Clinical oral investigations · 2025
Neutrophil activity compromises root caries remineralization and alters caries-affected-like dentin.
СтатьяПоддержка исследования: вне правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Trivedi Rinku K, Patel Riya H, Wazir Asma, Zamperini Camila A
Аннотация
OBJECTIVES: Root caries (RC) progression involves the dentin extracellular matrix (dECM) degradation by proteolytic enzymes. As neutrophil-derived enzymes have been systemically associated with ECM degradation, we hypothesized that neutrophil activity would: (i) inhibit RC remineralization; and (ii) alter the caries-affected-like dentin.
MATERIALS AND METHODS: In vitro RC were created on human dentin specimens. Half each lesion was covered to keep the initial lesion (IL). The other half (final lesion; FL) was exposed to one of the following groups (n = 10): Control (buffer solution; C); Neutrophils (human neutrophils; N); Collagenase (positive control; Col), and then remineralized by pH-cycling and sodium fluoride. RC remineralization was calculated using rhodamine infiltration and cross-sectional microhardness (CSMH). Collagen of the fully demineralized dentin was stained with picrosirius red. The physical properties of the caries-affected-like dentin were investigated by CSMH and loss of mineral density (MD).
RESULTS: Two-way ANOVA and Tukey showed only remineralization in the C group (p < 0.001). N did not show any remineralization (p = 0.588) between IL and FL. The N and Col groups exhibited changes in collagen integrity and organization. The N and Col groups' caries-affected-like dentin showed significantly lower CSMH (p < 0.001) than the C group, and significant losses (IL-FL) of MD (p = 0.012 and p = 0.042, respectively). In contrast, no MD loss was observed in the C group (p = 0.411).
CONCLUSIONS: Neutrophil-derived enzymes compromise RC remineralization and detrimentally affect the physical properties of the caries-affected-like dentin.
CLINICAL SIGNIFICANCE: Identifying proteolytic sources involved with dECM degradation during RC progression will pave new research directions.
MATERIALS AND METHODS: In vitro RC were created on human dentin specimens. Half each lesion was covered to keep the initial lesion (IL). The other half (final lesion; FL) was exposed to one of the following groups (n = 10): Control (buffer solution; C); Neutrophils (human neutrophils; N); Collagenase (positive control; Col), and then remineralized by pH-cycling and sodium fluoride. RC remineralization was calculated using rhodamine infiltration and cross-sectional microhardness (CSMH). Collagen of the fully demineralized dentin was stained with picrosirius red. The physical properties of the caries-affected-like dentin were investigated by CSMH and loss of mineral density (MD).
RESULTS: Two-way ANOVA and Tukey showed only remineralization in the C group (p < 0.001). N did not show any remineralization (p = 0.588) between IL and FL. The N and Col groups exhibited changes in collagen integrity and organization. The N and Col groups' caries-affected-like dentin showed significantly lower CSMH (p < 0.001) than the C group, and significant losses (IL-FL) of MD (p = 0.012 and p = 0.042, respectively). In contrast, no MD loss was observed in the C group (p = 0.411).
CONCLUSIONS: Neutrophil-derived enzymes compromise RC remineralization and detrimentally affect the physical properties of the caries-affected-like dentin.
CLINICAL SIGNIFICANCE: Identifying proteolytic sources involved with dECM degradation during RC progression will pave new research directions.