A clinically and genetically heterogeneous group of hereditary conditions characterized by malformed DENTAL ENAMEL, usually involving DENTAL ENAMEL HYPOPLASIA and/or TOOTH HYPOMINERALIZATION.
The elaboration of dental enamel by ameloblasts, beginning with its participation in the formation of the dentino-enamel junction to the production of the matrix for the enamel prisms and interprismatic substance. (Jablonski, Dictionary of Dentistry, 1992).
The proteins that are part of the dental enamel matrix.
Cylindrical epithelial cells in the innermost layer of the ENAMEL ORGAN. Their functions include contribution to the development of the dentinoenamel junction by the deposition of a layer of the matrix, thus producing the foundation for the prisms (the structural units of the DENTAL ENAMEL), and production of the matrix for the enamel prisms and interprismatic substance. (From Jablonski's Dictionary of Dentistry, 1992)
A major dental enamel-forming protein found in mammals. In humans the protein is encoded by GENES found on both the X CHROMOSOME and the Y CHROMOSOME.
A secreted matrix metalloproteinase that is the predominant proteolytic activity in the enamel matrix. The enzyme has a high specificity for dental enamel matrix protein AMELOGENIN.
A hard thin translucent layer of calcified substance which envelops and protects the dentin of the crown of the tooth. It is the hardest substance in the body and is almost entirely composed of calcium salts. Under the microscope, it is composed of thin rods (enamel prisms) held together by cementing substance, and surrounded by an enamel sheath. (From Jablonski, Dictionary of Dentistry, 1992, p286)
An acquired or hereditary condition due to deficiency in the formation of tooth enamel (AMELOGENESIS). It is usually characterized by defective, thin, or malformed DENTAL ENAMEL. Risk factors for enamel hypoplasia include gene mutations, nutritional deficiencies, diseases, and environmental factors.
The process whereby calcium salts are deposited in the dental enamel. The process is normal in the development of bones and teeth. (Boucher's Clinical Dental Terminology, 4th ed, p43)
Epithelial cells surrounding the dental papilla and differentiated into three layers: the inner enamel epithelium, consisting of ameloblasts which eventually form the enamel, and the enamel pulp and external enamel epithelium, both of which atrophy and disappear before and upon eruption of the tooth, respectively.
Any of the eight frontal teeth (four maxillary and four mandibular) having a sharp incisal edge for cutting food and a single root, which occurs in man both as a deciduous and a permanent tooth. (Jablonski, Dictionary of Dentistry, 1992, p820)
Any change in the hue, color, or translucency of a tooth due to any cause. Restorative filling materials, drugs (both topical and systemic), pulpal necrosis, or hemorrhage may be responsible. (Jablonski, Dictionary of Dentistry, 1992, p253)
One of a set of bone-like structures in the mouth used for biting and chewing.
Congenital absence of or defects in structures of the teeth.
The collective tissues from which an entire tooth is formed, including the DENTAL SAC; ENAMEL ORGAN; and DENTAL PAPILLA. (From Jablonski, Dictionary of Dentistry, 1992)
A condition in which certain opposing teeth fail to establish occlusal contact when the jaws are closed.
An amino acid-specifying codon that has been converted to a stop codon (CODON, TERMINATOR) by mutation. Its occurance is abnormal causing premature termination of protein translation and results in production of truncated and non-functional proteins. A nonsense mutation is one that converts an amino acid-specific codon to a stop codon.
Resorption of calcified dental tissue, involving demineralization due to reversal of the cation exchange and lacunar resorption by osteoclasts. There are two types: external (as a result of tooth pathology) and internal (apparently initiated by a peculiar inflammatory hyperplasia of the pulp). (From Jablonski, Dictionary of Dentistry, 1992, p676)
The most posterior teeth on either side of the jaw, totaling eight in the deciduous dentition (2 on each side, upper and lower), and usually 12 in the permanent dentition (three on each side, upper and lower). They are grinding teeth, having large crowns and broad chewing surfaces. (Jablonski, Dictionary of Dentistry, 1992, p821)
The process of TOOTH formation. It is divided into several stages including: the dental lamina stage, the bud stage, the cap stage, and the bell stage. Odontogenesis includes the production of tooth enamel (AMELOGENESIS), dentin (DENTINOGENESIS), and dental cementum (CEMENTOGENESIS).
Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC, TISSUE KALLIKREIN (EC, and PROSTATE-SPECIFIC ANTIGEN (EC
The teeth of the first dentition, which are shed and replaced by the permanent teeth.
The hard portion of the tooth surrounding the pulp, covered by enamel on the crown and cementum on the root, which is harder and denser than bone but softer than enamel, and is thus readily abraded when left unprotected. (From Jablonski, Dictionary of Dentistry, 1992)
Microscopy in which the object is examined directly by an electron beam scanning the specimen point-by-point. The image is constructed by detecting the products of specimen interactions that are projected above the plane of the sample, such as backscattered electrons. Although SCANNING TRANSMISSION ELECTRON MICROSCOPY also scans the specimen point by point with the electron beam, the image is constructed by detecting the electrons, or their interaction products that are transmitted through the sample plane, so that is a form of TRANSMISSION ELECTRON MICROSCOPY.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
Genes that influence the PHENOTYPE only in the homozygous state.

Immunohistochemical localisation of amelogenin-like proteins and type I collagen and histochemical demonstration of sulphated glycoconjugates in developing enameloid and enamel matrices of the larval urodele (Triturus pyrrhogaster) teeth. (1/128)

The presence of collagen in enameloid distinguishes it clearly from true enamel, but little is known about the phylogenetic relationship between these 2 tissues. It has previously been reported that amelogenins are the principal proteins of the enamel matrix, that type I collagen and chondroitin sulphates are the predominant matrices in dentine, and that amphibian and reptilian aprismatic enamels, contain no sulphated glycoconjugates, although certain sulphated substances are secreted into mammalian prismatic enamel during matrix formation. The larval urodele (Triturus pyrrhogaster) teeth are known to be composed of enameloid, dentine, and enamel-like tissue. To characterise the tooth matrices, the localisation of amelogenin-like proteins, type I collagen, and sulphated glycoconjugates was investigated. Chondroitin sulphates and fine fibrils immunoreactive for type I collagen were elaborated as the enameloid matrix inside the dental basement membrane. After the matrix had been deposited in full thickness, coarse collagen fibrils also immunoreactive for type I collagen and chondroitin sulphates were deposited below as the first dentine matrix. Further, enamel-like matrix with no collagen fibrils or sulphated glycoconjugates but strongly immunoreactive for amelogenins was deposited on the dentine. Although no immunolabelling for amelogenins was found over the enameloid matrix, at least at the formation stage, the zone of coarse collagen fibrils of dentine was partially immunoreactive as observed in mammalian mantle dentine. From the ontogeny and matrix constituents of larval urodele teeth, it is suggested that enameloid is originally a dentine-like tissue.  (+info)

