THE 6 YEAR OLD TOOTH
Introduction
The first permanent molar (FPM) due to its anatomophysiological characteristics and its importance in the dentition, has given rise to many qualifiers. Considered as the key to occlusion by Edwards H. Angle at the beginning of the 20th century, its anteroposterior position is the basis of the classification of malocclusions still used today. Its essential role in the growth and development of the dental arches and in occlusal functions, makes it the true cornerstone of the dental arch.
I. The physiology of the immature first permanent molar:
The physiology of PMPI plays a major role in the initiation and progression of caries disease. Indeed, the immaturity of its histological components, its occlusal anatomy and its eruption are all factors that contribute to the susceptibility of PMPI to this disease.
I.1. Histological immaturity:
The vulnerability of the post-eruptive first permanent molar is due largely to the immaturity of its histological components. Indeed, its porous enamel and wide dentinal tubules make it more susceptible to early formation and rapid progression of carious lesions.
I.1.a. Enamel immaturity:
When the tooth erupts into the oral cavity, the enamel has reached its final degree of mineralization, i.e. 96% of the weight, but has not yet benefited from its post-eruptive maturation.
Indeed, during the 2-3 years following its eruption, the immature permanent tooth must undergo subsurface remodeling that corresponds to demineralization-remineralization cycles. Continuously, but depending on local concentrations and the surrounding pH, exchanges of phosphate, calcium and fluoride ions occur at the enamel/biofilm junction.
I.1.b. Dentin immaturity:
The susceptibility of immature dentin is largely related to dentinogenesis, which is continuous but different throughout life. Thus, three types of dentin are formed and affixed at different periods of development: primary dentin (synthesized by odontoblasts during dental development and up to root formation), secondary dentin (from complete rhizagenesis and throughout life, under physiological conditions) and tertiary dentin (formed in response to an aggression, this is reactive or repair dentin).
The post-eruptive tooth therefore has neither secondary dentin nor a hypermineralized border of pericanacular dentin. Consequently, the obliteration of the canaliculi induced by the deposition of
Pericanacular dentin that has not yet occurred, the pulp ceiling consisting of 80% open canaliculi and the large periodontoblastic spaces invaded by tissue fluids make the dentin very permeable, which clinically results in rapid progression of the carious lesion into the dentin once the enamel-dentin junction is reached.
I.1.c. Pulporadicular immaturity:
Pulp immaturity is mainly characterized by significant vascularization and immature innervation which clinically translate into an absence of pain even in the presence of deep carious lesions.
Indeed, on the one hand, immature innervation makes the tooth less sensitive to external stimuli, on the other hand, during pulp inflammation, due to the absence of apical constriction, the nerve pathways are not compressed.
I.2. Occlusal anatomy: pits and fissures;
Occlusal surfaces represent only 12.5% of total dental surfaces. However, they are mainly affected by carious disease. Indeed, nearly 90% of carious lesions concern the pits and fissures of posterior permanent teeth and 100% of occlusal caries begin at the bottom of an anfractuous groove. The susceptibility of occlusal grooves is based on several aspects.
I.2.a- Histology:
Pits and fissures arise, during their mineralization, from junction zones (and not synthesis) of coalescence of enamel prisms. The presence of frequent defects of prismatic coalescence sometimes leads to direct exposure of the dentine at the bottom of the fissures.
I.2.b- Morphological anatomy:
The occlusal surface is composed of anatomical depressions that are highly vulnerable to caries. Its complex morphology is characterized by main and secondary grooves that constitute retention points for bacterial plaque. The depth and narrowness of these occlusal grooves (10 to 20 μ) promote the accumulation of food debris and bacteria, in an area where, compared to smooth surfaces, not only does the enamel not receive the same level of exogenous fluoride or the flushing effect of salivary flow, but it also escapes the finest bristles of the toothbrush and the buffering power of saliva. These crevices, ideal niches for the bacteria considered to be the most cariogenic, namely mutans streptococci and lactobacilli, therefore constitute privileged sites for the development of caries.
I.3- The eruption:
Due to its location, context and duration, the eruption of PMPI represents a key period, where the vulnerability of the tooth to carious disease is increased.
I.3.a- Location:
PMP emerges in the oral cavity behind the other temporary teeth already present. Its occurrence too often goes unnoticed by parents who are unfortunately not enough
informed. In addition, since the occlusal surfaces are located below the occlusal plane of the temporary molars, brushing is often deficient. Finally, the inflamed gingiva can bleed and be sensitive to brushing. The immature tooth is therefore subject to an accumulation of microorganisms for many months, before the tooth is in functional occlusion.
I.3.b- The period and the conditions:
The eruption of PMPs generally occurs between the ages of 4 and 8 years. In the majority of cases, the tooth develops quietly, without having been announced by the loss of a temporary tooth, at an age when the child often manages his or her own brushing, which is rarely effective.
I.3.c- Duration:
The eruption time between the appearance of the cusp tips in the oral cavity and functional occlusion is 5 to 32 months with an average of 15 months. During this time, the tooth does not participate in chewing and the absence of contact with the antagonist provides favorable conditions for the accumulation of bacterial plaque, thus increasing the risk of caries.
