Nicotine Pouches and Oral Mucosal Health: A Review of Cellular, Histopathological, and Potentially Malignant Changes
Nicotine pouches, oral epithelium, histopathology, oral potentially malignant disorders, in-vitro, in vivo.
AuthorsAbstractNicotine pouches (NPs) have seen a swift rise in adoption as tobacco-free nicotine delivery mechanisms, often marketed as harm-reduction substitutes for combustible tobacco. While their global prevalence continues to grow, the enduring impacts of NPs on oral mucosal health are still not fully understood. Preliminary experimental findings from both in vitro and in vivo investigations suggest that nicotine exposure, irrespective of combustion-related toxic substances, can trigger considerable cellular dysregulation and structural modifications within the oral epithelium. This review critically evaluates the current evidence regarding NP-related cellular alterations, histopathological changes, and their potential contribution to the emergence of oral potentially malignant disorders (OPMDs). Furthermore, the review examines the underlying biological processes, contrasts the oral effects of NPs with those of other nicotine delivery systems, and identifies significant deficiencies in the current body of research. A thorough comprehension of these impacts is crucial for the enhancement of clinical protocols and the formulation of public health strategies grounded in empirical evidence.
1. Introduction Nicotine pouches (NPs) are tobacco-free, flavoured delivery products of nicotine as a pharmaceutical-grade product in the oral vestibule, which combines pharmaceutical-grade nicotine, stabilizers and alkalizing agents.1 In contrast to conventional smokeless tobacco products, NPs are not made of tobacco leaf material and thus can be commonly promoted as being cleaner and having lower exposure to toxicants. The marketability and distribution of these products throughout the world in the past few years have been on rapid growth. The NP use of NPs is promoted under the harm-reduction models, and in the last five years, their prevalence has risen significantly among young adults and former smokers who seek the use of NP products as substitutes for combustible cigarettes and traditional oral tobacco.2 These products partially decrease the exposure to tobacco-specific nitrosamines (TSNAs) and combustion-based toxicants; however, they cannot be considered biologically inert. Their popularity creates significant issues concerning their effects on oral tissues in the long term, particularly with the oral cavity being the major location of placement and exposure. The first biological barrier that is exposed to nicotine pouch constituents is the oral mucosa. Direct absorption through epithelial tissues causes a direct delivery to the system, thus, at a high speed. Nevertheless, constant and prolonged use of the same intraoral location leads to consecutive local chemical contact, mechanical friction, and mucosal irritation. Notably, most NPs are developed at high alkalinity (pH > 8.5) to maximise absorption of free-base nicotine, this latter quality being itself a potential chronic chemical irritant and a contributor to focal mucosal alterations also known as nicotine pouch keratosis.3,4 Such lesions can be clinically expressed as white thickened formations or localised epithelial changes that cast doubt as to whether the •••••••••••••••••••••••••••••••• ejprd.org - Published by Dennis Barber Journals. Barber Ltd. All rights reserved
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