Proteinases in developing dental enamel. (2/128)

For almost three decades, proteinases have been known to reside within developing dental enamel. However, identification and characterization of these proteinases have been slow and difficult, because they are present in very small quantities and they are difficult to purify directly from the mineralizing enamel. Enamel matrix proteins such as amelogenin, ameloblastin, and enamelin are cleaved by proteinases soon after they are secreted, and their cleavage products accumulate in the deeper, more mature enamel layers, while the full-length proteins are observed only at the surface. These results suggest that proteinases are necessary for "activating" enamel proteins so the parent proteins and their cleavage products may perform different functions. A novel matrix metalloproteinase named enamelysin (MMP-20) was recently cloned from tooth tissues and was later shown to localize primarily within the most recently formed enamel. Furthermore, recombinant porcine enamelysin was demonstrated to cleave recombinant porcine amelogenin at virtually all of the sites that have previously been described in vivo. Therefore, enamelysin is at least one enzyme that may be important during early enamel development. As enamel development progresses to the later stages, a profound decrease in the enamel protein content is observed. Proteinases have traditionally been assumed to degrade the organic matrix prior to its removal from the enamel. Recently, a novel serine proteinase named enamel matrix serine proteinase-1 (EMSP1) was cloned from enamel organ epithelia. EMSP1 localizes primarily to the early maturation stage enamel and may, therefore, be involved in the degradation of proteins prior to their removal from the maturing enamel. Other, as yet unidentified, proteinases and proteinase inhibitors are almost certainly present within the forming enamel and await discovery.  (+info)

Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis. (3/128)

tabby and downless mutant mice have apparently identical defects in teeth, hair and sweat glands. Recently, genes responsible for these spontaneous mutations have been identified. downless (Dl) encodes Edar, a novel member of the tumour necrosis factor (TNF) receptor family, containing the characteristic extracellular cysteine rich fold, a single transmembrane region and a death homology domain close to the C terminus. tabby (Ta) encodes ectodysplasin-A (Eda) a type II membrane protein of the TNF ligand family containing an internal collagen-like domain. As predicted by the similarity in adult mutant phenotype and the structure of the proteins, we demonstrate that Eda and Edar specifically interact in vitro. We have compared the expression pattern of Dl and Ta in mouse development, taking the tooth as our model system, and find that they are not expressed in adjacent cells as would have been expected. Teeth develop by a well recorded series of epithelial-mesenchymal interactions, similar to those in hair follicle and sweat gland development, the structures found to be defective in tabby and downless mice. We have analysed the downless mutant teeth in detail, and have traced the defect in cusp morphology back to initial defects in the structure of the tooth enamel knot at E13. Significantly, the defect is distinct from that of the tabby mutant. In the tabby mutant, there is a recognisable but small enamel knot, whereas in the downless mutant the knot is absent, but enamel knot cells are organised into a different shape, the enamel rope, showing altered expression of signalling factors (Shh, Fgf4, Bmp4 and Wnt10b). By adding a soluble form of Edar to tooth germs, we were able to mimic the tabby enamel knot phenotype, demonstrating the involvement of endogenous Eda in tooth development. We could not, however, reproduce the downless phenotype, suggesting the existence of yet another ligand or receptor, or of ligand-independent activation mechanisms for Edar. Changes in the structure of the enamel knot signalling centre in downless tooth germs provide functional data directly linking the enamel knot with tooth cusp morphogenesis. We also show that the Lef1 pathway, thought to be involved in these mutants, functions independently in a parallel pathway.  (+info)

Dental enamel formation and its impact on clinical dentistry. (4/128)

The nature of tooth enamel is of inherent interest to dental professionals. The current-day clinical practice of dentistry involves the prevention of enamel demineralization, the promotion of enamel remineralization, the restoration of cavitated enamel where demineralization has become irreversible, the vital bleaching of dental enamel that has become discolored, and the diagnosis and treatment of developmental enamel malformations, which can be caused by environmental or genetic factors. On a daily basis, dental health providers make diagnostic and treatment decisions that are influenced by their understanding of tooth formation. A systemic condition during tooth development, such as high fever, can produce a pattern of enamel defects in the dentition. Knowing the timing of tooth development permits estimates about the timing of the disturbance. The process of enamel maturation continues following tooth eruption, so that erupted teeth can become less susceptible to decay over time. Mutations in the genes encoding enamel proteins lead to amelogenesis imperfecta, a collection of inherited diseases having enamel malformations as the predominant phenotype. Defects in the amelogenin gene cause X-linked amelogenesis imperfecta, and genes encoding other enamel proteins are candidates for autosomal forms. Here we review our current understanding of dental enamel formation, and relate this information to clinical circumstances where this understanding may be particularly relevant.  (+info)

Possible role of heat shock protein (Hsp) 25 in the enamel organ during amelogenesis in the rat molar. (5/128)

The postnatal expression of heat shock protein (Hsp) 25 during the amelogenesis of rat molars was investigated by immunocytochemistry and confocal microscopy. The localization pattern of Hsp 25-immunoreactivity in the inner enamel epithelium and ameloblast cell layer of the rat molars was almost identical to that in the rat incisors which we have previously reported: an intense Hsp25-immunoreactivity, which first appeared in the preameloblasts, was recognized in secretory ameloblasts and ruffle-ended ameloblasts with stage-specific immunointensity. Confocal microscopy with Hsp 25-antibody and rhodamine-labeled phalloidin clearly demonstrated the co-localization of Hsp 25 and actin filaments in the ameloblast layer, supporting our hypothesis that this molecule might serve to reinforce the ameloblast layer during enamel formation as well as the formation and maintenance of the ruffled border in ruffle-ended ameloblasts. Interestingly, the enamel free area cells, which essentially lack the ability for enamel formation, showed the Hsp 25-immunoreactivity during 4-11 days when they developed a ruffled border, but decreased in that immunoreactivity after postnatal 15 days following apoptosis. Since Hsp 25 has been shown to be a specific inhibitor of apoptosis, the enamel-free area cells contribute to determine the outline of dentin at the cusped area. These data support our previous hypothesis on the diverse functions of Hsp 25 in amelogenesis.  (+info)

Phospholipids in amelogenesis and dentinogenesis. (6/128)

