Abstract
Highlights
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- Fluoride does not cause DDH directly but increases its susceptibility by increasing hip capsular laxity.
- Hip laxity results from apoptosis occurring in capsular fibroblast after fluoride exposure.
- Fluoride-induced fibroblast apoptosis was triggered by oxidative stress via mitochondrial pathway.
The etiology of developmental dysplasia of the hip (DDH) is multifactorial, including breech presentation and hip capsular laxity. In particular, hip laxity is the main contributor to DDH by changing the ratio and distribution of collagens. Also, fluoride (F) affects collagens from various tissue besides bone and tooth. To investigate the association of DDH and excessive F intake, we conducted this research in lab on cell and animal model simultaneously. We established animal model of combination of DDH and F toxicity. The incidence of DDH in each group was calculated, and hip capsules were collected for testing histopathological and ultrastructural changes. The primary fibroblasts were further extracted from hip capsule and treated with F. The expression of collagen type I and III was both examined in vivo and in vitro, and the level of oxidative stress and apoptosis was also tested identically. We revealed that the incidence of DDH increased with F concentration. Furthermore, the oxidative stress and apoptosis levels of hip capsules and fibroblasts both increased after F exposure. Therefore, this study shows that excessive F intake increases susceptibility to DDH by altering hip capsular laxity in vivo and in vitro respectively. We believe that F might be a risk factor for DDH by increasing hip laxity induced by triggering fibroblast oxidative stress and apoptosis.
Graphical Abstract
