What Is Dentin Hypersensitivity?
Dentin hypersensitivity can be primarily defined as a sensation of short, sharp pain that arises when the dentinal tooth layer (the second tooth layer) is exposed to temperature-related (evaporative or thermal), pressure-related (tactile, or osmotic), or chemical stimuli. This dentinal pain cannot be attributed to any regressive tooth alteration or carious lesions involving the tooth structure; hence, it is not related to any other dental defect or disease. According to the widely accepted hydrodynamic theory, dentin hypersensitivity is, in fact, activated by the dentinal tubular fluid flow resulting from changes triggered by these stimuli. Patients complaining of dentin hypersensitivity may not only report pain primarily from cold drinks or certain foods but also experience discomfort during daily toothbrushing or consuming sweet foods.
Is Dentin Innervated?
With the advent and advances of modern-day neurophysiologic and anatomic techniques over the last few decades, dental researchers and clinicians have resolved the question regarding the innervation of dentin. Dentinal hypersensitivity, a common complaint among patients experiencing tooth pain or sensitivity due to changes in the environment, thermal stimuli (heat or cold), or taste, remains a primary concern addressed by dental surgeons.
As early as the 1970s, electron microscopy of dentin (the second layer of the tooth, located beneath the superficial enamel structure that makes up the tooth crown) revealed nerve-like endings or processes, which were observed to degenerate upon the experiment of transecting the inferior alveolar nerve. Studies involving neural tracing and modern-day histopathological examination of the dental pulp (the layer after dentin, also known colloquially as the root canals) consistently indicate that the nerve terminals extend only into the dental pulp region and travel a short distance, approximately 0.1 to 0.2 millimeters, into the dentinal tubules.
Where Does This Sensitivity Occur?
The innervation of this layer remains relatively superficial, with only a mild extension from the dental pulp. It is these areas of low-density dentin that are most susceptible to hypersensitivity, where patients complain of sensitive teeth in response to specific stimuli, and in severe cases, the sensitivity may be more generalized.
A typical example observed in most clinical cases is hypersensitive dentin at the junction of the tooth crown and root, known as the cervical dentin layer, which is highly sensitive to thermal, tactile, or pressure changes affecting the tooth in question. Dental research also suggests that the odontoblast processes within the dentin layer may potentially be related or coupled to the sensation relay with the pulpal nerve terminals. This relationship could be a contributing factor to hypersensitive dentin.
What Is the Hydrodynamic Theory of Dentinal Hypersensitivity?
Most investigators and researchers believe in the common hypothesis known as the hydrodynamic theory of dentinal hypersensitivity. According to this theory, dentinal stimulation is intensified by the flow of dentinal fluid within the dentinal tubules. When mechanical, thermal, or heat stimuli are applied, they may induce fluid movement within the dentinal tubules. This sudden or rapid flow can cause distortion of the dental pulp dentin tissue, specifically at the sensitive junctional area where the nerve endings lightly penetrate the dentin.
The fluid flow not only transmits pressure across the dentinal side but also the geometry of the dentinal tubules itself may facilitate this fluid movement, creating pressure or concentrating the stimulus on the pulpal side of the tubules. This mechanism, widely accepted and referred to as "induced fluid flow," explains both dentinal hypersensitivity and the subsequent amplification of stimulus transmission from the dentin to the pulpal nerve endings due to pressure, tactile, or environmental changes on the tooth.
Why Does Dental Pain or Sensitivity Occur?
Neurophysiologic experiments also suggest that dental pain or sensitivity experienced from the dentin region, which is the hypersensitive dentin layer, is a result of mechanical stimulation, such as probing, drilling, or air blasting. Upon mechanical or thermal stimulation, the A-delta fibers and the C fibers in the dental pulp are considered responsible for the perception of pain and the subsequent response. Furthermore, inflammation of the dental pulp can also induce changes within the dentinal layer, making it more sensitive and causing the nerve endings or terminals to become more responsive to environmental stimuli or fluctuations. These activated A-delta fibers and C fibers are the main contributors to enhanced dentinal stimulation. As a result, any functional changes occurring within a diseased tooth, whether due to hypersensitive dentin or inflamed or infected dental pulp, can further exacerbate the disease process. This is because these layers may remain exposed to the outer oral environment for an extended period, lasting several days or months, until the patient experiences severe pain or unbearable sensitivity.
Why Dental Checkups and Preventive Measures Are Important in Managing Sensitivity?
Due to dental fears, many people often delay visiting the dentist until the issue of sensitivity worsens and transforms into pain. However, by the time sensitivity becomes painful, the pulpal nerve endings are already sensitized, and the situation may require endodontic treatment rather than conservative or preventive restorations. This highlights the importance of timely prevention, frequent dental check-ups, and restorative management as recommended by the dentist. Measures such as fluoride treatments in children, fillings, anti-sensitive mouthwashes or gels, bioactive glass treatments, or lasers can play a crucial role in preventing hypersensitive teeth from progressing into severe pain cases. In situations where severe pain has already developed, endodontic treatment becomes necessary and appropriate. Therefore, proactive dental care and early intervention can significantly reduce the risk of hypersensitive teeth advancing to a point where more invasive treatments become essential.
Conclusion:
To conclude, research on dentinal hypersensitivity theories and the physiological mechanisms of dentinal tubules indicates that the sensitivity or pain originates from the innervated and sensitive dentin of the tooth. Timely prevention and dental management are crucial in effectively addressing dentinal hypersensitivity.
