Dental nerve endings in exposed dentine

Dental nerve endings in exposed dentine refer to the terminal sensory axons, primarily A-delta and C-type nociceptors, that originate in the dental pulp and extend into the dentinal tubules [1]. Under normal conditions, these nerves are protected by enamel or cementum; however, when dentine is exposed due to gingival recession or enamel erosion, these endings become vulnerable to external stimuli [2]. According to the widely accepted Hydrodynamic Theory, stimuli such as cold, heat, or osmotic pressure cause rapid fluid movement within the dentinal tubules, which mechanically distorts and activates these nerve endings, resulting in the sharp, transient pain known as dentin hypersensitivity [3]. Pharmacological management of this condition targets these nerve endings through two main strategies: the use of potassium salts (like potassium nitrate) to increase extracellular potassium concentration and depolarize the nerve membrane, thereby blocking signal transmission, or the use of occluding agents (like fluorides, oxalates, or arginine) to physically plug the tubules and stop fluid movement [4][5]. While 'Dental nerve endings' is an anatomical description rather than a single molecular target, it serves as the functional site for various desensitizing therapies in clinical dentistry [1].

Other names

Intradental nerve endingsPulpal nerve fibersA-delta fibersC-fibersDentine-pulp complex nervesNociceptors of the dental pulp

Nerve depolarization blockade (via potassium ions); Dentinal tubule occlusion (preventing hydrodynamic fluid movement); Protein precipitation; Nerve conduction inhibition.