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Journal of Science / Vol 8 / Issue 1 / 2018 / 19-25 Monika Rohilla. / Journal of Science / Vol 8 / Issue 1 / 2018 / 19-25. e ISSN 2277 - 3290 Print ISSN 2277 - 3282 Journal of Science Microbiology www.journalofscience.net Research article DISTURBANCES DURING APPOSITION OF DENTAL HARD TISSUES Monika Rohilla* PG Demonstrator in the Department of Pedodontics, PGIDS, Rohtak, Haryana 124514, India. ABSTRACT A series of factors influence the normal development of the occlusion, interfering in correct alignment of the teeth and harmonic relationship with the adjacent and antagonistic elements. Developmental disturbances of the teeth may manifest by variations in number, position, size, shape, eruption, structure. Such disturbances may occur in association with some more generalised disorder or may occur independently. The present study is undertaken to review the etiopathogenesis of various developmental disturbances during apposition of dental hard tissues. Keywords: Development, Hypoplasia, Apposition. Access this article online mutations in the AMEL-X gene which codes for Home page: Quick Response ameloblastin, enamelin, or tuftelin. In the case of http://journalofscience.net// code autosomal dominant type, the locus of defective gene is on chromosome 4q21 to which enamelin maps. The most DOI: common X-linked types are caused by a variety of defects http://dx.doi.org/10.21276/jos.2018.8.1.5 in the amelogenin genes and confusingly, it seems the same mutation can sometimes cause hypoplastic, Received:16.11.17 Revised:28.11.17 Accepted:06.12.17 hypomineralisation, or hypomaturation forms in different patients [2]. If there is disturbance of the first phase in which the Corresponding Author matrix is being formed the result is enamel hypoplasia Monika Rohilla and if it occurs during the second phase then the quality is PG demonstrator in the department of pedodontics, PGIDS, Rohtak, affected resulting in enamel hypomineralisation. Darling Haryana 124514, India. reported that in hypomineralisation the line of junction between mature and immature enamel runs roughly Email:- [email protected] parallel to the enamel surface. He stated that in some cases hypoplasia and hypomineralisation may occur INTRODUCTION together [4]. In the hypoplastic type ,the main patterns of It represents a group of hereditary disorders of inheritance are autosomal dominant and recessive, X- enamel unassociated with any other generalised defects. It linked and a X-linked dominant type. In the last there is is entirely an ectodermal disturbance since the almost complete failure of enamel formation in affected mesodermal components of the teeth are basically males, while in females the enamel is ridged [2]. In the normal[1]. AI is a group of conditions caused by defects hypomaturation type there are several variants of in the genes encoding enamel matrix proteins [2]. Many hypomaturation defects such as a more severe, autosomal authors have ascribed to Haldane the recognition of AI as dominant of hypomaturation combined with hypoplasia. the first X-linked dominant condition in man [3]. Its In the hypocalcified type there are dominant and recessive inheritance is mainly autosomal dominant, recessive or X- patterns of inheritance. linked. However the most common types have an autosomal inheritance and are thought to be caused by Enamel Hypoplasia Page | 19 Monika Rohilla. / Journal of Science / Vol 8 / Issue 1 / 2018 / 19-25. Enamel hypoplasia is the incomplete or defective disturbance is probably of an inhibitory nature, causing formation of dental enamel. It occurs as a result of a the cells to atrophy and to cease to function. The affected disturbance in the formation of enamel matrix, resulting cells will not recover, and when the disturbance is in a deficient amount of matrix. Two basic types of overcome, new cells adjacent to the atrophied ones will enamel hypoplasia exist: 1)a hereditary type described continue to form enamel. This leaves a defective space under amelogenesisimperfecta2)a type caused by between the old well formed and the newly formed environmental factors[1]. normal tissue, which may become partly repaired some enamel growing over it, but which will remain a visible Etiology scar and present a telltale mark when the tooth has During enamel formation, ameloblasts are erupted. Gottlieb, however, believes the defects to be due susceptible to various external factors that may be to collapse of normally formed but poorly calcified reflected in erupted teeth. Metabolic injury, if severe and enamel matrix, the atrophy of the ameloblasts being long enough, can cause defects in quantity and shape of secondary[4]. enamel or in the quality of enamel. Quantitatively defective enamel, in which normal amounts of enamel are Enamel hypoplasia due to congenital syphilis. produced but are hypomineralised, is known as enamel Congenital syphilis produces very specific duration of the factor’s presence and 3)the time at which changes in the teeth that are pathognomonic. Bradlaw the factor occurs during crown development. The factors (1053), pointed that