Phospholipids have been identified in enamel and dentin. Before demineralization, a group of phospholipids extracted by lipid solvents was associated with cell membranes and is therefore closely related to cell growth and intracellular regulations. After demineralization, a second group of phospholipids, associated with the extracellular matrix, was extracted; this group is probably linked to the mineralized phase. Using imidazole-osmium tetroxide fixation of rat incisors, we stained cellular unsaturated fatty acids, so that we could visualize the membrane domains, coated pits, and endocytic inclusions. Filipin, a probe for cholesterol, varied in density along the plasma membrane of secretory ameloblasts, and allowed us to visualize membrane remnants inside the forming enamel. With respect to phospholipids located in the extracellular matrix, the malachite-green-glutaraldehyde (MGA) method or iodoplatinate (IP) reaction retains and visualizes enamel and dentin phospholipids. In predentin, aggregates appearing as granules and filaments, or liposome-like structures, were located in the spaces between collagen fibrils. In dentin, organic envelopes coating the crystals, also named "crystal-ghost" structures, outlined groups of collagen fibrils. Histochemical data provided evidence that phospholipids are co-distributed or interact with proteoglycans. Radioautography after IP reaction established that [3H] choline was detected in dentin as early as 30 min after the intravenous injection of the labeled precursor, before any labeling was seen in odontoblasts and predentin. This suggests that blood-serum-labeled phospholipids pass between odontoblasts, cross the distal permeable junctional complex, and diffuse in dentin prior to any cellular uptake and phospholipid synthesis. Pharmacologically and genetically induced pathology also supports the suggestion that phospholipids play an important role in the formation and mineralization of dental tissues.  (+info)

Dental fluorosis: chemistry and biology. (7/128)

This review aims at discussing the pathogenesis of enamel fluorosis in relation to a putative linkage among ameloblastic activities, secreted enamel matrix proteins and multiple proteases, growing enamel crystals, and fluid composition, including calcium and fluoride ions. Fluoride is the most important caries-preventive agent in dentistry. In the last two decades, increasing fluoride exposure in various forms and vehicles is most likely the explanation for an increase in the prevalence of mild-to-moderate forms of dental fluorosis in many communities, not the least in those in which controlled water fluoridation has been established. The effects of fluoride on enamel formation causing dental fluorosis in man are cumulative, rather than requiring a specific threshold dose, depending on the total fluoride intake from all sources and the duration of fluoride exposure. Enamel mineralization is highly sensitive to free fluoride ions, which uniquely promote the hydrolysis of acidic precursors such as octacalcium phosphate and precipitation of fluoridated apatite crystals. Once fluoride is incorporated into enamel crystals, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral. In the light of evidence obtained in human and animal studies, it is now most likely that enamel hypomineralization in fluorotic teeth is due predominantly to the aberrant effects of excess fluoride on the rates at which matrix proteins break down and/or the rates at which the by-products from this degradation are withdrawn from the maturing enamel. Any interference with enamel matrix removal could yield retarding effects on the accompanying crystal growth through the maturation stages, resulting in different magnitudes of enamel porosity at the time of tooth eruption. Currently, there is no direct proof that fluoride at micromolar levels affects proliferation and differentiation of enamel organ cells. Fluoride does not seem to affect the production and secretion of enamel matrix proteins and proteases within the dose range causing dental fluorosis in man. Most likely, the fluoride uptake interferes, indirectly, with the protease activities by decreasing free Ca(2+) concentration in the mineralizing milieu. The Ca(2+)-mediated regulation of protease activities is consistent with the in situ observations that (a) enzymatic cleavages of the amelogenins take place only at slow rates through the secretory phase with the limited calcium transport and that, (b) under normal amelogenesis, the amelogenin degradation appears to be accelerated during the transitional and early maturation stages with the increased calcium transport. Since the predominant cariostatic effect of fluoride is not due to its uptake by the enamel during tooth development, it is possible to obtain extensive caries reduction without a concomitant risk of dental fluorosis. Further efforts and research are needed to settle the currently uncertain issues, e.g., the incidence, prevalence, and causes of dental or skeletal fluorosis in relation to all sources of fluoride and the appropriate dose levels and timing of fluoride exposure for prevention and control of dental fluorosis and caries.  (+info)

The structure of the rat ameloblastin gene and its expression in amelogenesis. (8/128)

Ameloblastin (also designated amelin and sheathlin) is an enamel matrix protein expressed within the ameloblast lineage. In this study we analyzed the structure of the rat ameloblastin gene and characterized its subtypes. The promoter sequence contains several E-box-like elements, and consensus sequences for AP1 and SP1. The gene is about 6 kb in length and contains 12 exons. Exon 1 was mapped by primer extension and encodes 90 bp of 5' untranslated leader sequence, followed by the coding sequences of exon 2 (309 bp), alternatively spliced exon 3a (45 bp), exon 3b (198 bp), exon 4 (36 bp), exon 5 (60 bp), exon 6 (45 bp), exon 7 (150 bp), and exon 8 (448 bp) containing coding sequence (426 bp) and 3' untranslated sequence (22 bp), followed by exon 9 (39 bp); exon 10 (143 bp); exon 11 (342 bp); and exon 12. Exon 3a, encoding YEYSLPVHPPPLPSQ, has a potential SH3 binding domain. Analysis of ameloblastin subclones showed that exon 3a and 11 were potential alternative splicing sites, producing 4 types of ameloblastin mRNA, from which ameloblastin I and II could be translated. Using in situ hybridization, immunohistochemistry, Western blot and RT-PCR methods we found that ameloblastin II, containing exon 3a, was more strongly expressed at the late maturation stage of ameloblasts than at the secretory stage, while a common probe for both ameloblastin subtypes showed wide expression throughout the presecretory, secretory and postsecretory stages. From the above results we propose that ameloblastin II plays an important role in the mineralization of ameloblasts during the maturation stages.  (+info)

1. Sensitive teeth: Teeth with AI may be sensitive to hot or cold temperatures due to the lack of enamel.
2. Tooth decay: Without adequate enamel, teeth with AI are more susceptible to decay.
3. Discolored teeth: Teeth with AI may appear grayish, yellowish, or brownish due to the defective enamel.
4. Difficulty chewing: Depending on the severity of the condition, people with AI may experience difficulty chewing or biting due to the sensitive teeth.
5. Aesthetic concerns: The discoloration and irregular shape of teeth can cause self-esteem issues and affect the overall appearance of the smile.
6. Dental problems: Teeth with AI are more prone to dental problems such as cavities, gum disease, and tooth loss.
7. Speech difficulties: In severe cases, AI can affect the development of the palate and cause speech difficulties.
8. Jaw pain: The improper alignment of teeth can lead to jaw pain and temporomandibular joint (TMJ) disorders.
9. Increased risk of oral infections: The lack of enamel can make teeth more susceptible to bacterial infections.
10. Dental anxiety: People with AI may experience dental anxiety due to the fear of undergoing dental procedures or the stigma associated with the condition.

