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Enamel Hypoplasia: a Concise Review of Its Factors & Pathogenesis

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Enamel Hypoplasia: a Concise Review of Its Factors & Pathogenesis Vanishree H.S and Anand S Tegginamani. / American Journal of Oral Medicine and Radiology. 2016;3(1):48-51. e - ISSN - XXXX-XXXX ISSN - 2394-7721 American Journal of Oral Medicine and Radiology Journal homepage: www.mcmed.us/journal/ajomr ENAMEL HYPOPLASIA: A CONCISE REVIEW OF ITS FACTORS & PATHOGENESIS Vanishree H.S.1* and Anand S Tegginamani2 Faculty of Dentistry, SEGi University, Kota Damansara, 47810 Petaling Jaya, Selangor, Malaysia. Article Info ABSTRACT Received 23/11/2015 Developmental disturbances of the teeth occur with the insult/trauma to the dental lamina. Revised 16/12/2015 The lesions may differ with the stages of the tooth development and the intensity of the Accepted 09/01/2016 trauma to the dental lamina. A considerable number of environmental factors have been reported to be capable of causing enamel defects and systemic disturbances consist of Key words:- intoxications, prenatal and postnatal problems, malnutrition, infectious diseases and a range Developmental of other medical conditions. This review is an attempt to factors and Pathogenesis disturbances of the associated to enamel hypoplasia, so all clinical features of enamel hypoplasia are not teeth, Enamel included. Hypoplasia, Fluoride, Systemic factors, Turners Hypoplasia. INTRODUCTION Disorders of development of teeth may be due to function of matrix production and initial mineralization. abnormalities in the differentiation of the dental lamina Matrix production involves the synthesis and secretion of and the tooth germs, causing anomalies in the number, the matrix proteins, amelogenin, enamelin, ameloblastin size and form of teeth (abnormalities of morpho and tuftelin, of which amelogenin accounts for about 90 differentiation) or to abnormalities in the formation of the per cent. Initial mineralization occurs immediately after dental hard tissues resulting in disturbances in tooth secretion. structure (abnormalities of histodifferentiation). • The maturation stage: There is withdrawal of protein and Abnormalities of histodifferentiation occur at a later stage water from the enamel accompanied by increase in in development than abnormalities of morpho mineral content before the tooth erupts. differentiation; in some disorders both stages of Most classifications of disturbances in enamel differentiation are abnormal Developmental disturbances formation distinguish between those that affect the of the teeth occurs with the insult/trauma to the dental secretory stage, resulting in deficient matrix production lamina. The lesions may differ with the stages of the tooth and thin hypoplastic enamel and those that affect the development and the intensity of the trauma to the dental maturation stage, resulting in deficient mineral deposition lamina [1]. and soft hypomineralized enamel [2-4]. Enamel normally develops in two stages Hypoplasia is defined as a quantitative defect of • In the secretory stage: The ameloblasts perform the dual enamel visually and is histomorphologically identified as an external defect involving the surface of the enamel and Corresponding Author associated with reduced thickness of enamel [5]. The cervical and the incisal borders of the defect have a Vanishree HS rounded appearance due to the prisms in the non-affected Email: - [email protected] enamel being bent, which may be attributed to a change in 48 | P a g e Vanishree H.S and Anand S Tegginamani. / American Journal of Oral Medicine and Radiology. 2016;3(1):48-51. the prism direction. The macro & microscopical homologous teeth of children with demarcated opacities appearances suggest that only some specific ameloblasts were affected to varying extents, and found it difficult to have ceased to form enamel, whereas others are partly or make any assumption about the severity of the insult completely able to fulfil their task [6]. because the damaging agent seemed to have been rather nonspecific in most of the children. Hence, they assumed Pathogenesis that two or more interacting factors were required to While the pathogenesis of the dental defects produce the defects [15]. remains unclear, it is probable that both systemic disturbances and local factors contribute to the aetiology Enamel Hypoplasia [7]. Developmental defects of enamel with a similar Both dentitions could be affected by enamel appearance are not necessarily caused by similar hypoplasia; however, the incidence is more severe in aetiological agents. Conversely, the same aetiological permanent dentition. The characteristics of clinical enamel factors can produce different defects at different stages of hypoplasia include unfavourable esthetics, higher dentin tooth development. Enamel defects may also