23.2 Pulpal Neurophysiology and Dentine Hypersensitivity
Key Takeaways
- A-delta fibres are myelinated, 1 to 5 micrometres in diameter, sited peripherally, and produce sharp, well-localised pain.
- C-fibres are unmyelinated, 0.4 to 1.2 micrometres in diameter, sited centrally, and produce dull, poorly localised throbbing pain.
- C-fibres resist hypoxia far better than A-delta fibres, so a tooth with a dying pulp may not respond to cold yet remains painful.
- Brannstrom's hydrodynamic theory attributes sensitivity to fluid movement within patent tubules deforming A-delta terminals.
- Tubule fluid can move at velocities up to 2 to 3 mm per second, with outward flow from evaporative or osmotic stimuli being the more painful direction.
Neurophysiology: A-Delta vs C-Fibres
The sensory innervation of the pulp-dentine complex is mediated by primary sensory afferent neurons of the trigeminal nerve (CN V), categorized into two functionally and anatomically distinct fibre populations: myelinated A-delta fibres and unmyelinated C-fibres.
| Characteristic | A-Delta (Aδ) Fibres | C-Fibres |
|---|---|---|
| Myelination | Thinly myelinated (type III sensory) | Unmyelinated (type IV sensory) |
| Conduction Velocity | Fast: 5 – 30 m/sec | Slow: 0.5 – 2.0 m/sec |
| Axon Diameter | 1 – 5 µm | 0.4 – 1.2 µm |
| Anatomical Location | Coronal periphery, subodontoblastic plexus of Raschkow, inner 100 µm of dentinal tubules | Deep central pulp core, radicular pulp |
| Pain Quality | Sharp, fast, pricking, well-localized lancinating pain | Dull, aching, throbbing, heavy, poorly localized, lingering, burning pain |
| Primary Stimuli | Thermal shifts (especially cold), mechanical probing, hyperosmotic fluids, drying air blasts | Prolonged noxious heat, tissue ischemia, inflammatory mediators (bradykinin, histamine, prostaglandins, capsaicin/TRPV1) |
| Threshold of Activation | Low electrical and thermal threshold | High threshold; requires intense tissue-damaging stimuli |
| Resistance to Hypoxia | Highly vulnerable to tissue ischemia and anoxia | Highly resistant to hypoxia, necrosis, and ischemia |
| Clinical Significance | Signifies intact, vital peripheral pulpal tissue; mediates dentine hypersensitivity and early reversible pulpitis | Signifies deep pulpal inflammation, irreversible tissue damage, and partial necrosis; pain radiates and lingers |
[!IMPORTANT] Survival of C-Fibres in Necrotic Teeth: Because unmyelinated C-fibres have minimal metabolic demands, they remain functional in hypoxic, ischemic, and even partially purulent tissue long after A-delta fibres have ceased conducting. Consequently, a patient with advanced irreversible pulpitis or partial coronal liquefaction necrosis may report excruciating, dull, throbbing nocturnal pain and retain sensitivity to heat testing, even when cold and electric pulp testing (which test A-delta fibres) yield no response.
Hydrodynamic Theory of Dentine Hypersensitivity
Formulated by Martin Brännström in the 1960s, the hydrodynamic theory remains the universally accepted mechanism explaining dentine sensitivity in the absence of direct nerve stimulation.
- Anatomical Substrate: Dentinal tubules traverse the full thickness of dentine, tapering from 2.5 µm in diameter at the pulpal border to 0.9 µm at the amelodentinal junction (ADJ), with tubule density increasing from ~20,000/mm² peripherally to ~45,000/mm² near the pulp. The tubules are filled with dentinal fluid (an ultrafiltrate of pulpal interstitial fluid).
- Mechanism of Transduction:
- Thermal, mechanical, evaporative, or osmotic stimuli applied to exposed dentine create rapid physical displacement of tubular dentinal fluid.
- Cold stimuli, air blasts, and hypertonic solutions (sweets/sugars) cause rapid outward fluid movement (away from the pulp) by capillary action and evaporation at velocities up to 2–3 mm/sec.
- Heat causes thermal expansion, producing inward fluid movement toward the pulp.
- Outward fluid movement generates substantial hydrodynamic shear stress and mechanical strain across the odontoblast cell bodies and adjacent subodontoblastic nerve endings in the plexus of Raschkow.
- This mechanical deformation activates mechanosensitive ion channels (PIEZO2, TREK-1, and transient receptor potential TRP channels) on peripheral A-delta sensory nerve fibres, firing action potentials that transmit sharp, fast pain to the trigeminal sensory nucleus.
Diagnosing Dentine Hypersensitivity
Dentine hypersensitivity is a diagnosis of exclusion, and that is the point most often examined. The classic presentation is a short, sharp pain arising from exposed dentine in response to thermal, evaporative, tactile, osmotic or chemical stimuli, which cannot be ascribed to any other dental defect or disease. Before accepting the diagnosis, the clinician must exclude caries, a cracked tooth or cusp, a fractured or leaking restoration, a recently placed restoration with an incomplete seal, marginal gaps, pulpitis, and postoperative sensitivity after periodontal instrumentation or bleaching. The examinable discriminator is duration and provocation: hypersensitivity stops the moment the stimulus is removed, whereas pain that lingers for seconds or minutes after a cold stimulus indicates pulpal inflammation and requires a different plan entirely.
Why the Dentine Became Exposed
Effective management begins with the aetiology rather than with a desensitising agent. Dentine becomes exposed either through gingival recession — from periodontal disease, periodontal treatment, traumatic toothbrushing, thin biotype, or orthodontic movement outside the alveolar envelope — or through loss of enamel from erosion, attrition or abrasion, most often in combination. Erosion is the dominant modern driver, and it also removes the smear layer and opens tubules, which is why patients with dietary or intrinsic acid exposure are disproportionately affected. Unless the acid source, the brushing technique or the parafunctional habit is addressed, desensitising products provide only temporary relief.
Mechanisms of Desensitising Agents
Treatments work in one of two ways, and candidates are expected to classify them. Tubule occlusion physically blocks fluid movement: strontium salts, stannous fluoride, calcium sodium phosphosilicate, arginine–calcium carbonate, oxalates, varnishes, bonding agents and glass ionomer restorations all act this way, as does the natural occlusion produced by salivary mineral deposition and by sclerotic dentine. Nerve desensitisation raises the excitability threshold of the intradental nerve: potassium salts, principally potassium nitrate in toothpastes, diffuse along the tubules and depolarise the nerve terminal, preventing repolarisation.
Management follows a sequence from least to most invasive: identify and remove the cause, advise on brushing technique and timing relative to acid intake, recommend a desensitising toothpaste used twice daily and rubbed into the affected area rather than rinsed away, apply professional agents such as fluoride varnish or a resin sealer, and finally consider restoration of the defect or, in severe localised recession, a mucogingival graft. Endodontic treatment for hypersensitivity is almost never justified and should be recognised as a distractor.