Volume 3, Issue 1 - Winter 2012

Enamel Hypoplasia

December 27, 2012

         Development of the tooth occurs in multiple stages. Initiation, commonly referred to as the bud stage, begins as early as the sixth week of embryonic life. Cells in the basal layer of the oral epithelium proliferate rapidly resulting in thickening, and the formation of the dental lamina. Proliferations of the cells continue during the cap stage. A shallow invagination appears on the deep surface of the bud and the shape of the tooth and enamel organ are formed. Next at the bell stage, histodifferentiation and morphodifferentiation occur. Cells of dental papilla differentiate into odontoblasts and cells of the inner enamel epithelium differentiate into ameloblasts. Apposition then occurs, as ameloblasts and odontoblasts deposit a layer like matrix. Finally calcification occurs and this involves the precipitation of inorganic calcium salts within the deposited matrix.[1]

            Tooth structure abnormalities result from disruption during the histodifferentiation,opposition, and the mineralization stages of tooth development. Amelogenesis occurs in two stages. In the first stage, the enamel matrix forms, and in the second stage, the matrix undergoes calcification. Local or systemic factors that interfere with normal matrix formation cause enamel surface defects and irregularities called enamel hypoplasia. Factors that interfere with calcification and maturation of the enamel produce a condition termed enamel hypocalcification. According to Jorgenson and Yost, they may be broadly classified as heritable defects or environmentally induced defects.[2]

Enamel hypoplasia may be mild and may result in a pitting of the enamel surface or in the development of a horizontal line across the enamel of the crown. If ameloblastic activity has been disrupted for a long period of time, gross areas of irregular or imperfect enamel formation occur. Enamel hypoplasia is often seen as one component of many different syndromes. Postnatal hypoplasia of the primary teeth is probably as common as hypoplasia of the permanent teeth, although postnatal hypoplasia is usually not as severe. Hypoplasia of the primary enamel that forms before birth is rare, however in its mildest form, a prenatal disturbance is seen as an accentuated neonatal ring inthe primary tooth. In the severe type of neonatal disturbance, enamel formation is sometimes arrested at birth or during the neonatal period.  Postnatal amelogenesis is confined to the portion of the crown located cervically from the enamel area present at birth. Slayton et al examined 698well-nourished and healthy children 4 to 5 years of age and found that 6% had at least one primary tooth with enamel hypoplasia.[3]

Amelogenesis Imperfecta (AI) is a classic example of heritable enamel defects. The four major AI categories are described according to the stages of tooth development in which each is thought to occur. Type I is hypoplastic, Type II is hypomaturation, Type III is hypocalcified and Type IV is hypomaturation, hypoplastic with taurodontism. Fourteen subgroup classifications of AI exist with multiple inheritance patterns. The only feature that distinguishes AI from other enamel defects is its distinct patterns of inheritance and the fact that it occurs alone without any other metabolic, or systemic condition.

Hereditary enamel defects occurring in the histodifferentiation stage of tooth development are exemplified by the hypoplastic type of AI wherein an insufficient quantity of enamel is formed. This occurs because some areas of the enamel organ are devoid of inner enamel epithelium, causing a lack of cell differentiation into ameloblasts. Both primary and permanent dentitions are affected, and the condition is inherited predominantly as an autosomal dominant trait depending on the subgroup pattern. Affected teeth appear small with open contacts, and areas of the clinical crowns contain very thin or nonexistent enamel resulting in high sensitivity to thermal stimuli.

The hypomaturation type of AI is an example of an inherited defect in enamel matrix apposition. It is characterized by teeth having normal enamel thickness but a low value of radio density and mineral content .The problem is related to the persistence of organic content in the rod sheath resulting in poor calcification, low mineral content, and a porous surface that becomes stained.

The hypocalcification type of AI is an example of an inherited defect in the calcification stage of enamel formation. Quantitatively, the enamel is normal, but qualitatively the matrix is poorly calcified with a resultant fracturing of the enamel surface. The hypocalcified enamel is soft and fragile, especially at the incisal regions, and is easily fractured, exposing the underlying dentin that produces an unaesthetic appearance. Increased calculus formation and marked delay in tooth eruption are consistent findings. Anterior open bite is also common in these patients.

