Enamel Structural Anomalies

 Developmental anomalies in tooth structure arise in the last stage of tooth development (Brook, 2009), which is histo-differentiation (William et al., 2006). Enamel problems are usually classified into hypoplastic or hypominerlized defects. Hypoplasia is usually a problem that arises in tissue apposition (Elfrink et al., 2012), which result in disruption during enamel matrix production (Weerheijm et al., 2003), so it is said to be a quantitative defect (Fearne et al., 2004). Clinically hypolpastic enamel is thin, grooved and possibly pitted (Elfrink et al., 2012; Welbury et al., 2012).

In hypomineralization it is considered to be a Qualitative defect (Jälevik & Norén, 2000), Problems of tissue hypomineralization usually occur due to the disruption during the initial mineralization or during prism crystallite maturation (Weerheijm et al., 2003; Welbury et al., 2012). However, in some cases the type of defect is clinically indistinguishable, as the two anomalies frequently occur together (Mitchell and Mitchell, 2014). Furthermore, the aetiology of enamel defects varies from genetic to environmental insults as follows:

Enamel defects due to environmental insults 

Dental hypoplasia

 Dental hypoplasia might affect a single tooth, which is named Turner tooth, or it can affect multiple teeth (Mitchell and Mitchell, 2014; Dean, 2015). Turner tooth appears in permanent dentition due to infection or trauma from the primary predecessor (Mitchell and Mitchell, 2014).

On the other hand, the hypoplasia might affect multiple teeth. In such a case, it follows a chronological pattern indicating the time at which the environmental insult occurred (Welbury et al., 2018). Some chronic diseases carry a particular high risk of such deformity. Celiac disease and dermatitis herpetiform are highly associated with hypoplastic defects in the permanent dentition (Koch et al., 2017). It is thought to occur because of acute episodes during childhood (Maloney et al., 2014), which result in an immunological reaction that affect tooth development (Koch et al., 2017). These insults are not exclusive to permanent dentition (Dean, 2015). It can be seen in the primary dentition due to problems that have aroused during pregnancy period. Low birth weight and preterm babies are of particular risk to develop such anomalies (Welbury et al., 2018). It is worth mentioning that several anomalies are seen in the latter two categories. These include delayed tooth eruption and yellow stained teeth due to hyper-bilirubinaemia (Cameron & Widmer, 2014). Lastly, chemical factors such as fluoride ingestion might result in fluorosis which can be accompanied by hypoplasia (Welbury et al., 2018).

The restorative management varies according to the extent and severity of the defect (Mitchell & Mitchell, 2014). Unfortunately, within the limitation of my search, there is no viable literature to cover treatment options for primary teeth. In permanent dentition, it is not uncommon to see the defect involving only the tip of permanent first molar, since it starts mineralizing early (Welbury et al., 2018). Small defects as such can be fissure sealed (Mitchell and Mitchell, 2014). Yet, if the defect is extensive, it can carry a significant risk of developing dental caries (Dean, 2015). Therefore, partially erupted teeth can be covered by GIC. For completely erupted teeth coverage by SSC or adhesive onlays are acceptable options if the teeth are disfigured. In some cases, extraction after taking orthodontic considerations is the best treatment option (Cameron and Widmer, 2013).

For anterior teeth, composite restorations are the most widely recommended (Mitchell and Mitchell, 2014). Yet, it might need to be preceded by bleaching or removal of the superficial enamel by rotary instrument.  The reason is that hypoplastic enamel is usually rough, it retains debris and stains which might jeopardise restoration aesthetics (Cameron and Widmer, 2013). Micro-abrasion can be an alternative in some cases as well (Dean, 2015).

Molar incisor hypomineralization (MIH)

Hypomineralization (MIH) is defined as a disease of systemic origin that leads to hypomineralization of one to four permanent first molars, it is frequently associated with incisors as well (Weerheijm et al., 2001). MIH does not appear to be a new phenomenon, but when caries prevalence was globally high, the developmental defect responsible for the initiation of cavitation was probably not diagnosed. After the reduction in caries prevalence in many countries, MIH aroused as a new entity (Weerheijm, 2004). In the previous literature, such molars were described and referred to as non-fluoride enamel opacities, internal enamel hypoplasia, non-endemic mottling of enamel, opaque spots, idiopathic enamel opacities, enamel opacities and cheese molars (Koch et al., 1987; Van Amerongen, 1995).

