## 1 Introduction  
The main etiological factor for periodontal disease is the disruption in the homeostasis of the host-bacterial interplay. Such an imbalance creates a conducive milieu for commensal and pathogenic bacteria to flourish, thus triggering an inflammatory cascade [1; 2]. It is a well-documented fact that polymorphonuclear neutrophils (PMNs), commonly referred to as neutrophils, are the foremost players in the immunological arena. The destruction of periodontal supporting tissues will be favoured if the functions of PMNs are compromised [3; 4]. Periodontal diseases are not only affected by immune cells, but various environmental risk factors can also act as a catalyst for the worsening of the condition. Smoking has already been established to have a causal relationship [5], whereas the influence of area nut chewing has not been explored much in the context of gingival and periodontal diseases. Areca nut has been rated as the fourth most widely abused substance, andis mainly consumed in East and South-East Asian countries in various forms [6]. Its users amount to 600 million people worldwide, which comprises of 10-20% of the total population of the world [7]. In India, tender area nuts are mainly consumed in the southern and north-eastern regions, while the ripe form is consumed in almost every part of the country. The ripe variant of the areca nut is commonly consumed as a preparation in piper betel leaves with or without additives. However, in Taiwan, tender areca nut is more often consumed without any accompaniment, like tobacco [8]. In the past, investigations have been carried outto study the deleterious impact of areca nut on the gingival epithelium [9; 10], fibroblast [11], and cementoblast [12]. Results have also shown radiographic changes in oral bone tissues [13]. These findings led us to contemplate that area nut usage could compromise gingival and periodontal health. Although periodontal disease is prevalent in area nut chewerscompared to non-chewers [13], its exact mechanism is nevertheless not well understood. The main culprit of gingival and periodontal disease is plaque, comprising colonies of microorganisms. With the advancement of the disease, there is a growth in colonies with the addition of various microbes, thus transforming the composition of the plaque and local environment [1; 2]. Concurrently, the body's immune mechanism is also preparing to combat the microbial intrusion by recruiting various progenitor and immune cells that will reach the site to impart their action [14]. During the progression of periodontal disease, various inflammatory cytokines playimportant roles [15]. PMNs, being the first favoured amongline of defence mechanismsm come into effect immediately. This makes them highlycrucial in the initial inflammatory response [16]. This rationale supports the idea that situations in which PMN actions are curbed will lead to the destruction of tissues far beyond the rate of the body's physiological repair. PMNs, which are available to the oral cavity, commonly known as oral PMNs, are distinctfromtheir counterparts seen in the peripheral blood [17]. Subsets of oral PMNs that exist in the gingival crevice, known as crevicular PMNs (cPMNs), are of paramount importance with regard to the gingival and periodontal diseases because of their proximity to the diseased tissues [18; 19]. PMNs derived from the peripheral blood of healthy subjects have been used to assess the effect of area nut extract (ANE) on its various function such as chemotaxis, phagocytosis and bactericidal activity [20; 21; 22]. However, only the phagocytic activity of cPMNs has been assessed [23]. Additionally, the emphasis has been placedon area nut usage in the development of potentially malignant disorders (oral submuc fibrosis) and oral cancer. However, the due attention has not been directed towardsits role in periodontal diseases.Based on the literature search, no in vivo longitudinal studies haveevaluated the bactericidal activity of cPMNs under the impact of area nut.