Enamel Defects in the Permanent Dentition: Prevalence and Etiology

Permanent tooth type
Calcification begins at
Crown formation completes at
Eruptiona
Maxillary
Mandibular
Central incisor
3–4 mo
4–5 y
7–8 y
6–7 y
Lateral incisor
Maxilla: 10–12 mo
4–5 y
8–9 y
7–8 y
Mandible: 3–4 mo
4–5 y
Canine
4–5 mo
6–7 y
11–12 y
9–11 y
First premolar
18–24 mo
5–6 y
10–11 y
10–12 y
Second premolar
24–30 mo
6–7 y
10–12 y
11–13 y
First molar
Birth
30–36 mo
5.5–7 y
5.5–7 y
Second molar
30–36 mo
7–8 y
12–14 y
12–14 y
Third molar
Maxilla: 7–9 y
 
>16 y
>16 y
Mandible: 8–10 y
mo months, y year
aIt is noteworthy that the sequence is not simply in rank order

Prevalence of DDE in the Permanent Dentition

Mouth and tooth prevalence are the most commonly used systems to report the prevalence data for DDE. Mouth prevalence is determined by the inclusion of any individual who has been found to have at least one tooth affected by the condition, while tooth prevalence illustrates the percentage of teeth affected per person. Mouth prevalence figures reflect the extent of the distribution of enamel defects in a population group because individuals who are mildly and severely affected are grouped together. Tooth prevalence indicates the proportion of teeth affected and hence reflects the severity of the condition [2].
Table 2.2 summarizes the prevalence of DDE in the permanent dentition as reported in the literature. Wide variations exist in the literature because of the use of various terminologies and the different diagnostic criteria employed to describe the enamel defects in the permanent dentition [21, 22, 24, 26]. Nevertheless, the majority of reports have failed to demonstrate any difference in the prevalence of enamel defects between girls and boys [12, 27]. Furthermore, for all types of enamel defects, the published mouth prevalence in the permanent dentition ranges from 9.8 % to 93 % [8, 26], while tooth prevalence figures range from 2.2 % to 21.6 % [26, 28].

Table 2.2

The prevalence figures, reported in the literature, for any type developmental defects of enamel in the permanent dentition of healthy children
Author
Year
Country
F level (ppm)
Age (years)
Prevalence %
Mouth
Tooth
Suckling et al. [3]
1985
New Zealand
1.0
12
56.6
18.8
Dooland and Wylie [4]
1989
Australia
1.0
8–9
25.5
0
   
15.6
Dummer et al. [5]
1990
UK
<0.1
15–16
50.1
5.71
26.2
11.8
Nunn et al. [6]
1992
UK
<0.2
15
64.1
38.7
   
57.5
1.0
 
78.9
59
   
83.9
1.0–1.3
 
83.9
66.2
   
81.5
Fyffe et al. [7]
1996
UK
13–14
48.7
Rugg-Gunn et al. [8]
1997
Saudi Arabia
0.25
14
75
0.80
 
82
2.71
 
93
Hiller et al. [9]
1998
Germany
<0.02
8–10
39.9
 
Dini et al. [10]
2000
Brazil
0.7
9–10
26.1
Jalevik et al. [11]
2001
Sweden
Low
7–8
33.3
Zagdwon et al. [12]
2002
UK
<0.1
7
14.5
7.2
Ekanayake and van der Hoek [13]
2003
Sri Lanka
<0.3
14
29
0.3–0.5
 
35
 
0.5–0.7
 
43
>0.7
57
Cochran et al. [14]
2004
Finland
<0.01
8
59
Greece
<0.01
43
Iceland
0.05
54
Portugal
0.08
49
UK
<0.1
48
The Netherlands
0.13
70
Ireland
1.0
69
Mackay and Thomson [15]
2005
New Zealand
9–10
51.6
Balmer et al. [16]
2005
UK
<0.1
8–16
27.3
Australia
0.9–1.1
51.6
Wong et al. [17]
2006
Hong Kong
1.0 (1983)
12
92.1
0.7 (1991)
55.8
0.5 (2001)
35.2
Hoffmann et al. [18]
2007
Brazil
12
46.4
Muratbegovic et al. [19]
2008
Bosnia and Herzegovina
<0.1
12
32.8
Arrow [20]
2008
Australia
0.8
7
22
Kanagaratnam et al. [21]
2009
New Zealand
9
35a
Seow et al. [22]
2011
Australia
0.1
13.5b
58
Casanova-Rosado et al. [23]
2011
Mexico
6–12
7.5
Robles et al. [24]
2013
Spain
0.07
3–12
52
8.3
Vargas-Ferreira et al. [25]
2014
Brazil
8–12
64
aBoth fluoridated and non-fluoridated areas
bMean age

Etiology of DDE in the Permanent Dentition

Enamel morphogenesis is a continuous, complex process that starts with the secretion of enamel matrix proteins followed by mineralization and finally maturation. This process has been shown to start at the cusps on the molars and the incisal part of the incisors, progressing to the cervical areas of the teeth [29]. However, there is still limited understanding of how mineralization progresses across the crowns of the teeth. This could be important in determining the timing of defects to relate to specific disturbances caused by systemic disorders. Disturbances in the different stages of enamel formation may result in a range of enamel defects with quite different clinical appearances and structural changes. Defective formation of the enamel matrix results in hypoplasia, a quantitative defect, depicted by generalized thinning or pitting types of defects (Fig. 2.1). Defective calcification of an otherwise normal fully developed organic enamel matrix results in hypomineralization, a qualitative defect (Fig. 2.2). This is seen clinically as changes in color and translucency of the enamel and presents as enamel opacities which can be either demarcated or diffuse [2, 30].