The pathological basis to hypominerlization in MIH is due to hypomaturatin of enamel crystals to its full thickness which is caused by protein retention (Fearne et al., 2004). One recent systematic review concluded that the global burden of MIH is on average 13% and the disease is considered pandemic (Schneider et al., 2018). The high prevalence of MIH in association with treatment complexity, warrants the need for preventative programs, which cannot be conducted unless the etiological factors are clarified (Jemâa et al., 2017). The condition is thought to occur due to environmental insults that disrupts enamel mineralization. It is assumed to take place within the first 3 years of life (Lygidakis et al., 2004). Thereby affecting the teeth that mineralizes at that time, which are the central incisors and the permanent first molars (PFM) (Fearne et al., 2004). Several etiological factors were suggested, examples are respiratory diseases and febrile illnesses (William et al., 2006).  Yet the specific aetiology is currently obscure (Silva et al., 2017).

Expression of MIH defects may vary from molar to molar within one patient (Alaluusua et al., 1996). Thus, the condition is usually asymmetrical (Cameron & Widmer, 2013). However, when one molar is severely affected, it is most likely that the contralateral tooth is also somehow affected (Alaluusua et al., 1996). Incisors are not always affected (Schneider et al., 2018). Yet if incisors are involved, it is most likely to affect maxillary teeth (Weerheijm et al., 2001). The risk of defects of the upper incisors increases when a greater number of first permanent molars have been affected. The defects of incisors are not usually associated with loss of enamel substance as in molars (Weerheijm et al., 2001). In some cases, second permanent molars are also affected (Anthonappa  & King, 2015).

Early identification of MIH patients and those who carry risk factors is paramount (Elhennawy and Schwendicke, 2016). One of the most important indicators is the primary dentition (Elfrink et al., 2012) since deciduous molars can also be affected by hypomineralization (Seow, 2015). The condition is named “hypomineralized second primary molars” (HSPM) (Elfrink et al., 2008) or “Deciduous Molar Hypomineralization” (DMH) (Elfrink et al., 2010). In primary dentition, the condition involves the canines and second molars as they develop at the same time (Smith, 1991). It seems that children affected by the condition in primary dentition are six times more likely to develop MIH in the permanent set of teeth (da Silva et al., 2017). Yet, the absence of these defects does not preclude its possibility to occur in the permanent dentition (Negre-Barber et al., 2016). Furthermore, the severity of the condition in permanent dentition is not related to the number of teeth involved in the primary dentition (da Silva et al., 2017).

Diagnosis:

Early diagnosis of MIH patients is crucial (Elhennawy and Schwendicke, 2016). Usually, MIH is diagnosed by the age of eight to nine years when the first permanent molars are fully erupted (Jälevik and Klingberg, 2002). According to the AAPD guidelines for diagnosing MIH put forward by Weerheijm et al. (2003), diagnosis can be established after examining wet incisors and molars for signs of post eruption breakdown (PEB), atypical restorations or demarcated opacities.

1-    Post eruption breakdown (PEB)

Generally, molars carry the most significant burden of both the disease and occlusal forces (Weerheijm, 2004). Hence, incisors are not usually exposed to PEB (Weerheijm, 2004). Molars break rapidly after eruption due to its inability to withstand the normal occlusal forces (Schneider et al., 2018). PEB can be largely unpredictable (Weerheijm, 2004).

Sometimes, post-eruptive enamel breakdown can mimic hypoplasia because the clinician might think that the enamel was not formed initially (Weerheijm, 2004).  However, in hypoplasia, the junctional borders to the normal enamel are smooth, whilst in post-eruptive enamel breakdown the borders to the normal enamel are irregular (Weerheijm, 2004; William et al., 2006).

2-    Atypical restorations

When a clinician sees the patient for the first time after series of previous dental treatment, atypical restorations can be one of the prime features that raises suspicion to MIH. Several factors combined are responsible for the occurrence of the atypical restoration. These teeth are highly prone to caries (Leppaniemi et al., 2001; Garcia‐Margarit et al., 2014), recurrent caries and PEB (Weerheijm, 2004; William et al., 2006). In one study by Jälevik and Klingberg, (2002) children suffering from MIH had 10 times more dental visits compared to normal controls. Recurrent caries and PEB were among the most common reasons for retreating those PFMs. Moreover, these children usually have multiple repeated restorations because the initial material bonding is not satisfactory (Schneider et al., 2018).

