Sensory transduction mechanisms responsible for pain caused by cold stimulation of dentine in man

Abstract

Objective

To determine the effects on the sensitivity of exposed dentine to cold that are produced when dentine is etched to remove the smear layer and when the tubules are blocked again with calcium oxalate. Separate in vitro observations were made on the effects of these procedures on fluid flow through the dentine.

Design

The experiments were carried out on 24 premolars in 17 subjects. Dentine was exposed at the tip of the buccal cusp and cold stimuli were applied by placing the tip of an ice stick on the cavity floor for 5 s under the following conditions: before etching the dentine, after etching, and after oxalate treatment. The subject indicated the intensity of any pain produced on a visual analogue scale (VAS). Fluid flow through the dentine was recorded under similar conditions in eight of the teeth in vitro.

Results

The mean VAS score produced by the ice before etching was 21.3 ± 19.5 mm (S.D.). This increased significantly to 85.4 ± 15.6 mm after etching (P < 0.01). After oxalate treatment, it decreased significantly to 8.5 ± 13.3 mm. The corresponding mean rates of fluid flow through dentine were 2.15 ± 1.02, 1.55 ± 0.84, and 2.29 ± 1.28 nL/s mm² exposed dentine, respectively. The mean after etching was significantly less than the other two values (P < 0.05).

Conclusion

If the pain was due to hydrodynamic receptors, their sensitivity to dentinal fluid flow changed when the tubules were opened or closed. Alternatively the pain was produced by receptors sensitive to some other change produced by the cold stimuli, such as specific cold receptors.

Introduction

Dentine is sensitive to the application of a wide range of different types of stimulus, which all cause pain. The types of stimulus that evoke pain include hot, cold, mechanical, osmotic and drying. Thermal stimulation of intact enamel also produces pain. It appears that all these different stimuli are capable of generating impulses in intradental nerves via a common sensory transduction mechanism, and that this mechanism detects movement of the contents of the dentinal tubules. It seems that the tubules act as hydraulic links between the site of stimulation and the nerve endings, which are located either in the pulpal ends of the tubules or in the underlying pulp. The evidence for this so-called hydrodynamic hypothesis is reviewed in references 1, 2, 3, 4. Recently, it has been shown that the transduction mechanism is more responsive to outward than inward flow through the tubules5, 6 but the precise mechanism whereby the flow generates nerve impulses is not known.

The evidence that responses to cold stimulation involve a hydrodynamic mechanism includes the observations that the latencies of sensory responses to cold stimulation in man⁷ and of neural response to cold in the cat⁸ are too short to be accounted for by a mechanism that is sensitive to temperature change in the pulp or at the pulp/dentine interface, where the nerve endings are located. In man, the estimated interval between the application of the cold stimulus and the neural discharge being evoked averaged 0.14 s; and the latency in the evoked discharge cat was 0.15–0.2 s. It is known that cold stimulation of enamel or exposed dentine causes outward flow in the underlying dentinal tubules.6, 9, 10, 11 This is assumed to be due to the fluid contents of the tubules undergoing a greater contraction (due to their a greater coefficient of thermal expansion) than the dentine matrix. With such a mechanism, the delay between the application of a cold stimulus to the tooth surface and the onset of fluid flow at the pulpal ends of the dentinal tubules would be very short, and compatible with the latency measurements referred to above. Further evidence that a hydrodynamic mechanism is responsible for the pain caused by cold stimulation is the observation that intradental nerves that respond to cold stimulation in the cat and dog also respond to other forms of stimulus, such a hydrostatic pressure change, that cause fluid flow through the tubules.12, 13, 14

However, it is difficult to explain on the basis of a hydrodynamic mechanism alone, the observation that oxalate treatment of hypersensitive dentine produces an immediate reduction in the sensitivity of the dentine to cold stimuli.15, 16 Hypersensitive dentine is associated with patent dentinal tubules17, 18 and occluding those tubules with insoluble calcium oxalate provides temporary symptomatic relief.15, 16 The depth of penetration of the calcium oxalate plugs, determined under conditions similar to those of the present experiments and using the same potassium oxalate preparation, was found to be around 6–7 μm.¹⁹ In other experiments in the dog, penetrations of 15–133 μm have been reported.20, 21 The reduction in sensitivity to mechanical, hydrostatic pressure and osmotic stimuli and to drying produced by this treatment is readily explained on the basis of a hydrodynamic transduction mechanism, but not the desensitisation to thermal stimuli. In the case of a tubule that was plugged peripherally by either enamel, a smear layer or calcium oxalate, the contraction of the tubule contents that resulted from the topical application of a cold stimulus would be accommodated largely by tissue fluid being sucked into the tubule from the pulp. On the other hand, if the peripheral end of the tubule was patent, some of the contraction would be accommodated by movement of fluid into the tubule from the outer dentine surface, with the result that the flow from the pulp into the opposite end of the tubule (where the nerve endings are situated) would be less than with an occluded tubule. Thus, if a hydrodynamic mechanism is responsible for the pain caused by cold stimulation of hypersensitive dentine, occlusion of the patent tubules by calcium oxalate might be expected to increase rather than decrease the sensitivity of the dentine to the cold stimuli.

It is unlikely that the effect of the calcium oxalate in reducing the sensitivity of dentine to cold is due to any thermal insulating effect because the layer is so thin.

One factor that may have affected the responses to cold stimuli in these experiments on hypersensitive dentine is the presence of pulpal inflammation. The pulp may be inflamed under the patent tubules of hypersensitive dentine, and this could have affected the properties of the nerve endings and transduction mechanism.

The present experiments were carried out to investigate further the transduction mechanisms responsible for the pain produced by cold stimuli in man. The specific aims of the experiments were (1) to determine the effects on the sensitivity of exposed human dentine to cold stimulation of removing the smear layer by etching and then occluding the tubules again with calcium oxalate, and (2) to measure the fluid flow through dentine produced by cold stimuli under similar conditions in vitro. This was done to check that our predictions on the effects of etching and of tubular occlusion on the fluid flow through dentine produced by cold stimuli were correct. It is not possible to measure the fluid flow through dentine during the application of a cold stimulus in vivo. The experiments were carried out on teeth with no pulpal inflammation.