There is no cure for AI, but various treatments can help manage the symptoms and prevent complications. These may include fluoride applications, dental fillings, crowns, and other restorative procedures to protect the teeth and improve their appearance. In some cases, orthodontic treatment or oral surgery may be necessary to correct bite problems and improve jaw alignment.

The most common symptoms of dental enamel hypoplasia are yellow or brown discoloration of the teeth, sensitivity to hot or cold foods and drinks, and an increased risk of cavities.

Treatment for dental enamel hypoplasia typically involves restorative procedures such as fillings, crowns, or veneers to repair and protect the affected teeth. In severe cases, extraction of the damaged teeth may be necessary. Preventive measures such as good oral hygiene practices, a balanced diet, and avoiding harmful substances like tobacco and excessive sugars can also help manage the condition.

Early detection and treatment of dental enamel hypoplasia are crucial to prevent further damage and improve the appearance and function of the teeth. Dentists may use specialized techniques such as radiographs and clinical examinations to diagnose this condition and recommend appropriate treatments.

There are several types of tooth discoloration, including:

1. Extrinsic stains: These are the most common type of tooth discoloration and are caused by factors such as coffee, tea, red wine, and smoking. These stains can be removed with professional cleaning and whitening treatments.
2. Intrinsic stains: These are deeper stains that occur within the tooth itself and can be caused by factors such as fluorosis, tetracycline staining, and overexposure to fluoride during childhood. These stains can be more difficult to remove and may require more advanced treatments such as porcelain veneers or teeth whitening.
3. Age-related discoloration: As we age, our teeth can become naturally more yellow due to the accumulation of calcium and other minerals on the surface of the teeth. This type of discoloration is more common in adults over the age of 40.
4. Trauma: A blow to the mouth or a injury to a tooth can cause discoloration.
5. Disease: Certain medical conditions such as bruxism, gum disease, and enamel defects can also cause tooth discoloration.

Tooth discoloration can be treated with various methods such as teeth whitening, dental bonding, porcelain veneers, and crowns. The choice of treatment depends on the severity and cause of the discoloration. It is important to consult a dentist if you notice any changes in the color of your teeth, as early diagnosis and treatment can help prevent further damage and improve the appearance of your smile.

1. Congenital abnormalities: These are present at birth and may be caused by genetic factors or environmental influences during fetal development. Examples include hypodontia (absence of one or more teeth), hyperdontia (extra teeth), or anodontia (absence of all teeth).
2. Acquired abnormalities: These can occur at any time during life, often as a result of trauma, infection, or other conditions. Examples include tooth decay, gum disease, or tooth wear and tear.
3. Developmental abnormalities: These occur during the development of teeth and may be caused by genetic factors, nutritional deficiencies, or exposure to certain medications or chemicals. Examples include enamel hypoplasia (thinning of tooth enamel) or peg-shaped teeth.
4. Structural abnormalities: These are irregularities in the shape or structure of teeth, such as anomalies in the size, shape, or position of teeth. Examples include crowded or misaligned teeth, or teeth that do not erupt properly.
5. Dental caries (tooth decay): This is a bacterial infection that causes the breakdown of tooth structure, often leading to cavities and tooth loss if left untreated.
6. Periodontal disease: This is an inflammatory condition that affects the supporting tissues of teeth, including the gums and bone, and can lead to tooth loss if left untreated.
7. Tooth wear: This refers to the wear and tear of teeth over time, often due to habits such as bruxism (teeth grinding) or acid reflux.
8. Dental anomalies: These are rare, genetic conditions that affect the development and structure of teeth, such as peg-shaped teeth or geminated teeth (two teeth fused together).

These are just a few examples of tooth abnormalities, and there are many more conditions that can affect the health and appearance of teeth. Regular dental check-ups can help detect and address any issues early on to ensure good oral health.

An open bite can lead to a range of dental problems, including:

* Tooth wear: The excessive wear on the upper and lower teeth can cause them to become weakened and sensitive.
* Gum recession: The continuous pressure on the gums can cause them to recede, exposing the roots of the teeth and increasing the risk of decay and sensitivity.
* Bone loss: The chronic open bite can lead to bone loss in the jaw, which can eventually result in a weakened jaw structure and an altered facial appearance.
* Difficulty chewing and biting food: An open bite can make it challenging to eat certain foods, leading to digestive problems and nutritional deficiencies.
* Aesthetic concerns: An open bite can also affect the appearance of the teeth and face, potentially leading to low self-esteem and confidence issues.

Treatment for an open bite usually involves a combination of orthodontic and restorative dental procedures, such as braces, Invisalign, or dental fillings to correct the alignment of the teeth and close the gap. Surgical options may also be considered in severe cases where the jaw structure needs to be realigned.

It is essential to seek professional dental care if you suspect that you have an open bite, as early treatment can help prevent more significant problems from developing and improve your overall oral health and well-being.

There are two types of tooth resorption:

1. External resorption: This type occurs when the resorption takes place on the surface of the tooth, and is usually caused by an infection or injury.
2. Internal resorption: This type occurs when the resorption takes place within the tooth structure, and can be caused by factors such as a crack or a cavity.

Symptoms of tooth resorption may include sensitivity to hot or cold foods and drinks, pain when biting down, and visible holes or pits on the surface of the tooth. Treatment options for tooth resorption depend on the severity of the condition and can range from fillings to root canal therapy or extraction.

Prevention is key in avoiding tooth resorption, by maintaining good oral hygiene practices such as brushing and flossing regularly, avoiding sugary foods and drinks, and visiting a dentist for regular check-ups. Early detection and treatment can help prevent further damage and save the tooth from being lost.

In conclusion, tooth resorption is a process where the body breaks down and reabsorbs the dentin layer of the tooth, leading to sensitivity, pain, and potentially significant damage to the tooth structure. It can be treated with various methods depending on its severity, but prevention through good oral hygiene practices and regular check-ups is key in avoiding this condition altogether.