3-    Demarcated opacities

MIH coronal opacities are smooth (Clarkson, 1992), porous and looks like discoloured chalk or old Dutch cheese (Weerheijm, 2004). The first challenge in managing this opacity is differentiation MIH from fluorosis and incipient lesion. The management of each differ greatly; fluorosis is caries resistant while MIH is caries prone (Weerheijm, 2004). Moreover, incipient caries should be identified early and controlled to prevent its progression into a cavitated lesion (Kidd & Fejerskov, 2016).

 

Caution should be taken when managing MIH opacities. Although surface enamel is intact (William et al., 2006), sub surface enamel is porous and soft (Clarkson, 1992). The colour of the opacity seems to be an important indicator; the more yellowish or darker it is, the more tendency to breakdown (Neves et al., 2018).

MIH associated tooth sensitivity and its clinical challenges

MIH molars can create several challenges for both, the dentist and the affected child. One of the major challenges is tooth sensitivity (William et al., 2006). The porous exposed enamel predisposes the pulp into a chronic state of inflammation. Thus, the child will experience pain and sensitivity, even when the enamel is visibly intact (Weerheijm, 2004). This neuroplastic pulpal defects are named hyperalgesia (Schneider et al., 2018). Eventually the pulp becomes unresponsive to anaesthetic agents (Croll, 2000; Jälevik and Klingberg, 2002; Fayle, 2003).

Caries is a dynamic process which is enhanced by the child inability to brush sensitive PFMs (Weerheijm, 2004; Mahoney and Morrison, 2011). Hence, those children suffer increased incidence of caries, which is directly correlated with the severity of MIH (William et al., 2006; Negre-Barber et al., 2018). Children with MIH are treated on average ten times as often as children without such molars (Jälevik and Klingberg, 2002).

For dentists, sensitivity problems are related to the child’s inability to maintain good hygiene, thus, unexpectedly rapid caries development in the erupting first permanent molar, besides the clinician’s inability to anaesthetize the MIH molar when treatment is indicated (Weerheijm, 2004). The use of air or water during clinical examination might be adequate to render the child uncooperative (Schneider et al., 2018). Because of previous painful dental experiences, MIH affected children displayed more dental fear and anxiety compared to the healthy normal children (Jälevik and Klingberg, 2002; William et al., 2006). Thus, to avoid recurrent problems of the same tooth in a child who can easily become uncooperative, it is generally recommended that the radical approach is favoured to the minimal invasive approach in managing those teeth (Kopperud et al., 2017). Yet, even if extraction is planned, sometimes the only way to extract those PFM is under GA (Schneider et al., 2018).

 

Clinical management: 

Before exploring the treatment options for MIH, there is no strong evidence and guidelines for the management of MIH, particularly for affected anterior teeth (Elhennawy and Schwendicke, 2016).

Restoring permanent incisors 

In many instances, poor aesthetics of MIH incisor teeth is a major concern for the parent and child (Weerheijm, 2004). Micro-abrasion can improve appearance, yet not always effective (Fayle, 2003). Bleaching with 5% sodium hypochlorite was proven to be effective in some cases (Wright, 2002). Sodium hypochlorite is preferred over hydrogen peroxide in young permanent teeth for several reasons (Wright, 2002). Sodium hypochlorite bleaches mainly by removing organic tooth material (Belkhir and Douki, 1991), which is relatively increased in MIH affected teeth. Secondly, sodium hypochlorite potentiates the efficiency of etching agents (Venezie et al., 1994), thereby, infiltrating resins can be used after bleaching to seal those surfaces (Wright, 2002). However, this “deproteinization” approach as described by Gandhi et al. (2012) should always be preceded by etching as well. This procedure is named: etch-bleach-etch-seal technique. Alternatively, infiltration with resins such as ICON-Infiltrant by DMG^® after 15% hydrochloric acid application produces satisfactory results in mild cases. However, its stability is doubted on the long run (Bhandari et al.,2018). These instable results are thought to be caused by chemical disintegration over time in adjunction with water sorption (Della Bona et al., 2003).

