8. Prevention of developmental defects in hard dental tissue



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8. Prevention of developmental defects in hard dental tissue


8.1. Introduction
Developmental defects in dental hard tissue result from the action of harmful agents or other factors that affect the normal course of mineralization during tooth development.

The most common developmental defects in dental hard tissue are enamel fluorosis, internal discolouration of teeth (particularly tetracycline-stained teeth), enamel opacity, enamel hypoplasia and genetic disorders such as amelogenesis imperfecta and dentinogenesis imperfecta.



Acquired defects of dental hard tissue result from the action of mechanical factors or harmful chemicals on the teeth after their eruption in the mouth. Such defects are sometimes called non-cariogenic changes in dental tissue.

The wide group of acquired defects of hard dental tissue particularly includes enamel attrition and abrasion, enamel erosion, the outer discolouration of tooth surface and some traumatic injuries to teeth.

This chapter will focus on the prevention of defects in dental hard tissue during tooth development.

In order to understand correctly the causes of developmental defects in dental hard tissue, it is necessary to have thorough knowledge of the individual stages of tooth development, particularly time differences and relationship between the development of temporary and permanent teeth. Clear understanding of individual developmental stages of temporary and permanent teeth will enable us to assess which clinical symptoms may occur when tooth development is affected at the certain age of a child, and which early preventive measures should be taken to minimize damage to dental tissue. For these reasons, we consider it useful to present a brief overview of developmental stages of temporary and permanent dentition.


Table 8.1. Stages of dental hard tissue development and the resorption of roots of temporary teeth



(according to Künzel, 1985)


Jaw/tooth

Mineralization and developmental stages

Beginning (emb. weeks)

Condition at birth

End of crown mineralization (months)

End of root mineralization (years)

Beginning of root resorption (years)

Upper

I

14

5/6

1.5

1.5

4

II

16

2/3

2.5

2

5

III

17

1/3

9

3.3

8

IV

15.5

United cusps

6

2.5

7

V

19

United cusps

11

3

8

Lower

I

14

3/5

2.5

1.5

4

II

16

3/5

3

1.5

5

III

17

1/3

9

3.3

8

IV

15.5

United cusps

5.5

2.3

7

V

18

United cusps

10

3

8

Table 8.2. Stages of the development of dental hard tissue of permanent teeth (according to Künzel, 1985)




Order

Mineralization and developmental stages

Lower jaw

Upper jaw

Beginning of mineralization (months)

End of crown mineralization (years)

End of root mineralization (age – years)

End of root development (age – years)

1




Perinatal

-3

10

10

2




3 - 4

4 - 5

9 - 11

9 - 11

3

(4)

4 - 8

4 - 5

10 - 11

10 - 11

4

(5)

4 - 5

6 - 7

13 - 14

13 - 14

5

(3)

18 - 24

5 - 6

12 - 13

12 - 13

6




24 - 28

6 - 7

13 - 14

13 - 14

7




30 - 36

7 - 8

14 - 17

14 - 17

8




8 – 10 years

12 - 16

17 - 20

17 - 20

Tooth development can be divided into four stages:

the development of tooth buds, crown and root mineralization, tooth eruption and the completion of root development. The first two stages of tooth development are crucial with regard to the prevention of congenital defects in dental hard tissue.



Buds of temporary teeth develop in the first trimester of pregnancy: the embryonic dental ledge is formed on Day 35 of pregnancy; buds of individual temporary teeth develop between Weeks 8 and 12 of the embryonic period.

Buds of permanent teeth are formed in the prenatal period (buds of the first permanent molars, central and lateral incisors, canines and first premolars are gradually being developed in a period between Month 4 and Month 9 of intrauterine development) and in the postnatal period (the buds of the second premolar and the second permanent molar are formed at the age of 9 months; the variable development of buds of wisdom teeth can be seen from the age of 4 years until the age of 15 years). The overview of the development of dental hard tissue is provided in Tables 8.1. and 8.2.

From a clinical practice point of view, it is also very important to know the period of mineralization of individual parts of crowns of permanent teeth in order to be able to determine exactly the period when a harmful agent had a negative effect on the normal course of amelogenesis. Such assessment was carried out using the results of a study published in 1982 that dealt with enamel hypoplasia caused by tetracycline. In this study, we describe tetracycline damage to the surface of dental crowns and use a computer programme to assign respective defects to a particular period of the application of a tetracycline antibiotic, on the basis of information obtained by means of a questionnaire from an attending paediatric physician. The results of our study deepened our knowledge of the course of enamel mineralization in permanent teeth on vestibular, oral and chewing surfaces of teeth (Figs. 8.1. and 8.2.).