result from a sensitivity, malocclusion and dental caries susceptibility combination of factors. It has been proposed that there are [16]. The treatment of challenge in this type of injury for a well over 90 different factors that may be responsible for complete oral rehabilitation in both esthetics and function causing developmental defects of enamel [8,9]. Disturbances during apposition of hard dental In the case of amelogenesis, it is not different tissues during growth of teeth leads to [1] cells doing different jobs, but the same cells at different (a) Enamel hypoplasia stages of maturation doing the different jobs. First they lay (b) Amelogenesis imperfecta down the organic matrix and then they lay down the (c) Dentinogenesis imperfecta hydroxyapatite crystals within this matrix and finally they (d) Dentinal dysplasia become quiescent and vestigial once the cells have (e) Shell teeth matured from one phase and moved to the next, they cannot go back and fix any defects. Anything that disrupts Hypoplasia are categorized into the following types the delicate ameloblasts during enamel production will [17] result in defective enamel which may be very porous and Type I hypoplasia: Enamel discoloration due to weak. This defective enamel is often present at eruption hypoplasia but will soon be lost to abrasive forces. This leaves an area Type II hypoplasia: Abnormal coalescence due to of exposed dentin and rough margins to the surrounding hypoplasia enamel. In some instances the enamel does not form at all Type III hypoplasia: Some parts of enamel missing due and so is missing as soon as the tooth erupts.[10] to hypoplasia A considerable number of environmental factors Type IV hypoplasia: A combination of previous three have been reported to be capable of causing enamel types of hypoplasia. defects. These systemic disturbances consist of intoxications, prenatal and postnatal problems, Other Factors for enamel Hypolasia malnutrition, infectious diseases and a range of other Intoxications, the one responsible for affecting medical conditions [11]. most people is probably fluoride.[11] The effect of Suckling suggested that the pathogenesis of each increasing the intake of fluoride during tooth development type of Developmental defects of enamel is different and upon the appearance of the enamel has been well- therefore should be considered separately. The stage of documented. Among the many hypotheses that have been amelogenesis at which time the dysfunction occurs, the proposed for the mechanism by which excess fluoride severity of the insult leading to temporary, or permanent affects degradation and removal of enamel matrix inactivity of the cells, the duration of the insult, the phase proteins, three are favoured by most researchers: of ameloblast activity during the relevant period, and the (i) fluoride might directly affect ameloblasts [18] specific agent involved, may affect the final appearance of (ii) proteins may be more tightly bound to fluoridated the defect [12] damage of secretory ameloblasts results in hydroxyapatite and, thus, proteinolysis might be more pathologically thin enamel. However, interference during difficult [19] (iii) fluoride might inhibit enamel the maturation stage can lead to defects which present as proteinases [20]. However, there is no conclusive proof bands, or patches of chalky opaque porous enamel [13] that fluoride alone, either in the form of an excessive Suga suggested that ameloblasts were very sensitive to intake, or of an abnormal metabolic process in the disorders at an early stage of maturation. Hence, if a cell is presence of a low or normal intake, is responsible for all damaged by a systemic or local disorder at this stage, it the enamel changes of diffuse opacities. cannot easily recover from dysfunction during the long Other systemic factors operating over a long period of maturation. Therefore, he hypothesized that period of tooth development such as malnutrition, chronic demarcated opacities were due to a disturbance in the illness (diabetes insipidus) & hypervitaminosis D process of matrix degradation [14]. It’s observed that the [11,21,22]. 49 | P a g e Vanishree H.S and Anand S Tegginamani. / American Journal of Oral Medicine and Radiology. 2016;3(1):48-51. Children with low birth-weights, i.e. 2000g or the formation of enamel. Because of the location of the below, have also been shown to have a much higher permanent tooth's developing tooth bud in relation to the prevalence of enamel opacities in the first permanent primary tooth, the most likely affected area on the molars and lateral incisors than children who had a normal permanent tooth is the facial surface. White or yellow birth-weight [23]. Since anti-neoplastic therapy affects all discoloration may accompany Turner's hypoplasia [31]. cells, it is not surprising that developmental defects of
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