The unrestored discoloured anterior tooth: when to intervene

Aetiology

The optical properties of a tooth are modulated by the composition and thickness of the enamel, dentine and pulp, which in turn are influenced by the age of these tissues and their relative health or disease status.

Pathological states that may contribute to the (dis)colouration of a tooth include developmental disease, caries, cracks, fractures, pulpal injury (and its various sequelae such as pulpal haemorrhage and haemolysis, calcific metamorphosis and necrosis with or without endodontic infection), and internal coronal or external cervical resorption.

A tooth may experience many pathological insults over time, with associated changes in colour. For example, a traumatic dental injury (TDI) may result in cracks that can appear brown owing to ingress of both bacteria and extrinsic stains (internalized discolouration).¹

In conjunction with any disruption to pulpal blood supply, cracks that extend deeper into the tooth structure may enable bacteria to drive low-grade inflammation within the pulp tissue, potentially stimulating progressive calcific metamorphosis (yellow discolouration) or pulp necrosis (grey discolouration).

The discolouration of a single tooth in the absence of caries or a deep restoration should raise suspicion of previous physical injury. TDIs may arise via excessive forces, applied via a fleeting impact (such as blunt force trauma during an accident or assault) or over prolonged time periods (via excessive forces during orthodontic treatment). Parafunctional habits, such as bruxism, may also play their part.

In addition, the (dis)colouration of a tooth will be modified by the presence and nature of any surface stains. This tends to be a more generalized problem, and is not discussed further here.

The annual global incidence of dental trauma is estimated to be up to 4.5%, although this varies considerably depending on country and culture.² Up to 25% of adolescents/young adults will receive at least one TDI, with a higher risk to upper anterior teeth with an increased overjet, and in those leading more active lifestyles and taking part in contact sports.² However, many of these incidents will be minor and result in the lower end of severity and damage. As a result, it is estimated that only one-third present to a dentist within 24 hours, with the other two-thirds delaying for up to 1 year.³ The true incidence of TDIs is therefore undoubtedly under-reported.

This means that many who receive a minor knock to a front tooth never report this to their dentist, with the majority experiencing no long-term sequelae, and it is suspected that the patient eventually forgets about such incidents. However, calcific metamorphosis is common after concussion and luxation injuries (up to 35%), resulting in gradual discolouration of the tooth over many years, even though the patient may be completely unaware of any problems.⁴

The general relationship between specific key findings of diagnoses and tooth discolouration is summarized in Table 1.

Service evaluation of management

Triggered by curiosity, the lead author conducted a service evaluation to assess the management of UDAT identified in military patients presenting to him for routine dental inspection over a 32-month period. The service evaluation was registered within Defence Primary Healthcare's audit register.

Patients identified with UDAT had their history taken alongside a retrospective review of their clinical records to assess whether the UDAT had previously been identified and investigated.

The clinical examination involved pulp sensibility testing of affected teeth using both cold (Roeko Endo-Frost, Coltène Whaledent, Germany) and electrical pulp testing (Digitest 3, Parkell, New York, USA). Clinical photographs and long cone peri-apical (LCPA) radiographs were taken using a direct digital imaging sensor with evaluation using VixWin Platinum software (Gendex Dental Systems, PA, USA).

Clinical management depended on the underlying aetiology of the UDAT and patient preference. Patient consent was given for the storage of the pertinent findings in an Excel database (Microsoft, WA, USA) and for the use of clinical photographs and copies of radiographs.

Results

During the study period, 21 discoloured incisors (12 upper and six lower centrals; 86%), and one upper and two lower laterals (14%) were identified in 19 patients. Only nine patients (47%) could recall an episode of previous dental trauma as a possible cause for their discoloured tooth; these included significant events such as assaults, sports injuries, a traffic accident and a swimming pool incident.

Fourteen of the 21 teeth (67%) had received no previous radiograph, and 15 had not been subjected to any previous sensibility tests (71%). Of the 14 UDATs with no previous radiograph, five were found to have undiagnosed apical disease (36%), and one was found to have a root fracture (~7%). One of the teeth, discovered to have a large apical radiolucency, was a non-discoloured lateral incisor adjacent to a UDAT (Case 5).

Twelve teeth (57%) required further monitoring only, eight required endodontic treatment (38%) and one required extraction and prosthetic replacement (~5%).

This indicates a significant underdiagnosis of dental morbidity, and serves to underline the importance of applying assessment and monitoring guidelines for traumatized teeth as set out by the International Association of Dental Traumatology, which maximize the probability of achieving the most favourable outcome.^{14,15,16,17,18} Findings from the service evaluation are summarized in Table 2 and a selection of representative cases is shown in Table 3.

History taking and clinical examination

A full and robust history should be taken for any patient presenting with a UDAT, followed by thorough extra-oral and intra-oral examination.

Specifically, history taking should screen for:

The examination should include:

Given the importance of special tests in ascertaining the diagnosis, sensibility testing and radiographic imaging are discussed in greater detail.