... is the formation of enamel on teeth and begins when the crown is forming during the advanced bell stage of tooth ... Amelogenesis is considered to have three stages. The first stage is known as the inductive stage, the second is the secretory ... This is in contrast to dentin formation which occurs throughout life (secondary dentin production). Ameloblast Amelogenesis ... therefore after amelogenesis, enamel production has been finalized. ...
... as a result of abnormal enamel formation via amelogenesis. People with amelogenesis imperfecta may have teeth with abnormal ... The prevalence of amelogenesis imperfecta in non-human animals has not been explored, however its presence has been noted. This ... Amelogenesis imperfecta (AI) is a congenital disorder which presents with a rare abnormal formation of the enamel or external ... A manifestation of amelogenesis imperfecta known as "snow capping" is confined to the outer prismless enamel layer. It may ...
AmelogenesisAmelogenesis imperfecta • Amelogenin • American Academy of Cosmetic Dentistry • American Academy of ...
Amelogenesis will then follow. The cervical portion of the enamel organ then gives rise to the Hertwig Epithelial Root Sheath ( ... Furthermore, because IgG can be transported across the placenta, the amelogenesis process is disturbed from the intrauterine ... Formation of dentine (dentinogenesis) precedes enamel formation (amelogenesis). It occurs first as along the future ... Enamel mineral will increase daily (apposition growth) during the secretory stage of amelogenesis (enamel formation). ...
This protein is formed by ameloblasts during the early secretory to late maturation stages of amelogenesis. Although not ... Pandya M, Diekwisch TG (December 2021). "Amelogenesis: Transformation of a protein-mineral matrix into tooth enamel". Journal ... Mutations in AMBN cause amelogenesis imperfecta, a disease characterized by abnormal enamel formation resulting in discolored, ... April 1997). "Ameloblastin gene (AMBN) maps within the critical region for autosomal dominant amelogenesis imperfecta at ...
During tooth development there are strong similarities between keratinization and amelogenesis. Keratin is also present in ... Toto PD, O'Malley JJ, Grandel ER (1967). "Similarities of keratinization and amelogenesis". Journal of Dental Research. 46 (3 ... Enamel formation is called amelogenesis and occurs in the crown stage (advanced bell stage) of tooth development. "Reciprocal ...
FAM83H Amelogenesis imperfecta, type IB; 104500; ENAM Amelogenesis imperfecta, type IC; 204650; ENAM Amelogenesis imperfecta, ... AD5 Amelogenesis imperfecta, hypomaturation type, IIA3; 613211; WDR72 Amelogenesis imperfecta, hypomaturation-hypoplastic type ... with taurodontism; 104510; DLX3 Amelogenesis imperfecta, hypoplastic/hypomaturation type; 301200; AMELX Amelogenesis imperfecta ... type IIA1; 204700; KLK4 Amelogenesis imperfecta, type IIA2; 612529; MMP20 Aminoacylase 1 deficiency; 609924; ACY1 Amish ...
"Entrez Gene: amelogenin (amelogenesis imperfecta 1". "AceView: Gene:AMELX, a comprehensive annotation of human, mouse and worm ... Lee SK, Seymen F, Kang HY, Lee KE, Gencay K, Tuna B, Kim JW (Jan 2010). "MMP20 hemopexin domain mutation in amelogenesis ... Mutations in AMELX result in amelogenesis imperfecta. It has been shown that mice with a knocked-out AMELX gene will present ... Hart PS, Hart TC, Simmer JP, Wright JT (Apr 2002). "A nomenclature for X-linked amelogenesis imperfecta". Archives of Oral ...
Ameloblastin Amelogenin Amelogenesis Amelogenesis imperfecta GRCh38: Ensembl release 89: ENSG00000132464 - Ensembl, May 2017 ... It is one of the key proteins thought to be involved in amelogenesis (enamel development). The formation of enamel's intricate ... Mutations in the ENAM gene can cause certain subtypes of amelogenesis imperfecta (AI), a heterogenous group of heritable ... Kida M, Ariga T, Shirakawa T, Oguchi H, Sakiyama Y (November 2002). "Autosomal-dominant hypoplastic form of amelogenesis ...
Mutations in enamel ECM proteins result in enamel defects such as amelogenesis imperfecta. Type-I collagen is thought to have a ... March 2005). "ENAM Mutations in Autosomal-dominant Amelogenesis Imperfecta". Journal of Dental Research. 84 (3): 278-282. doi: ... 2003). "Relationship of phenotype and genotype in X-linked amelogenesis imperfecta". Connective Tissue Research. 44 (1): 72-78 ...
The following is a list of symptoms that this disorder causes: Amelogenesis imperfecta Biconcave vertebrae Wide ribs ... Only one of them had amelogenesis imperfecta. "OMIM Entry - 610319 - RHIZOMELIC DYSPLASIA, SCOLIOSIS, AND RETINITIS PIGMENTOSA ...
Wang X, Jung J, Liu Y, Yuan B, Lu Y, Feng JQ, Qin C (Nov 2013). "The specific role of FAM20C in amelogenesis". Journal of ...
Amelogenesis, or enamel formation, occurs after the first establishment of dentin, via cells known as ameloblasts. Human enamel ... There are 14 different types of amelogenesis imperfecta. The hypocalcification type, which is the most common, is an autosomal ...
mutations in WDR72 is thought to play a role in amelogenesis imperfecta People who suffer from amelogenesis imperfecta have ... 2010). "Ultrastructural analyses of deciduous teeth affected by hypocalcified amelogenesis imperfecta from a family with a ... 2008). "FAM83H mutations in families with autosomal-dominant hypocalcified amelogenesis imperfecta". Am. J. Hum. Genet. 82 (2 ... 2009). "Phenotypic variation in FAM83H-associated amelogenesis imperfecta". J. Dent. Res. 88 (4): 356-60. doi:10.1177/ ...
Two types of amelogenesis imperfecta (AI) have been seen in KTS patients. The first is Hypoplastic which is caused by the ... Amelogenesis Imperfecta is known to be caused by other genetic mutations. Two examples are in chromosome 4 open reading frame ... The most prominent symptom is amelogenesis imperfecta which gives the teeth a stained brown-yellow color. The enamel is thin, ... Because the tooth discoloration caused by amelogenesis imperfecta is often thought to be caused by environmental factors or ...
Mutations in AMELX can cause amelogenesis imperfecta, a disorder of tooth enamel development. Bansal, Ajay Kumar; Shetty, Devi ... They are involved in amelogenesis, the development of enamel. Amelogenins are type of extracellular matrix protein, which, ... Wright JT (December 2006). "The molecular etiologies and associated phenotypes of amelogenesis imperfecta". American Journal of ... it is known that amelogenins are abundant during amelogenesis. Developing human enamel contains about 70% protein, 90% of which ...