In some cases, the only real option would be direct composite veneers (Weerheijm, 2004). Placement of composite should be considered as the first treatment option if PEB affected anterior teeth (Weerheijm, 2004). Yet, unlike micro-abrasion and bleaching, veneers should not be prepared except in fully erupted teeth (Wright, 2002). Special consideration should be given to the irregular prism structure seen in MIH (Chan et al., 2010; Fagrell et al., 2010). Bonding of MIH enamel to composite is extremely doubtful (Koch et al., 2017). Fortunately, although dentine can be affected by the condition in severe cases (Jälevik and Norén, 2000), the bond strength of resins to the dentine can be comparable to the normal tooth structure (Krämer et al., 2018).

Lastly, since enamel bonding strength to resins is weekend, these teeth are poor candidates for orthodontic bracketing (Veereshi et al., 2013; Schneider et al., 2018). Moreover, debonding these brackets can cause a serious damage to the tooth (Cochrane et al., 2017).

Restoring permanent first molars 

Normally, the mineral content of enamel decreases towards the dentine, which is a less mineralized structure (Miller, 2012). In MIH the mineral gradient is reversed (Fearne et al., 2004). Thus, the first step in managing these teeth is supersaturating the external enamel with minerals to prevent its breakdown (Reynolds, 2005). Also, remineralisation decreases tooth sensitivity (Fayle, 2003). Fluoride varnish, tooth mousse application and GIC fissure sealants are recommended as soon as tooth erupts (Simonsen, 2002). However, remineralizing enamel and applying GIC restorations was found to decrease the rate of PEB, rather than completely stopping the process (Fragelli et al., 2015).

If these teeth need to be restored, several considerations should be taken (William et al., 2006). Firstly, general considerations as child ability to cope with the treatment and severity of defects should be assessed (Mahoney, 2001; Fayle, 2003). Secondly, some considerations should be taken during cavity preparation. All defective and porous enamel must be removed (Weerheijm et al., 2001). The preparation margins should stop only when good resistance to the bur is felt, otherwise, the restoration margins are threatened by breakdown (William et al., 2006). However, prophylactic removal of defected enamel was argued by Fragelli et al., (2015) who recommend preserving conservative approach and avoiding unnecessary enamel removal. Furthermore, sodium hypochlorite was suggested to pre-treat molars before filling them to remove enamel proteins (Wright, 2002).

Amalgam is the least acceptable restorative material. Reasons are the atypical restoration margins and decreased retention in shallow cavities (Fayle, 2003). On the other hand, GIC is easier to place, chemically bonds to the tooth and releases fluoride (Mahoney, 2001). Yet, it is known by it weak mechanical properties. The mechanical properties can be improved by using RMGIC instead of GIC (Croll and Nicholson, 2002). Yet, both materials are only considered interim for permanent teeth and cannot be used in stress bearing areas (Mahoney, 2001; Berg, 2002).  Composite is the material of choice to restore non-cuspal supra-marginal defects (Fayle, 2003).

When moderate to severe PEB is witnessed, stainless steel crowns are recommended (Weerheijm, 2004; Kotsanos et al., 2005). They would help in maintaining the remaining tooth structure and alleviating tooth sensitivity (Mahoney, 2001; Fayle, 2003). However, SSC are mainly considered interim restorations until future casted restorations can be obtained (Radcliffe and Cullen, 1991; Hunter, and Stone, 1997). Indirect composite onlays was described as an alternative to SSC in a case series by Dhareula et al. (2018). Yet, in my opinion, a significant limitation of such treatment protocol is the excessive crown reduction to provide shoulder margins which might extend sub-gingivally as described by Dhareula et al. One case report by Orellana and Pérez, (2017) used orthodontic band around MIH severely affected molars after building it with GIC. Yet, it does not seem efficient compared to extraction. In severe cases, extraction after taking orthodontic considerations might be the only realistic treatment approach (Jalevik Klingberg, 2002) and the most cost effective in MIH molars (Elhennawy et al., 2017). Particularly if more than one molar is affected and the child is at optimal age (William et al., 2006).

Enamel defects that are genetically determined: 

 Amelogenesis imperfecta (AI)

Amelogenesis imperfect is a developmental anomaly associated with dental enamel malformation. One recent study by Kammoun et al. (2018) suggested that AI extends to include dentine and cementum as well, which become hypominerlized and non-homogenous in nature. Yet the enamel is the most severely involved and all teeth in both dentitions are affected (Regezi et al., 2016). AI is not associated with any systemic disorders (Wright and Thornton, 1983; Wright et al., 2011). The only exception is if taurodontism was associated with hypoplastic-hypomaturation type, then tricho-dento-osseous syndrome would be suspected (Hart et al., 1997).

