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When baby teeth and adult teeth come in is more heritable than most people would guess — twin studies put it above 80%. Nine variants across three large studies mark some of that heritability, in genes that also shape height and facial width.
When teeth erupt — both the primary ("baby") set in infancy and the permanent set that replaces it through childhood — is a highly heritable trait. Twin and family studies have typically put that heritability above 80%, higher than most people would guess for something so easily written off as random.
Pillas et al. 2010 studied time to first tooth eruption and number of teeth at one year in 4,564 Finnish and 1,518 British infants, finding five genome-wide-significant loci, including rs8079702 near KCNJ2. The same paper notes that tooth agenesis — teeth that never form — is the most common developmental anomaly in humans, and that a variant in the HOXB gene cluster tracked with occlusion problems serious enough to need orthodontic treatment by age 31.
Fatemifar et al. 2013 scaled this up considerably: 5,998 to 6,609 British children and 5,403 Finnish children, testing 2,446,724 variants. They found 15 independent loci — 10 for age at first tooth, 11 for number of teeth — together explaining 6.06% and 4.76% of the variation in each trait. The strongest single signal was rs17563 in BMP4 (P = 9.08 × 10⁻¹⁷). Six of this page's nine variants come from this study: rs1799922 (CALU), rs10740993 (CACNB2), rs997154 (AJUBA), rs1994969 (IGF2BP1), rs11796357 (FAM155E), and rs4937076 (CDON), alongside BMP4. Three of the loci — HMGA2, AJUBA and ADK — also associated with craniofacial distances, particularly facial width: the same genes that time a tooth's arrival also help shape the face around it.
Geller et al. 2011 studied permanent tooth eruption in 5,104 Danish girls and replicated the finding in 3,762 more children from the US and Denmark, with every combined p-value below 10⁻¹¹. One of the four loci, rs12424086 in HMGA2, is on this page. The effect was large enough to matter directly: children carrying 6 to 8 delay-associated alleles across all four loci had, on average, 3.5 fewer permanent teeth (95% CI 2.9–4.1) at ages 10 to 12 than children carrying 0 or 1 — a genuine developmental-timing difference, not a statistical abstraction.
Tooth eruption timing is tracked by a dentist or paediatrician against normal developmental ranges, not by genotype. The variants on this page describe ordinary variation in timing within those ranges — they are not a test for a disorder, and no guideline uses them to decide anything about a child's dental care.
Genuinely delayed eruption, or teeth that fail to form at all (tooth agenesis, the most common human developmental anomaly per Pillas et al. 2010), are evaluated clinically — by a dentist, and sometimes a geneticist when agenesis is extensive or runs in a family. That evaluation is not what these nine common variants are for; each shifts timing or count by a small amount within the range of normal development, the same way common height variants shift height without diagnosing anything.
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 9 of 9 linked studies with a resolved discovery ancestry.
Databases, guidelines and references
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Tooth Eruption Timing. MyGeneLog™. https://www.mygenelog.com/conditions/tooth-development
Not usefully for an individual. Each variant shifts average timing or count by a small amount across a population; none of them is diagnostic or predictive for one child.
Twin and family studies typically put it above 80% — higher than most people expect for something that looks like random variation.
Three of them do, genuinely: HMGA2, AJUBA and ADK are associated with craniofacial distances, particularly facial width, in addition to tooth eruption timing — the same developmental genes appear to do both jobs.
Tooth agenesis is when a tooth never forms at all — the most common developmental anomaly in humans. It is a distinct clinical finding evaluated by a dentist or geneticist, not something these nine timing variants are used to assess.
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