Abstract
The aim of the study was to examine the efficacy of cold atmospheric plasma (CAP) on the mineralization and cell proliferation of murine dental cementoblasts. Cells were treated with CAP and enamel matrix derivates (EMD). Gene expression of alkaline phosphatase (ALP), bone gamma-carboxyglutamate protein (BGLAP), periostin (POSTN), osteopontin (OPN), osterix (OSX), collagen type I alpha 1 chain (COL1A1), dentin matrix acidic phosphoprotein (DMP)1, RUNX family transcription factor (RUNX)2, and marker of proliferation Ki-67 (KI67) was quantified by real-time PCR. Protein expression was analyzed by immunocytochemistry and ELISA. ALP activity was determined by ALP assay. Von Kossa and alizarin red staining were used to display mineralization. Cell viability was analyzed by XTT assay, and morphological characterization was performed by DAPI/phalloidin staining. Cell migration was quantified with an established scratch assay. CAP and EMD upregulated both mRNA and protein synthesis of ALP, POSTN, and OPN. Additionally, DMP1 and COL1A1 were upregulated at both gene and protein levels. In addition to upregulated RUNX2 mRNA levels, treated cells mineralized more intensively. Moreover, CAP treatment resulted in an upregulation of KI67, higher cell viability, and improved cell migration. Our study shows that CAP appears to have stimulatory effects on regeneration-associated cell functions in cementoblasts.
Highlights
Traumatic dental injuries (TDI) are common events in the dental field
cold atmospheric plasma (CAP) led to increased mRNA levels of crucial cementoblast- and mineralizationspecific genes 24 h after treatment
CAP-treated cells demonstrated similar results to enamel matrix derivates (EMD) treatment, which was used as a positive control (ALP: 2.3 ± 0.3-fold; POSTN: 2.6 ± 0.3-fold; OPN: 2.3 ± 0.2-fold; Figure 1a)
Summary
Traumatic dental injuries (TDI) are common events in the dental field. It has been shown that approximately 900 million people in the world population of 2016 had at least one dental traumatic event [1]. When a tooth is injured, often anatomical structures such as cementum, periodontal ligament, alveolar bone, and gingiva are damaged and require to regenerate. Another reason for the pathological loss of these anatomical structures is periodontitis. The pathological biofilm triggers and keeps periodontitis active, leading to progressive and irreversible loss of periodontal ligament, cementum, and alveolar bone [4]. Conventional treatment only results in periodontal repair; in certain circumstances, regenerative treatment approaches such as enamel matrix derivates (EMD)
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