene mutations had to be confirmed by a proper genotyping or sequencing method. Studies assessing participants with syndromic TA, oral cleft defects, or missing third molars only were excluded.

2.3. Information Sources

Regarding electronic search, MEDLINE (via PubMed), Scopus, and Web of Science were assessed. Handsearching was conducted on Google Scholar, whereas opengrey.eu was deployed to assess gray literature. The detailed search strategy on MEDLINE can be seen in Supplementary Table S1.

2.4. Study Records

Search records were inserted into Mendeley, where duplicates were removed. Data were exported from Mendeley and imported into the Rayyan platform [37]. Records were assessed according to their title and abstract, and the next step involved full-text assessment. Study selection was performed by two independent reviewers (F.B.K., I.T.), with disagreements resolved by a third one (E.K.). Figure 1 provides a detailed overview of the process using a PRISMA 2020 flow diagram.

2.5. Data Items

Data extraction was performed by two independent reviewers (F.B.K., I.T.) and verified by a third independent reviewer (E.K.). The data were inserted into a Microsoft Excel spreadsheet under the following categories:
  • PMID, first author, year of publication, age, sex, gene of interest, single-nucleotide polymorphisms (SNPs) of interest, sample size, TA cases and controls, number of TA cases and controls with mutations, number of missing teeth, phenotype, diagnostic method of TA, and verification method of gene mutations.

2.6. Risk of Bias

The quality of included studies was assessed via the Newcastle–Ottawa Scale. Biases were judged as “low”, “high”, or “unclear” in each of the three domains (criteria), namely, selection, comparability, and exposure bias [38]. This step was performed by two independent reviewers (F.B.K., I.T.), with a third reviewer (E.K.) solving any differences.
Prosthesis 07 00142 g001
Figure 1. PRISMA 2020 flow diagram.
Figure 1. PRISMA 2020 flow diagram.
Prosthesis 07 00142 g001

3. Results

The electronic search of the three databases yielded 106 records. After duplicate removal, 62 records were screened according to title and abstract, and 20 of them progressed toward full-text evaluation. The final number of studies eligible for the systematic review was 15 [39,40,41,42,43,44,45,46,47,48,49,50,51,52,53]; however, a meta-analysis could not be performed due to the complexity and heterogeneity of the numerical results of gene mutations in cases of TA and their controls. Table 1 and Table 2 present the characteristics of the included studies, and Table 3 lists the full-text studies excluded from the review and the reasons for exclusion.

3.1. Demographic Characteristics

Table 1 contains the general demographic characteristics of the included studies. In total, 11 out of 15 studies were published in the decade 2010–2020. Four studies were conducted on Chinese populations, while Brazil followed closely behind with three studies.

3.2. Gene Mutations, Samples, and Methods of Detection

Table 2 provides detailed information about the genes of interest, the number of TA cases and controls, and methods of detecting TA and gene mutations. Among the genes examined, MSX1 has attracted considerable attention, as nine studies refer to it, followed by WNT10A and six studies. A total of 77 SNPs have been reported across the studies, with MSX1 rs12532 appearing to be the most common, as it was found in seven publications. The total sample size was 5186, comprising 1576 TA cases and 3610 controls. TA was confirmed by clinical and radiographic examination (13 studies each), and gene aberrations were detected by DNA extraction and genotyping (14 studies).

