Dental development or odontogenesis is a complex process in which teeth are formed from embryonic cells, grow, and erupt into the mouth. For human teeth having a healthy oral environment, all parts of the tooth should develop during the proper stage of fetal development. Primary teeth (infants) begin to form between the sixth week and eight prenatal developments, and permanent teeth begin to form in the twentieth week. If the tooth does not begin to develop at or near this time, the tooth will not develop at all, resulting in Hypodontia or Anodontia.
A large number of studies have focused on determining the process that initiates dental development. It is widely accepted that there is a factor in the network of the first pharyngeal arch necessary for dental development.
Video Human tooth development
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Dental germs are the cell aggregation that eventually forms the tooth. These cells originate from the ectoderm of the first pharyngeal arch and the ectomesenchyma of neural crystals. Dental germs are arranged into three parts: the enamel organ, the dental papilla and the tooth sac or follicle.
The enamel organ consists of the outer enamel epithelium, the inner enamel epithelial, the stellate reticulum and the intermedium stratum. These cells give rise to ameloblasts, which produce enamel and become part of the reduced enamel epithelium (REE) after enamel ripening. The location where the outer enamel epithelium and the inner enamel epitelium join are called cervical loops. The growth of cervical loop cells into the deeper tissues forms the Hertwig Epithelial Root Sheath, which determines the root shape of a tooth. During dental development there is a strong similarity between keratinization and amelogenesis. Keratin is also present in epithelial cells of dental germs and keratin thin films present in newly erupted teeth (Nasmyth membrane or enamel cuticle).
The tooth papilla contains cells that develop into odontoblasts, which are dentin-forming cells. In addition, the intersection between the dental papilla and the inner enamel epith determines the shape of the dental crown. Mesenchyme cells in the dental papilla are responsible for dental pulp formation.
The tooth sac or follicle raises three important entities: cementoblast, osteoblasts, and fibroblasts. Cementoblasts form cementum teeth. Osteoblasts grow alveolar bone around tooth roots. Fibroblasts are involved in developing a periodontal ligament that connects the teeth to the alveolar bone through the cementum.
NGF-R is present in ectomesenchymal cell condensation of dental papillae on early stage germicide stamp and plays a double role during morphogenetic events and cytodifferentiation in the teeth. There is a relationship between tooth agenesis and the absence of trigeminal peripheral nerves (see Hypodontia).
All stages (buds, caps, bells, crowns), dental growth and morphogenesis are governed by a protein called sonic porcupine.
The various phenotypic inputs modulate the size of the teeth.
Parathyroid hormone is needed for tooth eruption.
Development schedule of human teeth
The following table presents the timeline for the development of human teeth. The times for initial calcification of primary teeth are for weeks in utero . Abbreviations: wkÃ, = Ã, week; moÃ, = Ã, month; yrÃ, = Ã, year.
Maps Human tooth development
Stages
Dental development is usually divided into the following stages: the initiation stage, the shoot stage, the lid stage, the bell stage, and finally the maturation. Staging dental development is an attempt to categorize the changes that occur along the continuum; it is often difficult to decide what stage should be given to certain developing teeth. This determination is more complicated by the emergence of different histological sections of the same developing teeth, which may appear to be different stages.
Initiation Phase
One of the earliest signs of microscopically visible tooth formation is the difference between vestibular laminae and dental lamina. The dental lamina connects the development of tooth buds to the epithelial layer of the mouth for significant time. This is considered a stage of initiation.
Phase Bud
Phase shoots are characterized by the appearance of bud shoots without clear cellular arrangement. The stage is technically started after epithelial cells proliferate into the ektomesenkim jaw. Usually, this happens when the fetus is about 8 weeks old. Dental shoots themselves are a group of cells on the periphery of the lamina tooth.
Along with the formation of dental lamina, 10 rounded epithelial structures, each referred to as the bud, develops on the distal aspect of dental lamina of each arch. This corresponds to the 10 primary teeth of each dental arch, and they signify the stage of budding development of the tooth. Each bud is separated from ectomesenchyme by a basement membrane. The ectomesenchymal cells cluster deep in the bud, forming a group of cells, which are the initiation of condensation ektomesenkim. The remaining ectomesenchymal cells are arranged in a more or less uniform and haphazard manner.
