## 2 Etiology of Dentin Hypersensitivity  
Based on the hydrodynamic theory of dentin sensitivity, thermal, osmotic, tactile (from probe pressure), and drying-induced evaporation stimuli transmit sensations to the pulp nerves through the dentin tubules. These tubules contain fluid, originating from pulp fluids. Dentin hypersensitivity typically occurs when external stimuli are applied to the surface of exposed dentin with open tubules. Different stimuli lead to rapid fluid movement within the tubules, creating pressure changes that activate pressure receptors located close to the pulp. This activation results in immediate acute pain [14]. Unlike other stimuli, heat causes a gentle movement of the dentinal tubule fluid toward the pulp, leading to a milder activation of the pressure receptors and consequently causing less pain [14].  
It has been discovered that clinically hypersensitive teeth exhibit an exposed dentin tubule count approximately eight times higher and a dentin tubule diameter around two times larger in comparison to non-sensitive teeth [15; 16]. This discrepancy in dentin tubule diameter between hypersensitive and non-sensitive teeth appears to hold clinical significance [14]. Two prerequisites are necessary for DH to occur on a tooth's surface. Firstly, there must be exposure and removal of dentin, which can result from enamel loss or a combination of receding gums and the loss of root cement. Secondly, the dentinal tubules must become accessible, allowing external stimuli to activate the sensory mechanism present on the dentin surface [6].  
Gum recession and dentin exposure can be attributed to excessive brushing, improper brushing techniques, and periodontal disease, often arising after either surgical or non-surgical treatment [14]. While regular brushing typically does not lead to substantial enamel loss, the combination of acid erosion from acidic foods and beverages with brushing can result in significant tooth tissue loss across all tooth surfaces, with a particular impact on cervical regions [17]. During the removal of tartar from root surfaces, it is common for scalers to inadvertently eliminate a thin layer of cementum (20-40 \(\upmu\)m), giving rise to the creation of a smear layer containing blood and saliva that covers the underlying dentin [18].  
[PERSON] and [PERSON] (2012) [18] demonstrated that dentin tubule fluid gradually permeates the smear layer and moistens the dentin surface. However, the smear layer presents significant resistance (86%) to the outward flow of fluids through the dentin [18; 19]. Generally, the presence of the smear layer offers patients protection against dentin sensitivity, as it effectively seals the dentin tubules, even more efficiently than the resin infiltrations formed by bonding agents [20; 21]. This smear layer, however, does not persist on the dentin surface for an extended period. Over approximately 7-10 days, microbes accumulate on it, forming a biofilm that produces acids capable of dissolving the smear layer [20]. The loss of the smear layer leads to increased dentin permeability, resulting in the emergence of dentin sensitivity. In some instances, the level of sensitivity can escalate further, progressing to the state of hypersensitivity from the prior condition of simple dentin sensitivity.