Role of Plaque
The effectiveness of clients’ plaque removal should be assessed when evaluating causes of tooth sensitivity. However, the role of plaque in the initiation and/or persistence of cervical hypersensitivity is controversial. Logic would suggest that plaque deposits would likely demineralize tooth structure and perhaps lead to gingival/periodontal pathology, and initiate gingival recession as a precursor to hypersensitivity. The clinical reality is that the teeth with the most extensive recession and hypersensitivity usually have been subjected to excessive buccal tooth cleaning, and therefore exhibit little to no plaque.

Further evidence against the role of plaque in hypersensitivity comes from reports of sensitivity following periodontal surgery where chemical agents such as chlorhexidine have rendered the teeth nearly plaque free.86 Additionally, some people with periodontal disease often harbor copious amounts of plaque on their teeth and report no sensitivity. Following periodontal therapy, they demonstrate relatively plaquefree tooth surfaces, yet report experiencing hypersensitivity. This post-surgical sensitivity frequently occurs several days after surgery rather than immediately.44,52

However, plaque has been shown to play a role in the patency of dental tubule orifices. One study found that when plaque was not removed from teeth the diameter of the tubule orifices increased to three times their original size within three weeks.87 With plaque control, the orifices became less than 20% of their original diameter within one week, suggesting that plaque control can occlude tubules. These investigators concluded that plaque removal does play a key role in the patency versus occlusion of dentinal tubules and thus the process of hypersensitivity.87

Bacteria have been shown to diffuse into open dentin tubules and may diffuse into the pulp resulting in hypersensitivity.88 However, the diffusion would be
against the outward flow of dentinal fluid. Such bacterial penetration could occur as a result of marginal leakage or secondary decay around restorations. The deleterious effect of the bacterial toxins would be inflammation of the pulp. If hypersensitivity is defined as a reaction to a non-noxious stimulus, then plaqueinduced dentin sensitivity would not be categorized as true hypersensitivity.


Self-Care Strategies

Clinical research issues

 

To date, research evidence that supports an ideal intervention for dentinal sensitivity that works 100% of the time with all patients, for all teeth, even within the same mouth, regardless of whether the strategy is self or professional care has not been reported. Well-designed clinical trials to compare treatment approaches are difficult to formulate because it is hard to standardize stimuli and pain reactions. Consequently, the evidence demonstrating superiority of any desensitizing agent over any other is not available. It is readily apparent that study design must be carefully considered when claims are made that improvements in hypersensitivity resulted from either therapeutic or natural resolution.

Designing studies to evaluate treatment approaches to relieve the pain of hypersensitivity is complicated for a variety of reasons. Pain, a subjective phenomenon, is difficult to quantify and measure. Lack of standardization in applying the stimulus agent can also lead to inconclusive or contradictory results. As a result of faulty research designs, many early studies do not provide reliable findings.7 These studies often did not include necessary controls or use an adequate sample size, and lacked reliable evaluation methods. Additionally, some reports in the literature resemble testimonials provided by the clients of the operator who developed the treatment. Because the scientific method was not used in these studies, the results are inconclusive. Because of questionable early clinical trials, the ADA formed an ad hoc Advisory Committee on Dentinal Hypersensitivity in 1986. This group was asked to quantify the variables associated with pain perceptions and to assist in standardizing study protocols.55

It has been suggested that a well designed hypersensitivity study should include three groups: a control group that receives no treatment, a group that receives a placebo, and a group that is treated with the agent or procedure being tested.43 This design would address the placebo effect that has proven problematic in hypersensitivity research.56-58 The literature now provides guidance for designing a hypersensitivity clinical trial.7,59

Continued research is needed to compare various therapeutic interventions. When selecting treatment options, clinicians will want to utilize an evidence-based approach that incorporates careful scrutiny of the available scientific literature, clinician judgment, and client preferences. A systematic approach will encourage individualized treatment (Figure 9).