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Traumatic occlusion aggravates bone loss during periodontitis and activates Hippo‐YAP pathway
Author(s) -
Pan Weiyi,
Yang Li,
Li Jinle,
Xue Lili,
Wei Wei,
Ding Handong,
Deng Shibing,
Tian Ye,
Yue Yuan,
Wang Min,
Hao Liang,
Chen Qianming
Publication year - 2019
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.13065
Subject(s) - periodontitis , medicine , hippo signaling pathway , dentistry , clinical attachment loss , occlusion , cardiology , immunology , effector
Aim This study aimed at exploring changes in YAP expression and their effect on periodontitis (PD) combined with traumatic occlusion (TO). Materials and Methods BALB/cJ mice were used to establish a PD model by local administration of Porphyromonas gingivalis ( P.g , ATCC 33277) and a TO model by occlusal elevation (OE) using composite resin bonding on the bilateral maxillary molar. The mouse fibroblast cell line (L929) and pre‐osteoblast cell line (MC3T3‐E1) were subjected to cyclic tensile/compressive stress and inflammatory stimuli (lipopolysaccharide from Escherichia coli ) to verify in vivo results. Results Severe bone resorption was observed by microCT scanning in OE with P.g group, when compared to OE only and P.g only groups. Mechanical stress caused by OE activated the Hippo‐YAP pathway in periodontal tissues and upregulated the expression of JNK/AP‐1. OE with P.g further promoted the expression of YAP and JNK/AP1, leading to the upregulation of the JNK/AP‐1 related inflammatory cytokines TNF‐α and IL6. Similar results were obtained when osteoblasts were subjected to mechanical stress in vitro. Conclusions Our study demonstrated that periodontitis with TO caused severe inflammation‐induced bone resorption. Activation of YAP and upregulation of JNK/AP‐1 induced by TO potentially aggravated the symptoms of PD.