Diagnosis:  

Usually, the diagnosis is made by exclusion (Crawford et al., 2007). Fluorosis and AI can present initially similarly, yet in fluorosis the history of fluoride intake can be detrimental for diagnosis (AAPD, 2009). Fluorosis is a dose dependant disease that develop due to excessive fluoride consumption, while in AI there is usually a strong family history of the condition (Mitchell and Mitchell, 2014; Welbury et al., 2018). Since the exposure in fluorosis occurs in a certain period of life, not all teeth are affected equally. Usually, fluorosis misses the teeth that develops lately (Welbury et al., 2018) e.g. second molars and premolars (AAPD, 2009).

Genetic etiology and classification: 

Gene screening does not affect clinical management. It is mainly used for research purposes (Crawford et al., 2007). Moreover, it can be necessary for absolute confirmation of the condition. Furthermore, understanding genetic aetiology will enhance our understanding of the disease itself. The most common genes responsible of the condition are divided broadly into two categories. The first one would include amelogenin (AMELX) and enamelin (ENAM) which are responsible for matrix deposition (Hu and Simmer, 2007). The second category include kallikrein4 (KLK4), (MMP-20) and (FAM83H) which are responsible for matrix resorption to allow mineral deposition (Aldred et al., 2003). Problems with the first gene group results in enamel hypoplasia while interruption of the second genetic group results in enamel hypomineralization (Brook, 2009). Lastly, newly identified genes anomalies like (WDR72) results in inability of enamel mineral to grow to its full size, thus hypomaturation phenotype appears (Wright et al., 2011). Accordingly, AI is classified into hypoplastic, hypocalcified, hypomaturation or mixed hypoplastic and hypomaturation type (Hart et al., 1997). Yet, the classification is very controversial, and several attempts were made in the literature to propose other classifications that describe the association between clinical manifestation, genetic aetiology and pattern of inheritance (Aldred et al., 2003). 

Clinical problems associated with AI 

Surprisingly, children with AI exhibit low caries susceptibility (Yip and Smales, 2003; Poulsen et al., 2008). Yet, as any treatment plan formulated to any child, it must begin with emphasizing preventive dental care (Neville et al., 2002). Also, Radiographs can be indicated periodically. Not just to assess the possible presence of caries, but to evaluate enamel thickness and structure (McDonald et al., 2012).

The main problem in AI is that the teeth are threatened by two types of disintegrations; post eruptive breakdown by attrition, and pre-eruptive disintegration by resorption (Crawford et al., 2007). Attrition is commonly seen (Poulsen et al., 2008). In selected cases, surgical crown lengthening is convenient to allow coronal covering restoration obtain an acceptable retention to those short crowns (Yip et al., 2003).

Pre-eruption breakdown or resorption is commonly seen in AI patients (Wright et al., 1992; Seow, 1995), particularly if eruption is delayed (Poulsen et al., 2008). Moreover, resorption can be progressive and involve both the crown and roots (Yip and Smales, 2003). To avoid the possibility of resorption, periodic radiographic follow-up is recommended (Welbury et al., 2018). Unfortunately, it is not uncommon to see delayed eruption pattern in those patients (Poulsen et al., 2008). Delayed eruption should be always addressed, the teeth might be assisted surgically and orthodontically to erupt (Poulsen et al., 2008). In partially erupted permanent teeth, the operculum around unerupted teeth can be removed to accelerate its eruption and GIC is placed over the tooth (McDonald et al., 2012).

 

Commonly associated anomalies that must be addressed in treatment plan:

Moreover, those children problem list extends beyond tooth surface loss. Several dental conditions and occlusal anomalies are highly related to AI (Crawford et al., 2007; Poulsen et al., 2008). Usually, the eruption timing is either accelerated or delayed (Poulsen et al., 2008). It is common to detect absence of teeth, particularly second molars (Yip et al., 2003). Other anomalies seen include impacted teeth (Wright et al., 1992; Seow, 1995) and enlarged dental follicles (Poulsen et al., 2008).