The mutual topography of temporary and permanent dentition is also of major clinical importance enabling one to assess some defects of dental hard tissue in a period from temporary to permanent dentition. The relationship between the roots of temporary teeth and the developing buds of permanent teeth is very intimate. Mutual relationships between the teeth and dental buds in a four-year-old child are illustrated in Fig. 8.3. A and B.

It follows from the position of teeth in the scheme that traumatic damage to the buds of permanent incisors can only occur if the roots of temporary incisors are dislocated as a result of trauma in an oral direction and that inflammatory periapical changes in the roots of temporary gangrenous molars can damage the crown of premolars that is undergoing mineralization.




8.2 Prevention of developmental defects in dental hard tissue
8.2.1. Enamel fluorosis
Enamel fluorosis is a typical kind of damage affecting the development of enamel (dental hard tissue) that is caused by an excessive intake of fluorine in the period of enamel mineralization. Fluorosis is characterized by the following clinical symptoms: the presence of feeble, opaque, whitish spots on the enamel, sometimes with streaking and mottling, the uneven surface of the tooth, the pitting of teeth. In severe cases, the pitting of the tooth’s surface is observed, with some patches of enamel hypoplasia (Fig. 8.4.).

There are several types of classification to describe the seriousness of enamel fluorosis. In 1934, Dean was the first scientist to define six classes of this enamel defect. Besides the normal enamel, he described the boundary-type, very mild, moderate and severe form of fluorosis. He also reported that brownish spots on the enamel appear in a mild form of fluorosis, with the intensity of staining increasing towards more serious forms.





months


the cervical third of the crown

the middle third of the crown

the initial or occlusal third of the crown

the mineralization of tooth crowns according to literature data


UPPER JAW

B - buccal surface

P - palatinal surface

Fig. 8.1. The course of the mineralization of crowns in permanent teeth – upper jaw (a study on tetracycline-stained teeth – Handzel, Srajer, 1982)


the cervical third of the crown

the middle third of the crown

the initial or occlusal third of the crown

the mineralization of tooth crowns according to literature data


LOWER JAW

months


B - buccal surface

L - linqual surface

Fig. 8.2. The course of the mineralization of crowns in permanent teeth – lower jaw (a study on tetracycline-

stained teeth – Handzel, Srajer, 1982)

Fig. 8.3. A – Topography of the roots of temporary teeth and the buds of permanent teeth in a four-year-old child – Anterior view; b – Relationships between temporary and permanent teeth in a four-year-old child – lateral view




In 1974, Jackson recommended the following classification of six types of fluorosis based on the objective description of the appearance of affected enamel:

Type A: White spots, sized not more than 2 mm in a diameter;

Type B: White spots, sized more than 2 mm in a diameter

Type C: Brownish spots, sized not more than 2 mm in a diameter

(regardless of the potential presence of white spots);

Type D: Brownish spots, sized more than 2 mm in a diameter

(regardless of the potential presence of white spots);

Type E: Horizontal white streaks, regardless of the potential presence of other white

non-linear patches;

Type F: Brownish or white spots or streaks linked by pits or hypoplastic areas.

Enamel fluorosis is a defect acquired during enamel mineralization and is therefore irreversible. Enamel fluorosis cannot occur after the completion of enamel mineralization, i.e. approximately after the age of 8 years. Theoretically, the prevention of enamel fluorosis is based on preventing the excessive intake of fluorine in the body during enamel mineralization. A double of the optimum level of fluorine in drinking water in a particular geographical area is considered too high. The optimum level of fluorine in drinking water in our country is 0.8 – 1.2 mg of fluorine per litre.

Fig. 8.4. Symptoms of fluorosis in the permanent dentition
The practical importance of fluorosis prevention will increase when the caries prevention and control programme based on fluorine tablets will resume. In the past, the prevention programme based on fluorine tablets which was intended for children up to the age of 2 years was ensured by paediatricians. Nowadays, this responsible role should be overtaken by a dentist (from the child’s age of 6 months) according to the applicable Health Rules of Order. The prevention of enamel fluorosis requires that the dentist knows the level of fluorides in drinking water that is used for the preparation of food for young children and that he/she is also able to evaluate the contribution of other potential sources of fluorine such as food, the environment, fluoridated tooth pastes used, etc. Once he does such an assessment, he/she can define the prophylactic dose of fluorine to be given in form of fluoride tablets.

