Journal of endodontics · 2013
Overlapping protective and destructive regulatory pathways in apical periodontitis.
СтатьяПоддержка исследования: вне правительства СШАОбзорНазвание 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.
Márton Ildikó J, Kiss Csongor
Аннотация
INTRODUCTION: Protective and destructive immunoreactions take place simultaneously in apical periodontitis. However, the same reactions defending the periapical area from infection-derived damage may also result in host tissue injury.
METHODS: The inflammatory reaction of the periapical tissues is self-limited. Regeneration of the injured tooth-supporting structures may follow elimination of the causative microbial irritation.
RESULTS: Recent experimental and clinical observations have identified important interplay between positive and negative regulatory pathways. A network of stimulatory and inhibitory feedback loops may influence the intensity of the defense and inflammatory responses and the balance between bone resorption and regeneration, resulting in lesion expansion or healing of apical periodontitis.
CONCLUSIONS: We critically discuss research data on regulatory mechanisms that control the activity of host effector cells and signaling molecules during interactions with pathogenic microbes.
METHODS: The inflammatory reaction of the periapical tissues is self-limited. Regeneration of the injured tooth-supporting structures may follow elimination of the causative microbial irritation.
RESULTS: Recent experimental and clinical observations have identified important interplay between positive and negative regulatory pathways. A network of stimulatory and inhibitory feedback loops may influence the intensity of the defense and inflammatory responses and the balance between bone resorption and regeneration, resulting in lesion expansion or healing of apical periodontitis.
CONCLUSIONS: We critically discuss research data on regulatory mechanisms that control the activity of host effector cells and signaling molecules during interactions with pathogenic microbes.