## 3 Pain Mechanism of Dentin Hypersensitivity  
While considerable knowledge has been acquired regarding DH since its initial documentation, there remains a deficiency in clinical evidence-based research, particularly concerning the underlying pain mechanisms, which remain incompletely understood [22]. The theory that continues to hold the most widespread acceptance posits that sensitive dentin arises from the stimulus-triggered fluid flow within the dentin tubules, leading to the subsequent activation of nociceptors at the border between the pulp and dentin [23]. It is believed that intradental myelinated A-\(\beta\) fibers and some A-\(\delta\) fibers respond to stimuli that displace the fluid within the dentin tubules, culminating in the distinct, brief, and sharp pain experienced in cases of DH [24]. Despite the fact that the inner diameter of dentin tubules measures about 1 \(\upmu\)m, their hydrodynamic behavior, influenced by collagen fibers and calcium phosphate salts within them, resembles that of tubules with a functional diameter of less than 0.1 \(\upmu\)m [21]. Consequently, while microbial penetration through the dentin tubules into the pulp is unlikely, microbial byproducts, including endotoxins and exotoxins, can readily traverse the tubules and reach the pulp [25; 26]. In cases where toxins induce localized inflammation of the pulp, an escalation in pulpal pressure occurs, consequently increasing fluid outflow. This process ultimately leads to increased sensitivity of the pulp nerves beyond normal levels. Furthermore, localized pulp inflammation can prompt the proliferation of nerve endings located close to the dentin tubules, intensifying the overall sensitivity of the pulpo-dental complex [21; 27]. The proliferation of nerve endings is triggered by inflammation mediators, such as histamine, bradykinin, prostaglandandins, neuropeptides, and others. These mediators induce the proliferation of fibroblasts, aiming to restore the damaged collagen within the pulp's connective tissue due to inflammation [28; 29; 30]. Furthermore, the cell membrane receptors on the newly formed nerve branches identify microbial antigens and inflammatory byproducts. This recognition activates mechanisms for generating new protein factors that subsequently stimulate sodium channels. As a result, these channels are further stimulated, leading to an increased sensitivity of the pulp [31]. It has been noted that DH can, in certain instances, gradually subside without external therapeutic intervention, often following a period of exacerbation [32; 33]. Experimental studies conducted in vivo by [PERSON] et al. [30] offered insight into this phenomenon. When cavities were created in dog teeth and dentin permeability was measured hourly over an 8 h span, a decline of 15% in permeability occurred each hour in living teeth, in contrast to pulpless teeth [33]. The researchers deduced that this decrease in permeability resulted from the release of plasma proteins from the pulp into the fluid of the dentin tubules, leading to a reduction in tubule diameter. The significance of fibrinogen, the largest plasma protein, in reducing dentin permeability after cavity preparation was also experimentally confirmed in dogs [34]. Additionally, other researchers discovered that immunoglobulins, such as IgG, can induce a gradual reduction in dentin permeability over time [35]. Consequently, microbial toxins originating from saliva and plaque have the capability to infiltrate the pulp, prompting pulp irritation, elevating pulp pressure, stimulating new neuron growth, and increasing nerve sensitivity [21]. These toxins are believed to underlie the sustained presence of DH within a subset of patients who initially experienced it. It is plausible that this persistence of hypersensitivity is linked to multiple episodes of localized pulpitis in these patients, which eventually resolves through pulpal eschar formation [21].