The administration of fluoride tablets follows the following rule: If the content of fluorine in drinking water is below or equal to 0.3 mg/l, the recommended dose for prevention in children from the age of 6 months to the age of 14 years should comply with the prophylactic dose of fluorine; if the fluorine level in drinking water varies in a range of 0.3 – 0.7 mg/l, the level should be reduced to one half of the prophylactic dose of fluorine in all age groups; if drinking water contains more than 0.7 mg/l, the application of a prophylactic fluorine supplement is not necessary.

The treatment of teeth affected by fluorosis is limited to the procedures that improve the aesthetic appearance of teeth. However, every dentist who also provides dental care to children should know relevant measures to prevent such irreversible damage to teeth. Fluorides administered generally or applied locally are currently still unmatched, effective means of caries prevention, and will remain such in the future. The Dean’s ingenius idea of using minimal fluorosis, which is clinically negligible, to achieve effective caries prevention requires the permanent active participation of a dentist who will keep this relation in a proper ratio for a long period of time.
8.2.2. Enamel opacities
Enamel opacities occur sporadically or on more than one permanent tooth, rarely on temporary teeth. The clinical symptoms of the defect include white, opaque, sometime brown-yellow spots. The enamel on these spots is usually glossy and smooth, with marked wear in the middle, particularly in the case of large defects.

The etiology of enamel opacities has not yet been fully explained. Originally, it was assumed that enamel opacities represent a mild form of enamel hypoplasia. However, if this hypothesis was adopted, it would mean that the factors causing enamel hypoplasia should also cause enamel opacities, but this is in conflict with clinical experience. Nowadays, etiological factors associated with enamel defects are divided into two groups: factors that cause localized defects only on one or several teeth, and harmful substances that cause generalized damage to most teeth or all teeth.

Localized changes can be caused by injury, infection, dental ankylosis (reinclusion) or irradiation. Generalized defects caused by environmental factors can occur as a result of infection, endocrine disorders, nutritional problems, haemolytic disorders, exogenic intoxication, or cardiac, renal or gastrointestinal disorders occurring in the prenatal, perinatal or postnatal period. Congenital defects of the enamel can only damage teeth or may only be a single manifestation of a systemic disease. There are more than 90 factors known to cause enamel opacity, with the excessive intake of fluorine during enamel mineralization being just one of them.

The classification schemes for fluorosis were used to evaluate and classify non-carious changes. Besides the Dean’s fluorosis index and its multiple modifications, the TF index (according to Thylstrup and Fejereskov) or the Horowitz index were also used. However, the use of different indices does not allow us to compare the results from other studies. In the early 1980s, the FDI commission in cooperation with WHO experts developed the DDE index (Developmental Defects of Enamel Index). This index was also modified for screening purposes to five basic codes (Clarkson and O’Mullane, 1989).

Modified DDE index:

1. Healthy enamel 0

2. Single opacities 1

3. Diffuse opacities 2

4. Hypoplasia 3

5. Other defects 4

The DDE Index defines opacity as a qualitative change in the enamel. Hypoplasia is then considered a quantitative change associated with the disorder in the development and mineralization of the enamel.

From a prevention point of view, patients with enamel opacities must avoid all harmful agents causing localized changes, and the patients with generalized defects must be subjected to dispensarisation. In the second group of patients, it is suitable to choose some of the intensive preventive programmes aimed at the prevention of dental caries.


8.2.3. Enamel hypoplasia

Enamel hypoplasia occurs when a harmful agent has acted in the apposition phase. Secondarily, this also affects the course of the next stage, i.e. mineralization. This results in shape abnormalities of different degree which are accompanied with qualitative changes in the enamel. The appearance of hypoplastic teeth is very variable, usually being characterized by hypoplastic pits, oval-shaped crater-like defects, grooves or ringlets, with the thin, rugged or rough enamel of brown-yellow to dark brown colour.

Clinically, it is relatively easy to determine whether it was caused by a harmful agent or whether hypoplastic defects have occurred in response to a metabolic disorder or systemic disease. Changes in individual teeth result from the action of local effects, particularly traumatic damage or chronic inflammation. Diffuse hypoplastic changes in all teeth which were in the mineralization stage at the moment of the action of a harmful agent, are usually caused by fever of different origin, diarrhoea associated with metabolic disorders, severe organ diseases, disorders of vitamin metabolism, some endocrine diseases and perhaps also by the action of some drugs.

The prevention of enamel hypoplasia due to the local action of a harmful factor - traumatic action of intruded temporary incisors as the most common cause - relies on early diagnosis and the choice of non-intervention therapy such as the intruded temporary incisor is allowed to join spontaneously the dental arch. The prevention of the chronic effect of periapical lesion of temporary gangrenous tooth (usually in temporary molars) on the developing bud of the permanent tooth relies on the radical treatment of the dentition and on the initiation of a suitable caries prevention and control programme at patient dispensarisation.