Cap stage
The first signs of the cell arrangement in the dental bud occur in the cap stage. A small group of ectomesenchymal cells stops producing extracellular substances, which results in the aggregation of cells called dental papilla. At this point, the tooth buds grow around the ectomesenchymal aggregation, taking the appearance of the lid, and into the organ of enamel (or teeth) covering the dental papilla. Ectomesenchymal cell condensation called a tooth sac or follicle surrounds the enamel organ and limits the dental papilla. Finally, the enamel organ will produce enamel, the dental papilla will produce dentine and pulp, and the tooth sac will produce all the supporting structures of the tooth, periodontium.
Bell stage
The bell stage is known for the histodifferentiation and morphodifferentiation that occurs. Organs are bell-shaped during this stage, and most of the cells are called reticulum stellata because of their star-shaped shape. The bell stage is divided into the early stages of the bell and the final bell stage . Cells on the periphery of separate enamel organs into four important layers. The cytopoid cells at the edges of the tooth organ are known as the outer enamel epithelial (OEE). The columnar cells of the enamel organ adjacent to the enamel papilla are known as the inner enamel epithelium (IEE). The cells between the IEE and the stellate reticulum form a layer known as the intermedium stratum. The rim of the enamel organ in which the outer and inner enamel epithelium is joined is called the cervical loop. In short, layers in the deepest order to the outermost consist of dentine, enamel (formed by IEE, or 'ameloblasts', as they move outward), deep enamel epithelials and stratum intermediates (stratum cells supporting the synthetic activity of the inner enamel epitelium ) The following is part of the original 'enamel organ', its center consisting of a stellate reticular cell that serves to protect the enamel organ. These are all enclosed by the OEE layer.
Other events occur during the bell stage. The dental lamina is destroyed, leaving the developing tooth completely separated from the oral epithelial of the mouth; both will not merge again until the last tooth eruption to the mouth.
Dental crowns, which are affected by the inner enamel epithelial form, are also formed during this stage. Throughout the mouth, all the teeth undergo this same process; it is still uncertain why teeth form different forms of crowns - for example, incisors versus canine teeth. There are two dominant hypotheses. The "field model" proposes no component for any type of tooth form found in ectomesenchyme during dental development. Components for certain types of teeth, such as incisors, are localized in one area and disappear quickly in different parts of the mouth. Thus, for example, "incisors" have factors that develop teeth into the form of incisors, and this area is concentrated in the central incisor area, but decreases rapidly in the canine area. Another dominant hypothesis, the "clonal model", proposes that the epithelium categorizes a group of ectomesenchymal cells to produce a tooth in a particular shape. This group of cells, called clones, persuades the dental lamina into the development of the tooth, causing the tooth buds to form. The growth of dental lamina continues in an area called the "development zone". After the progress zone has covered a certain distance from the first tooth bud, the second tooth bud will begin to develop. Both of these models are not always mutually exclusive, as are the widely accepted dentistry that it is so: postulated that both models influence the development of teeth at different times.
Other structures that may appear on the developing teeth at this stage are enamel nodes, enamel cables, and enamel niches.
Advanced bells level
Hard tissue, including enamel and dentine, develops during the next stage of dental development. This stage is called the crown, or the maturation stage, by some researchers. Important mobile changes are happening right now. In the previous stage, all IEE cells divide to increase the overall size of the dental bud, but rapid division, called mitosis, stops during the crown stage at the site where the cusps are formed. The first mineralized mineralized tissue is formed at this location. At the same time, IEE cells change from cuboid to columnar and become preameloblasts. The nuclei of these cells move closer to the intermedium stratum and away from the dental papilla as they become polarized.
The adjacent cell layers in the dental papilla suddenly increase in size and differentiate into odontoblasts, which are the cells that make up the dentin. The researchers believe that odontoblasts will not be formed if not for the changes occurring in the IEE. When changes in the IEE and odontoblast formation continue from the tip of the valve, odontoblasts secrete the substance, the organic matrix, into the vicinity. The organic matrix contains the material needed for dentine formation. When odontoblasts store an organic matrix called predentine, they migrate to the center of the dental papilla. So, unlike tooth enamel, dentine begins to form on the surface closest to the outside of the tooth and goes inside. The cytoplasmic extension is abandoned when the odontoblast moves inward. The unique tubular microscopic appearance of dentine is the result of dentine formation around this extension.
After dentine formation begins, cells from the IEE secrete the organic matrix to dentine. This matrix is ​​immediately mineralized and becomes the initial layer of tooth enamel. Beyond dentine is a newly formed ameloblast in response to dentin formation, which is a cell that continues the process of enamel formation; therefore, enamel formation moves outward, adding new material to the outer surfaces of developing teeth.
