Dentin hypersensitivity: the Canadian Advisory Board consensus (2003), a diagnosis of exclusion with a first-line treatment the trials never quite confirmed

What it says#

The Canadian Advisory Board on Dentin Hypersensitivity met in Toronto in June 2002 because two things were true at once: the condition was common, and the profession was managing it badly. The board was dentists and dental hygienists from general practice, specialist practice, academia and research across Canada, plus two international subject matter experts. It worked from a MEDLINE and hand search of 1966 to 2002 and from a 66-item questionnaire mailed to a random sample of 5,000 dentists and 3,000 hygienists. Where the science was deficient, the board says plainly, it wrote consensus positions drawn from its members' own backgrounds. The output is six pages, an algorithm, and a list of recommendations.

The definition does the heavy lifting. The board adopted Holland's wording with one change, substituting "disease" for "pathology": a short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical, and which cannot be ascribed to any other form of dental defect or disease. That last clause is the whole entry. It makes dentin hypersensitivity a diagnosis of exclusion, and the algorithm's second box is a list of what must come off first: cracked tooth syndrome, fractured restorations, chipped teeth, dental caries, gingival inflammation, post-restorative sensitivity, marginal leakage, pulpitis and palatogingival grooves. The diagnostic tools listed are an air jet, a cold water jet, other thermal tests, a dental explorer, a periodontal probe, radiographs if needed, percussion, assessment of occlusion and bite stress tests, with selective anesthesia and transillumination as further aids.

The mechanism is Brannstrom's hydrodynamic theory: fluid flow within the dentinal tubules is increased or redirected by a stimulus near the exposed surface, stimulating the A-delta fibers around the odontoblasts. That requires tubules open both at the dentin surface and at the pulp. The board's supporting numbers come from Absi and colleagues: sensitive teeth had about 8 times as many open tubules per unit area at the root surface as nonsensitive teeth, and tubule diameters averaging 0.83 micrometers against 0.4. Because Poiseuille's law makes flow proportional to the fourth power of the radius, diameter alone would give 16 times the flow; combined with the tubule count, the board estimates roughly 100 times the fluid flow in a sensitive tooth.

Two processes are required: dentin has to become exposed, by enamel loss or gingival recession (lesion localization), and the tubules have to be open to both the mouth and the pulp (lesion initiation). Erosion, abrasion, attrition and possibly abfraction expose the tubules. Enamel resists abrasion from brushing with or without toothpaste but is very vulnerable to acid, so brushing acid-softened enamel is what does the damage. Gingival recession is the other route, with overzealous brushing, necrotizing ulcerative gingivitis, self-inflicted injury and periodontal procedures as its main predisposing factors.

The survey results are the most useful part of the paper for an owner, because they describe the office, not the tooth. Prevalence was underestimated: about 70% of respondents thought their sensitivity patients were between 35 and 50, while an independent survey of 683 Canadian adults found about 30% prevalence across the 18 to 64 band, including 28% of 18 to 24 year olds. Screening was not routine, done only when a patient raised it. Fewer than half of respondents considered a differential diagnosis at all. Sixty-four percent of dentists and 77% of hygienists named bruxism and malocclusion as triggers, neither of which has been identified as a major causative factor. Only 7% of dentists and 5% of hygienists named erosion as a primary cause, and 60% overall named gingival recession, which is a predisposing factor rather than the cause. Eighty-five percent of dentists and 94% of hygienists blamed toothbrush abrasion for continued tubule exposure. Half said they lacked confidence managing the pain, and only half tried to modify predisposing factors at all. Fifty percent of dentists and 73% of hygienists believed fluoride compounds were the most popular desensitizing ingredient, when the most widely available is potassium nitrate; only 10% knew that potassium nitrate works by interfering with pain transmission rather than by occluding tubules.

