The scientists claimed that various toxic materials enter the body through the oral cavity. These toxic substances significantly affect different structures in the body, such as the oral mucosa.
Studies have shown that when a person smokes a cigarette, the oral mucosa is directly exposed to smoke, which causes many oral pathologies, such as leukoplakia, oral mucosal dysplasia, and carcinoma.
Study: Cannabis smoke condensate induces damage to human gingival epithelial cells through apoptosis, autophagy, and oxidative stress. Image credit: HQuality / Shutterstock
Fund
Previous in vitro studies have revealed that smoking cigarettes inhibits the growth of epithelial cells and increases the risk of cell death through necrotic and apoptotic pathways. In addition, researchers have reported that DNA damage occurs in cells exposed to cigarette smoke.
Previous studies have indicated that tobacco and cannabis smoke consists of different organic and inorganic chemical compounds that negatively affect cannabis smokers. Cannabis sativa is a common cannabis plant that contains 60 different phytocannabinoids, including cannabinol, cannabigerol, cannabidiol, cannabichromene, and tetrahydrocannabinol.
Studies have shown that cannabis smoke contains many chemicals, such as benzopyrenes, hydrocarbons, tar, and nitrosamines. The scientists revealed that when cannabis smoke comes in contact with the oral cavities, it causes dry mouth, burning red papilloma and nicotinic-like spots.
A high prevalence of oral candidiasis and dental caries has been associated with cannabis smokers. Compared to non-smokers, a high growth of Candida albicans has been observed in the mouths of cannabis smokers. Previous studies have also revealed that frequent candida smokers suffer from increased gingivitis, gingival hyperplasia, and alveolar bone loss because the smoke affects the structure and functioning of gingival tissue. However, the precise effect of cannabis smoke on gingival epithelial cells is unclear.
A new study
In a new study published in Archives of Oral Biology, scientists evaluated the effect of cannabis smoke condensate (CSC) on gingival epithelial cells. They determined the effect of CSC on cell shape, adhesion, and viability, at 30-minute, 60-minute, 2-hour, and 24-hour intervals, by microscopic observations and lactate dehydrogenase activity assays. In addition, they determined how CSC affected the release of lactate dehydrogenase (LDH) and phosphorylated signaling pathway proteins by flow cytometry. The effect of CSC on autophagy, oxidative stress, and cell apoptosis was studied by gene expression using an RT2 -PCR matrix.
Discoveries
Gingival epithelial cells exposed to these CSCs caused alterations in their morphology and a decrease in cell adhesion. The current study revealed that CSC is toxic to gingival epithelial cells. It decreases cell viability and its metabolic functions. Similar cases have been reported with cigarette smoke condensate. Scientists have related the adverse effects of CSCs to high levels of lactate dehydrogenase (LDH) in the cell culture medium.
Most cells contain LDH, which is a soluble cytoplasmic enzyme, which is released into the extracellular space when the plasma membrane is damaged. The present study reported that CSC damaged the membrane of gingival epithelial cells, leading to the release of LDH into the culture medium.
Previous studies reported that DNA is damaged due to excessive oxidative stress, which sometimes leads to cell apoptosis. In the current study, researchers reported that CSC initiates oxidative stress in cells, due to the detection of a higher number of reactive oxygen species (ROS) in epithelial cells. positive gingivitis, compared with control cells. An increase in the level of ROS increases the risk of cell death by apoptosis and autophagy, by simulating different apoptotic genes.
The current study reported that when cells are exposed to 20% CSC, activation of different apoptotic genes (e.g., BCL2-like 11) occurred, leading to cell death. Gene activation caused gingival epithelial cells to bind to anti-apoptotic proteins, which in turn released hijacked pro-apoptotic molecules. These molecules eventually caused cell death.
Scientists showed that cannabis smoke caused higher expression of several genes, including the TNF superfamily (TNFSF) and the NLR family apoptosis inhibitor protein, which facilitated cell death. gingival epithelial by apoptosis. They also claimed that reduced CD40L gene expression caused disruption of cellular communications and indirectly promoted cell apoptosis.
CSC facilitated autophagy of gingival epithelial cells by increasing the expression of CDKN1B, TMEM74, and GABARAPL1 genes. The finding of this study is in line with previous studies that reported that the GABARAPL1 gene was associated with autophagic flow. The authors reported that CSC deregulates the behavior of gingival epithelial cells by suppressing the phosphorylation of these signaling proteins (e.g., P38, STAT5, NF-κB, and ERK1 / 2).
Future perspective
The authors stated that the current study assessed gene expression of gingival epithelial cells at 20% CSC; however, the adverse effect of CSC was found at other concentrations, such as 5 and 10% as well. Therefore, in the future, a genetic analysis of gingival epithelial cells exposed to lower concentrations of CSC should be performed. The researchers believe that because epithelial cells play a key role in innate immunity, their response to CSC exposure could have a substantial effect on the immune response. This hypothesis should be addressed in future studies. Additionally, the results obtained in this study are based on monolayer cell cultures, which must be subsequently validated by animal studies.