Hard network formation
Enamel
The formation of enamel is called amelogenesis and occurs at the stage of the crown (advanced stage of the bell) of dental development. "Reciprocal induction" regulates the relationship between dentin and enamel formation; dentine formation should always occur before enamel formation. Generally, enamel formation occurs in two stages: the secretory and maturation stage. Organic proteins and matrix form partial mineralized enamel in the secretory stage; the maturation stage completes the enamel mineralization.
At the secretion stage, ameloblasts release an enamel protein that contributes to the enamel matrix, which is then partially mediated by the alkaline phosphatase enzyme. This mineralization phase occurs very early around the 3rd or 4th month of pregnancy. This marks the appearance of the first enamel in the body. Ameloblasts make emails in locations where the tooth cusps are located. Enamel grows outward, away from the center of the tooth.
At the maturation stage, ameloblasts remove some of the substances used in enamel formation of enamel. Thus, the ameloblast function changes from enamel production, as occurs in the secretory stage, to the transport of the substance. Most of the material transported by ameloblasts at this stage is the protein used to complete the mineralization. The important proteins involved are amelogenins, ameloblastins, enamelins, and tuftelins. At the end of this stage, the enamel has completed the mineralization.
Residues can form on new eruptive teeth that can leave extrinsic stained teeth. This gray-green residue, Nasmyth's membrane, consists of fused tissue of reduced enamel epithelium and oral epithelium, as well as tooth cuticles placed by ameloblasts on the surface of the newly formed enamel. The nasym membrane then easily picks up stains from the leftovers and is difficult to remove except with selective polishing. Adults who supervise a child may need to be reassured that it is just an extrinsic stain on a new erupted child's teeth.
Patients with osteopetrosis exhibit email abnormalities, suggesting that the a3 gene mutations found in V-ATPase also play a role in the development of hipopliner and hypoplastic enamel.
Dentin
The formation of dentin, known as dentinogenesis, is the first feature that can be identified at the dental development stage. Dentin formation should always occur before enamel formation. Various stages of dentin formation produce various types of dentine: dentine mantle, primary dentine, secondary dentine, and tertiary dentine.
Odontoblasts, dentin-forming cells, differentiate from dental papilla cells. They begin secreting the organic matrix around the area directly adjacent to the inner enamel epithelium, closest to the cusp tooth area in the future. The organic matrix contains collagen fibers with large diameter (0.1-0.2 m diameter). Odontoblasts begin to move toward the center of the tooth, forming an extension called the odontoblast process. Thus, the formation of dentin continues into the interior of the tooth. The odontoblast process causes the secretion of hydroxyapatite crystals and the mineralization of the matrix. This mineralized area is known as the dentine mantle and is usually a layer of about 150 m thick.
While the dentine coat is formed from the basic substance already present from the dental papilla, the primary dentine is formed through a different process. Odontoblasts increase size, eliminating the availability of extracellular resources to contribute to the organic matrix for mineralization. In addition, larger odontoblasts cause collagen to be secreted in smaller amounts, resulting in more dense heterogeneous nucleation, used for mineralization. Other substances (such as lipids, phosphoproteins, and phospholipids) are also secreted.
Secondary dentine forms after root formation is complete and occurs at a much slower rate. It does not form at a uniform level along the teeth, but it forms faster along the sections closer to the dental crown. These developments continue throughout life and contribute to smaller areas of the pulp found in older individuals. Tertiary dentine, also known as reparative dentine, is formed as a reaction to stimuli, such as dental caries or attrition.
Cementum
The cement formation is called sementogenesis and occurs late in dental development. Cementoblas is the cell responsible for cementogenesis. Two types of cementum form: cellular and aseluler.
The first aselular cementum form. The cementoblast differentiates from follicular cells, which can only reach the root surface of the tooth after Hertwig's Epithelial Root Sheath (HERS) has begun to deteriorate. The cementoblasts secrete fine collagen fibrils along the root surface at right angles before migrating away from the teeth. As the semenoblast moves, more collagen is stored to lengthen and thicken the fibers. Non-collagen proteins, such as bone sialoprotein and osteocalcin, are also secreted. The acellular factor contains the secreted protein and fiber matrix. As the mineralization progresses, the sementoblasts move away from the cementum, and the fibers remaining along the surface eventually join the formation of a periodontal ligament.
The cellular factor develops after most of the formation of teeth is completed and after the occlusion teeth (in contact) with the teeth in the opposite arch. This type of cementum is formed around the fiber bonds of the periodontal ligament. The cementoblasts form the cementum of the cell to become trapped in the cementum they produce.
