From Volume 47, Issue 6, June 2020 | Pages 494-499
This article is the first of a two-part series on cracked tooth syndrome (CTS). It seeks to aid the clinician in understanding the pathogenesis and clinical features of the condition and review established and new diagnostic tests that will allow greater confidence and predictability in diagnosing teeth with CTS.
Cracked tooth syndrome refers to the signs and symptoms of pain in a posterior tooth with a vital pulp, that is directly attributable to an incomplete fracture involving the dentine, which occasionally extends into the pulp or periodontal ligament.1 It commonly presents with sharp pain on chewing and thermal sensitivity, and can be difficult to distinguish from other pulpal and periapical conditions2 (see later).
A crack has been defined by Oxford Dictionaries as, ‘a line on the surface of something along which it has split without breaking apart’. At this point it could be described as an incomplete fracture (Figures 1 and 2), as there is no visible separation of the segments divided by the crack. Cracks can be symptomatic, which would support a diagnosis of CTS (Figure 1), or asymptomatic, which would not (Figure 2). A complete fracture would demonstrate visible separation and independent movement of one or more segments (Figure 3).
A diagnosis of CTS relies on the presence of a painful crack within dentine, not necessarily the overlying enamel, and the presence of an enamel crack does not necessarily indicate that the underlying dentine is cracked3 (Figure 4). Cracks are mainly initiated and propagated by occlusal loading, with some progressing internally from an initiation point on the external aspect of the tooth, whilst others develop from internal stress concentrators, such as the line angles of cavities and propagate externally (Figure 5). Such cracks are not always associated with visible crack-lines in enamel, which may complicate diagnosis, classification and appropriate clinical management (see later).
Dentine is a tough, resilient material, and will resist crack propagation through the formation of micro-cracks ahead of the main crack. These serve to dissipate energy and can lead to ‘crack blunting’. Unbroken ‘ligaments’ of intertubular collagen behind the tip of the crack also serve to resist propagation4 (Figure 5).
Critically, this suggests that a tooth with a dentine crack is still capable of functioning without fully removing the crack.
Cyclical loading has a greater propensity to propagate cracks than static loading,5 suggesting bruxists may fare worse than clenchers. Hydration of dentine improves crack blunting,4 suggesting that root-filled teeth and teeth with non-vital pulps may be at greater risk, above and beyond their structural compromise. Ageing beyond around 30 years also reduces fracture resistance.6
Suggested predisposing factors for CTS include previous cavity preparation, restorative material compaction or bonding procedures, tooth morphology, cervical tooth surface loss, function, parafunction and trauma, all of which may lead to crack initiation or propagation.1,7
Diagnosis can be difficult, with many CTS affected teeth originally misdiagnosed.2 Commonly, there is a history of pain on chewing, and sensitivity that can range from transient to lingering. Sensitivity is often elicited by thermal stimuli (mainly cold) or sweet food and drinks.8
A crack can lead to secondary involvement of the pulp or periodontium. The history, clinical examination and any tests should look to assess their potential involvement, whilst considering other aetiologies in the differential diagnosis.
Clinical examination and visual inspection may be enhanced by magnification and transillumination.7 The presence of an enamel crack is often not diagnostic in the absence of other clinical signs. Visible crack separation, which would give a diagnosis of a complete fracture, can be assessed by attempting to separate cusps manually (Figure 3). A probe catch, or bubbles forming at the gingival margin adjacent to a crack as it opens and closes under digital or biting pressure, can be an early sign of a complete fracture. Crack extension to the periodontium may result in localized deep periodontal probing depths.9
Tests should look to reproduce the presenting symptoms predictably and localize the source of the pain.
Air from a 3-in-1 often elicits symptoms from cracked teeth. Pulp sensibility testing is advised, and an exaggerated response from the affected tooth may aid diagnosis.10 The pulp may present in variable states. Assessing whether a pulpitis is reversible or irreversible will guide management, however, this may be difficult until after the crack is stabilized,11 and these clinical diagnoses may not accurately represent the histological diagnosis.12 Of teeth presenting with CTS that exhibited pain lingering for up to 45 seconds after ethyl chloride application, 98% were successfully managed, resolving pain on biting and maintaining pulp vitality at one year.13
Percussion in an occluso-apical direction is often painless, whilst lateral percussion can elicit characteristic symptoms.1 Rebound pain on release of pressure is classically described as being highly suggestive of a diagnosis of CTS,14 however, data suggests that pain on application of pressure is more common than pain on release, or the presence of both phenomena.2 Each can cause fluid movement within or outwith the tubules and consequent pain.15 Common tools used to elicit these responses are the Tooth Slooth (Professional Results, Inc, California, USA) (Figure 6), the FracFinder (Denbur, Oak Brook, Illinois), and cotton wool rolls. Biting on cotton wool rolls has limited application because cotton is non-rigid, and rolls are usually too large to be applied in a controlled manner to individual cusps. Each cusp of all teeth in the affected area should be assessed, and painful responses should be checked for reproducibility. It is important to consider opposing teeth, as these are inadvertently loaded during testing.