Hypoplastic/ hypomaturation AI with taurodontism is an example of inherited defects in both apposition and histodifferentiation stages of enamel formation. The enamel appears mottled with a yellow-brown color and is pitted on the facial surfaces, exemplifying the features of both hypoplasia and hypomaturation previously described. Molar teeth demonstrate taurodontism, and other components of the dentition have enlarged pulp chambers.[4]

Examples of environmentally induced enamel hypoplasia can result from systemic or local causes. Examples of systemic causes producing generalized enamel hypoplasia include nutritional deficiencies, particularly in vitamins A, C, and D as well as in calcium and phosphorus. Sarnat and Schour observed that, in a group of 60 children who had adequate medical histories, two thirds of the hypoplastic disturbances occurred during infancy (birth to the end of the first year). Approximately one third of enamel hypoplasia was found in the portion of teeth formed during early childhood (13 to 34 months) Less than 2% of enamel defects found originated in late childhood (35 to80 months).[5]

Severe infection, such as exanthematous diseases and fever-producing disorders, particularly during the first year of life, can directly affect ameloblastic activity, resulting in enamel hypoplasia as well. Rubella embryopathy has a high correlation with prenatal enamel hypoplasia in the primary dentition. Syphilis caused by the spirochete Treponema pallidum produces classic patterns of hypoplastic dysmorphic permanent teeth. The tapered and notched incisal edges of anterior teeth with screwdriver shapes are called Hutchinson’s incisors, and the crenated occlusal patterns of posterior teeth known as mulberry molars are classic clinical findings for prenatal syphilis infection.

Hypoplasia is also shown to be related to brain injury and neurologic defects. Herman and McDonald studied 120 children with cerebral palsy between 2.5 and 10.5 years of age to determine the prevalence of dental hypoplasia. The researchers compared them with 117 healthy children in the same age group and observed enamel hypoplasia in 36% of the group with cerebral palsy and in 6% of the group without the disorder.[6]

Children with asthma also demonstrate a higher prevalence of enamel hypoplasia than children without asthma. Premature childbirth and excess radiation exposure have been shown to disrupt the ameloblastic matrix formation or subsequent mineralization and are also additional causes of systemic enamel hypoplasia. Lai and Seow et al completed a longitudinal study investigating the enamel defects in a group of 25 Caucasian preterm low birth weight children with a mean gestational age of 27 +/- 1.9 weeks in comparison with 25 randomly selected full term control children born at the same hospital. The children were examined at 30 months, 44 months and 52 months of age. At all ages, the preterm children had significantly higher prevalence of enamel hypoplasia when compared to the normal birth weight children. At the last recall examination, 96% of low birth weight group, and 45% of the normal birth weight group had at least one tooth with an enamel defect. The defect identified to be most significantly associated with dental caries was a variant showing both enamel hypoplasia and opacity. In spite of a high prevalence of enamel defects, the overall prevalence of dental caries in the low birth weight children was not significantly different from that of normal birth weight controls at all three examinations.[7]

Sheldon, Bibby, and Bales tried to determine whether defects in enamel were related to the incidents of systemic diseases. They examined ground sections of95 teeth from 34 patients for whom detailed medical histories were available. In more than 70% of the individuals a positive correlation was established between the time of formation of a band of defective enamel and the existence of some systemic disability. However, defects in enamel occurred in 23% of patients who had no history of systemic conditions that might have produced enamel defects. No enamel changes occurred in 6% of patients who had histories of disabilities that had produced enamel changes in other patients. Deficiencies of vitamins A, C, and D, calcium, and phosphorus were the most common causes of defective enamel formation.[8]

Purvis et al, in a study of 112 infants with neonatal tetany in Edinburgh, observed that

63 (56%) later showed severe enamel hypoplasia of the primary teeth. Histologic examinations revealed a prolonged disturbance of enamel formation in the 3 months before birth. An inverse relationship was demonstrated between the mean daily hours of bright sunshine in each calendar month and the incidence of neonatal tetany 3 months later. This observation suggested that enamel hypoplasia and neonatal tetany can be manifestations of vitamin D deficiency during pregnancy and are most likely the result of secondary hyperparathyroidism in the mother. A significantly higher mean maternal age and a preponderance of lower social class was also seen in the mothers of those in the tetany group.[9] Another study in Edinburgh indicated that only1% of pregnant mothers took vitamin D supplements.

Apparently in some children a mild deficiency state or systemic condition without clinical symptoms can interfere with ameloblastic activity and can produce a permanent defect in the developing enamel.

            Enamel hypoplasia resulting from a deficiency state or a systemic condition will be evident on all the teeth that were undergoing matrix formation and calcification at the time of the insult. The hypoplasia will follow a definite pattern. Individual permanent teeth often have hypoplastic or hypocalcified areas on the crown that result from infection or trauma. Turner first described this localized type of hypoplasia. He noted defects in the enamel of two premolars and traced the defects to apical infection of the nearest primary molar. Enamel hypoplasia resulting from local infection is called Turner tooth.[10]A traumatic injury to an anterior primary tooth that causes its displacement apically can also interfere with matrix formation or calcification of the underlying permanent tooth. The trauma or subsequent periapical infection frequently produces defects on the labial surface of the permanent incisor. The permanent tooth may develop hypoplastic defects or potential necrosis subsequent to trauma.