The origin of formative sementoblasts is believed to be different for the cementum and cementum cementum. One of the main hypotheses today is that cells producing cementum migrate from adjacent bone regions, while cells producing acyl celtum emerge from tooth follicles. However, it is known that cellular cementum is not usually found in teeth with one root. In premolars and molar, the cellular cementum is found only in the roots closest to the apex and in the interadicular area between many roots.
Formation of periodonsium
Periodonsium, which is a tooth supporting structure, consists of cementum, periodontal ligament, gingiva, and alveolar bone. Cementum is the only one that is part of the tooth. The alveolar bone surrounds the tooth root to provide support and create what is commonly called a "socket". Periodontal ligaments connect the alveolar bone to the cementum, and the gingiva is the surrounding tissue seen in the mouth.
Periodontal ligament
The cells of the tooth follicle cause a periodontal ligament (PDL). Specific events that lead to the formation of periodontal ligaments vary between primary and permanent teeth and between different animal species. However, the formation of a periodontal ligament begins with ligament fibroblasts of the tooth follicle. This fibroblast secretes collagen, which interacts with the fibers on the surface of the bone and adjacent cementum. This interaction leads to an attachment that develops when the teeth burst into the mouth. Occlusion, which is the arrangement of teeth and how the teeth in the opposite arc are in contact with each other, continuously affecting the formation of periodontal ligaments. The creation of persistent periodontal ligaments leads to the formation of fiber groups in different orientations, such as horizontal and oblique fibers.
Alveolar bone
When the formation of roots and cementum begins, bone forms in adjacent areas. Throughout the body, the bone-forming cells are called osteoblasts. In the case of the alveolar bone, these osteoblasts are formed from the tooth follicles. Similar to the formation of the primary cementum, collagen fibers are made on the nearest surface of the tooth, and they remain there until they are attached to the periodontal ligament.
Like other bones in the human body, alveolar bone is modified throughout life. Osteoblasts create bones and osteoclasts destroy them, especially if strength is placed in the teeth. Just as when tooth movement is attempted through orthodontics using ribbons, wires, or equipment, the bone area under the compressive force of the gear that moves toward it has a high osteoclast level, resulting in bone resorption. The bone area that receives the strain from the periodontal ligament attached to the tooth that moves away from it has a high amount of osteoblasts, which results in bone formation. Thus, the teeth or teeth slowly move along the jaws so as to reach the teeth that work in harmony. In this way, the width of space between the alveoli and the root is kept almost the same.
Gingiva
The relationship between the gingiva and the tooth is called the dentogingival junction. This intersection has three types of epithelium: gingival, sulcular, and junctional epithelium. These three types are formed from the mass of epithelial cells known as cuff epithms between the teeth and the mouth.
Much about gingival formation is not fully understood, but it is known that the hemidesmosome is formed between the gingival epithelium and the teeth and is responsible for the primary epithelial attachment . Hemidesmosomes provide anchors between cells through a small filament-like structure provided by the remains of ameloblasts. After this occurs, the junctional epithelium is formed from the loss of the enamel epithelium, one of the products of the enamel organ, and divides rapidly. This results in an increasing size of the junctional epithelial layer and the isolation of ameloblast residues from nutrient sources. When the ameloblases are degenerated, the gingival sulcus is formed.
Neural and vascular formation
Often, the nerves and blood vessels run parallel to each other in the body, and the formation of both usually occurs simultaneously and in the same way. However, this is not the case for the nerves and blood vessels around the teeth, due to different developmental levels.
Neural formation
The nerve fibers begin to approach the teeth during the developmental stages of the teeth and grow toward the tooth follicle. Once there, the nerve develops around the teeth buds and enters the dental papilla when dentin formation has begun. The nerves never proliferate into the enamel organ.
Vascular Formation
The blood vessels grow in the tooth follicle and enter the tooth papillae at the close stage. Groups of blood vessels are formed at the entrance of the dental papilla. The number of blood vessels reaches its maximum at the beginning of the crown stage, and the dental papilla eventually forms in the dental pulp. Throughout life, the amount of pulp tissue in the tooth declines, meaning that the blood supply to the teeth decreases with age. The enamel organ has no blood vessels because of its epithelial origin, and the mineralized tissue of enamel and dentine does not require nutrients from the blood.
