**1. Introduction**

The "perfect" and healthy tooth is properly designed to cope with the rough environment in the oral cavity, since virtually cleanses itself in an inside-out manner. Dental caries is supposed to be a result of the phenomenon that a tooth's fluid flow has been halted or even reversed, thus compromising tooth's defense system. It is well known that the local enamel demineralization process, aided by bacterial acid, is vastly stimulated by nutritional conditions, specifically by today's refined carbohydrates (sucrose and corn syrup = free glucose + fructose). Hence, the ensuing process renders the tooth vulnerable, and part of this process begins in the hypothalamus, resulting in alterations of the fluid flow passing through the dentine layer [1]. Not to forget: in this context, nutritional phenomena play very important roles (both systemically and locally).

**2. Backing of a new concept**

**2.2. How the tooth develops caries**

**2.1. Oral and systemic stress responses with common denominators**

"dentinitis" represents this local inflammatory response.

The definition of the stress concept dates back some 60–70 years [7]. It was meant to feature the process of how irritants caused a bodily reaction, and how the body dealt with it. If a stressor was defined as local, e.g. acid-induced enamel demineralization or irritation of the periodontal tissues by plaques, the body might provoke a specific, but local reaction. This would be controlled inflammatory responses that will remain similar throughout the entire body. Hence, they are defined as "local adaptation syndromes" (LAS). In the dentin of a tooth,

Vitamin K2 and Its Impact on Tooth Epigenetics

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A focal reaction is often mild, but resides rather quickly. However, this limited response may develop into a systemic and an exaggerated variant, thus "threatening" the entire body via the endocrine system. The present response is named "GAS" ("general adaption syndrome"), because its "attack" on the organism pretty much resembles the systemic type reaction, even though it represents a local type of stress reaction [7]. The hypothalamus/pituitary/adrenal

The essence of the problem resides with the ingestion of refined carbohydrates (i.e., mono and disaccharides in particular) that locally escalate the growth of microorganisms within the oral cavity and their production of acid. This inflammation causes a rapid loss of minerals, such as dental enamel, and it is named "dentinitis" and serves as a local adaptation, being a part of an LAS.

However, subsequent to this local reaction, small-molecular sugar entities (like sucrose, glucose, and fructose) exert a major impact on the body, when absorbed. Blood-sugar spikes are therefore counteracted by emerging dentinal fluid flows through the tooth by coordinated signals emanating from the hypothalamus. This adaptation (GAS) is chiefly endocrine, and affects the entire body. Hence, the present hypothalamic-parotid axis serves as the endocrine axis that is instrumental in maintaining the dental health [8]. The essence of it is the following: local irritation is magnified in the presence of a GAS response [7, 9]. Sugar molecules (mostly monosaccharides), with their marked effect on the whole organism, magnifies the local acid attack by triggering the GAS response. As a consequence, the tooth is rendered more vulnerable to the acid exposure [1], whether the acid is produced from sugar entities (via bacteria) or comes from various carboxylic acids in the diet.

The tooth is fed by the alimentary elements delivered by fluid flow through the dentin which may be halted or reversed, when impacted by a systemic stressor, like excessive sugar intake [10, 11]. This allows bacteria in the oral cavity to attach to the tooth, where they enhance the local concentration of acid, leading to the well-known demineralization of the enamel surface. Consequently, the flow of fluid through the tooth is enhanced by parotid hormone [8]. The secretion of parotid hormone, as well as the secretion of insulin [12, 13] is regulated by the hypothalamus, influencing GAS, and eventually affecting the adrenal glands. Finally,

axis serves as the mechanism in charge of the body's general, untoward reactions.

In the aftermath of acid-induced enamel demineralization of the breakdown of the dentin layer is accomplished by the body's own matrix metalloproteinase (MMP) enzymes [2, 3], a process which follows as a result of an untoward and galloping inflammatory response to an enhanced acid secretion. The present caries process begins as a more or less dormant, but reversible inflammation ("dentinitis"), while developing into a nonreversible dentin phase of caries after a while. This biological phenomenon is very much like reversible versus irreversible pulpitis and the terms gingivitis and periodontitis, while referring to the periodontium only [4].

However, there is a consensus that the process of dental caries recognization is multifactorial, as well as systemically based. It may not be sufficient to decrease the detrimental process rendered by the sugar intake with the ensuing enhancement of bacterial number and strains, but also boost the body's defense mechanisms with an antioxidant-rich diet that may be composed of fruits and vegetables, as well as vitamin K2.

Some research reports document that vitamin K2 can assist in significantly reducing dental caries [5, 6]. A larger body of research, however, is necessary in order to establish the mode, by which this vitamin may augment local defense mechanisms by altering saliva composition, while also systemically, via influencing the hypothalamus, as well as endocrine aspects of the parotid gland.

This concept of systemically delivered impact underscores an important shift in paradigm, from a traditional 'acid theory' explaining the development of dental caries that carries a plethora of implications for the prevention of dental decay in the future. Furthermore, it will necessary to document, via the mechanism of action of vitamin K2, how this small molecule affects gene regulation of the intimate play of osteoblast- and osteoclast-like cells in the organ layers constituting developing and full-frown teeth. The present chapter attempts to create a synthesis of current knowledge and recent research reports and ongoing research projects, with the intention of shedding new light on the impact of K2 on dental health.