Excess ingestion of fluoride can affect the ameloblasts during the tooth formation stage and can cause dental fluorosis commonly referred to as mottled enamel. The appearance of enamel that is affected in its formation by excessive fluoride varies considerably. Although the more severe cases of dental fluorosis are associated with a high level of fluoride consumption, there is apparently a great deal of individual variation. The affected enamel is often limited superficially to the most outer surface and presents a white or brown opaque and/or pitted appearance. Dental fluorosis is most often seen in permanent teeth, but it has also been observed in primary teeth. Levy et al observed fluorosis of primary teeth in 12.1% of 504 children.[11] It was observed most often on second primary molars. The middle of the first year of life seemed to be the most important time with regard to the development of fluorosis in the primary dentition based on their estimates of fluoride ingestion prenatally and during the first year of life in these children.

The controversy that hypoplastic teeth are more susceptible to dental caries than normal teeth has little evidence to support it. However, carious lesions do develop in the enamel defects and in the areas of the clinical crown when dentin is exposed. Small carious and precarious areas can be restored with resin or glass ionomer, leaving the restoration confined to the area of involvement.[12] Hypoplastic primary and permanent teeth with large areas of defective enamel and exposed dentin may be sensitive as soon as they erupt. Topical application of fluoride has been found to decrease the sensitivity of the tooth until a restoration can be completed.

            Isolated hypoplastic white or yellowish brown spots can be improved by enamel microabrasion or by composite resin restorations. Microabrasion is the preferred technique whenever possible due to the fact that it requires less enamel removal and does not necessitate placement of a restoration. For many years some dentists have advocated the application of hydrochloric acid as an effective method for removing the staining in the mottled enamel. McClosky described a technique that used 18% hydrochloric acid on the affected enamel surface.[13] Croll proposed a modified procedure called enamel microabrasion in which a specially prepared abrasive compound is applied to the discolored enamel areas, similarly to prophylaxis paste, using a synthetic rubber cup applicator in a 10:1gear-reduction hand piece. Frequent water rinsing and reevaluation of the tooth for color correction are required. This is continued until the undesirable coloration is removed or until a noticeable amount of enamel is being removed when the tooth is viewed from the incisal. Finally, the abraded teeth are polished with a fine fluoridated prophylactic paste and given a 4-minute fluoride treatment.[14]

            In more severe cases of enamel hypoplasia, composite resin or porcelain veneers provide an aesthetic treatment option. The use of hybrid and microfilled composite has been shown to be used to conservatively rehabilitate a smile.[15]

            Enamel hypoplasia is a multifaceted tooth structure abnormality that ranges from mild to severe in form. There are numerous diverse causes that come into play including hereditary, systemic and local environmental factors. It is commonly seen in our population, and various restorative techniques exist to improve the aesthetic appearance and overall outcome of the involved teeth.

 

 

 


[1]Pinkham,Casamassimo,Fields; Pediatric Dentistry: Infancy through adolescent, 4thed2005

[2]Jorgenson RT, Yost C: Etiology of enamel dysplasias. J Pedod 6:316-329,1982.

[3]Slayton RL et al: Prevalence of enamel hypoplasia and isolated opacities

in the primary dentition, Pediatric Dent 32:32-36, 2001.

[4]Chaudhary M, Dixit S, Singh A, Kunte S.Amelogenesis imperfecta: Report of a case and review of literature.J Oral MaxillofacPathol. 2009 Jul;13(2):70-7.

[5]Sarnat BG, Schour I: Enamel hypoplasia (chronologic enamel aplasia) in relation to systemic disease: a chronologic, morphologic, and etiologicclassification, J Am Dent Assoc 28:1989-2000, 1941; 29:67-75, 1942.

[6]Herman SC, McDonald RE: Enamel hypoplasia in cerebral palsied children, J Dent Child 30:46-49, 1963.

[7]Lai, Seow,Tudehope, Rogers:Enamel Hypoplasia and dental caries in very low birthweightchildren:a case controlled longitudinal study, Pediatric Dentristy19(1):42-9, 1997 Jan-Feb.

[8]Sheldon M, Bibby BG, Bales MS: Relationship between microscopic enamel defects and infantile disabilities, J Dent Res 24:109-116, 1945

[9]Purvis RJ et al: Enamel hypoplasia of the teeth associated with neonatal tetany: a manifestation of maternal vitamin D deficiency, Lancet 2:811-814, 1973

[10]Turner JG: Two cases of hypoplasia of enamel, Br J Dent Sci 55:227-228,

1912.

[11]Levy SM et al: Primary tooth fluorosis and fluoride intake during the first year of life, Community Dent Oral Epidemiol 30:286-295, 2002.

[12]McDonald,Avery,Dean; Dentistry for the child and adolescent, 8thedmosby 2004

[13] McCloskey RJ: A technique for removal of fluorosis stains, J Am Dent Assoc 109:63-64, 1984.

[14]Croll TP, Helpin ML: Enamel microabrasion: a new approach, J EsthetDent 12:64-71, 2000.

[15]Soares,Fonseca,Martins,Giannini:Esthetic rehabilitation of anterior teeth affected by enamel hypoplasia:a case report:J EsthetRestor Dent. 14(6):340-8, 2002.