Amelogênese imperfeita (AI) é um grupo de distúrbios congênitos que envolvem a formação anormal do esmalte dentário, a camada externa da coroa dos dentes. A amelogênese imperfeita pode não estar relacionada a quaisquer condições sistêmicas ou generalizadas ou pode fazer parte de uma condição sindrômica. O esmalte saudável e totalmente formado consiste em aproximadamente 96% de mineral em peso e se forma ao longo de meses a anos em seres humanos, dependendo do dente em questão.
Introdução
O que você precisa saber de cara
Visão geral
Sinais e sintomas
As manifestações clínicas da condição incluem características orais e dentárias específicas, como hipoplasia do esmalte, fóssulas no esmalte dentário, amelogênese imperfeita, dentes cariados e descoloração amarelo-acastanhada dos dentes, além de outras anormalidades na cor dentária e hipomineralização do esmalte.[1][2]
Também são observadas alterações morfológicas e anatômicas, como microdontia generalizada, dentes amplamente espaçados, anormalidade da dentina, taurodontia, sobremordida e má oclusão de mordida aberta anterior. Há ainda o registro de anormalidade da pele associada ao quadro fenotípico.[1][2]
Causas genéticas
Diagnóstico
O diagnóstico pode ser investigado e confirmado com o auxílio de testes genéticos, existindo atualmente 11 testes genéticos catalogados para a avaliação da condição.[1][3][4]
Na base de dados ClinVar, constam 432 variantes registradas e associadas à condição, contribuindo para a interpretação molecular e identificação de mutações patogênicas.[1][3][4]
Tratamento e manejo
Tratamentos citados na literatura
Em levantamentos de mineração da literatura biomédica, são registradas menções aos seguintes compostos e substâncias: Composite Resins (1 publicação), Fluconazole (1 publicação) e phosphoric acid (1 publicação). Ressalta-se que estas citações representam unicamente associações mineradas em publicações científicas e não constituem recomendação ou prescrição de tratamento.[4]
Conteúdo informativo gerado e mantido automaticamente a partir de fontes oficiais (Orphanet, HPO, OMIM, SUS). Não substitui avaliação médica.
A **amelogênese imperfeita, tipo hipoplástica** é uma alteração genética rara que atinge a camada protetora dos dentes, fazendo com que o esmalte se desenvolva fino ou incompleto. Geralmente, a família percebe dentes menores que o esperado, pequenas depressões na superfície, coloração amarelada ou amarronzada e maior risco de cáries. O cuidado principal é odontológico, visando proteger e reconstruir a estrutura dentária para garantir a mastigação. No Brasil, esta condição não conta com um protocolo clínico (PCDT) próprio nem remédios específicos dispensados pelo SUS, sendo o suporte fornecido pela rede de saúde bucal.
Amelogênese imperfeita (AI) é um grupo de distúrbios congênitos que envolvem a formação anormal do esmalte dentário, a camada externa da coroa dos dentes. A amelogênese imperfeita pode não estar relacionada a quaisquer condições sistêmicas ou generalizadas ou pode fazer parte de uma condição sindrômica. O esmalte saudável e totalmente formado consiste em aproximadamente 96% de mineral em peso e se forma ao longo de meses a anos em seres humanos, dependendo do dente em questão.
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Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Partes do corpo afetadas
+ 4 sintomas em outras categorias
Características mais comuns
Os sintomas variam de pessoa para pessoa. Abaixo estão as 14 características clínicas mais associadas, ordenadas por frequência.
Linha do tempo da pesquisa
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Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
6 genes identificados com associação a esta condição.
Curadoria gene-doença
fontes oficiaisAmelogenesis imperfecta 1J
A form of amelogenesis imperfecta, a disorder characterized by defective enamel formation. The enamel may be hypoplastic, hypomineralized or both, and affected teeth may be discoloured, sensitive or prone to disintegration. AI1J is an autosomal recessive form characterized by hypoplastic enamel, enamel discolorization ranging from yellow to black, and normal dentin.
Amelogenesis imperfecta 1B
An autosomal dominant defect of enamel formation. Clinical manifestations may be variable. Some cases present with generalized enamel hypoplasia resulting in small, smooth, yellow and widely spaced teeth (smooth hypoplastic AI). Others show horizontal rows of pits, grooves or a hypoplastic area in the enamel (local hypoplastic AI).
Amelogenesis imperfecta 1K
A form of amelogenesis imperfecta, a disorder characterized by defective enamel formation. The enamel may be hypoplastic, hypomineralized or both, and affected teeth may be discoloured, sensitive or prone to disintegration. AI1K is an autosomal dominant form characterized by hypoplastic enamel in all teeth.
Amelogenesis imperfecta 1F
A form of amelogenesis imperfecta, a disorder characterized by defective enamel formation. The enamel may be hypoplastic, hypomineralized or both, and affected teeth may be discoloured, sensitive or prone to disintegration. AI1F is characterized by hypoplastic enamel of the primary and secondary dentition.
Amelogenesis imperfecta 1H
A disorder characterized by defective enamel formation, resulting in hypoplastic and hypomineralized tooth enamel that may be rough, pitted, and/or discolored.
Epidermolysis bullosa, junctional 1B, severe
A form of epidermolysis bullosa, a genodermatosis characterized by recurrent blistering, fragility of the skin and mucosal epithelia, and erosions caused by minor mechanical trauma. Junctional epidermolysis bullosa is characterized by blistering that occurs at the level of the lamina lucida in the skin basement membrane. JEB1B is an autosomal recessive, severe form characterized by bullous lesions appearing at birth, and extensive denudation of skin and mucous membranes that may be hemorrhagic. Death occurs usually within the first six months of life. Occasionally, children survive to teens.
