Spots on Tooth Enamel: What's New?

DOI: 10.1051/odfen/2013306 J Dentofacial Anom Orthod 2013;16:404 Ó RODF / EDP Sciences

Spots on tooth enamel: what’s new?

Muriel DE LA DURE-MOLLA, Chantal NAULIN-IFI, Katia JEDEON, Ariane BERDAL, Sylvie BABAJKO

ABSTRACT Enamel is the most visible tissue of the tooth. It gives the tooth its whiteness, its brilliance and is the main focus of our attention from an esthetic point of view. Unfortunately, it is not uncommon to see alterations in this enamel, whether they are simple localized discolored spots, or more extensive loss of tooth substance. The etiologies, then, are multiple: toxicity during the mineralization of the bud, hyperthermia or a genetic abnormality. As professionals, making an etiological diagnosis and reassuring the parents is a challenge that we must address on a daily basis.

KEY WORDS

Dysplasia Amelogenesis Hypomineralization Enamel

Even though the enamel is the hardest comprised of three distinct entities: hypo- tissue of the tooth, paradoxically, it is also plasias, hypomineralizations and hypoma- biologically the most brittle. In fact, defects turations (Fig. 1). in the enamel presenting most often as –Hypoplasiasare quantitative altera- spots or as loss of tooth substances are tions caused by a defect of secretion much more frequent than abnormalities of of the enamel matrix. Clinically, this the dentin or cement. From a terminologi- leads to a loss of localized tooth cal standpoint, any alteration in the enamel substance, or a decrease in thickness can be designated by the generic term of enamel layer. The remaining enamel, ‘‘enamel dysplasia’’. This dysplasia is

Address for correspondence: Article received: 03-2013 Muriel de La Dure Accepted for publication: 04-2013 Private practice 1 121 boulevard Jean Jaure`s 92100 Boulogne Bilancourt [email protected] Article available at http://www.jdao-journal.org or http://dx.doi.org/10.1051/odfen/2013306 MURIEL DE LA DUREMOLLA, CHANTAL NAULIN-IFI, KATIA JEDEON, ARIANE BERDAL, SYLVIE BABAJKO

therefore complains about signif- icant pain with changes in tem- perature and when chewing hard foods. Each of these alterations corresponds to a histological defect occurring during specific stage of anamelogenesis. Hypoplasias arise during the secretion stage, hypomaturations during the ma- turation stage and hypomineralizations during the enamel extracellular matrix mineralization5. The prevalence of defects in the enamel is greater in permanent teeth than in deciduous teeth, but extremely vari- Figure 1 able from one study to the next. In fact, Summary diagram of the different clinical alterations the prevalence is from 24% to 49% in the enamel. (40.2% in Spain) for temporary teeth and from 9% to 63% (52% in Spain) for 6 on the other hand, is very hard permanent teeth . Of course, enamel and its coloring is normal or defects arising in the permanent denti- slightly yellow. tion concern parents the most, espe- – Hypomaturations and hypomi- cially when they appear in the anterior neralizations are, conversely, sectors. Parents are concerned about qualitative defects where the various issues: the esthetics, the risk of very mineralization process itself seeing other teeth affected and the risk is altered. The organic matrix is for brittleness of the affected tooth. But therefore excessive. Strictly the first question that the parents ask is speaking, with hypomaturation, often ‘‘where did it come from’’? the decrease in mineralization is The etiologies are then extremely less severe than in hypominera- variable: traumatic, systemic and ge- lization. Hypomaturation gener- netic. Clinical examination, medical ally shows up as an alteration in history, questioning of the parents the color of the enamel varying concerning the growth, life style and from chalky white to dark brown. the home environment of the child On the other hand, there is no provide information for positive and loss of enamel in the affected differential diagnosis. The first step area. of this diagnosis is to determine how – Hypomineralization is the most many teeth are affected. severe alteration of the enamel. – When a single tooth is affected, The degree of mineralization is the etiological factor is therefore reduced which leads to brittle, local. It is necessary to discover if soft when probed and rapidly there was an earlier trauma that worn enamel. It is a dark yellow occurred to the primary tooth or even orange color. The patient (especially, a traumatic intrusion).

2 De La DureMolla M., Naulin-Ifi C., Jedeon K., Berdal A., Babajko S. Spots on tooth enamel:what’s new? SPOTS ON TOOTH ENAMEL: WHAT’S NEW?