3.3. Tooth Agenesis Patterns and Phenotype

Table 2 provides information about missing teeth in TA cases. Based on 13 studies that provided relevant data, 5164 teeth were missing in total. With regard to TA types, Figure 2 depicts the percentage of TA cases with one, two, or at least three missing teeth in each study [39,41,44,45,49,50,52]. The publication of Chen et al. [46] was not included in Figure 2 due to the classification of cases into different groups regarding the number of missing teeth (one to five: 5.36%; six or more: 94.64%).
Table 2. List of included studies—study samples, missing teeth, and genes of interest.
Table 2. List of included studies—study samples, missing teeth, and genes of interest.
Genes of InterestSNPs of InterestSample SizeTooth Agenesis Cases/Control GroupTotal Number of Missing TeethMeans for Tooth Agenesis DiagnosisHow Were the Mutations Investigated?
1AXIN2, MSX1, EDAAXIN2: rs4128941, rs4791171. MSX1: rs8670, rs12532, rs1042484, rs36059701, rs3775261,
rs3821949, rs186861426. EDA: rs1160315, rs12853659,
rs2274469, rs2428151, rs2520378, rs62604271		36061/299141Clinical examination, X-ray, dental historyDNA extraction and genotyping
2EDA, WNT10AEDA: rs1160315, rs2428151, rs2520378, rs12853659, rs5936523. WNT10A: rs11680244, rs2385199, rs7349332306102/204188Clinical examination, X-rayDNA extraction and genotyping
3EDAR, EDARADDEDAR: rs151195196, rs759735008, rs61761321, rs3749108, rs3749098, rs3749099, rs200267845, rs10432616, rs3827760, rs146567337. EDARADD: rs966365, rs60808129, rs200569815, rs604070, rs777172467, rs753890063, rs74942492, rs753408117224112/1121766Clinical examination, X-ray, dental historyDNA extraction and genotyping
4WNT10Ars1476802161386191/1195502Clinical examination, X-ray, dental historyDNA extraction and genotyping
5AXIN2, WNT10AAΧΙΝ2: rs190687283, rs2240308, rs9915936, rs1133683, rs63533624, rs139316692, rs35415678, rs143243661. WNT10A: rs77583146, rs147680216, rs12190812010860/48136Clinical examination, X-ray, medical history, family historyDNA extraction and genotyping
6MSX1, AXIN2MSX1: rs12532. AXIN2: rs2240308, rs2240307, rs35415678469209/260363 (in hypodontia group)Clinical examination, X-ray, family historyDNA extraction and genotyping
7MSX1rs8670, rs125326131/3080X-ray, dental history, family historyDNA extraction and genotyping
8MSX1rs1253221053/15796Clinical examination, X-rayDNA extraction and genotyping
9AXIN2, EDAR, EDARADD, MSX1, WNT10AAXIN2: rs2240308. EDAR: rs3749096, rs3749110, rs3827760, rs6749207. EDARADD: rs966365, rs3916983, rs6428955, rs7513402. MSX1: rs12532, rs3821947, rs3821949. WNT10A: rs1057306, rs6744926, rs34972707473273/200585Clinical examination, X-rayDNA extraction and genotyping
10WNT10Ars121908119, rs121908120587157/430801Clinical examination, X-ray, medical history, family historyDNA extraction and genotyping
11MSX1rs8670, rs1095, rs125325035/1566Clinical examination, X-rayDNA extraction and genotyping
12MSX1N/A10050/50N/AX-ray, dental historyDNA extraction and genotyping
13MSX1N/A4020/20N/AClinical examination, X-ray, medical history, family historyDNA extraction and sequencing
14MSX1, EDA, EDARMSX1: rs62636562, rs1042484, rs10213286, rs13127820, rs12532. EDA: rs760041, rs6625561, Hcv992421, rs2804361, rs6625546, hCV27026158. EDAR: hCV790922, rs3827760, rs13029834, rs7585138, rs12992554, rs899259, rs1726948746593/372175Clinical examinationDNA extraction and genotyping
15WNT10Ars116998555, rs147680216347129/218265Clinical examination, dental historyDNA extraction and genotyping
Table 3. List of excluded studies.
Table 3. List of excluded studies.
First Author et al., YearCitationReason for Exclusion
1Wang, 2010[54]No English language
2Wong, 2014[55]No English language
3Ross, 2023[56]Population: No tooth agenesis cases and controls
4Wang, 2013[57]No gene mutations of interest
5Wang, 2016[58]Only on family members
In Figure 3, information is given about the distribution of missing teeth between the maxilla and mandible, based on nine studies that provided relevant data [40,41,46,47,48,49,50,51,52]. The total number of missing maxillary and mandibular teeth was 1865 and 1917, respectively.
Figure 4 depicts the distribution of missing teeth among tooth groups, based on seven studies that provided data [40,41,45,49,50,52,53]. Furthermore, Figure 5 illustrates the relevant findings from the study by Chen et al. [46], as the composition of their sample appears to vary, with 94.64% of TA cases identified as oligodontia.

