**2.6 Hypersalivation**

The quantity of salivation and the quality of saliva can be an indicator of a certain disease of the oropharynx and esophagus or it can be an indicator of the complication of such conditions. Saliva is produced by the parotid, submandibular and sublingual glands and the small salivary glands. Sialoreia usually occurs in neurological diseases, such as Parkinson's and Wilson's disease, Angelman's syndrome, infections, heavy metal poisoning, and can also occur in the secretory phase of the menstrual cycle or as idiopathic paroxysmal sialoreia. Increased salivation can be caused by systemic consumption of drugs with a cholinergic effect (clozapine, risperidone, nitrazepam, lithium and bethanekol), and it also occurs as a subtle manifestation of gastroesophageal reflux disease in the form of 'water

brash'. However, hypersalivation, although uncomfortable and disruptive, does not necessarily have to be negative since saliva plays an important role in protecting the esophageal mucosa. There are studies on the importance of ingested saliva that neutralizes the pH of gastric acid regurgitated into the esophagus [21] and on the buffering of gastric acid that enters the esophagus by reflux [22]. The acid that accumulates in the upper part of the esophagus reflexively initiates the formation of saliva [23], which is not the case when the acid accumulates in the lower part of the esophagus [24].

#### **2.7 Dental erosion**

Chronic regurgitation of gastric acids in patients with gastroesophageal reflux and related condition - laryngopharyngeal reflux may cause dental erosion which can, in combination with attrition or bruxism, lead to extensive loss of coronal tooth tissue. Dental erosion is typically a slowly-progressing and ireversibile phenomenon defined as the loss of tooth substance by chemical processes (acid exposure) not involving bacteria [25]. The literature shows a strong correlation between GERD and dental erosion, with a median prevalence of 24% in a large range of age groups. The degree of erosion due to GERD is related to the duration of the disease, frequency of reflux, the pH and type of acid, and the quality and quantity of saliva. Demineralisation and the loss of calcium and phosphate ions from the mineral surface of the teeth result in visible defects, and cause significant reduction in microhardness which makes the softened surface more prone to mechanical damage [26]. It is recognized that refluxed acid attacks the palatal surfaces of the upper incisor teeth first, later, if the condition continues, erosion of the occlusal surfaces of the posterior teeth in both arches and the labial or buccal surfaces [27].

#### **2.8 Halitosis**

Halitosis is an unpleasant odor from the oral cavity and is a condition that affects a large number of people [28]. The prevalence of halitosis is 8–46% [29]. The pathophysiological mechanism of halitosis is still not completely clear and is mainly attributed to oral pathology due to microbial activity in the interdental space, between the teeth and periodontium, and on the dorsal side of the tongue. Published data suggest that halitosis may correlate with chronic sinusitis, upper and lower respiratory tract diseases, various systemic diseases, gastroenterological diseases, and consumption of certain drugs in patients without oral pathology. It has been stated that mouth breathing, too, can be the cause of halitosis [30]. Although halitosis has previously been considered a rare consequence of gastrointestinal disorders [31], recent literal data have shown that it is common in gastrointestinal pathology and is significantly more common in patients with gastroesophageal reflux disease than in healthy individuals [32]. Furthermore, the symptom is often present in patients with verified infection with Helicobacter pylori, a bacterium that is among the major pathogenic factors of inflammatory and ulcerative changes on the gastric mucosa [33–36]. In addition, a high correlation has been demonstrated between halitosis and gastroesophageal reflux disease and peptic ulcer disease [37], and some authors have linked halitosis to volatile sulfur compounds [30, 38, 39] and to the chemical compounds cadaverine, some types of indoles [30]. Cadaverine (1,5-pentanediamine) is a toxic diamine formed by tissue putrefaction. Indole (benzopyrrole) is a heterocyclic compound formed by the breakdown of the amino acid tryptophan in the digestive tract, however, it is also used in the production of certain drugs, fragrances and essential oils [40]. An organic compound from the indole family associated with halitosis is skatol (3-methylindole), which occurs naturally

in faeces, it is also present in flowers and essential oils (orange and jasmine) in low concentrations, and is used as a fixative in many perfumes [41]. A 2006 study by Lee et al. reported that Helicobacter pylori produces hydrogen sulfide and methyl mercaptan that contribute to halitosis [42], and the bacterium itself is one of the main factors in the manifestation of gastrointestinal diseases.