Dental eruption
Teeth eruption occurs when the teeth enter the mouth and become visible. Although researchers agree that tooth eruption is a complex process, there is little agreement on the identity of the mechanisms that control eruptions. Some general theories that have been proven to be incorrect over time include: (1) the tooth is pushed up into the mouth by the root growth of the tooth, (2) the tooth is pushed upward by the growth of the bone around the tooth, (3) the tooth is pushed up by the vascular pressure, and (4) the tooth is pushed upward by a soft hammock. The soft hammock theory, first proposed by Harry Sicher, was taught extensively from the 1930s to the 1950s. This theory postulates that the ligaments beneath the tooth, which Sicher observes under a microscope on a histologic slide, are responsible for the eruption. Then, the "ligaments" Sicher observed were determined only as artifacts created in the process of preparing the slides.
The most recently held theory is that while some forces may be involved in eruptions, periodontal ligaments provide a major boost to the process. Theorists hypothesize that the periodontal ligament promotes eruption through the shrinkage and crosslinking of their collagen fibers and their fibroblast contractions.
Although a tooth eruption occurs at different times for different people, a general eruption timeline exists. Typically, humans have 20 primary teeth (infants) and 32 permanent teeth. Dental eruption has three stages. The first, known as the stage of the deciduous tooth, occurs when only the primary teeth are visible. After the first permanent tooth erupts into the mouth, the teeth are in a mixed (or transition) tooth. After the last deciduous teeth fall out of the mouth - a process known as exfoliation - the teeth are in permanent teeth.
The primary tooth begins at the arrival of the mandibular central incisor, usually at eight months, and lasts until the first permanent molars appear in the mouth, usually at six years. The main teeth usually erupt in the following order: (1) central incisor, (2) lateral incisors, (3) first molar teeth, (4), and (5) second molar. As a general rule, four teeth erupt for every six months of life, mandibular teeth erupt before the maxillary teeth, and teeth erupt faster in women than men. During the primary tooth, permanent tooth buds are formed under the primary tooth, close to the ceiling or tongue.
Tooth mixing begins when the first permanent molars appear in the mouth, usually at six years, and last until the last primary tooth is lost, usually at the age of eleven or twelve. The permanent teeth in the maxilla erupt in a different order from the permanent teeth of the mandible. The maxillary teeth erupt in the following order: (1) first molar (2) central incisor, (3) the lateral incisor, (4) first premolar, (5) second premolar teeth, (6) canine teeth, (7) molar second, and (8) third molar. Mandibular teeth erupt in the following order: (1) first molar (2) central incisor, (3) lateral incisor teeth, (4) canine teeth, (5) first premolar, (6) second premolar teeth, (7) molar second, and (8) third molar. Since there is no premolar tooth on first teeth, the oldest molars are replaced with permanent premolars. If there are missing primary teeth before the permanent teeth are ready to replace them, some posterior teeth may drift forward and cause lost space in the mouth. This can cause crowding and/or misplacement after permanent teeth erupt, which is usually referred to as a malocclusion. Orthodontics may be required in such circumstances for an individual to achieve a set of straight teeth.
The permanent tooth begins when the last primary tooth is lost, usually at 11 to 12 years, and lasts for the rest of a person's life or until all the teeth are gone (edentulism). During this stage, the third molar (also called "wisdom tooth") is often extracted from decay, pain or impact. The main reasons for tooth loss are decay and periodontal disease.
As soon as the enamel eruption is covered by a specific film: the Nasmyth membrane or 'enamel cuticle', the embryological origin structure consists of the keratin that causes the enamel organ.
Nutrition and dental development
As with other aspects of human growth and development, nutrition has an effect on developing teeth. Essential nutrients for healthy teeth include calcium, phosphorus, and vitamins A, C, and D. Calcium and phosphorus are needed to form the right hydroxyapatite crystals, and their levels in the blood are maintained by Vitamin D. Vitamin A is necessary for the formation of keratin, C is for collagen. Fluorides, though not nutrients, are incorporated into the hydroxyapatite crystals of the developing tooth and bone. Dental theories are low levels of fluoride and fluorosis combined so lightly that teeth are more resistant to demineralization and subsequent decay.
Lack of nutrients can have various effects on the development of teeth. In situations where calcium, phosphorus, and vitamin D are deficient, hard tooth structure may be less mineralized. Vitamin A deficiency can lead to reduced enamel formation.