The root of the primary tooth will exert force on the bud of the permanent tooth during morphogenesis and therefore disturb the amelobastics layer. This type of trauma most frequently involves the incisors. The 2nd possible local etiological factor is infection. In fact, if an infection presents on a primary molar and propagates to Figure 2 the succesional tooth during its Intraoral view of a patient with mild to morphogenesis, this will cause an moderate dental fluorosis. abnormality in the permanent tooth that is then referred to as a mineralization at that age, namely the ‘‘Turner’s tooth’’. The premolars permanent incisors, the 1st perma- are teeth most affected by this nent molars, some of the canines disorder. and premolars. The 2nd molars are – When several teeth are affected, very rarely affected by fluorosis. the etiology to consider therefore Since this pathology is well known is systemic toxicity, that’s mean now, its prevalence decreased con- prolonged exposure to a factor that siderably ranging from 3.9% in 1991 alters amelogenesis. to 2.73% in 1998 in France. – Fluorosis: Fluoride was the first enamel toxin – MIH: Molar Incisor Hypominer- described. In fact, an overdose of alization: fluoride, namely an intake of fluoride In 2001, Weerheijm defined MIH greater than 1.5 mg/j, is responsible as being a ‘‘hypomineralization of for dental fluorosis. This dosage is systemic origin frequently affecting reached very quickly. In fact, by way 1-4 permanent first molars whether of comparison, drinking water has a associated or not with affected per- 9 fluoride content on average varying manent incisors’’ . The damage can From 0.3 to 0.5 mg/l. The prophylac- be mild, moderate or severe. In the tic dose is 0.05 mg/kg/j. The serious- mild forms, we see limited white or ness of enamel alteration varies, light yellow spots. from ‘‘very mild’’ forms to ‘‘severe’’ In moderate forms, these spots forms according to Dean classifica- are more extensive, ranging from tion in 1942. The mildest form is white to brown. And in the severe characterized by limited small opaque forms, these spots are associated areas affecting at least half of the with hypoplasias. The severity of dental surface and the severe form is the damage to the incisors generally characterized by brown or even black indicates the severity of the molar in- stains combined with areas of hypo- volvement, whereas the converse is plasia (Fig. 2). Excessive intake of not true. Generally, the spots are fluoride generally occurs during the well-defined on the incisors, espe- first years of a child’s life. Fluorosis cially impacting the buccal surface. then affects all the teeth during At the level of the molars, on the

Rev Orthop Dento Faciale 2014;17:404. 3 MURIEL DE LA DUREMOLLA, CHANTAL NAULIN-IFI, KATIA JEDEON, ARIANE BERDAL, SYLVIE BABAJKO

Figure 3 a-b: Intraoral views showing un incisor and a permanent molar affected by MIH. The incisors present white and yellows stains that are well defined. The molar presents a localized brown spot on the occlusal surface combined with a hypoplasia of the enamel on the bucco-distal surface of the cuspid. c: Microscopic photograph of a cut of a tooth presenting a localized white spot on the palatal surface. d: Scanning electron microscope photograph of the pre- vious cut that visualizes a deformation in the thickness of the enamel in the area affected by MIH as well as a decrease in mineralization (dark gray areas).

other hand, they are more diffuse Different criteria should be taken and especially affecting the occlusal into account for the diagnosis: surface and the buccal surface. The – the presence of well-defined damage is not symmetrical either in opacities either white, yellow or relation to the affected tooth nor in brown in color; relation to the severity of the damage – post-eruptive losses of enamel from one tooth to the other in the due to abrasion of the hypomi- same patient. All the other perma- neralized enamel; nent teeth are healthy, only the inci- – atypical restorations; sors and permanent first molars are – extractions of the first molars affected. These hypomineralizations combined with damage to the make the enamel extremely suscepti- incisors in a patient who presents ble to wear and to caries (Fig. 3). The a low risk for caries. molars are the teeth most affected When the incisors are the only by this phenomenon of a carious le- teeth affected, MIH can be ruled out. sion that then will develop very ra- The etiology of MIH is still un- pidly. It is not uncommon to see known. Numerous epidemiological caries approaching the pulp on teeth studies have been carried out, with- that are still erupting. An histological out really pinpointing any causal analysis of these teeth confirms factor. The only certain finding is that hypomineralization of the enamel in one or more toxic factors occurred the affected area. Prisms are then during the end of pregnancy or separated from one another by the during the first years of life of the non-degraded organic matrix render- child. In fact, this period corresponds ing the enamel permeable to micro- to the period of mineralization of organisms3. these affected teeth. The different The damage is always asymmetri- possible causes that have been men- cal.

