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 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

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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

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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. were localized in the occlusal third of the primary canines Irving (1943), suggested that fluoride acts primarily by and first molars[1, 8]. altering the composition of the blood and that the mineralization changes produced are variants of the Hypoplasia associated with lead poisoning (Plumbism) normal process. Feeding of sodium fluoride also produces Pearl and Roland have pointed out that the fetus marked disturbances of mineralization in the enamel, the of a lead- poisoned mother can be affected because lead effects varying from loss of pigmentation to severe readily crosses the placenta during pregnancy. They enamel hypoplasia, the latter occurring with larger doses observed significant delays in development and eruption given more frequently[4]. of the primary teeth in the child of a lead-poisoned mother. Hypoplasia due to hypocalcemia and vitamin D deficiency Hypoplasia caused by local infection and trauma Tetany, induced by a decreased level of calcium Turner (1912) first described this localized type in the blood, may result from several conditions, the most of hypoplasia. Enamel hypoplasia resulting from local common being vitamin D deficiency and parathyroid infection is called "Turner tooth". The infection fails to deficiency (Staz, 1943). In tetany the serum calcium level stimulate the development of a fibrous wall that would may fall as low as 6 to 8 mg per 100 ml and at this level localize the lesion8. Instead, the infection spreads enamel hypoplasia is frequently produced in teeth diffusely through the bone around the buds of the developing concomitantly. This type of enamel successors and thereby affects the important protective hypoplasia is usually of the pitting variety and thus does layer of the young enamel, the united enamel epithelium. not differ from that resulting from a nutritional Bauer (1932) found that in some cases the united enamel disturbance or exanthematous disease[1, 6]. epithelium was destroyed and the enamel was exposed to inflammatory edema and to granulation tissue8. The Hypoplasia due to birth injuries granulation tissue later eroded the enamel and deposited a The neonatal line or ring, described by Schour in well-calcified, metaplastic, cementum-like substance on 1936 and present in deciduous teeth and first permanent the surface of the deep excavation. molars, may be thought of as a type of hypoplasia because there is produced in the enamel and in the dentin as well, Hypoplasia relating to endocrinal influences a disturbance indicative of the trauma or change of It is generally known that certain glands have environment at the time of birth. In traumatic births the specific regulatory functions; for instance, the formation of enamel may even cease at this time[1]. parathyroids are influential in calcium and phosphorus utilization. Because of their primary influence in the Hypoplasia related to brain injury and neurologic maintenance of calcium and phosphorus ratios in the defects blood stream and, therefore, in the calcification A definite relationship between the time of mechanism, the parathyroid glands, through their occurrence of the possible factors that could have caused secretion, parathormone, are of importance in the brain damage and the apparent time of origination of the occurrence of hypoplastic defects in teeth. Many general enamel defect (based on its location in enamel on crown diseases, particularly those in which there is interference of tooth) was established for 70% of the affected teeth of with the body temperature and heat regulatory children with cerebral palsy[8]. Cohen and Diner mechanisms during active odontogenesis, may be observed that enamel defects occurred with greatest responsible for hypoplastic defects, influencing, the frequency in children with low intelligence quotients and calcification mechanism through parathyroid disturbance a high incidence of neurologic defects. [6].

