Special Aspects in Children and the Young: 21 How to Maintain Sound Teeth: an Individualized Population Strategy for Children and Adolescents


Special Aspects in Children and the Young: 21 How to Maintain Sound Teeth: an Individualized Population Strategy for Children and Adolescents

Kim R. Ekstrand

Based on the previous chapters, the focus here is on how to control the caries disease in children and adolescents by timely application of noninvasive and microinvasive treatments. These include any measure undertaken toward the individual patient, aiming to prevent visible sign of caries and arrest ongoing caries, without resorting to minimally invasive treatment.1

This chapter will elaborate on:

  • The multifactorial concept of caries

  • Relevant epidemiology

  • A program related to dental age and caries risk

  • Documentation of caries experience in Denmark

Then Chapter 22 will focus on microinvasive and, in particular, minimally invasive treatment possibilities toward the individual patient in pediatric dentistry.

The Multifactorial Concept of Caries

Figure 21.1 shows one way to visualize the multifactorial concept of the caries disease.2 The following five factors in this model are considered necessary for the development of caries:

  • the tooth structure (1);

  • microorganisms adhering to the teeth (2), particularly when situated in

  • plaque stagnation areas (PSA) (3)

  • fermentable carbohydrate (4), which comes from the dietary intake and from the saliva in the form of glycoproteins; and

  • time (5)

Apart from the tooth structure, the other necessary factors are presented in bold type ( Fig. 21.1 ).

Facultative or strictly anaerobic bacteria in the plaque produce lactic acid if a sufficient amount of fermentable carbohydrate is accessible,3 resulting in pH drops that may demineralize the dental hard tissues over time. In Fig. 21.1 this is illustrated by the pH going up and down. If little or no fermentable carbohydrate is available, the bacteria in the plaque produce other types of weak acids3 which are not harmful to the dental hard tissues. The factors next to the teeth indicate the many biological determinants influencing the caries process at the tooth surface level, while the more external determinants (income, etc.) act at the individual/population level.

However, none of the determinants influencing the caries progression rate are in themselves capable of either initiating or arresting caries. From Fig. 21.1 it is obvious that if one of the necessary factors (e.g., the microorganisms or plaque) is eliminated, no caries can develop, or an already established lesion will arrest. Thus, the most realistic way to control the caries disease is to disturb or to remove the biofilm trying to adhere to teeth on a regular basis by means of tooth brushing and dental flossing. The tooth brushing should be performed with fluoride toothpaste (influences one of the biological determinants). In the dental office this can be combined with dietary advice on reducing the intake of fermentable carbohydrate (influences one of the necessary factors). Finally, the dentist can effect professional plaque removal (influences one of the necessary factors), apply a high concentration of fluoride (influences one of the biological determinants), or apply sealants (influences several of the necessary factors)—the latter two measures are only effective locally (at the tooth surface level). All individuals need the same type of noninvasive interventions to control the caries disease, but some people need certain treatments more often than others, according to individual needs.4 The best term for this is “individualized population strategy,” 4,5 which is in contrast to both strict population and strict individual strategies (Chapter 13).

Model to describe the caries disease. The tooth structure, microorganisms, fermentable carbohydrate, plaque stagnation areas (PSA), and time are all considered to be necessary factors for caries to develop. The biological determinants decreasing or increasing the caries progression rate are in italics. In the outer perimeter are the external determinants. (Modified after Fejerskov and Manjii.2)


Individualized population strategy within cariology: All people require the same types of noninvasive intervention, but some people need certain interventions more often than others, according to individual needs.

Fig. 21.2 The distribution of filled and sealed surfaces in 9-year-olds in Denmark.6O: occlusal; M: mesial; B: buccal; D: distal; L: lingual.
The distribution of decayed, filled, and sealed surfaces in 15-year-olds in Denmark.10 O: occlusal; M: mesial; B: buccal; D: distal; L: lingual.

Relevant Epidemiology

Chapter 8 dealt with the epidemiology of caries disease worldwide. This section goes into more detail about caries risk surfaces in relation to age, how long it takes for caries to penetrate the enamel in deciduous (primary) and in permanent teeth, and the length of eruption periods of different teeth at risk of caries.

