Cannabis smoke condensate induces human gingival epithelial cell damage through apoptosis, autophagy, and oxidative stress

Abstract

Objectives: This study aims to investigate the effects of cannabis smoke condensate (CSC) on the adhesion, growth, and signaling pathways of human gingival epithelial cells.

Design: The effects of CSC on cell shape and adhesion, and viability were evaluated after 30 min, 60 min, 2 h, and 24 h of exposure using microscopic observation, cell metabolic activity, and lactate dehydrogenase activity assays. The effects of CSC on cell apoptosis, necrosis, autophagy, and oxidative stress were determined through flow cytometry, while apoptotic and autophagic gene expression were identified via an RT²-PCR array. Phosphorylated signaling pathway proteins were measured using flow cytometry.

Results: CSC deregulated gingival epithelial cell shape and adhesion, decreased cell viability, and increased lactate dehydrogenase release. Its toxic effects included apoptosis, autophagy, and oxidative stress. Moreover, it modulated seven specific apoptotic and six autophagic genes. Furthermore, it decreased phosphorylation in signaling proteins, such as STAT5, ERK12, P38, and nuclear factor κB.

Conclusions: CSC has notable adverse effects on gingival epithelial cells. This finding indicates that cannabis smoke could impair gingival epithelial cell innate immune function, leading to gingivitis and periodontitis. Oral health professionals may need to document observed modifications in the oral cavity of patients who smoke cannabis and consider these potential changes during clinical care.

Keywords: Apoptosis; Autophagy; Cannabis smoke; Human gingival epithelial cell; Necrosis; Oxidative stress.