Amelogenesis imperfecta hypomaturation type with taurodontism are often confused. Amelogenesis imperfecta of the hypomaturation ... Amelogenesis imperfecta, an abnormal formation of the enamel or external layer of the crown of the tooth, may also be present ... The presence of this hair texture type is a defining characteristic between a diagnosis of TDO verses amelogenesis imperfecta ... There are several clinical subsets of amelogenesis imperfecta, but common to TDO is the hypoplastic-hypomaturation subtype; the ...
"Amelogenesis imperfecta in the dentition of a wild chimpanzee". ResearchGate. Retrieved 12 January 2019. Herculano‐Houzel, ...
2005). "Dentin sialoprotein and dentin phosphoprotein overexpression during amelogenesis". J. Biol. Chem. 280 (36): 31991-8. ...
The first reported case was in 2013 following whole genome sequencing of a 7-year-old girl with amelogenesis imperfecta, a ... Some mice also develop amelogenesis imperfecta, a disorder causing the teeth to develop abnormally. Integrin αvβ6 is found ... While multiple patients with Amelogenesis Imperfecta have since been found to have ITGB6 mutations, there were no other ... April 2014). "ITGB6 loss-of-function mutations cause autosomal recessive amelogenesis imperfecta". Human Molecular Genetics. 23 ...
Jalili, I K; Smith, N J (1988). "A progressive cone-rod dystrophy and amelogenesis imperfecta: A new syndrome". Journal of ... Jalili, I K; Smith, N J (1988). "A progressive cone-rod dystrophy and amelogenesis imperfecta: A new syndrome". Journal of ... Jalili syndrome is a genetic disorder characterized by the combination of cone-rod dystrophy of the retina and amelogenesis ... Jalili, I.K. Cone-rod dystrophy and amelogenesis imperfecta (Jalili syndrome): phenotypes and environs. Eye (2010) 24, 1659- ...
2009). "Mutations in the beta propeller WDR72 cause autosomal-recessive hypomaturation amelogenesis imperfecta". Am. J. Hum. ... Mutations in this gene cause autosomal-recessive hypomaturation amelogenesis imperfecta. GRCh38: Ensembl release 89: ... "Mutations in the beta propeller WDR72 cause autosomal-recessive hypomaturation amelogenesis imperfecta". Am. J. Hum. Genet. 85 ...
This protein is formed for a short time during amelogenesis. The function of tuftelins is under contention, but it is proposed ...
Towle I, Irish JD, De Groote I (April 2018). "Amelogenesis imperfecta in the dentition of a wild chimpanzee" (PDF). Journal of ... Hereditary causes of enamel hypoplasia include: Primary abnormalities in enamel development, such as amelogenesis imperfecta ...
2004). "Mutation in kallikrein 4 causes autosomal recessive hypomaturation amelogenesis imperfecta". J. Med. Genet. 41 (7): 545 ...
2005). "DLX3 mutation associated with autosomal dominant amelogenesis imperfecta with taurodontism". Am. J. Med. Genet. A. 133 ... and amelogenesis imperfecta with taurodontism. GRCh38: Ensembl release 89: ENSG00000064195 - Ensembl, May 2017 GRCm38: Ensembl ...
... in Ameloblastoma Amelogenesis imperfecta Dentin Enamel Odontoblast Tooth development List of human cell types derived ... The differentiation from preameloblasts to ameloblasts occurs during the first stage of amelogenesis, called the pre-secretory ... implications for amelogenesis and dental fluorosis". Cells. 1 (3): 631-45. doi:10.3390/cells1030631. PMC 3671616. PMID 23745169 ... 103 These stages occur during the third and final stage of amelogenesis, called the maturation phase. There are various factors ...
2006). "MMP-20 mutation in autosomal recessive pigmented hypomaturation amelogenesis imperfecta". J. Med. Genet. 42 (3): 271- ... has been associated with amelogenesis imperfecta. Enamel in the absence of MMP-20 is hypoplastic (thin), contains less mineral ...
Amelogenesis imperfecta is a rare condition that affects the formation of enamel (amelogenesis). The enamel is fragile, the ...
Normally, amelogenesis involves a period of enamel matrix formation and a rest period. In case of any disturbance, the rest ...
Amelogenesis imperfecta is a disorder of tooth development. Explore symptoms, inheritance, genetics of this condition. ... Genetic Testing Registry: Amelogenesis imperfecta, hypocalcification type *Genetic Testing Registry: Amelogenesis imperfecta ... Mutations in the AMELX, ENAM, MMP20, and FAM83H genes can cause amelogenesis imperfecta. The AMELX, ENAM, and MMP20 genes ... Other cases of amelogenesis imperfecta result from new gene mutations and occur in people with no history of the disorder in ...
Clinical aspects and treatment of amelogenesis imperfect: a case report Authors. * Bruna Mandrá da Cunha Universidade de ... Amelogenesis imperfecta, Dental enamel, Glass ionomer cements, Radiography panoramic Abstract. Objectives: This study discusses ... Amelogenesis imperfecta: the importance of early diagnosis for adolescent health and development: Case report. Rev Adolesc ... Ceyhan D, Kirzioglu Z, Emek T. A long-term clinical study on individuals with amelogenesis imperfecta. Niger J Clin Pract. 2019 ...
... compatible with hypocalcified amelogenesis imperfecta. Final considerations: changes during amelogenesis may cause disorders in ... BERALDO, Cibele Batista de Siqueira et al. Amelogenesis imperfecta: clinical case report. RFO UPF [online]. 2015, vol.20, n.1, ... Keywords : Amelogenesis Imperfecta; Dental Enamel; Diagnosis; Panoramic Radiography.. · abstract in Portuguese · text in ... Early diagnosis of Amelogenesis Imperfecta is imperative to a more conservative treatment focused on preventing the effects of ...
A Suite of Mouse Reagents for Studying Amelogenesis.. Wald, Tomas; Verma, Adya; Cooley, Victoria; Marangoni, Pauline; Cazares, ... Amelogenesis, the formation of dental enamel, is driven by specialized epithelial cells called ameloblasts, which undergo ... Our understanding of amelogenesis and developmental pathologies is rooted in past studies using epithelial Cre driver and ...
Amelogenesis imperfecta causes tooth enamel to develop irregularly. With the right care, dogs with amelogenesis imperfecta can ... Serious dental conditions like amelogenesis imperfecta can cause pain and difficulty eating for your dog. ... Amelogenesis Imperfecta. Amelogenesis imperfecta is an inherited condition in which the tooth enamel doesnt fully develop. It ... Amelogenesis imperfecta causes tooth enamel to develop irregularly. With the right care, dogs with amelogenesis imperfecta can ...
13-year-old suffering from Amelogenesis Imperfecta.. Amelogenesis Imperfecta, caused by a chromosomal defect, causes teeth to ... Composite Bonding For Amelogenesis Imperfecta. Case ID: 46271. Individual results may vary. Case Details. Published articles on ... Amelogenesis Imperfecta is a development disorder of the teeth that can present in many ways. Fourteen forms of AI have been ...
