According to the researchers, the common tissue origin of skin and teeth means that genetic mutations associated with atopic dermatitis may share a pathogenic pathway with abnormalities in tooth development.
Skin and teeth share a common origin from ectodermal tissues, and a number of studies have demonstrated an association between atopic dermatitis and dental abnormalities such as hypomineralization and hypodontia. A recent review aimed to identify possible links between atopic dermatitis and dental agenesis, and the researchers suggested that these conditions may be related through a common mechanistic pathway of protein interactions.
Researchers from institutes in China and Singapore examined numerous examples in the scientific literature that showed similarities between chronic inflammatory skin disease and abnormalities in tooth structure. They pointed to a 2017 Singapore cohort study that found that children with atopic dermatitis were three times more likely to develop dental caries by age 3. A 2021 cross-sectional nationwide study among adults in South Korea found a similar association, finding that the prevalence of decayed, missing, and filled teeth was strongly associated with a diagnosis of atopic dermatitis.
Based on these and other findings, the investigators in the review wrote that an “ectodermal subclinical developmental defect” was hypothesized due to a common tissue origin of skin and teeth, and that genetic mutations associated with atopic dermatitis may share a pathogenetic pathway with developmental anomalies. teeth.
The review did not find a direct match between genes associated with epidermal barrier defects in atopic dermatitis and dental agenesis, prompting researchers to analyze the protein interactions between these conditions in order to further explore possible common developmental pathways. They identified potential protein-protein interactions between proteins known to be associated with these conditions, in particular desmosomal proteins that are involved in maintaining the skin barrier, and β-catenin, which regulates cell growth and adhesion between cells and is involved in odontogenesis, among others. functions.
“The specific mechanism by which the two diseases interact in this way remains unclear, and more evidence is needed,” the researchers wrote. “However, these results help to narrow down possible common pathogenic pathways for future research in this new field and help support the hypothesis that common genetic mutations in the structure of the epidermis may increase the risk of dental agenesis, thus linking structural defects in the skin barrier and the formation teeth,” they concluded.