Diffuse hypoplastic changes in the enamel of permanent teeth resulting from generally acting pathological conditions cannot be prevented with the methods of primary prevention. However, we are using the method of secondary and tertiary prevention based on complete preservation or prosthetic treatment. Aesthetic fillings or prosthetic replacements are usually made in two stages: child undergoes primary mid-term treatment, a definitive aesthetic fully complying filling or prosthetic replacement is then made at the end of the adolescent age. Patients with diffuse enamel hypoplasia should also be subjected to dispensarisation because of prevention.


8.2.4. Internal discolouration of teeth
Tetracycline-stained teeth are among major defects listed in the group of defects manifested by internal discolouration of teeth. Tetracycline antibiotics induce changes in dental hard tissue particularly in the permanent dentition, rarely in temporary teeth. Such changes manifest themselves by yellow to dark brown-yellow colour; sometimes, tetracycline deposited deep in the enamel and dentin may cause dental tissue to turn grey. Major damage is seen in children who were treated with tetracycline during their first years of life (the earlier is the application, the greater is the damage). Stained teeth also show different degrees of enamel hypoplasia (Fig. 8.5.). Damage to temporary or permanent teeth may also occur in children whose mothers received tetracycline antibiotics in the last trimester of pregnancy or during breast-feeding.

Epidemiological studies on tetracycline-stained teeth have shown that only approximately 40% of children treated with tetracycline develop typical symptoms associated with the administration of tetracycline antibiotics. The presence of tetracycline-induced changes depends on several factors such as the total dose of an antibiotic, the child’s age at the time of antibiotic treatment, the respective phase of tooth mineralization and general aspects such as a kind and seriousness of underlying condition, the effect of fever on the sensitization of ameloblasts in the secretion phase.

The problem of tetracycline-stained teeth resulting from antibiotic therapy was discussed intensively in the 1960s and 1970s when tetracycline was a widely used antibiotic. In order to prevent tetracycline-induced changes in the child’s dentition, tablets of sodium fluoride tested with relative success, being co-administered with tetracycline. The aim was to diminish staining and hypoplastic changes in the enamel.

However, the most successful method in the prevention of tetracycline-stained teeth is to use alternative antibiotics. The methodological guideline of 1981 issued by the Commission for

Practical Pharmacotherapy of the Ministry of Health that time recommended paediatric physicians to prescribe tetracycline antibiotics in children less than 8 years of age only in vital indications, and was widely accepted among paediatricians, leading practically to the elimination of tetracycline-induced damage to teeth. This positive trend in antimicrobial therapy was also supported by the development of a number of novel antibiotics that could replace the use of tetracycline in paediatric patients. Thanks to such developments, tetracycline-induced damage to teeth is unlikely to continue beyond the year of 2000.


Fig. 8.5. Damage to permanent teeth caused by tetracycline antibiotics (tetracycline-stained teeth)

8.2.5. Amelogenesis imperfecta and dentinogenesis imperfecta
Both defects are rare abnormalities that usually affect the whole dentition in a diffuse fashion. They show autosomal dominant inheritance (Fig. 8.6.). Although both conditions differ by pathological changes in hard dental tissues, the therapeutic approach to both conditions is similar from a clinical point of view: early prevention is necessary to protect teeth against abrasion with cap crowns.



Fig. 8.6. Amelogenesis imperfecta in three family members in temporary (A), mixed (B) and permanent (C) dentition




Particularly, necrobiotic changes in dentinogenesis imperfecta in the dental pulp resulting from excessive abrasion are undesirable since the endodontic treatment of obliterated root canals is very difficult or even impossible in many cases. The aesthetic correction of these serious cosmetic defects is one of demanding and long-term tasks, associated with a number of aspects to prevent the carious destruction of weakened dental crowns (Fig. 8.7. A, B).




F
Fig. 8.7. B – Panoramic image of the same patient at the age of 27: A total of 10 retained permanent teeth were treated; vast fixed bridges in both jaws were used to bridge the gaps after upper canines and two lower incisors and reconstruct congenital defects in the enamel; both fixed bridges are not only functional but also satisfactory from an aesthetic point of view, in 11 years.

ig. 8.7. A – Panoramic image of the dentition with amelogenesis imperfecta with multiple retentions of permanent teeth, showing a tendency to form follicular cysts in both jaws in a 13-year-old boy


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