Fluoride ingestion has been noted to delay the eruption of teeth by a year or more from the date of eruption received since the early fluoridation experiments of the 1940s. The researchers theorize that delay is a manifestation of the effects of fluoride depression on thyroid hormone. Delayed eruptions have been suggested as the reason for the apparent differences in decay among youngest children. Swallowing fluoride during dental development can lead to a permanent condition known as fluorosis with varying degrees of severity, a result of fluoride disorder with normal osteoblast development.
Undiagnosed and untreated celiac disease often causes tooth enamel damage and may be the only manifestation of the disease, in the absence of gastrointestinal symptoms or signs of malabsorption.
Bisphenol A (BPA) is a hormone that interferes with hormones that have been implicated in negative effects on human health, including, but not limited to, the development of the fetus. As shown in studies on animals that mimic human enamel, the consumption of maternal products with BPA during pregnancy can lead to the development of discontinued teeth in children. The children proved susceptible to incisors and hypomineralization of the first molar, the weakened enamel state. In addition, it is important for mothers to avoid BPA during pregnancy, but also avoid using BPA in child products until the age of five months.
Although reason is not fully understood, high levels of cheese consumption during pregnancy can reduce the risk of childhood caries. Reducing childhood caries leads to a higher quality of life by reducing pain and discomfort.
Developmental breakdown
Anodontia is a lack of dental development, and hypodontia is lack of some tooth development. Anodontia is rare, most commonly occurring under a condition called Hypohidrotic ectodermal dysplasia, while hypodontia is one of the most common developmental disorders, affecting 3.5-8.0% of the population (excluding the third molar). The absence of a third molar is very common, occurring in 20-23% of the population, followed by the prevalence of second premolar teeth and lateral incisors. Hypodontia is often associated with the absence of dental lamina, which is susceptible to environmental forces, such as drug infection and chemotherapy, and is also associated with many syndromes, such as Down syndrome and Crouzon syndrome.
Hyperdontia is the development of foreign teeth. It occurs in 1-3% of Caucasians and is more common in Asians. About 86% of these cases involve an additional tooth in the mouth, most commonly found in the upper jaw, where the incisor is located. Hyperdontia is believed to be associated with excess lamina teeth.
Dilaceration is the abnormal curvature found in teeth, and is almost always associated with trauma that moves the developing tooth buds. When the tooth is formed, a force can move the tooth from its original position, leaving the rest of the tooth to form at an abnormal angle. A cyst or tumor adjacent to the tooth bud is a force known to cause welding, such as a primary tooth pushed up by trauma into the gingiva where it moves the teeth of a permanent dental tooth.
Hypoplastic enamel or hypomineralization is a defect in the tooth caused by a disturbance in the formation of an organic enamel matrix, clinically seen as an email defect. It may be caused by nutritional factors, some diseases (such as undiagnosed and untreated celiac disease, chickenpox, congenital syphilis), hypocalcemia, fluoride consumption, birth, premature birth, infection or trauma from deciduous teeth.
Some systemic conditions may cause delayed tooth development, such as nutritional factors, endocrine disorders (hypothyroidism, hypopituitarism, hypoparathyroidism, pseudohypoparathyroidism), undiagnosed and untreated celiac disease, anemia, prematurity, low birth weight, renal failure, heavy metal toxicity or tobacco smoke, among others.
Regional odontodisplasia is rare, but most likely in the maxillary and anterior teeth. The cause is unknown; a number of causes have been postulated, including disturbances to neural crest cells, infections, radiation therapy, and decreased vascular supply (the most widely held hypothesis). Teeth exposed to regional odontodisplasia nevAmelogenesis imperfecta is an autosomal dominant disease characterized by defects in tooth enamel formation. Teeth are often free of enamel, small, defective, and brown. The cause of this disorder is due to mutations in email expression. Dental patients with this disease should be very careful and often visit their dentist.
Christmas and neonatal teeth are anomalies involving teeth that erupt in the newborn's mouth earlier than usual. The incidence ranged from 1: 2,000 to 1: 3,500 births. Christmas teeth are more common, about three times more common than neonatal teeth. Some authors report a higher prevalence in women than men. The most common location is the mandibular area of ​​the central incisor. Christmas teeth and neonatal teeth are associated with genetics, developmental disorders and known syndromes. Additional names for this condition include premature teeth, baby teeth, and milk teeth.
See also
- Polyphyodont
- Teeth regeneration
- Development of animal teeth
References
Additional references
External links
- A database of different gene expression in the developing gear.
- Embryology at UNSW Notes/skin4a - Integumentary Dental Development, by Dr. Ir. Mark Hill
Source of the article : Wikipedia
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