A313082_1_En_2_Fig1_HTML.jpg
Fig. 2.1

Hypoplasia of the maxillary central incisors
A313082_1_En_2_Fig2_HTML.jpg
Fig. 2.2

Hypomineralization and hypoplasia of the maxillary and mandibular incisor teeth
Although the etiology of enamel defects may be attributed to local, systemic, genetic, or environmental factors, most are likely to be multifactorial in nature. This makes it difficult to identify a single cause for many cases of DDE. The time frame of exposure and the mechanism underpinning the causative factors determine the presentation of these defects. Defects on a single tooth or only a few teeth suggest a local etiological factor e.g. a defect in a permanent tooth due to damage (trauma or infection) to its primary predecessor (Fig. 2.3a–c). Alternatively, a systemic factor (both short and longer term) may affect all the teeth that are developing during the time of the insult and lead to what is described as a chronological defect. Genetic factors can be considered separately. Defects caused by genetic factors are most often (although not always) generalized in distribution, affecting both the primary and permanent dentitions. They may present as either enamel defects alone as seen in amelogenesis imperfecta (see Chap.​ 5) or as enamel defects associated with other general genetic disorders/syndromes (see Chap.​ 4).

A313082_1_En_2_Fig3_HTML.jpg
Fig. 2.3

(a) Caries in the mandibular second primary molar has led to the intra-radicular infection which has resulted in hypoplasia of the developing second premolar. (b) Hypoplasia of the maxillary permanent canine as a consequence of infection of the primary predecessor. (c) Hypoplasia in the form of missing enamel is exhibited by this mandibular second premolar following infection of the primary second molar
Enamel defects can be classified clinically as demarcated and diffuse opacities and hypoplasia. The location of isolated defects depends on the stage of amelogenesis at the time of the insult or injury [31]. The general consensus regarding the etiology of isolated opacities, which may be demarcated or diffuse and present as white, creamy, or yellow in color, is that amelogenesis is affected by a disturbance during the mineralization phase. It remains unclear why this would involve only an isolated patch of enamel on the crown and not the whole surface. Conversely, hypoplasia occurs when there is a disturbance during the secretory stage of amelogenesis while the enamel is only partly mineralized. Thus, enamel defects with similar presentations may have been caused by a variety of etiological factors. Furthermore, the same etiological factor can produce enamel defects with different presentations depending on the timing of the insult. Examples of this are commonly seen following primary tooth trauma. When a maxillary anterior primary tooth is intruded in infancy (during the first year of life), the crown of the permanent successor may suffer severe structural damage with missing enamel and even dilaceration of the root or the crown, while an intrusion in the later preschool years may only cause an isolated labial hypomineralized enamel opacity on the permanent successor (Fig. 2.4a, b).

A313082_1_En_2_Fig4_HTML.jpg
Fig. 2.4

(a) Hypoplasia of the maxillary permanent incisor tooth as a consequence of trauma to the predecessor. (b) Hypomineralization and hypoplasia of the maxillary central incisor teeth as a consequence of trauma to the predecessor

Determining the Etiology

Based on the number of teeth affected, the possible etiological factors for DDE in permanent teeth can be categorized as being local or general. However the evidence is equivocal, with the majority of published reports being animal studies or case reports of children with specific systemic disorders. The putative etiological factors reported in the literature are summarized in Table 2.3. Only a few of these factors have good evidence supporting a direct causal effect, e.g., trauma to a primary predecessor or high levels of ingested fluoride during early childhood.

Table 2.3

List of etiological factors, reported in the literature, responsible for the formation of enamel defects in the permanent dentition
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Local
Systemic
Hereditary conditions
Perinatal and neonatal
Postnatal
Trauma
Neonatal hypocalcemia
Nutritional and gastrointestinal disturbances resulting in hypocalcemia and vitamin D deficiency
22q11 deletion syndrome
 Primary tooth
 Surgery
 Distraction osteogenesis
 Tooth forceps
Chronic periapical infection in a primary tooth
Severe perinatal and neonatal hypoxic injury
Bacterial and viral infections associated with high fever
Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy
Cleft lip and palate
Prolonged delivery
Exanthematous diseases
Candidiasis endocrinopathy syndrome
Radiation
Prematurity
Juvenile hypothyroidism
Cleidocranial dysostosis
Burns
Low birth weight
Hypothyroidism
Celiac disease
Osteomyelitis
Twins
Hypogonadism
Congenital adrenal hyperplasia
Jaw fracture
Cerebral injury
Phenylketonuria
Congenital contractual arachnodactyly
Neurological disorders
Alkaptonuria
Congenital unilateral facial hypoplasia
Hyperbilirubinemia
Renal disorders
Ectodermal dysplasias
Prolonged neonatal diarrhea and vomiting
Oct 30, 2015 | Posted by in General Dentistry | Comments Off on Enamel Defects in the Permanent Dentition: Prevalence and Etiology
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