Pulp sensibility testing

Sensibility is the ‘capacity for sensation or feeling; responsiveness or susceptibility to sensory stimuli’.²⁰

Sensibility testing of teeth provides a surrogate measure of pulpal health, estimated by the knowledge that an intact nerve supply (indicated by a positive sensibility test) correlates to the presence of an intact vascular supply (e.g. vital pulp). However, this correlation is imperfect, and there is the possibility of both false negative and false positive results, particularly if a TDI has been experienced within the past 12 months.^21,22

The most common sensibility tests used in dental practice are cold testing (e.g. using a refrigerant, such as Endo-Frost (Coltène Whaledent), sprayed onto a cotton wool pledget and held on a tooth with tweezers), and electric pulp testing (EPT). Pulp sensibility test results are recorded as ‘positive’ or ‘negative’.

Additionally, as contemporary EPT devices provide arbitrary numbers to indicate the amount of current flow, this can be recorded in the clinical notes for reference at follow-up as required. However, the clinician should not put too much emphasis on the number itself, as variations between EPT devices (if more than one is used in practice), electrode positioning on tooth, the nature of electrolyte medium (if used), as well as modulation of the psychological state of the patient will influence the point at which they will indicate a positive test. Reasons for false negative results include, but are not limited to:

Under-developed neural networks in immature teeth;

TDI resulting in direct damage to the neural supply;

Calcific metamorphosis (see below), where the additional dentine thickness acts as both a thermal (Figure 1) and an electrical insulator.^14,22

Reasons for false positive results include, but are not limited to:

The persistence of functioning nociceptor fibres within dying or necrotic pulp;

Transmission of stimulus to nociceptors within the periodontal ligament via fluid in crown-root cracks or fractures in a non-vital tooth;

Inadvertent stimulation of the pulp in an adjacent tooth.

It should be noted that while a positive response shortly after a TDI is considered a good predictor of pulp survival, a negative response is not necessarily associated with subsequent pulp necrosis.²²

Despite some disadvantages, EPTs are still a valuable resource to clinicians and their use in cases of UDAT is recommended to aid diagnosis and to provide a baseline reference against which to monitor any change over time.

True vitality tests, such as laser Doppler flowmetry and pulse oximetry, have been used in isolated cases to assess revascularization and changes in pulp microcirculation of traumatized teeth. Both technologies have yet to be refined to the point of application in real-world dentistry, but the latter in particular offers a promising objective assessment of arterial blood flow that, with more research, might be beneficial in future dental practice.²³

Diagnosis

Following history-taking and clinical/radiographic examination, information is synthesized and definitive (or provisional) diagnoses are formulated. Diagnosis statements for UDAT will often mention discolouration (type), cracks/fractures in the crown/root (if applicable), the presence of resorption (if applicable) and endodontic and periodontal status.

When to intervene

It is beyond the scope of this article to categorize and provide detailed management advice for every TDI or resorption variant; comprehensive guidance on these topics has been published elsewhere.^{14,15,16,24,25} However, in Table 4, the authors offer a summary of suggested clinical situations for when intervention for the UDAT may be justified.

While the rationale for endodontic treatment of teeth with symptoms, frank peri-apical disease or progressive resorption is relatively clear, the pros and cons of intervention in cases of the more common sequelae of calcific metamorphosis can often provoke debate.²⁷

Up to 75% of calcific metamorphosis cases are symptom free and have no apical pathology, so require no treatment other than radiographic review.¹² If monitored in this way then, unless rapidly progressive, prophylactic treatment of calcific metamorphosis ‘does not seem to be justified’, ‘should only be considered in rare circumstances’ or is even ‘contraindicated’.^24,28,29 The risks of endodontic intervention in asymptomatic cases without apical radiolucency may often outweigh any perceived benefits, as shown in Figure 1.

How to intervene

Ideally, the patient should be fully informed of the rationale and relative advantages and disadvantages of different treatment approaches to support their decision-making and enable the consent process.

While there are multiple options for treating UDAT, a minimally invasive approach should always be considered in the first instance. This includes:

Summary

The causes of minor trauma involving anterior teeth are varied, and any sequelae may not manifest for many years, if at all.³⁶ The gradual discolouration of an affected tooth may be subtle, with patients often unaware of the problem.

In the authors' experience, UDATs are frequently not picked up at routine examinations. Possible reasons for this during a busy day in practice may include colour vision deficiency (which affects 8% of men and 0.5% of women), variations in hue, value and chroma changing under differing light sources (metamerism), fatigue and occasional time constraints.³⁷ If extra time is required to carry out more detailed history-taking and further tests, the authors recommend rescheduling the patient for such additional investigations.

Questions that may also help improve the clinical mindset for identifying a UDAT during a whole-mouth examination include:

Conclusion

Effective recognition and diagnosis of UDAT enables appropriate treatment and potentially reduces the risk of a patient experiencing a dental emergency.

In the presence of more complex contributing disease, such as calcific metamorphosis plus apical periodontitis, extensive inflammatory root resorption or root fracture, onward referral may be warranted.^12,38,39,40