It is always prudent to check both the static and dynamic occlusion and consider occlusal trauma in the differential diagnosis. A study reported non-resolution of symptoms from a tooth initially diagnosed with CTS and managed with an adhesive composite restoration.16 Subsequent occlusal adjustment resolved the pain.
Where doubt exists over the diagnosis, a trial direct composite splint (DCS) (also called a direct supra-coronal resin onlay restoration or direct coronal onlay splint) can be useful.17 If the pain resolves after the application of non-bonded composite, that wraps over and constrains the cusps (Figure 7), the clinician may be confident of a CTS diagnosis. If the pain on biting does not resolve, it is prudent to reconsider the diagnosis. Differential diagnoses may include apical periodontitis, irreversible pulpitis (uncomplicated by a crack) and occlusal trauma.
Radiographs are useful to identify other pathologies that may be confused with CTS, such as pulpitis associated with caries, or symptomatic apical periodontitis, but are of limited value in diagnosing undisplaced dentine cracks.
Many attempts have been made to classify cracks.9,18 An ideal system would allow prevalence data to be recorded in defined populations and guide clinical decision-making for individual patients. One recent system of crack classification9 stated that the ‘location and extent of the crack determines the treatment plan’. However, in CTS it is often impossible to know the location and extent of the crack at presentation. Diagnostic testing often gives no indication of the location or extension of the crack(s) (Figure 8). Even when the tooth is operatively explored, by removing existing restorations (Figures 1 and 8), the true extension is often unclear. A classification system should therefore not overreach by including clinically unknowable variables.
All that can really be ascertained (and again this may only be possible following operative exploration), is if cracks run obliquely (Figures 1b and 9) or vertically (Figures 2 and 8b). An oblique crack that can be seen both internally in dentine and externally in the overlying enamel (Figure 9) may have clinical relevance, and is therefore prudent to include in a crack classification. Unrestored teeth with a suspected crack should ideally not be opened for investigation but managed by non-destructive means, if possible (see Part 2).
The extension of a crack, in the absence of frank manifestations of pulpal or periodontal pathology, or an observable exit point, is always unknown. Any attempts to quantify the extension are therefore unhelpful in formulating a treatment plan. This is most often the situation faced when a diagnosis of CTS is made. Cracks commonly harbour biofilm,19 and may extend to the pulp or the periodontium, but might not necessarily manifest pulpal or periodontal disease. This is reliant on the presence and nature of the biofilm, and the host response to it, which may often be in equilibrium. Subtle shifts in quantity or quality of the biofilm, or in the host response, can easily change this balance, favouring either health or disease. The complex dynamics seen in the shift from biofilm-influenced health to disease are not fully understood.20
Cracked tooth syndrome is most commonly seen in mandibular molars, followed by maxillary molars and then maxillary premolars, with non-functional cusps more commonly affected than functional cusps.8 Finite element analysis has helped to explain this observation by showing that non-functional cusps generally sustain more damaging tensile stresses, whilst functional cusps generally sustain more favourable compressive stresses.21 The restorative status of affected teeth varies considerably between studies, with the proportion of unrestored teeth ranging from 5–60%.22,23
There are few good data on the incidence or prevalence of CTS in defined populations. Hilton et al reported a ‘very high’ prevalence of cracked teeth in an American population,24 though this is likely to have included cracks confined to enamel or ‘craze lines’, and asymptomatic cracks which are therefore not teeth with CTS. Cracks in dentine are also often asymptomatic25 (Figure 2). One study in an American population of patients with observable cracks suggested that the greatest chance of a tooth being symptomatic CTS was seen in patients who had the combination of a molar tooth with an observable distal crack that blocked transilluminated light, though the increase in likelihood was modest at just over 20%. Stained cracks were less likely to be symptomatic.7 This data does highlight the problem of visually differentiating crack lines which are confined to enamel from those which extend into dentine, and ascribing causation to a visible crack in a painful tooth (Figure 4).
Patients with CTS may present with a confusing collection of symptoms. Successful clinical management of cracked teeth does not always require the removal of the crack or a segment of tooth tissue. Current classification systems are not always helpful in guiding clinical management. Classification of cracks in CTS should be limited to known parameters.
Current diagnostic methods may be inconclusive but, when supported by the provision of a diagnostic DCS that resolves the patient's symptoms, may reassure both the patient and practitioner of the diagnosis.
The second article in this series looks at the effective clinical management of teeth, with a confirmed diagnosis of CTS, including a discussion of when to bond the diagnostic DCS in supra-occlusion, when it may not be appropriate to do so, and what to do if it is not. The development of a decision tree seeks to clarify the decision-making process.