II- Pathologies of the immature first permanent molar:
II.1- Caries disease:
Clinical forms:
Two clinical forms mainly concern PMPI: progressive caries of the grooves, pits and fissures and the so-called hidden or surprise carious lesion (hidden caries).
The first is located, as its name indicates, at the level of the pits and fissures of the occlusal surface of immature permanent teeth. Indeed, the caries begins at the bottom of the V-shaped, I-shaped or teardrop-shaped crevices inaccessible to the mechanical and chemical actions of oral hygiene. The diagnosis of these early lesions, invisible both clinically and radiologically, is delicate and calls upon new diagnostic aid techniques based on fluorescence.
The second form is a very extensive subtype of the first. The location is the same but the lesion continues its development in depth in the pulpal direction and in width under the entire surface of the enamel, with a rapid and quiet evolution of the dentin damage. In fact, the bacteria infiltrate the enamel up to the dentin where their progression has no limit due to a lower density. Clinically, the enamel surface appears intact or mini-perforated but the lesion is visible radiologically (bite-wings).
II.2- Molar-Incisor Hypomineralization (HMI or MIH in English):
Molar-Incisor Hypomineralization, defined as the most common structural anomaly, corresponds to a qualitative defect of the enamel, of systemic origin, affecting one or more permanent molars, associated or not with hypomineralization of the permanent incisors. This particular structural anomaly was first described in the 1970s in Sweden. Since then, many terms have been used in the literature to name this same anomaly, thus causing some confusion. It was in 2001 that the acronym MIH for “Molar
Incisor Hypomineralization” still used today was proposed by Weerheijm and his collaborators.
The use of a unique terminology and a definition with very precise criteria established by consensus have enabled the progress of research work on the subject.
II.2.a- Clinical aspects and diagnosis:
The clinical examination highlights the presence of well-defined enamel opacities which correspond to well-defined and circumscribed defects on the occlusal surfaces, with irregular contours, the color of which varies from white to brown (creamy-white, yellow-brown).
The damage is assessed on each tooth separately. Depending on the severity, three types of alterations are differentiated: mild, which corresponds to simple changes in the color of the enamel, moderate, which presents post-eruptive fractures of the enamel, and finally severe, where enamel loss is associated with dentin loss and therefore severe dental sensitivities.
Overall, a degree of mineralization that decreases from the enamel/cementum junction towards the occlusal surface and then increases again on the cusps has been described.
Additionally, affected teeth exhibit increased enamel porosity, disorganization of hydroxyapatite crystals in hypomineralized regions, and decreased surface microhardness.
Soft, porous, chalky enamel is therefore very fragile and increases susceptibility to carious disease. In addition, as soon as it erupts, the enamel will quickly cleave in places, exposing the underlying dentine, thus causing hyperesthesia. This post-eruptive enamel disintegration is linked to its high porosity, accentuated by the carious process and masticatory forces, responsible for severe damage to weakened tissues and leading to atypical restorations.
Finally, the clinical involvement of MIH can be confused with other structural anomalies such as amelogenesis imperfecta in its hypoplastic form (quantitative defect of the enamel due to a disturbance in the secretory phase of amelogenesis) and dental fluorosis (due to an excess of fluoride absorption during dental mineralization). It therefore appears essential to establish a differential diagnosis with these two clinical forms for optimized management.
II.2.b- Etiology:
The major problem with MIH is the lack of precise identification of the causes, which makes it impossible to implement targeted and appropriate prevention. Since the complex origin of this anomaly has still not been clearly identified, hypotheses have multiplied in recent years. It would seem that several presumed factors come into play during the first four years of life. To date, no consensus regarding the etiology of MIH has been validated, but the authors agree on a multifactorial origin that is currently based only on hypotheses.
Genetically determined dental development is sensitive to environmental perturbations. Thus, perinatal and postnatal systemic perturbations such as neonatal hypoxia, cesarean delivery, birth hypotrophy, disorders of
calcium metabolism, childhood diseases such as recurrent infectious diseases or frequent fevers, antibiotic therapy with amoxicillin or macrolides and environmental pollutants such as dioxins, chlorinated tricyclic aromatic compounds or even industrial pollution or other toxins passing through breast milk seem to be involved. Similarly, the involvement of bisphenol A is increasingly suspected.
More generally, these systemic disorders occur during the first years of life, between birth and the age of 4, which corresponds to the critical window of development and mineralization of the germs of the first permanent molars and incisors. Enamel mineralization defects would therefore result from disturbances occurring during the crown mineralization phase.
THE 6 YEAR OLD TOOTH
III. Preventive strategies:
In cariology, the management of immature permanent teeth must take into account the vulnerability of the dental tissues that compose them. Indeed, their immaturity plays an important role in their rapid and voluminous decay. This is why prevention remains the best strategy.
III- Prevention:
The preventive approach is established from the first consultation and is based on three objectives: avoiding the initiation of the disease (primary prevention), intercepting the progression of lesions (secondary prevention) and avoiding recurrences (tertiary prevention). In order to implement targeted preventive actions, the identification of patients at risk is essential.