Caries in the Primary Dentition

Data from Denmark6 show that the prevalence of early childhood caries (defined as caries in children less than 3 years of age, see Chapter 8) in cavitated stages is as low as 2% of the child population at age 3 years. In other countries, early childhood caries is a bigger problem.7,8 Data from several countries6,8,9 show that the primary first molars, in particular the distal surfaces, are the most often restored, followed by the occlusal surfaces of both primary first and second molars, followed by the mesial surfaces of primary second molars ( Fig. 21.2 ). Detailed analyses6 disclosed that 52% of 9-year-olds in Denmark in 2005 had one or more filled approximal surfaces in primary molar teeth.

Caries in the Permanent Dentition

From the ages of around 6–15 years the most caries-affected tooth in the permanent dentition is the permanent first molar. In one study from Denmark ( Fig. 21.3 ) dealing with 15-year-olds,10 25% of all occlusal surfaces of permanent first molars were restored, followed by the mesial and buccal surfaces (8%) for the same teeth. In addition, more than one-third of the occlusal surfaces in permanent first molars were sealed. This was also the case for the occlusal surfaces of permanent second molars, indicating that this tooth surface can be considered as being at a higher risk as well. Very few occlusal surfaces of premolar teeth were sealed or restored.

Caries Progression Rate through the Enamel

Radiographically, studies show that the median time for caries to penetrate the enamel of primary molar teeth was 2.5 years.11 Studies from Sweden12 revealed that the median time for caries penetration through the enamel in permanent premolar and molar teeth was double (5 years) that of primary teeth. However, it was also found that 10% of the lesions penetrated into dentin within 2.5 years. In both dentitions the progression rate in dentin was faster than in enamel (Chapter 20). Studies also show that the progression rate seems faster just after the eruption of the tooth than after the tooth has been in the mouth for a couple of years.12 In one Swedish study the median time for caries penetrating through the enamel was 4 years at the age of 10–11 years versus more than 7 years for 17–22-year-olds.13

Eruption Time for Teeth in the Two Dentitions

The times for tooth emergence in the oral cavity for the individual teeth in the primary dentition14 and for the permanent teeth15 were described in Chapter 1 (see Fig. 1.2a, b ). Two other pieces of information are of interest in the perspective of caries initiation and eventual control of caries in the child population.16,17

First, the primary second molar erupts at the age of about 2 years. On average, it takes about 1 year before firm approximal contact with the primary first molar is established.16 This means that the chance of developing approximal caries distally on primary first molars and mesially on the primary second molars increases by about the age of 3 years. If the progression rate through the enamel is estimated to be around 2.5 years (see above), the child can have approximal dentin caries at the age of about 5.5 years, occasionally even earlier.

Besides, data shows that the time for emergence of permanent first molars varies greatly from an age of less than 5 years to around 8 years. Similarly, the time for emergence of permanent second molars varies from an age of about 8 to 14 years.15 This variation in emergence time was confirmed in a more recent study,17 which also disclosed that the time it takes from the emergence of the permanent first molar until firm occlusal contact with the antagonist is on average 1 year. However, some children get contact after 4 months, while in others it can be after 32 months.17 Corresponding data for the permanent second molars are 24 months to reach firm contact with a variation of 8–48 months.17 These long-lasting eruption periods of the permanent molar teeth are a predominant risk factor for caries of their occlusal surfaces.1821 In contrast, the eruption time to full occlusion for permanent premolar teeth is relatively short.


In children and adolescents caries-risk teeth are molar teeth in both dentitions. Risk surfaces on these teeth are distally on primary first molars, mesially on primary second molars, and occlusally on both types of primary molar teeth. In the permanent dentition it is the occlusal surfaces of both types of molar that are vulnerable to caries, including buccal and lingual pits.

Only gold members can continue reading. Log In or Register to continue

May 23, 2020 | Posted by in General Dentistry | Comments Off on Special Aspects in Children and the Young: 21 How to Maintain Sound Teeth: an Individualized Population Strategy for Children and Adolescents
Premium Wordpress Themes by UFO Themes