A critical size volumetric muscle loss model in mouse masseter with impaired mastication on nutrition

Author:

Zhao Ning12ORCID,Huang Yixuan12,Cheng Xu1,Xie Li1,Xiao Wenlin3,Shi Bing12,Li Jingtao12

Affiliation:

1. State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases Sichuan University Chengdu China

2. Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology Sichuan University Chengdu China

3. Department of Stomatology The Affiliated Hospital of Qingdao University Qingdao China

Abstract

AbstractOrofacial muscle defect due to congenital anomalies, tumour ablation or traumatic accident that exceeds endogenous regeneration capacity may lead to sustained deficits in masticatory function and nutrition intake. Functional recovery has always been the goal of muscle tissue repair, but currently, there is no suitable model for quantitative analyses of either functional consequences or treatment efficacy of orofacial muscle defect. This study proposed a critical size volumetric muscle loss (VML) model in mouse masseter with impaired mastication on nutrition. Full‐thickness VML defects in diameter of 1.0, 1.5, 2.0 and 3.0 mm were generated in the centre of the mouse masseter using a biopsy punch to determine the critical size for functional impairment. In the VML region, myogenesis was dampened but fibrogenesis was activated, as long with a reduction in the density of the neuromuscular junction and an increase in vascular density. Accordingly, persistent fibrosis was observed in the centre region of VML in all diameters. The 2.0 mm diameter was the critical threshold to masticatory function impairment after VML in the masseter. VML of 3.0 mm diameter led to a significant impact on nutrition intake and body weight gain. Autologous muscle graft effectively relieved the fibrosis and functional deficit after VML injury in the masseter. This model serves as a reliable tool in studying functional recovery strategies for orofacial muscle defects.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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