The recommendations follow from that. Screen every dentate patient. Exclude the mimics. Take a detailed dietary history assessing erosive influences, which the board calls essential. Remove or modify the predisposing factors first, because otherwise treatment gives only short-term success: cut the dietary acids, brush remote from meals and preferably before them, and stop overly frequent or aggressive brushing. Then treat, reversible procedures before irreversible ones. Everyday use of a desensitizing toothpaste is the noninvasive, inexpensive, efficacious first line, and brushing with it at least twice daily is, in the board's words, the only clinically supported method of application; there is no published evidence for dabbing it on, which 39% of respondents were recommending. If it persists, review the diagnosis to exclude periodontal, neuropathic and referred pain and chronic pain syndrome, then consider mucogingival surgery, resins or, last, pulpectomy, with referral to a specialist ideally before that point.

What the board could not do is tell you which agent works. Its own line is that there is little evidence to determine the superiority of one desensitizing agent over another. The reviews since have not fixed that. Cochrane's 2006 review of potassium containing toothpastes pooled six studies and found a statistically significant effect on air blast sensitivity at 6 to 8 weeks (standardized mean difference -1.25, 95% CI -1.65 to -0.851) and on tactile sensitivity, but no significant effect on the subjective assessment, and concluded that the evidence rests on a small number of individuals, varies with the assessment method, and gives no clear support for potassium containing toothpastes. Karim and Gillam's 2013 systematic review screened 94 papers, accepted seven, and concluded there is insufficient evidence to state categorically whether strontium or potassium salts are effective. The newest pooling, Saxena and colleagues in 2026, took 31 trials of newer modalities and meta-analyzed 25: advanced treatments beat conventional or placebo comparators at a pooled SMD of -1.02 (95% CI -1.32 to -0.73), with lasers largest at -2.11 but with I-squared of 93%, and with resin and varnish systems and oxalates not significantly better than controls. That team explicitly declined to run a GRADE assessment, saying the interventions were too heterogeneous for reliable certainty judgments.

Who it applies to#

Every dentate patient in a hygiene chair, which is why the board made screening universal. The operational owner of this in a practice is the hygienist, and the board's survey says the hygienists in it were, if anything, further from the evidence than the dentists on mechanism and on causes. The paper is Canadian and voluntary; it is not a standard of care anywhere, and the American organizations have not published an equivalent.

It does not reach pain that is not dentin hypersensitivity, and it is deliberate about that: the algorithm's exits are "seek other causes," "treat other causes," "refer patient to appropriate specialist" and "no further treatment required" as often as they are "treat." It also predates the whole modern shelf of bioactive glass, nano-hydroxyapatite, arginine and stannous formulations, so its material recommendations are a category, not a product list.

What changed#

Before 2003 there was no consensus document a general practice could work from, and the board's survey shows what filled the gap: a belief that sensitivity is caused by recession and abrasive toothpaste and driven by bruxism, treated by dabbing paste on a tooth. The consensus replaced that with a diagnosis of exclusion, an acid-first causal story, and a dosing instruction.

What has not changed is the weakness underneath. Twenty-three years of reviews have not produced clear evidence that the first-line agent works, and the 2026 pooling of newer agents came with I-squared of 93% on the laser subgroup and no certainty rating at all. My own view: that is an argument for the first half of the algorithm, not against the second. The part of this protocol with the strongest reasoning behind it is the differential diagnosis and the removal of dietary acid, and that part costs nothing but chair time.

Where the source is#

The document is Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity, Canadian Advisory Board on Dentin Hypersensitivity, Journal of the Canadian Dental Association 2003, volume 69, number 4, pages 221 to 226, peer reviewed, with Dr. James R. Brookfield as correspondent and eleven other named board members including Martin Addy and Howard C. Tenenbaum. The CDA rebuilt its website and the original JCDA archive path now returns a 404, so the link under the title opens an archived copy of the CDA's own PDF from the Internet Archive; that six-page PDF was read in full for this entry, algorithm and references included. PubMed carries the abstract. The acknowledgment states that the board was funded by an educational grant from GlaxoSmithKline Consumer Healthcare Inc. The three later reviews quoted here were read directly: the Cochrane review from its record on PubMed Central, and the 2013 and 2026 systematic reviews in full text on Europe PMC, both open access.