3.4. Risk of Bias Assessment

The Newcastle–Ottawa Scale was assessed to evaluate the quality of the evidence. In most of the studies, the risk of bias was characterized as “high” because of the “comparability bias” domain, whereas two studies had a low risk of bias (Figure 6 and Figure 7).

4. Discussion

The present study aimed to investigate the association between NSTA and the MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD mutations, focusing on phenotypic patterns. Our findings highlight the clinical relevance of identifying gene mutations associated with NSTA, as they can inform diagnosis and genetic counseling. The identification of specific patterns may contribute to the development of standardized guidelines for optimal design and manufacturing of prosthetic appliances [26]. By gaining a better understanding of the connection between NSTA phenotypes and the underlying gene mutations, dental prosthodontists will be better equipped to assess the pattern and severity of missing teeth and select restorative approaches tailored to each patient’s genetic and developmental profile. [11].
Although the current systematic review included 15 studies, a meta-analysis could not be performed due to the variability and heterogeneity of the data. Nearly all studies define TA cases as “participants with at least one permanent tooth, excluding third molars,” aligning with the accepted standard. Many studies specify the type of tooth examined, such as “participants with at least one missing (permanent) lateral incisor or premolar,” among others. One study [41] deviates from this standard by including third molars in the count of missing teeth. By analyzing the published data, we were able to include the cases from this study that involved missing teeth other than third molars. Additionally, variability is evident in the cut-off points used across studies, with common thresholds being one, two, or three or more missing teeth. No studies employed a cut-off at the boundary between hypodontia and oligodontia—specifically, six missing teeth—which marks the point where clinical consequences typically become more severe.
This outcome aligns with the report of Rakhshan [59], who also attempted a meta-analysis and characterized the results of the studies as controversial, stating that differing definitions of TA and the absence of standardized cut-offs are fundamental factors contributing to heterogeneity. Therefore, to make a proper quantitative synthesis of the results, it is preferable that the papers apply the definition of TA in a uniform manner and present the number of TA cases and controls with or without gene mutation. Such a presentation would facilitate the synthesis of the results among studies dealing with the same genes and SNPs, e.g., rs12532 located in the MSX1 gene and appearing in 7 of the 15 included studies.
To assess all the available information on a rare condition, such as TA, it was considered necessary to include case–control studies. However, this fact could introduce bias into the research. As most of the included studies were judged as “high risk”, meta-analyses would not offer reliable results, even if it was possible to be conducted [60]. Given that systematic reviews represent the qualitative synthesis of multiple primary studies, a high risk of bias in most of the selected studies could negatively impact the overall reliability of the systematic review [61]. However, it is important to emphasize that presenting the heterogeneous findings of these studies—despite their high risk of bias—highlights the lack of robust evidence and underscores the necessity for well-designed research, as well as the adoption of a standardized definition of TA and universally accepted cut-off values.
This systematic review highlighted MSX1 as the most studied gene and SNP rs12532 as the most examined SNP. It is widely recognized that MSX1 is essential in the early stages of odontogenesis [62], and it has attracted considerable interest from the scientific community. Recent research indicates that MSX1, particularly the rs12532 variant, is linked to the agenesis of the second premolar and third molar [62,63]. However, no statistically significant relationship has been identified between MSX1 rs12532 and TA to date [51,64]. Additionally, MSX1 has been studied in relation to cleft defects, cardiovascular diseases, and various syndromes [63,65,66].
In the studies examined, the proportion of cases with fewer than three missing teeth ranged from 61.29% to 84.9%, suggesting that the samples predominantly consisted of individuals with mild TA. This range is in total agreement with the data provided by Khalaf et al. [16], in which the percentage of participants with less than three missing teeth was 81.6%.
The source of the cases was not specified as a sampling criterion, and the studies we included encompassed both general population samples and exclusively orthodontic patients. Although it may be hypothesized that orthodontic patients might be associated with more severe cases of TA, research has shown that their epidemiology does not differ from that of the general population [16,59,67].
The present study noted a slight difference in favor of mandibular missing teeth. This finding is consistent with the outcomes of an earlier systematic review conducted by Polder et al. [15]; however, the systematic review by Khalaf et al. [16] observed a greater prevalence of missing maxillary teeth. It appears that there is no significant difference in the prevalence of TA between the upper and lower jaws, as both are susceptible to TA, and neither is more affected than the other.
In one of the included studies [40], all participants had maxillary lateral incisor agenesis (MLIA); thus, the calculated results of our study were biased toward maxillary TA. Nevertheless, the prevalence of mandibular tooth agenesis remained unchanged, even after excluding the data from this specific study.
Our findings indicate that lateral incisors and second premolars are the most commonly absent teeth. This observation aligns with the typical distribution of missing teeth in TA cases, irrespective of their genetic background [15,16]. The total counts of missing lateral incisors and second premolars are comparable, with the latter being slightly lower (791 lateral incisors compared to 747 second premolars). In a study by Alves-Ferreira et al. [40], where the sample consisted entirely of cases of MLIA, the number of missing lateral incisors was considerably higher compared to the missing second premolars, with 165 lateral incisors missing compared to 15 premolars. By excluding this study, the count of second premolars exceeds that of lateral incisors (626 lateral incisors compared to 732 premolars), consistent with the findings from previous publications [15,16].
The evaluation of the six genes that have been thoroughly investigated as underlying factors of TA and the assessment of current research findings are the strengths of this systematic review. Although the results were diverse, the review effectively summarized the main research findings, with an emphasis on the resultant phenotypes. Conversely, some limitations are recognized, specifically the limited number of included studies and the inability to conduct meta-analyses because of the heterogeneity and high risk of bias. In addition, the inability to clarify which mutation types are associated with the severity of phenotypic patterns of TA is an additional limitation of this study.

