## 1 Introduction  
Dental hypersensitivity (DH) is a challenging condition in dental practice, representing one of the most widespread dental problems and symptoms in the world population [1]. Thanks to the increasing life expectancy and to the greater attention to oral health, with healthy functional natural dentition present even in older age, it is also reasonable to assume a further increase in DH prevalence among the population. Currently, DH presents an incidence of about 35% of the population worldwide and occurs mainly between 20 and 50 years of age. Regarding prevalence, DH seems to affect women in higher number compared to men in an age range from 30 to 40 years old [2, 3]. DH is also found between 72% and 98% of patients presenting gingival recession and/or periodontal disease [4]. DH is conventionally defined as an episode of short sharp pain arising from exposed dentin after the application of thermal, tactile, chemical, osmotic, or evaporative stimuli, which cannot be caused by any other dental pathology and/or defect [5]. This condition impacts oral health-related quality of life [3], causing significant impairment on patients' daily life such as speaking, eating, drinking, and toothpushing [6, 7, 8]. In the literature, many etiopathogenice theories to try and explain DH such as the neural theory, the odontoblastic transduction theory, and the hydrodynamic theory; the latter is considered the most accepted pain theory [9, 10]. According to the hydrodynamic theory, dental hypersensitivity is caused by the fluid flow in the dental tubules caused by the stimulus, and the consequent activation of nociceptors in the pulp/dentine border area. Therefore, the main cause of DH is the exposure of dentinal tissue with unobstructed dentinal tubules, which allows the hydrodynamic mechanism to occur [11; 12]. In the literature, two other etiological theories are currently discussed: odontoblast transducer theory and neural theory. Current evidence highlights the fundamental role in DH pain mechanism of odontoblasts, representing a mechanosensory system, working as sensor cells. According to the neural theory, dental primary afferent neurons were found to respond to heat by the expression of TRP channels (temperature-sensitive transient receptor potential channels), suggesting that they may transduce only high temperatures. Odontoblasts too were found to express the same receptors class. This evidence leading to the identification of TRP channels as potential receptors provides a key information that may justify all the molecular mechanisms on which all the three DH etiological recognized theories are based [13]. Since consistent correlation is reported between tubules density and pain responses, dentinal tubules' patency seems to be a needed condition in sensitive dentine. [11; 12; 13]. Several other dental defects and/or pathologies can cause similar DH pain symptoms [13; 14], therefore a differential diagnosis other similar conditions is key. Some of these conditions are: chipped teeth, fractures in restorations and pulpal sensitivity response to cavities or restorative therapies [15]. An exposed dentine surface may be caused by: gingival recession, anomalies in the cementoenamel junction (CEJ) leaving uncovered areas of dentine surface, erosive phenomena, and removal or loss of tooth enamel [13; 16]. Before discussing and applying any of the available DH treatment options, it is necessary to eradicate the eventual causative etiological factors that may be present in the patient, to prevent recurrence of the condition [13; 14; 15; 16]. Treatment options can be classified according to administration modality (home treatment or professional treatment) and/or mechanism of action (modification/blocking of the pulpal nerve response or fluid flow alteration in the dentinal tubules). From the application of the latter, the effect on the clinical symptoms of DH is perceived only after a couple of weeks. A more direct approach to DH-associated pain is given by dentinal tubule orifice occlusion.