See also amelogenesis; dentinogenesis.Further Reading:Hamdan M. A., Sawair F. A., Rajab L. D., Hamdan A. M., Al-Omari I. K. ... See also amelogenesis; dentinogenesis.. Further Reading:. Hamdan M. A., Sawair F. A., Rajab L. D., Hamdan A. M., Al-Omari I. K ...
... characterized by significant short stature with brachyolmia and hypoplastic amelogenesis imperfecta (AI) with almost absent ... Amelogenesis imperfecta in two families with defined AMELX deletions in ARHGAP6.. Project description:Amelogenesis imperfecta ( ... Phenotype and Variant Spectrum in the LAMB3 Form of Amelogenesis Imperfecta.. Project description:Amelogenesis imperfecta (AI) ... LAMB3 mutations causing autosomal-dominant amelogenesis imperfecta.. Project description:Amelogenesis imperfecta (AI) can be ...
Our previous study showed that, although suffering from a severe Amelogenesis Imperfecta, the K14-cre;Bmp2f/f;Bmp4f/f mice ( ... However, when Bmp2 and Bmp4 were both inactivated by K14-cre, the mice exhibited not only the compromised amelogenesis (Xie et ... 2016). Abrogation of epithelial BMP2 and BMP4 causes amelogenesis imperfecta by reducing MMP20 and KLK4 expression. Sci. Rep. 6 ... 2015). Bmp2 deletion causes an amelogenesis imperfecta phenotype via regulating enamel gene expression. J. Cell. Physiol. 230, ...
... amelogenesis imperfecta, and dentinogenesis imperfecta. The patients medical, demographic and dietary history would aid in ...
Three basic types of amelogenesis imperfecta are recognized:. *. Hypoplastic type in which there is defective formation of ...
They are involved in amelogenesis, the development of enamel.. Is amelogenin an STR? ...
As teeth grow, they form a hard outer substance, called enamel, through a process called amelogenesis. During amelogenesis, ...
Amelogenesis imperfecta. Amelogenesis imperfecta is a genetically inherited defect of enamel that affects primary and permanent ... The earlier the diagnosis of amelogenesis imperfecta is confirmed, the better the outcome is. Optimal treatment approaches ... Intrinsic stains may be caused by trauma to a developing permanent tooth, tetracycline, fluorosis, amelogenesis and ... Diagnosis, treatment planning, and full-mouth rehabilitation in a case of amelogenesis imperfecta. Contemporary Clinical ...
Amelogenesis imperfecta. Definition. Amelogenesis imperfecta is a tooth development disorder in which the teeth are covered ... Amelogenesis imperfecta is passed down through families as a dominant trait. That means you only need to get the abnormal gene ...
Amelogenesis G7.700.320.500.325.377.750.190 G7.345.500.325.377.750.190 Aminacrine D3.494.46.250.200 D3.633.300.46.250.200 ...
Amelogenesis Imperfecta - Preferred Concept UI. M0000886. Scope note. A clinically and genetically heterogeneous group of ...
Amelogenesis imperfecta Dr. Sandeep Kaur, Dr. Kirandeep Kaur, Dr. Neha Mahajan and Dr. Abhiroop Singh ...
Anatomsko-histološke karakteristike zuba sa dijagnozom amelogenesis imperfecta  Anđelković, Katarina (Univerzitet u Beogradu, ...
Use of Dental Volumetric Tomography for Dental Phenotyping In Amelogenesis Imperfecta  Murillo Knudsen, Gina; Cob Castro, ...
Molecular strategies of tooth enamel formation are highly conserved during vertebrate evolution. - Texas A&M University (TAMU) Scholar profile, educations, publications, research, recent courses, and student works
Amelogenesis imperfecta From NCATS Genetic and Rare Diseases Information Center. * Amelogenesis imperfecta hypomaturation type ... Amelogenesis imperfecta nephrocalcinosis From NCATS Genetic and Rare Diseases Information Center. * Amelogenesis imperfecta ... Genetic testing for amelogenesis imperfecta: knowledge and attitudes of paediatric dentists. McDowall F et al. British dental ... Amelogenesis imperfecta hypoplastic/hypomaturation X-linked 1 From NCATS Genetic and Rare Diseases Information Center ...
Amelogenesis imperfecta is defined as a hereditary alteration of the enamel, which affects both dentitions, and also can cause ... Amelogenesis imperfecta refers to a group of development anomalies of the teeth (also referred as hereditary dysplasia) that ... According to study10, although amelogenesis imperfecta is a rare disease, where the formation of enamel is affected, the ... Clinical case number three, represented by the amelogenesis imperfecta, was the most difficult lesion to diagnose for group one ...
Maekawa, K., Ikeuchi, T., Shinkai, S., Hirano, H., Ryu, M., Tamaki, K., Yatani, H., Kuboki, T., Kimura-Ono, A., Kikutani, T., Suganuma, T., Ayukawa, Y., Gonda, T., Ogawa, T., Fujisawa, M., Ishigaki, S., Watanabe, Y., Kitamura, A., Taniguchi, Y., Fujiwara, Y., & 12 othersEdahiro, A., Ohara, Y., Furuya, J., Nakajima, J., Umeki, K., Igarashi, K., Horibe, Y., Kugimiya, Y., Kawai, Y., Matsumura, H., Ichikawa, T. & Ohkawa, S., Jun 1 2020, In: Geriatrics and Gerontology International. 20, 6, p. 607-614 8 p.. Research output: Contribution to journal › Article › peer-review ...
amelogenesis imperfecta type 1B. MONDO:0019507. amelogenesis imperfecta. http://identifiers.org/hgnc/3344. ENAM. HP:0000006. ...
1 Amelogenesis Imperfecta. *1 Anterior crossbite. *1 Antibiotics. *1 Antibiotics delivery/release ...
medicalkidunya. USA Board Exams Study Guide and Practice Tests ...
  • Researchers have described at least 14 forms of amelogenesis imperfecta. (medlineplus.gov)
  • The genetic basis of non-syndromic autosomal recessive forms of amelogenesis imperfecta (AI) is unknown. (omicsdi.org)
  • The panoramic radiograph showed squared-shaped crowns on incisors and low undefined cusps of molars and premolars, and a radiolucent image on crowns of all permanent teeth, including those in formation, compatible with hypocalcified amelogenesis imperfecta. (bvsalud.org)
  • Professors and students of the Dentistry course had difficulty in making treatment decisions on teeth with amelogenesis imperfecta, with mild dental fluorosis and ease on teeth with hypoplasia and dental caries. (bvsalud.org)
  • Defects in this gene are a cause of amelogenesis imperfecta type 3 (AI3). (nih.gov)
  • Witkop CJ Jr. Amelogenesis imperfecta, dentinogenesis imperfecta and dentin dysplasia revisited: problems in classification. (usp.br)
  • In recent years, a rare form of autosomal recessive brachyolmia associated with amelogenesis imperfecta (AI) has been described as a novel nosologic entity. (omicsdi.org)
  • Novel ENAM mutation responsible for autosomal recessive amelogenesis imperfecta and localised enamel defects. (omicsdi.org)
  • Here, we report on four families, three of them consanguineous, with an identical phenotype, characterized by significant short stature with brachyolmia and hypoplastic amelogenesis imperfecta (AI) with almost absent enamel. (omicsdi.org)