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Hypoplasia associated with cleft lip and palate type (discovered in the triracial Brandywine in Maryland). Among patients in the repaired unilateral and In this only dental defects occur similar to type II but with bilateral complete cleft lip and palate group, 66% of those some clinical and radiographic variations [5, 10]. with maxillary anterior primary teeth had one or more primary teeth affected with enamel hypoplasia, 92% of those with erupted maxillary anterior permanent teeth had Dentin dysplasia is an unusual developmental one or more permanent teeth affected with enamel disorder affecting the orientation of dentin tubules[11]. It hypoplasia[1]. is a condition characterized by teeth with a defective root form, partial or complete obliteration of pulp chambers by Hypoplasia caused by X-radiation and chemotherapy a whorl-like dentinal pattern and a predisposition to Leist (1926) demonstrated the effect of large abscess and cyst formation without an obvious inciting doses of x-rays on development of teeth. He stated that factor[12]. In 1957, Zellner was impressed with the ameloblasts are somewhat resistant to x-radiation. hereditary predisposition for the defect and considered the However, a line of hypoplastic enamel that corresponds to lesion a mesodermal formation syndrome, dentinogenesis the stage of development at the time of therapy may be imperfect radicularis hereditaria. seen. Radiotherapy will have a more severe effect on the development of the dentin and root formation will be Etiology stunted [8]. One of the hypotheses advocates that ectopic deposition of mineral salts, probably of vascular origin, DENTINOGENESIS IMPERFECTA induces mesenchymal cells to form odontoblasts and Also known as Hereditary Opalescent Dentin [9]. subsequent deposition of dentine. The second hypothesis Hereditary opalescent dentin remains a challenge to the advocates that epithelial clones from the developing dental profession because of its poor physical quality, its enamel organ in the dental papillae induce mesenchymal ugly coloration and its easy subjection to severe . cells to transform into odontoblasts. This concept is based Opalescent dentin has been reported as the most prevalent upon the hypothesis that the formation of odontoblasts hereditary dystrophy affecting the structure of the teeth - can be induced only by epithelial cells [12]. 1:8, 000 [10]. Keeler (1935) pointed out the typical In dentinal dysplasia, the exact mechanism is dominant mendelian unit character of the occurence of the unknown, but historically it has been hypothesized that disturbance [8]. displacement of inner cells of the developing dental organ In this condition the primary disturbance is due proliferate into the dentinal papillae at the level of the to imperfect development of the dentin, which is developing crown, inducing ectopic dentin formation. An discoloured, the development of the enamel being normal. opposing view, that of Logan and associates, propose that There is a marked hereditary factor. Wilson and the etiology of the defect is related to multiple Steinbrecher (1929) reported the pedigree of a family in degenerative foci within the dentinal papillae, leading to which the condition was traced through four generations reduced growth and final obliteration of the papillae and and was considered to be inherited as the result of a single formation of sporadic true dentine about calcified foci12. autosomal dominant gene. Dentinogenesis imperfecta is Hereditary predisposition for the defect has also been thought to be an autosomal dominant disorder in which considered. dentin is affected selectively (Witkop 1973, Bixler Shields et al classified dentin dysplasia into : 1976)[9]. Defects in the genes COL1A1 and COL1A2, for Type 1 : Also called “radicular dentin dysplasia” (witkop the procollagen alpha helix, prevent polymerization into et al). It primarily affects the root portions of both normal type 1 collagen. According to Herold (1972), primary and permanent teeth and produced teeth with dentinogenesis imperfecta is caused by incomplete shortened roots and periapical radiolucencies. Because of differentiation of odontoblasts, resulting in cells which the shortened roots this condition is sometimes spoken of fail to form fine fibrillar collagen. Eastoe et al (1973) as being characterized by “rootless teeth”. A sub suggest a collagen - carbohydrate complex may be classification of DD1 into “total”, characterized by produced which may restrict access of calcium and diminutive roots and considerably reduce or obliterated phosphate ions to the immediate sites of pulp spaces and “subtotal”, characterized by intermediate mineralization[9]. root lengths [13, 14]. O Caroll (1991) categorized DD1 Shields et al classified dentinogenesis imperfecta into 4 radiographic variations based on the amount of into three types : Type 1 - The abnormality occurs in obliteration of the pulp chambers, root development and patients with concomitant osteogenesis imperfecta. In this periapical radiolucent areas. DD1 a, there is complete form, primary teeth are more severely affected than obliteration of the pulp, no root development and many permanent teeth (Naito, 1924; Becks, 1931; Noyes, periapical radiolucent areas. DD1 b and DD1 c have less 1935)[6], Type 2 - Patients have only dental abnormalities pulpal obliteration and feature crescent shade radiolucent and no bone disease, Type 3 - Also called as Brandywine areas in the chamber, more root development and less

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frequent periapical radiolucencies. In DD1 d, the pulp Cinically these teeth are lost prematurely and appear to be chambers are distinct, with pulp stones in the coronal shed without apparent cause21. third of the root canal, the roots have significant In a hereditary metabolic disease called development and there are few, if any, periapical hypophosphatasia, there is hypoplasia of the cementum radiolucencies, Type 2 : Also called “coronal dentin and the deciduous teeth are prematurely lost without root dysplasia” (Witkop et al). It is characterized by large resorption (Beumer J, 1973). In the severe form, impaired coronal pulp chambers containing denticles in permanent calcification of bone, reduced tissue and plasma alkaline teeth and total obliteration of pulp chambers in primary phosphatase, and rickets like changes in the skeleton are teeth[16, 17]. seen [21].

