Карієс тимчасових зубів: анатомічна і генетична схильність

Abstract

Серед генів, які ідентифіковані чи підозрюються як такі, що призводять до карієсу зубів, виділено групу тих, що відповідають за структуру емалі та дентину, і проаналізовано, яким чином може реалізуватися цей генетичний вплив на анатомічному і мікроструктурному рівнях у тимчасових зубах. Наразі відсутні дослідження щодо поширеності та значення генів, які підвищують ризик карієсу зубів у дітей української популяції. Такі відомості необхідні для пошуку нових мішеней і стратегій профілактики та лікування.; Среди генов, которые идентифицированы или подозреваются в качестве предрасполагающих к кариесу зубов, выделена группа ответственных за структуру эмали и дентина, и проанализировано, каким образом может реализоваться это генетическое влияние на анатомическом и микроструктурном уровнях во временных зубах. В настоящее время отсутствуют исследования распространенности и значения генов, которые повышают риск кариеса зубов у детей украинской популяции. Такие сведения необходимы для поиска новых мишеней и стратегий профилактики и лечения. ; Dental caries results from specific tooth-adherent microbial biofilms that demineralize tooth structure by metabolizing dietary sugars to produce acid. Fermentable carbohydrates enrich cariogenic bacteria, including Streptococus mutans, S. sobrinus, and Lactobacillus species, in the biofilm leading to dental decalcification. Severe-early childhood caries, affecting multiple smooth tooth surfaces before age 5, can lead to pain, abscess formation, and loss of teeth; associated with more new carious lesions and emergency room visits, increased treatment costs, delayed development, and diminished ability to learn. Childhood caries prevalence varies by socio-economic status, environmental factors, including dietary composition, access to fluoride and dental care, and oral hygiene practices influence. But host factors including salivary composition, enamel structure, taste preferences, and immune responses vary among children and may be genetically determined. Review aims to literature analyzing how can be realized a genetic predisposition to caries on anatomical and micro structural organization level of temporary teeth. Database PubMed Central® (PMC) was used as a source for literature review because of analogues studying lack among Ukrainian population. Childhood caries has strong heritability, with strongest effect in primary dentitions as revealed. Human models, including studies with twins, provide evidence that caries has a genetic component. Of two genome-wide association studies (GWAS) of permanent dentition caries, one found two significant loci, LYZL2 which involves anti-bacterial defenses, and AJAP1 which may influence tooth development, and the other found no significant associations but both studies identified several novel loci with non-significant associations. One of two GWAS childhood caries found no variants with significant associations, and suggestive associations did not replicate in independent populations, and the other found significant association between KPNA4 and replicated the association with AJAP1. Inconsistent associations have been reported for childhood caries and genetic variants involved in enamel/dentin mineralization, salivary composition, and matrix metalloproteinases. Although one may envision risk stratification for S-ECC at diagnosis of first smooth surface lesions to guide intervention opportunities, investigators have appropriately questioned the clinical utility of genetic information in management of at-risk populations.Another study by multi-dimensional prioritization of dental caries candidate genes and its enriched dense network modules provided insights into the molecular mechanisms underlying dental caries. Candidate genes were prioritized according to the magnitude of evidence related to dental caries, then authors searched for dense modules enriched with the prioritized candidate genes through their protein-protein interactions (PPIs). They identified 23 modules comprising of 53 genes. Functional analyses of these 53 genes revealed three major clusters: cytokine network relevant genes, matrix metalloproteinases (MMPs) family, and transforming growth factor-beta (TGF-β) family, all of which have been previously implicated to play important roles in tooth development and carious lesions. Comparison of data from genetic and histological studies of primary dentition caries can indirectly indicate that structural genetic features are identical to both, but a genetic predisposition to caries is primary teeth can be clinically more visible through anatomical features of these teeth, e.g. thinner enamel, dentine, enamel-dentin junction, that can explain more expressive reaction of pulp cells at the slightest enamel injury. Obviously, primary dentition caries genetic management unlikely could be routine of clinical practice in the near future. Genetic studies to finding dental caries candidate genes among Ukrainian population are needed.