Overview
Tooth hypersensitivity is characterized by a short, sharp pain arising from exposed dentin (i.e., the mineralized tissue of teeth internal to crown enamel and root cementum) in response to a stimulus (thermal, chemical, or physical) that cannot be ascribed to any other form of dental defect or disease. Two processes are essential for the development of dentin hypersensitivity:
1. Dentin must become exposed (lesion localization) through erosion of tooth enamel or gingival recession.
2. The dentin tubules must be open to both the oral cavity and the pulp (lesion initiation).
When stimuli such as heat, cold, pressure, or acid touch exposed dentin or reach an open tubule, fluid flow in the dentinal tubule is increased and the underlying nerves are stimulated, resulting in pain.
Although tooth hypersensitivity is self-treatable, toothache is not. It is critical for pharmacists to differentiate between these two conditions (see Table 1) and advise patients with suspected toothache to seek professional dental assistance as soon as possible.
| Tooth Hypersensitivity | Toothache |
Etiology | Exposed and open dentin tubules | Bacterial invasion to the pulp |
Pathophysiology | Stimuli (heat, cold, pressure, acid) cause fluid in the dentinal tubules to expand and shrink, stimulating pulp nerve fibers and resulting in pain | Inflammatory response to invading bacteria stimulates free nerve endings in the pulp |
Causes | Attrition, abrasion, erosion, tooth/restoration fracture, faulty restoration, or gingival recession | Cavitation/decay present in tooth/teeth under existing restoration, tooth/restoration fracture, or trauma to the dentition |
Symptoms | A quick, fleeting, sharp, or stabbing pain on stimulation by thermal, chemical, or physical stimuli, which stops after stimuli are no longer present | Intermittent, short, and sharp pain on stimulation may indicate reversible damage; continuous, dull, and throbbing pain without stimulation usually indicates irreversible damage |
Assessment |