REGIONAL ODONTODYSPLASIA HYPERCEMENTOSIS McCall and Wald first described the condition as Hypercementosis is an abnormal thickening of arrested tooth development in 1947. In 1954, the term cementum. It may be diffuse or circumscribed. Types: “shell teeth” was introduced by Rushton[16]. Zegarelli Cemental hypertrophy - If the overgrowth improves the and Kutscher introduced the term odontodysplasia in functional qualities of the cementum it is termed as 1963[17, 18]. is a rare cemental hypertrophy, Cemental hyperplasia - If the developmental anomaly with an unknown cause and overgrowth occurs in nonfunctional teeth or if it is not involves both the ectodermal and mesodermal dental correlated with increased function, it is termed cemental layers. It more commonly affects the maxillary anterior hyperplasia[22]. teeth, and occurs in females twice as often as in males[19]. Etiology This condition frequently is found in teeth that Etiology are exposed to great stress that provides a larger surface Regional odontodysplasia is a condition of area for the attaching fibres and a firmer anchorage of the unknown aetiology. The condition is not hereditary and it tooth to the surrounding alveolar bone is assured. appears to be the result of local factors affecting the tooth Localized hypercementosis may sometimes be observed forming tissues during development. Several factors have in areas in which enamel drops have developed on the been suggested as causes in the literature, such as the dentin. The hyperplastic cementum covering the enamel activation of a latent viral infection of the tooth germ drops occasionally is irregular and sometimes contains during development, local trauma or ischaemia, round bodies that may be calcified epithelial rests. irradiation, metabolic and nutritional disturbances, neural Hyperplasia of cementum may occasionally be observed damage, hyperpyrexia, vitamin deficiency, rhesus on many teeth of the same dentition and is, at least in incompatibility, local somatic mutation, genetic some cases, the sequela of injuries to the cementum. The transmission, medications taken during pregnancy, failure radiographic features are characteristic, showing bulbous of migration of the neural crest cells, and local vascular enlarged roots. Generalized hypercementosis is seen in defects and haemangiomas [16-18]. However, no one conjuction with a ground glass or cotton wool appearing factor has been positively identified as the single cause of alveolar bone in osteitisdeformans [22, 23]. the condition. It is characterized by defective dentine and INTERGLOBULAR DENTIN enamel formation, calcifications within the dental pulp Sometimes mineralization of dentin begins in and dental follicle and often by a failure of the teeth to small globular areas that fail to fuse into a homogenous erupt fully. The teeth appear discolored, hypocalcified, mass. This results in zones of hypomineralization between and hypoplastic and tend to have short roots, open apices the globules. These zones are known as interglobular and wide pulp chambers[20]. dentin [22]. Cases of regional odontodysplasia are diagnosed by the combination of clinical, radiographic, and Etiology histologic features. Nearly all the teeth affected by the Interglobular dentin forms in the crowns of teeth disorder must be extracted and replaced either by fixed or in the circumpulpal dentin just below the mantle dentin removable prosthesis to allow proper function and and follows the incremental pattern (Nylen, 1960). It is esthetics [19]. seen in patients with numerous conditions e.g. physical or bacterial trauma to a developing tooth, rickets, chicken CEMENTAL HYPOPLASIA pox or any other exanthematous fever. The dentinal This rare condition affects the deciduous and tubules pass uninterruptedly through interglobular dentin, permanent dentitions and is characterized by significant thus demonstrating a defect of mineralization and not of reduction in the amount and rate of cementum formation. matrix formation.

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Fig 1. Enamel Hypoplasia Fig 7.Interglobular dentin

Fig 2.Dentinogenisis Imperfecta Fig 8. Enamel pearl

Fig 3. Dentin Dyplsia ENAMEL PEARL The enamel pearl is a circular mass of calcified material that appears primarily on the furcation of maxillary molars and is attached to the external surface of the tooth21. It also has other names enamel drop, enamel nodule and enameloma[24].

Etiology

Ectopic enamel originates from ameloblasts Fig 4. Regional odontodyplsia differentiating in the inner layer of Hertwig’s epithelial sheath which induces odontoblast differentiation in the root. The conditions needed for local differentiation and function of ameloblasts in this ectopic position are not fully understood [25]. Possibly, a composite enamel pearl may form in relation to a local bulging of the odontoblastlayer. Another theory is that it may develop from proliferating buds of epithelium that have become separated at the margin of enamel structure [26]. The rarity of the internal enamel pearl may also Fig 5.Cemental hypoplasia be attributable to a mechanism of development that differs from the external pearl. Possible sources for odontogenic epithelium that might give rise to an internal enamel pearl include: The enamel knot is a temporary proliferation of epithelial cells within the developing dental organ. It might be possible for these epithelial cells to move into the dental papilla as there is no intervening calcified tissue at that time. A proliferating bud of the cervical loop could become entrapped within the dentin matrix and Fig 6.Hypercementosis provide the nidus for an internal pearl, type B enamel lamellas contain cellular debris that are thought to be remnants of the enamel organ. This organic material may become calcified and act as a matrix for crystal deposition. Oehlers (1958) theorized that if enamel pearls could be caused by proliferation of the root sheath toward the periodontal membrane, it would be possible to see enamel within the root if the root sheath proliferated inwards. The extent of the invagination would depend on

the degree of proliferation, traumatic implantation of

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ameloblasts into the dental papilla is not a likely cause ACKNOWLEDGEMENT because there is no evidence of damage to the external Nil surface of the teeth. CONFLICT OF INTEREST No Interest

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Cite this article: Monika Rohilla. Disturbances During Apposition of Hard Tissues. Journal of Science, 2018; 8(1): 19-25. DOI: http://dx.doi.org/10.21276/jos.2018.8.1.5

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