Abstract

Smokers have high plaque accumulation that initiates gingival inflammation and progresses to periodontitis. Thus, oral hygiene to control microbial plaque formation is an effective method of preventing gingivitis. Medicinal plants such as Moringa oleifera Lam. (MO) and Cyanthillium cinereum (Less.) H. Rob. (CC) have an anti-inflammatory effect that might improve oral health in smokers. This study evaluated the effect of MO leaf and CC extracts using MO lozenges and a combination of MO + CC lozenges on oral inflammation and gingivitis in volunteer smokers. Lozenges consisting of MO and CC extracts were developed and studied in vivo. The results showed that lozenges significantly reduced oral inflammation and gingivitis in volunteers. The gingival index (GI) of group III (MO + CC lozenges) significantly decreased, while the percentage decrease of oral inflammation in group II (MO lozenges) was significantly higher than the other groups. The percentage decrease of GI values in group II (MO lozenges) and group III (MO + CC lozenges) were significantly higher than the placebo group I. Our findings indicated that MO and MO + CC lozenges reduced oral inflammation and gingivitis and showed potential to improve oral health in smokers.

Highlights

  • Cigarette smoke contains a complex mixture of over 5300 chemical substances including nicotine and other carcinogens

  • Herbal lozenges consisting of M. oleifera leaf extract and over ground parts of C. cinereum extract were developed for investigation of oral inflammation and gingivitis in volunteer smokers at the smoking cessation clinic, Wang Thong Hospital, Phitsanulok, Thailand

  • Our results showed Moringa oleifera Lam. (MO) leaf extract, CC extract, MO lozenges and MO + CC lozenges contained high total phenolic contents with greater DPPH radical scavenging activity compared to the control as dimethyl sulfoxide (DMSO) (p < 0.001)

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Summary

Introduction

Cigarette smoke contains a complex mixture of over 5300 chemical substances including nicotine and other carcinogens. Cigarette smoke induces inflammation by activation of IκB kinase (IKK), leading to the phosphorylation and proteasomal degradation of nuclear factor kappa B (NF-κB) inhibitor. This allows the translocation of NF-κB to the nucleus, where it regulates the expression of pro-inflammatory genes such as tumor necrosis factor (TNF)-α, interleukin (IL)-8, and cyclooxygenase (COX)-2 [3,4]. Subgingival bacteria and dental plaque accumulation initiate gingival inflammation. If left untreated, this causes gingivitis and eventually progresses to periodontitis, with destruction of the underlying supporting tissue and alveolar bone [8,9]

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