Abstract
Nicotine acts as a potent modulator of normal cellular responses through the nicotinic acetylcholine receptor subtype alpha7. In a mouse genetic model of alpha7 receptor dysfunction, alpha7E260A:G, 85 percent of 18 month-old mice exhibit an age-associated spontaneous loosening or complete loss of 3rd molars that was not present in the control mice. The adjacent soft tissues appeared largely unaffected. Further analysis including micro-CT revealed evidence of bone loss surrounding the 3rd molars with areas of cavitation and/or sponge-like (cancellous) bone remodeling in the mandible. The mandible microbiome was examined using 16S-rRNA sequencing. The results show the alpha7E260A:G oral microbiome included increased landscape complexity indicative of dysbiosis, and a significant increase of some bacteria, particularly Staphylococcus. These results suggest that normal alpha7 function plays a relevant role in maintaining normal gene expression and oral microbiome stasis. Consequently, this mouse model suggests there are consequences to ongoing alpha7 receptor dysfunction and oral health, as can occur from chronic exposure to nicotine as expected from electronic nicotine delivery systems (ENDS or “vaping”), that may not be seen until older age.
Highlights
The response to nicotine is promoted through targeting and interacting with a variety of genetically-related nicotinic acetylcholine receptors whose function varies dependent upon the individual receptor subunit composition and where they are expressed [e.g., [1,2,3]]
Additional screening of the mandibular microbiome using 16S-rRNA sequencing revealed alterations to the α7E260A:G microbiome landscape including altered complexity, bacterial abundance and the disproportionate increase in members, most notably Staphylococcus. These results suggest that normal α7 function provides an extended and diverse role in oral health that is relevant to maintenance of local gene expression and microbiome stasis
Nicotine, when delivered through the more traditional route of cigarette smoking, interacts with nicotine acetylcholine receptors that both leads to addiction, and changes many physiological processes in peripheral systems
Summary
The response to nicotine is promoted through targeting and interacting with a variety of genetically-related nicotinic acetylcholine receptors (nAChRs) whose function varies dependent upon the individual receptor subunit composition and where they are expressed [e.g., [1,2,3]]. The α7E260A:G mouse has proven applicable in resolving the effects of nicotine-α7 interaction on local cellular responsiveness during a variety of processes ranging from tooth and enamel development to allergen response mechanisms by both macrophages and epithelial cells in the lung [8, 10, 13, 15]. It has proven valuable in distinguishing receptor specific signaling mechanisms from those imparted by cigarette smoke [10, 11]
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