Furthermore, poor oral hygiene in AI patients is extremely common (Yip and Smales, 2003). Thus, periodontal disease is usually seen in those children (Lindunger and Smedberg, 2005) that is manifested as gingivitis and gingival hyperplasia (Poulsen et al., 2008). Tips to improve oral hygiene includes the use of topical fluoride and desensitizing agents, oral rinses and scaling. Since teeth can be sensitive, brushing can be encouraged using warm water (Marinho, 2009; McDonald et al., 2012). These measures should promote good periodontal health and help alleviate sensitivity problems (Sapir and Shapira, 2007; Hicks and Flaitz, 2007). Generally, several reasons interplay to result in this poor oral hygiene in AI patients. One of them is decreased brushing efficiency due to tooth hypersensitivity (Rowley et al., 1982; Yip and Smales, 2003). Plaque and calculus accumulation is increased around the rough irregular enamel surfaces (Mitchell and Mitchell, 2014). Lastly, mouth breathing is an added problem, it is associated with open bites (Yip and Smales, 2003). About half of the children with AI suffer an open bite as well (Aren et al., 2003; Crawford et al., 2007). Liaison with other departments to correct this occlusal problem and assess the need for future orthognathic surgery is indicated (Bäckman and Adolfsson, 1994; Williams, 2000).

Restorative treatment options:

For anterior teeth if the enamel is intact but the only complaint is discolouration. Bleaching and micro-abrasion can be done (AAPD, 2009). Yet, in my opinion, the clinician must be cautious regarding procedures that might damage the already compromised enamel. Nevertheless, composite veneers are widely used in such cases (Witkop, 1957; Türkün, 2005). Yet, debonding of composite veneers is frequent (Yoshida et al., 2001; Yip et al., 2003). GIC base can be applied to enhance adhesion. In cases of frequent debonding even when a GIC base is made, removal of defected enamel to bond the restoration to dentine can be useful (Yip et al., 2003). Alternatively, indirect restorations in such instances can be an option (Takagi and Sasaki, 1988; Ashkenazi and Sarnat, 2001).

For posterior teeth, casted restorations seem preferable if multiple teeth need to be covered (Sengun and Özer, 2002). Permanent molars in mixed dentition can be restored by two ways. The first one is by SSC which can be constructed in a single visit and requires minimum patient cooperation (McDonald et al., 2012). In my opinion, it is a feasible option since SSCs are cheap and readily available in any dental practice. The second option is gold crowns. It has the advantage over SSC that its margins can be left supra-gingivally as a definitive treatment (Zagdwon et al., 2003). Also, gold crowns are more conservative if preparation is needed. Moreover, it is more retentive in comparison to SSC (Lumley and Rollings, 1993; Yip et al., 2003). However, when applicable, placing a crown should be done without preparation. Crown preparation might compromise the enlarged pulp in immature permanent dentition (McDonald et al., 2012). In many unfortunate cases, over dentures can be the only realistic option. Over-dentures represent the second treatment option proposed for AI. On such occasions it can be used as a reservoir to release fluoride by applying fluoride gel onto it (Yip et al., 2003).

Lastly, some factors might complicate the treatment plan, such as loss of facial height and attempting to treat young children on the chair.  To re-establish the facial height in the case of full mouth rehabilitation, occlusal splints might be advisable (Yip and Smales, 2003; Kwok-Tung and King, 2007). Also, in anxious and young children the treatment delivery might be troublesome. Thus, interim procedures might be acceptable (McDonald et al., 2012). One example is covering both anterior and posterior teeth with GIC (Kwok-Tung and King, 2007).

AI affected children attitude towards dental treatment: 

AI is a psychological pressure on its own. It is noticeable that many of those children end uncooperative even if they do not have negative previous dental experience (McDonald et al., 2012). Adults who survived through AI describe their childhood experience painfully (Welbury et al., 2018). There are several cases where adolescent patients used to cover their teeth by chewing gums, sticking papers, or even attempting to steal to fund aesthetic dental treatment (Aldred et al., 2003). Inability to socialize is an important consideration that begins in young age (Crawford et al., 2007).

Since most of AI patients need continuous follow up for lifetime, achieving positive dental attitude is paramount (McDonald et al., 2012). It is important for the clinician to use words as “ordinary” instead of “normal” when describing the treatment plan for the child (Welbury et al., 2018). Although clinicians might not agree, most adolescent would prefer the most aesthetic restorations over the conservative ones, which must be respected (Crawford et al., 2007). Lastly, general anaesthesia is an acceptable option for treatment even in the absence of pain (Poulsen et al., 2008; McDonald et al., 2012).

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