5. Conclusions

  • Few case–control studies have investigated the association between TA and gene mutations, and many of these exhibit a high risk of bias, indicating concerns about their quality.
  • The distribution of missing teeth by jaw or type of tooth is in accordance with that reported for all TA cases, whether syndromic or non-syndromic. Therefore, the phenotype associated with mutations of the genes related to NSTA is similar to that observed in all TA cases.
  • The varying sampling methods and the lack of clear cut-off points do not permit the extraction of valid and clinically relevant results.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/prosthesis7060142/s1, Table S1: Search strategy in MEDLINE (PubMed).

Author Contributions

Conceptualization, F.B.-K., I.T., and E.K.; methodology, F.B.-K., I.T., and E.K.; software, F.B.-K., I.T., and E.K.; validation, F.B.-K., I.T., and E.K.; formal analysis, F.B.-K., I.T., and E.K.; investigation, F.B.-K., I.T., and E.K.; resources, F.B.-K., I.T., and E.K.; data curation, F.B.-K., I.T., and E.K.; writing—original draft preparation, F.B.-K., I.T., and E.K.; writing—review and editing, F.B.-K., I.T., and E.K.; visualization, F.B.-K., I.T., and E.K.; supervision, E.K. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Data were derived from previously published studies included in the systematic review and are available from the corresponding author upon reasonable request.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 2. Percentage (%) of tooth agenesis cases with one, two, or at least three permanent missing teeth (excluding third molars) [39,41,44,45,49,50,52].
Figure 2. Percentage (%) of tooth agenesis cases with one, two, or at least three permanent missing teeth (excluding third molars) [39,41,44,45,49,50,52].
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Figure 3. Distribution of permanent missing teeth between maxilla and mandible (excluding third molars) [40,41,46,47,48,49,50,51,52].
Figure 3. Distribution of permanent missing teeth between maxilla and mandible (excluding third molars) [40,41,46,47,48,49,50,51,52].
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Figure 4. Distribution of permanent missing teeth among tooth groups (excluding third molars). CI: central incisor, LI: lateral incisor, C: canine, PM1: first premolar, PM2: second premolar, M1: first molar, M2: second molar [40,41,45,49,50,52,53].
Figure 4. Distribution of permanent missing teeth among tooth groups (excluding third molars). CI: central incisor, LI: lateral incisor, C: canine, PM1: first premolar, PM2: second premolar, M1: first molar, M2: second molar [40,41,45,49,50,52,53].
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Figure 5. Distribution of permanent missing teeth among tooth groups in the study of Chen et al., 2017 [46] (excluding third molars). CI: central incisor, LI: lateral incisor, C: canine, PM1: first premolar, PM2: second premolar, M1: first molar, M2: second molar.
Figure 5. Distribution of permanent missing teeth among tooth groups in the study of Chen et al., 2017 [46] (excluding third molars). CI: central incisor, LI: lateral incisor, C: canine, PM1: first premolar, PM2: second premolar, M1: first molar, M2: second molar.
