Abstract
Molar incisor hypomineralization (MIH) is an endemic pediatric disease with an unclear pathogenesis. Considering that saliva controls enamel remineralization and that MIH is associated with higher saliva flow rate, we hypothesized that the protein composition of saliva is linked to disease. To test this, we enrolled 5 children aged 6–14 years with MIH showing at least one hypersensitive molar and 5 caries-free children without hypomineralization. Saliva samples were subjected to proteomic analysis followed by protein classification in to biological pathways. Among 618 salivary proteins identified with high confidence, 88 proteins were identified exclusively in MIH patients and 16 proteins in healthy controls only. Biological pathway analysis classified these 88 patient-only proteins to neutrophil-mediated adaptive immunity, the activation of the classical pathway of complement activation, extracellular matrix degradation, heme scavenging as well as glutathione -and drug metabolism. The 16 controls-only proteins were associated with adaptive immunity related to platelet degranulation and the lysosome. This report suggests that the proteaneous composition of saliva is affected in MIH patients, reflecting a catabolic environment which is linked to inflammation.
Highlights
Molar incisor hypomineralization (MIH) is an endemic pediatric disease with an unclear pathogenesis
We performed a mapping of the proteome of MIH saliva and respective controls from healthy individuals
Our findings show that out of 618 proteins, 88 and 16 proteins were exclusively detected in MIH saliva and control saliva, respectively
Summary
Molar incisor hypomineralization (MIH) is an endemic pediatric disease with an unclear pathogenesis. Considering that saliva controls enamel remineralization and that MIH is associated with higher saliva flow rate, we hypothesized that the protein composition of saliva is linked to disease. This report suggests that the proteaneous composition of saliva is affected in MIH patients, reflecting a catabolic environment which is linked to inflammation. Chronic subclinical pulpal inflammation is a consequence of increased enamel porosity and reduced hardness in MIH9. It is conceivable that the protein-composition of MIH saliva may exhibit characteristic changes that cause or contribute to the clinical symptoms of this disease. As changes in saliva composition are associated with oral diseases, it is reasonable to assume that compared to healthy children, the saliva of MIH children experiencing subclinical inflammation might be altered. We employed high-resolution shotgun proteomics to identify protein signatures unique to MIH patients
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