4 De La DureMolla M., Naulin-Ifi C., Jedeon K., Berdal A., Babajko S. Spots on tooth enamel:what’s new? SPOTS ON TOOTH ENAMEL: WHAT’S NEW?

tioned are: respiratory infections, involved in the process enamel complications at birth, dioxin, low formation could alter the synth- birth weight, low oxygenation at esis, the mineralization or the birth, phosphocalcic disorders, early architecture of the extracellular childhood sicknesses, antibiotics and enamel matrix. This pathology is prolonged maternal breastfeeding4. called hereditary amelogenesis This pathology is becoming a real imperfecta1. The enamel defect public health problem in recent years is as severe in the primary denti- with an average prevalence of 18%, tion as in permanent dentition and as high as 37.5% in certain stu- and the alteration of the enamel dies. is visible as soon as the tooth Children affected by MIH are very erupts into the oral cavity (Fig. 4). anxious during consultation. The Although no epidemiological data main reason is the pain that their mo- are available in France, the pre- lars cause after they erupt. Brushing valence of amelogenesis imper- is difficult, and the treatment for fecta in other parts of the world is these teeth is 10 times more fre- very low ranging from 1/700 to 1/ quent than for any other tooth. The 14000 individuals. More than 10 practitioner has to manage the child’s genes could be the cause of anxiety and at the same time deal amelogenesis imperfecta. Since with technical difficulties: difficulties genetic testing is not routinely for the anesthesia, difficulties with performed in France, the diagno- the restoration (unclear limits be- sis remains exclusively clinical. tween the healthy enamel and the From a therapeutic point of view, pathological enamel). The treatment there are multiple objectives: to for the molars is the most challen- prevent pain, to protect the per- ging. The least affected teeth can be manent teeth (by maintaining the restored with composite materials. If primary teeth) and functionally the occlusal morphology is altered, and esthetically rehabilitate the pediatric crown can be placed. On arches. In a surprising way, these the other hand, when the pulpal vital- patients do not present a high ity of a tooth is affected for a child risk for caries. From an orthodon- under the age of 9, long apexification tic standpoint however, we no- procedures have to be performed ticed a greater prevalence of since the first molars are still imma- skeletal open bite. ture. If a panoramic xray shows that Orthodontic or orthopedic treat- the permanent third molar is present, ments are in no way contraindicated it’s then better to extract the first for enamel dysplasia or even for molar and let the remaining two mo- cases of amelogenesis imperfecta. lars develop mesially. Nonetheless, it is preferable to rehabilitate the teeth before beginning – When all the teeth are affected, treatment. In fact, it has been shown and this includes primary as well that alterations in the enamel in- as permanent dentition, a genetic crease the risk for caries7. In the mo- abnormality is the only possible lar sectors, the pediatric crowns etiology. A mutation of the gene

Rev Orthop Dento Faciale 2014;17:404. 5 MURIEL DE LA DUREMOLLA, CHANTAL NAULIN-IFI, KATIA JEDEON, ARIANE BERDAL, SYLVIE BABAJKO

Figure 4 Intraoral photograph of a female patient in young adult dentition presenting the hypomineralized and hypoplastic type of hereditary amelogenesis imperfect.

make it possible to protect the teeth minute) in order to eliminate any or- and not interfere with the placement ganic material8. of brackets. As for the bonding, it Spots on the enamel are common can be done with glass ionomer ce- but are discret most of the time. ment or composites following tradi- They are frequently the main reason tional protocol. For hypomature spots for the concerns of the parents and it (brown), certain authors recommend is important to be able to reassure to complete the acid etch with a so- them not only on the cause but also dium hypochorite rinse (5% for 1 on the various treatments.

REFERENCES

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6 De La DureMolla M., Naulin-Ifi C., Jedeon K., Berdal A., Babajko S. Spots on tooth enamel:what’s new? SPOTS ON TOOTH ENAMEL: WHAT’S NEW?

5. Molla M, Naulin-Ifi, C, Berdal A. Enamel defects: frequence, aetiology and therapeutic aspect. Arch Pediatr 2010;17:758-759. 6. Robles MJ, Ruiz M, Bravo-Perez M, Gonzalez E, Penalver MA. Prevalence of enamel defects in primary and permanent teeth in a group of schoolchildren from Granada (Spain). Medicina Oral, Patologia Oral y Cirugia Bucal 2013;18:e187-193. 7. Targino AG, Rosenblatt A, Oliveira AF, Chaves AM, Santos VE. The relationship of enamel defects and caries: a cohort study. Oral Diseases 2011;17:420-426. 8. Venezie RD, Vadiakas G, Christensen JR, Wright JT. Enamel pretreatment with so- dium hypochlorite to enhance bonding in hypocalcified amelogenesis imperfecta: case report and SEM analysis. Pediatric Dentistry 1994;16:433-436. 9. Weerheijm KL. Molar incisor hypomineralisation (MIH). Eur J Paediatr Dent 2003;4:114-120.

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