  • Amelogenesis imperfecta: clinical case report. (usp.br)
  • Mutations in the AMELX , ENAM , MMP20 , and FAM83H genes can cause amelogenesis imperfecta. (medlineplus.gov)
  • In most cases, males with X-linked amelogenesis imperfecta experience more severe dental abnormalities than females with this form of this condition. (medlineplus.gov)
  • Final considerations: changes during amelogenesis may cause disorders in dental enamel development, affecting enamel's quality and quantity. (bvsalud.org)
  • Amelogenesis , the formation of dental enamel , is driven by specialized epithelial cells called ameloblasts , which undergo successive stages of differentiation. (bvsalud.org)
  • Serious dental conditions like amelogenesis imperfecta can cause pain and difficulty eating for your dog. (dailypuppy.com)
  • With the right care, dogs with amelogenesis imperfecta can have strong dental health for years. (dailypuppy.com)
  • It is concluded, therefore, that the presence of respiratory problems in early childhood, can interfere in amelogenesis, providing disturbances for the formation of normal enamel, causing defects or irregularities in the surface of the dental enamel, such as hypoplasias and hypo mineralization. (bvsalud.org)
  • In genetic conditions such as amelogenesis imperfecta (AI) in which certain enamel proteins are mutated, the teeth of these children are weak and often require repeated and increasingly progressive restorations to regain partial function. (nih.gov)
  • Genetic manipulation and proteomic tools have revealed many of the major players in amelogenesis, and both animal models and cell lines have proven useful. (nih.gov)
  • Complex morphological and molecular genetic examination of amelogenesis imperfecta: a case presentation of two Czech siblings with a non-syndrome form of the disease. (nel.edu)
  • Amelogenesis imperfecta (AI) is a clinically and genetically heterogeneous group of inherited defects of enamel formation. (omicsdi.org)
  • The purpose of this Funding Opportunity Announcement (FOA) is to encourage studies aimed at developing physiologically relevant models of amelogenesis that are robust and validated so that they can advance studies of healthy and diseased human conditions involving teeth. (nih.gov)
  • Amelogenesis Imperfecta is a development disorder of the teeth that can present in many ways. (hamptondentalassociates.com)
  • Amelogenesis Imperfecta, caused by a chromosomal defect, causes teeth to be unusually small, discolored, pitted or grooved, and prone to rapid wear and breakage. (hamptondentalassociates.com)
  • Amelogenesis imperfecta is a tooth development disorder in which the teeth are covered with thin, abnormally formed enamel. (nglf.net)
  • Amelogenesis imperfecta refers to a group of development anomalies of the teeth (also referred as hereditary dysplasia) that affects the genome of the individual and is related to at least one of the stages of enamel formation, being a hereditary characteristic that affects both the deciduous as the permanent dentition. (bvsalud.org)
  • The condition may be caused by illness, injury or, in the case of amelogenesis imperfecta, genetics. (dailypuppy.com)
  • A number of different environmental factors can lead to symptoms similar to those of the genetics-caused amelogenesis imperfecta. (dailypuppy.com)
  • Early diagnosis of Amelogenesis Imperfecta is imperative to a more conservative treatment focused on preventing the effects of this pathology. (bvsalud.org)
  • A Novel Homozygous WDR72 Mutation in Two Siblings with Amelogenesis Imperfecta and Mild Short Stature. (omicsdi.org)
  • The objectives of this concept are to 1) generate new or improved models for the study of amelogenesis that accurately reflect the developmental stage or physiological process they are intended to represent, and 2) validate those models to ensure they are robust and reproducible. (nih.gov)
  • Our understanding of amelogenesis and developmental pathologies is rooted in past studies using epithelial Cre driver and knockout alleles . (bvsalud.org)
  • Amelogenesis imperfecta can have different inheritance patterns depending on the gene that is altered. (medlineplus.gov)
  • Amelogenesis imperfecta is a disorder of tooth development. (medlineplus.gov)
  • Other cases of amelogenesis imperfecta result from new gene mutations and occur in people with no history of the disorder in their family. (medlineplus.gov)
  • When Do Symptoms of Amelogenesis imperfecta Begin? (nih.gov)
  • Additionally, amelogenesis imperfecta can occur alone without any other signs and symptoms or it can occur as part of a syndrome that affects multiple parts of the body. (medlineplus.gov)
  • Objectives: This study discusses the clinical characteristics of a case of type IIA amelogenesis imperfecta (hypomatured with diffuse pigmentation), presenting the treatment methods and how this condition affects the patient's quality of life. (usp.br)
  • Trentesaux T, Rousset MM, Dehaynin E, Laumaillé M, Delfosse C. 15-year follow-up of a case of amelogenesis imperfecta: importance of psychological aspect and impact on quality of life. (usp.br)
  • If there is any change in the initiation anomalies of structure (imperfect amelogenesis) can occur5. (bvsalud.org)
  • The objectives of this FOA are two-fold: 1) generate new and improved models that closely mimic physiological enamel development and maturation to enable studies of amelogenesis, and 2) validate those models to ensure they are robust and accurately reflect human physiology and pathology. (nih.gov)
  • They are involved in amelogenesis, the development of enamel. (david-cook.org)
  • Enamel formation occurs through the process of amelogenesis, during which ameloblast cells form and secrete the extracellular matrix which eventually matures into the outer hydroxyapatite layer of the tooth. (nih.gov)
  • The rodent with its continuously erupting incisor has been a model organism for the study of the continuum of amelogenesis where all the enamel formation stages are visible at once. (nih.gov)
  • Amelogenesis imperfecta (AI) is an overarching term for a group of rare inherited disorders of hard tooth tissues. (nel.edu)
  • Amelogenesis imperfecta: clinical aspects and treatment. (usp.br)
  • 17. N6-methyladenosine (m6A) RNA methylation mediated by methyltransferase complex subunit WTAP regulates amelogenesis. (nih.gov)
  • About 5 percent of amelogenesis imperfecta cases are caused by mutations in the AMELX gene and are inherited in an X-linked pattern. (medlineplus.gov)