Abstract
BackgroundGermline mutations in APC and AXIN2 are both associated with colon neoplasia as well as anomalous dental development. We tested the hypothesis that congenitally missing teeth may occur more commonly in individuals diagnosed with colorectal cancer than in individuals without this diagnosis.MethodsVia a survey conducted on 1636 individuals with colorectal cancer (CRC) and 2788 individuals with no colorectal cancer from the Colon Cancer Family Registry, self-reported information on congenitally missing teeth was collected. The frequency of missing teeth between cases and controls was compared using Pearson’s chi-squared test or Fisher’s exact test.Results4.8% of cases and 5.7% of controls reported having at least one missing tooth (p = 0.20). When we stratified by recruitment site, gender, and mutation status where available, frequency of missing teeth was not statistically significantly different between cases and controls.ConclusionsThis study did not provide support for there being a general predisposition to missing teeth among a large cohort of CRC patients. The study neither addresses nor excludes the possibility, however, that individuals presenting with notable hypodontia/oligodontia might still have an increased risk for colorectal neoplasia.
Highlights
Germline mutations in adenomatous polyposis coli (APC) and axis inhibition protein 2 (AXIN2) are both associated with colon neoplasia as well as anomalous dental development
A second family, in Finland, with the same AXIN2 mutation was reported by Renkonen et al [4] as part of their study of 29 polyposis families in which no adenomatous polyposis coli (APC) mutation was found
Women were reported to have more missing teeth than men in both cases and controls (OR = 1.56; 95% Confidence interval (CI) = 1.09-2.27; p = 0.01; Table 2)
Summary
Germline mutations in APC and AXIN2 are both associated with colon neoplasia as well as anomalous dental development. We tested the hypothesis that congenitally missing teeth may occur more commonly in individuals diagnosed with colorectal cancer than in individuals without this diagnosis. A Finnish family was described in 2004 [3] in which a nonsense mutation in axis inhibition protein 2 (AXIN2) was found to co-segregate with an oligodontia (severe tooth agenesis) phenotype. Further characterization of the family identified adenomatous colorectal polyps and cancer as part of the phenotype. A second family, in Finland, with the same AXIN2 mutation was reported by Renkonen et al [4] as part of their study of 29 polyposis families in which no adenomatous polyposis coli (APC) mutation was found. The APC gene, mutations of which cause Familial Adenomatous Polyposis, is a key component
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