THE 6 YEAR OLD TOOTH
III.A- Primary prevention:
III.A.1- Oral hygiene:
The effectiveness of brushing, the twice-daily rhythm and the fluoride dosage of the toothpaste are the three main points to remember.
Until the age of eight, tooth brushing should be supervised by parents. Since children are unable to effectively brush the first molars that are erupting, it is essential that parents complete the cleaning. From the age of eight, even if the child becomes more independent, parents remain responsible for monitoring the effectiveness of brushing and its regularity.
Finally, the concentration of fluoride in toothpaste, its frequency of use and the quality of brushing supervision reinforce the preventive effect of toothpaste. From 6 years of age, the recommended concentration is 1000 to 1500 ppm for patients with low RCI. This concentration can be increased to 2400-2800 ppm, with parental supervision before the age of 10, if the risk is high.
III.A.2- Eating habits:
The main thing is to detect children who nibble, to ban soft and sticky foods that promote demineralization and to intercept the daily consumption of sweets and sugary drinks that currently represent the most cariogenic dietary factors. In addition to the risk
carious, these sugary and acidic drinks present a risk of erosion. Regular intake of carbohydrates prevents the saliva buffer system from playing its protective role. In a child who nibbles, the demineralization time can reach 11 hours, it is better to eat a lot of carbohydrates at once than a few several times a day.
III.A.3- Fluoride prevention:
The different forms that exist are: toothpastes, gels, rinsing solutions and varnishes, the latter being the most effective, in addition of course to twice-daily brushing with fluoride toothpaste.
III.A.4- Sealing the furrows:
Fissure sealing is recommended for all permanent molars in subjects with high RCI and for all molars with anfractured fissures, regardless of the subject’s RCI. When it is impossible to isolate the tooth satisfactorily, two solutions exist: the application of fluoride varnish while waiting for sealing or the placement of a glass ionomer cement-based material.
III.B- Secondary prevention:
It is based on the screening, diagnosis and early interception of carious disease, as well as the remineralization and/or sealing of initial non-cavitated carious lesions.
It requires monitoring in order to control the effectiveness of the measures put in place. Thus, these lesions will be monitored over time quarterly on a clinical level and half-yearly on a radiological level. In addition, the fluorescence laser can be used to supplement the radiological examination in order to monitor the progression of remineralization and the evolution of the lesions underlying the seal.
III.B.1- Early diagnosis of lesions:
Even today, high-level evidence studies affirm that the ideal tool for the early detection of carious lesions, which should demonstrate both high sensitivity (ability to detect a lesion that exists: carious tooth) and high specificity (ability to affirm the absence of a lesion: healthy tooth), still does not exist. Indeed, conventional diagnostic tools, which are visual, tactile and radiographic examination, have good specificity but average sensitivity and are relatively “operator dependent”.
Even if the combination of visual examination/retrocoronary images allows in many cases optimal sensitivities and specificities, it is not totally reliable for the detection of non-cavitary lesions. This is why it is interesting to associate with the standard clinical approach new diagnostic aid tools such as the fluorescence laser.
III.B.2- Interception and remineralization of lesions:
On the one hand, numerous clinical studies have demonstrated the effectiveness of fissure sealants in intercepting initial carious lesions. This procedure represents a non-invasive solution for these lesions. However, many practitioners faced with colored fissures still too often take an invasive approach requiring a restoration with a fluid resin. On the other hand,
Remineralization strategies aim to stop the carious process and remineralize the lesions (fluorides, phosphopeptides). To stop carious activity, it is possible to add xylitol and chlorhexidine. In addition, the prophylactic paste has an indirect role: by polishing the enamel, it temporarily reduces bacterial adhesion.
THE 6 YEAR OLD TOOTH
IV- Therapeutic decisions and treatment plan in the presence of decay of the immature first permanent molar:
This component will depend on the stage of root development as well as pulp vitality.
If the tooth is mature, its treatment will be done as for any other mature tooth.
In the case where the tooth has not completed its root growth, and is therefore immature, we will turn to therapies that preserve pulp vitality first. Namely apexogenesis which will allow the root edification of this tooth to continue in the case where the tooth is alive and there is no irreversible pulp inflammation. In the case where the tooth is necrotic or there is irreversible pulp inflammation, we will turn to the apexification protocol which will allow us to immediately close the apex either with a plug of MTA or Biodentine, or by inducing the formation of a mineral barrier thanks to the action of calcium hydroxide in the canal.
THE 6 YEAR OLD TOOTH
Conclusion :
The first permanent molar in children is a very important tooth during this period of growth, it allows space to be maintained for the growth and establishment of other teeth as well as allowing occlusal balance. Its maintenance in the arch is therefore essential.
Baby teeth need to be taken care of to prevent future problems.
Periodontal disease can cause teeth to loosen.
Removable dentures restore chewing function.
In-office fluoride strengthens tooth enamel.
Yellowed teeth can be treated with professional whitening.
Dental abscesses often require antibiotic treatment.
An electric toothbrush cleans more effectively than a manual toothbrush.