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Figure 6. Risk of bias summary: Review of authors’ judgments about each risk of bias for each included study, based on Newcastle–Ottawa Scale [39,40,41,42,43,44,45,46,47,48,49,50,51,52,53].
Figure 6. Risk of bias summary: Review of authors’ judgments about each risk of bias for each included study, based on Newcastle–Ottawa Scale [39,40,41,42,43,44,45,46,47,48,49,50,51,52,53].
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Figure 7. Risk of bias graph: Review of authors’ judgments about each risk of bias item presented as percentages across all included studies, based on Newcastle–Ottawa Scale.
Figure 7. Risk of bias graph: Review of authors’ judgments about each risk of bias item presented as percentages across all included studies, based on Newcastle–Ottawa Scale.
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Table 1. List of included studies—demographic data.
Table 1. List of included studies—demographic data.
PMIDFirst AuthorYearCitationNationalityAge (in Years)Sex (M/F)
132772440Al-Ani 2021[39]New ZealandMean (SD). Hypodontia cases: 17.1 (4.8)/Controls: 19.3 (7.3)146/214
224554542Alves-Ferreira2014[40]PortugalN/A114/192
328808699Chen2017[46]ChinaN/AN/A
434878701Fan2023[47]ChinaMean (SD). Tooth agenesis cases: 16.60 (7.56)/Controls: 17.64 (4.65)460/926
530555066Grejtakova2018[48]SlovakiaN/AN/A
623964635Jobbagy-Ovari2014[49]HungaryMean (SD). Hypodontia cases: 18.9 (7.7)/Oligodontia cases: 21 (6.1)/Controls: 26.2 (13.4)161/308
728040065Kirac2016[50]TurkeyN/AN/A
831568994Lancia2020[51]BrazilMean (SD). Tooth agenesis cases: 25 y 6 m (10 y 8 m)/Controls: 27 y (8 y 1 m)62/148
922984994Liu2012[52]ChinaRange. Hypodontia cases: 15–38/Controls: 17–30225/248
1023167694Mostowska2013[53]PolandN/AN/A
1121111400Paixão-Côrtes2011[41]BrazilN/AN/A
1224324300Reddy2013[42]IndiaN/AN/A
1317559452Seifi2007[43]IranRange: 14–27N/A
1423549991Vieira2013[44]BrazilN/AN/A
1527050986Zhang2016[45]ChinaMean (SD). Hypodontia cases: 25.23 (8.16)/Controls: 32.04 (8.16)159/188
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Bakouros-Kouroupakis, F.; Tsolianos, I.; Kotsiomiti, E. The Association Between Non-Syndromic Tooth Agenesis and MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD Gene Mutations: A Systematic Review. Prosthesis 2025, 7, 142. https://doi.org/10.3390/prosthesis7060142

AMA Style

Bakouros-Kouroupakis F, Tsolianos I, Kotsiomiti E. The Association Between Non-Syndromic Tooth Agenesis and MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD Gene Mutations: A Systematic Review. Prosthesis. 2025; 7(6):142. https://doi.org/10.3390/prosthesis7060142

Chicago/Turabian Style

Bakouros-Kouroupakis, Fotios, Ioannis Tsolianos, and Eleni Kotsiomiti. 2025. "The Association Between Non-Syndromic Tooth Agenesis and MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD Gene Mutations: A Systematic Review" Prosthesis 7, no. 6: 142. https://doi.org/10.3390/prosthesis7060142

APA Style

Bakouros-Kouroupakis, F., Tsolianos, I., & Kotsiomiti, E. (2025). The Association Between Non-Syndromic Tooth Agenesis and MSX1, AXIN2, WNT10A, EDA, EDAR, and EDARADD Gene Mutations: A Systematic Review. Prosthesis, 7(6), 142. https://doi.org/10.3390/prosthesis7060142

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