## 1 Introduction  
An international workshop describes Dentin Hypersensitivity (DH) as follows: \"Dentin Hypersensitivity is characterized by short, sharp pain arising from exposed dentin in response to stimuli, typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other dental defect or pathology\" [1]. DH frequently affects individuals aged 30 to 40 years old and is often associated with non-carious cervical lesions (NCCLs) [2; 3; 4]. It occurs when dental tubules are exposed to the oral environment, and this is well explained by the hydrodynamic theory of [PERSON] [5]. This theory suggests that, when one of these stimuli are applied to the fluid within the patent denntal tubules, the resulting pressure changes activate the mechanical receptors causing the transmission of the stimulus to the pulpal nerves [5; 6]. The severity of symptoms does not depend on the breadth and depth of lesions, but on the number of non-occluded tubules exposed to the oral cavity, consequently, the sealing of exposed and patent tubules should reduce or eliminate the pain and discomfort of the patient. Several treatments belonging to the tubule-occluding agent family [7] have been proposed including protein binding and calcium compounds deposition within tubules with casein phosphopeptide [8; 9], peritubular mineral deposition, and sodium fluoride (NaF). Sometimes, these treatments, as well as the use of nerve depolarization therapies (topical potassium nitrate), could be ineffective or might produce short-lived desensitizing effects [10]. However, a recent systematic review comparing DH treatments on the based on its efficacy and effect duration confirms the following: for an immediate (until 7 days) DH reduction, the use of glutaraldehyde with HEMA, glass ionomer cement, and a laser is significant; the use of stannous fluoride, glutaraldehyde with HEMA, hydroxyapatite, glass ionomer cement, and a laser provides a medium-term (until 1 month) DH decrease; for a more long-term DH reduction, the use of potassium nitrate, arginine, glutaraldehyde with HEMA, hydroxyapatite, adhesive systems, glass ionomer cement, and a laser is significant. Overall, the review shows the efficacy of all active ingredients in reducing DH at different time points, but the treatments must be completely in-office to achieve an immediate and persisting efficient DH decrease [11]. In a meta-analysis by [PERSON] et al., all types of lasers showed a greater desensitizing effect on DH than the negative controls, both in the immediate and long term [12]. Regrettably, there are conflicting pieces of evidence amongst the authors on which laser achieves the best outcome for the treatment of DH. In fact, [PERSON] et al. (2011) [13] reported an equal desensitizing effect for a diode laser and Er,Cr:YSGG lasers, while [PERSON] et al. (2009) [14] stated that an Nd:YAG laser is more efficient than a diode laser. In a recent study by [PERSON] et al. (2019), a split-mouth randomized clinical study compared Er, Cr:YSGG and diode laser effects on DH using a pulse width of 140-200 us. The study findings showed that the DH reduction after an Er,Cr:YSGG laser application was considerably higher than that after a diode laser application at a 1-month postoperative interval [15].  
It seems that a diode laser with different output powers range (low and high) could act on DH by two different mechanisms: high-power lasers could cause a melt of the external surface peritubular dentin, while low-power lasers could induce anti-inflammatory effects with an increase in the metabolic activity of odontoblasts causing the production of new dentin [14].  
The aim of this study was to evaluate the effectiveness of a diode laser on pain caused by DH associated with NCCLs by comparing three different laser therapy protocols: high and low power used individually and a combined method using first a low- and then a high-power laser.