treponemapallidum has not been that lead to ameloblast damage are highly varied, reported in the foetus of less than 16 to 18 and this would although the clinical signs of defective enamel are the explain why the deciduous teeth are unaffected as their same[3-5]. tooth germs are fully differentiated by the tenth week of Etiological factors may occur locally, affecting uterine life [4]. only a single tooth, or they may act systemically, Congenital syphilis is better termed prenatal affecting all teeth in which enamel is being formed. For syphilis to denote that it existed in the fetus before birth. systemic factors to have an effect on developing The treponemapallidum is transmitted from the mother to permanent teeth, they must occur after birth and before the fetus by way of the blood stream. Here foci of the age of 6 years. During this time the crowns of syphilitic infection occur which extend to the fetal permanent teeth(with the exception of third molars) circulation and thus infect the fetal tissues. The greatest develop. Because most enamel defects affect anterior damage is done by syphilis during the second part of teeth and first molars, systemic factors must have intrauterine life and the first months after birth. The teeth, occurred predominantly during the first year and a half of which at this time are beginning to be formed, are most second year. Primary teeth and possibly occlusal tips of affected[7, 8]. first permanent molars and permanent central incisors This hypoplasia involves the maxillary and may reflect ameloblast dysfunction occurring in utero, as mandibular permanent incisors and the first molars. The these are the teeth undergoing calcification during this anterior teeth affected are sometimes called period. The specific causes of systemically induced “Hutchinson’s teeth,” while the molars have been referred enamel defects are often obscure but are usually attributed to as “mulberry molars” (Moon’s molars, Fournier’s to childhood infectious diseases. Other cited causes molars, mulberry or bud molar of Pfluger). include nutritional defects such as rickets, exanthematous Characteristically, the upper central incisor is disease (measles ,chickenpox), congenital syphilis, “screw-driver” shaped. In addition, the incisal edge is hypocalcemia, birth injury, prematurity, Rh haemolytic usually notched (crescent notch), sometimes it appears as disease, local infection or trauma, ingestion of chemicals a deep fissure on both the labial and lingual aspects and idiopathic cause. (Bradlaw, 1953).The cause of the tapering and notching of the maxillary incisor has been explained on the basis of Hypoplasia Due To Nutritional Deficiency And the absence of the central tubercle or calcification center. Exanthematous Fevers The crowns of the first molars are irregular and the In general it might be stated that any serious enamel of the occlusal surface and the occlusal third of nutritional deficiency or systemic disease is potentially the tooth appears to be arranged in an agglomerate mass capable of producing enamel hypoplasia, since the of globules rather than in well-formed cusps[1]. ameloblasts are one of the most sensitive groups of cells in the body in terms of metabolic function [6]. The Enamel hypoplasia due to fluoride: Mottled enamel mineralisation is an intermittent process with alternate Mckay and Black (1916) and McKay (1918, periods of activity and rest, so that if there is a short acute 1919) demonstrated that the defect was found in the bout of fever during the period of rest, the tooth will not inhabitants of certain areas in Colorado and Northwest be affected4. The defects are produced by a disturbance of Taxas. Smith, Lanz and Smith (1931) established the fact the ameloblastic activity of the enamel organ. The that the presence of an excessive amount of fluorine in the Page | 20 Monika Rohilla. / Journal of Science / Vol 8 / Issue 1 / 2018 / 19-25. water is the primary etiologic factor in the mottling of Hypoplasia associated with nephrotic syndrome enamel. Drinking water with a content of 0.5 to 0.75 part Oliver and Owings observed enamel hypoplasia per million caused no defects. The water of wells which in permanent teeth in a high percentage of children with caused mottled enamel contained 1 to 7 parts per nephrotic syndrome and found a correlation between the million[6, 8]. The severity of the mottling increases with time of severe renal disease and the estimated time at an increasing amount of the fluoride in the water. Thus which the defective enamel formation occurred. there is little mottling of any clinical significance at a level below 0.9 to1.0 part per million of fluoride[1, 4]. Hypoplasia associated with allergies De Eds (1941) suggested that the disturbance in Rattner and Myers discovered a correlation mineralization may be due to a deposition of calcium between enamel defects of the primary dentition and the fluoride in the tissue instead of calcium phosphate, and to presence of severe allergic reactions. The enamel lesions a disturbance of the phosphatase system of mineralization.
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