Dentinal hypersensitivity (DH)

Dentinal hypersensitivity (DH) is a clinical condition characterized by short, sharp pain arising from exposed dentin in response to stimuli, typically thermal, evaporative, tactile, osmotic, or chemical, which cannot be ascribed to any other dental defect or pathology (StatPearls, 2023). The most widely accepted pathophysiological explanation is the 'Hydrodynamic Theory,' which proposes that external stimuli cause the movement of fluid within open dentinal tubules, subsequently stimulating baroreceptors in the pulp's A-delta nerve fibers (Journal of Conservative Dentistry, 2014). While DH is a disease state rather than a single molecular target, the underlying biological mechanism involves the activation of ion channels such as Transient Receptor Potential Vanilloid 1 (TRPV1) and voltage-gated sodium channels (e.g., Nav1.7) on pulpal nociceptors (Nature Scientific Reports, 2017). Management strategies focus on either occluding the tubules to prevent fluid movement using agents like fluorides and arginine-calcium carbonate or chemically interfering with nerve conduction using potassium salts. DH remains a significant challenge in restorative dentistry and periodontology, impacting patient quality of life and necessitating the development of durable, long-acting desensitizing agents.

Other names

Dentin hypersensitivityCervical dentin hypersensitivitySensitive teethRoot sensitivity

Therapeutic agents typically work via two main mechanisms: 1) Nerve desensitization by using potassium salts to increase extracellular potassium ion concentration, thereby depolarizing the nerve membrane and blocking signal transmission; or 2) Tubule occlusion by using various salts or polymers to physically block the dentinal tubules, preventing the hydrodynamic fluid flow that triggers mechanoreceptors.