Abstract：
The prevalence of mouth breathing is high in children and adolescents. It causes various changes to the respiratory tract and, consequently, craniofacial growth deformities. However, the underlying mechanisms contributing to these effects are obscure. Herein, we aimed to study the effects of mouth breathing on chondrocyte proliferation and death in the condylar cartilage and morphological changes in the mandible and condyle. Additionally, we aimed to elucidate the mechanisms underlying chondrocyte apoptosis and investigate any variations in the related pathways. Subchondral bone resorption and decreased condylar cartilage thickness were observed in mouth-breathing rats; further, mRNA expression levels of Collagen II, Aggrecan, and Sox 9 were lower in the mouth breathing group, while those of matrix metalloproteinase 9 increased. TdT-mediated dUTP nick end labelling staining and immunohistochemistry analyses showed that apoptosis occurred in the proliferative and hypertrophic layers of cartilage in the mouth breathing group. TNF, BAX, cytochrome c, and cleaved-caspase-3 were highly expressed in the condylar cartilage of the mouth-breathing rats. These results suggest that mouth breathing leads to subchondral bone resorption, cartilage layer thinning, and cartilage matrix destruction, inducing chondrocyte apoptosis via both the extrinsic and mitochondrial apoptosis pathways.
摘要：
儿童和青少年的口呼吸患病率很高。它会引起呼吸道的各种变化，因此,颅面生长畸形。然而,导致这些影响的潜在机制是模糊的。在这里，我们旨在研究口呼吸对髁突软骨细胞增殖和死亡以及下颌骨和髁突形态变化的影响。此外,我们旨在阐明软骨细胞凋亡的潜在机制，并研究相关通路的任何变化。在张口呼吸的大鼠中观察到软骨下骨吸收和髁突软骨厚度的减少；此外，胶原II的mRNA表达水平,Aggrecan,Sox9在口腔呼吸组中较低，而基质金属蛋白酶9的含量增加。TdT介导的dUTP缺口末端标记染色和免疫组织化学分析表明，口呼吸组软骨的增殖层和肥大层中发生了细胞凋亡。TNF,巴克斯，细胞色素c,cleaved-caspase-3在口呼吸大鼠的髁突软骨中高表达。这些结果表明，口呼吸导致软骨下骨吸收，软骨层变薄，和软骨基质的破坏，通过外源性和线粒体凋亡途径诱导软骨细胞凋亡。
