Periodontal Conditions & Alveolar Bone Destruction

Clinical Studies have reported adverse toxic reactions in the epithelial cells in conjunction with extracts in ONPs, affecting gingival attachment loss and gingival recession. Disruption of the oral microenvironment, triggers an inflammatory response, leading to increased periodontal destruction.¹ Recent studies revealed when exposed to nicotine, the nicotinic acetylcholine receptors (nAChR) are activated, which in turn suppresses the periodontal ligament (PDL) fibroblast cells, and compromises the integrity of stem cells.¹ Additional studies have shown destruction of alveolar bone, in correlation to nicotine products, creating significantly deeper periodontal probe depths that harbor and host periodontal disease-causing pathogens such as Staphylococcus, Streptococcus, Aggregatibacter and Actinomyces are noted, along with increased furcation involvement.¹ The effect nicotine has on cytokine levels can also be a contributing factor to the progression of periodontal disease.¹ To further elaborate, additional studies have also discussed the risk of early onset periodontal disease among our youth population to be related to tobacco and nicotine use, such as combustible cigarettes, smokeless tobacco (snuff), cannabis, e-cigarettes and now ONPs, however, more research is indicated. While oral nicotine pouches (ONPs) carry a lower risk, their use can lead to dual dependency, elevating susceptibility among vulnerable youth populations.²⁰