MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1016/j.mehy.2009.09.044

Медицинская библиотека · Medical hypotheses · 2009

Possible key role of immune system in Schmorl's nodes.

Zhang Ning, Li Fang-Cai, Huang Yi-Jiang, Teng Chong, Chen Wei-Shan

СтатьяПеревод пока не подготовлен

Аннотация

Schmorl's nodes (SNs) are common abnormalities in the human spine, which represent herniation of the nucleus pulposus of the intervertebral disc into the adjacent cartilaginous endplate of the vertebra. However, the principle mechanism of SNs is still not fully understood. And the relationship of SNs in the spine and their clinical significance as a source of low back pain in the general population remains unknown. It is therefore important to get better understanding of this. Here, we review the clinical and experiment evidence on inducing of the SNs and correlative back pain, and propose a possible mechanism. Studies showed that once the nucleus pulposus enters into vascular tissue, the immune system could recognize it as a foreign body, and induces the immunological reaction. Then, there would be osteoimmunology action, a crosstalk between the immune system and bone, leading to bone loss by dysregulating T-lymphocyte function, and resulting to the bone absorption. Furthermore, the cytokines are involved in the development of immunological reactions and could be responsible for the significant pathology of symptomatic SNs. Given the above background, we hypothesize that immune system could be a key role in SNs and result in the pain.

Для цитирования: Zhang Ning, Li Fang-Cai, Huang Yi-Jiang, Teng Chong, Chen Wei-Shan. Possible key role of immune system in Schmorl's nodes.. Medical hypotheses. 2009. DOI: 10.1016/j.mehy.2009.09.044.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

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.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.