Variantes genéticas (ClinVar)
432 variantes patogênicas registradas no ClinVar.
Vias biológicas (Reactome)
17 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Amelogênese imperfeita, tipo hipoplástica
Selecione um estado ou use sua localização para ver resultados.
Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Pesquisa e ensaios clínicos
Nenhum ensaio clínico registrado para esta condição.
Publicações mais relevantes
Intra-familial phenotype variant in hypoplastic amelogenesis imperfecta under a complex genetic component: a family report, whole-exome sequencing, and literature review.
Amelogenesis imperfecta (AI) encompasses a group of conditions characterized by abnormalities in the development or function of tooth enamel. Clinical manifestations include different forms and degrees of enamel frailty, associated with sensitivity, tooth fractures, stains, abnormal tooth morphology, missing teeth, etc. AI is genetically heterogeneous, with over 70 genes associated with autosomal dominant, autosomal recessive, X-linked, and oligogenic inheritance. To identify genetic variants associated with AI in a single family. We describe the clinical findings of a family affected by AI, composed of five individuals: four affected (the father and three daughters) and one unaffected (the mother). The observed segregation pattern suggests a dominant, X-linked inheritance. Genetic variants were screened using whole-exome sequencing. The initial bioinformatic analysis was conducted using Qiagen QCI, and variants were selected based on their presence in all four affected family members and absence in the unaffected mother. Search terms included "amelogenesis imperfecta," "tooth," and "enamel." Several types of software were used to classify variants according to pathogenicity. Candidate variants were identified in six genes. Three of these variants were detected in autosomal genes: NM_031889.3(ENAM):c.1726T>C (p.F576L), NM_022168.4(IFIH1):c.1764dupA, (p.A589fs*21), and NM_032383.5(HPS3):c.1897A>T (p.M633L). Three variants were detected in X-linked genes: NM_006150.5(PRICKLE3):c.8C>G (p.A3G), NM_004484.4(GPC3):c.584A>G (p.N195S), and NM_152787.5(TAB3):c.1936G>A (p.V646M). None of these variants were classified as pathogenic or likely pathogenic in AI. Among the identified genes, only ENAM has previously been associated with AI; however, IFIH1, PRICKLE3, and GPC3 are associated with dental/enamel development. The relatively high number of candidate genes and variants detected may reflect an oligogenic component already proposed for AI. This study provides a set of new candidate genes and genetic variants for AI. Despite sharing the same variants, AI-affected family members show considerable phenotypic variant, suggesting the involvement of non-shared genetic or environmental factors.
Unique Dental and Craniofacial Manifestations of Hypoplastic Amelogenesis Imperfecta in a Patient With Prune Belly Syndrome: A Rare Case Report.
Introduction: Prune belly syndrome (PBS) is a rare congenital disease characterized by hypoplastic abdominal wall muscles, urological abnormalities, and bilateral cryptorchidism. This report describes a rare case of aberrant hypoplastic amelogenesis imperfecta in a patient with PBS. Case Presentation: A 10-year-old boy with PBS presented with difficulties in speech and mastication. Oral and radiological examinations revealed aberrant hypoplastic enamel defects, mandibular hypoplasia and retrusion, maxillary constriction, and anterior open bite. Conclusion: Although dental manifestations are not frequent in PBS, rare cases may present with aberrant hypoplastic amelogenesis imperfecta.
Amelogenesis imperfecta: Analysis of the genetic basis and treatment with a digital workflow: A clinical report.
A 20-year-old woman with type I hypoplastic amelogenesis imperfecta (AI) experiencing esthetic concerns and hypersensitivity is presented. The treatment was aimed at both functional and esthetic aspects, focusing on complete mouth rehabilitation using a fully digital workflow. In an interdisciplinary approach, a multigene panel analysis was performed. Digital intraoral scans and a face scan facilitated precise virtual planning, guiding minimally invasive preparations. Long-term interim restorations milled from high-performance polycarbonate preceded definitive restorations in translucent zirconia. This approach resulted in a time- and cost-efficient treatment, helped the patient to understand her disease by highlighting the pivotal role of genetics, and demonstrated the success of collaborative dental interventions. A strict recall program will be most important for the long-term success of this patient with AI and a pathogenic frameshift variant in the AMELX gene.
Full-mouth rehabilitation with lithium disilicate ceramic crowns in hypoplastic amelogenesis imperfecta: a case report and review of literature.
Amelogenesis imperfecta (AI) is a group of genetic disorders characterized by tooth discoloration and enamel defects. Patients with AI always exhibit generalized attrition and defective tooth structure, leading to the loss of occlusal vertical dimension (OVD). Appropriate rehabilitation is challenging and essential to improve patients' aesthetics and function. This case report presents a comprehensive management of a 30-year-old woman with hypoplastic AI. A 52-month follow-up revealed satisfactory full-mouth rehabilitation performances of lithium disilicate ceramic crowns after clinical crown lengthening, with increased vertical dimension. Patients with severe hypoplastic AI require proper full-mouth rehabilitation. Using full-crown lithium disilicate restorations to increase the OVD by 2‒4 mm is a safe and predictable recommendation for such cases. In addition, patients with AI require complex and comprehensive management. The long-term effects of full-mouth rehabilitation with lithium disilicate ceramic crowns still necessitate further follow-ups.
Mini-implant assisted palate expansion and digital design in junctional epidermolysis bullosa and amelogenesis imperfecta: Case report.
Junctional epidermolysis bullosa (JEB) is one of the four major types of EB caused by genetic variants in the genes coding the proteins of the lamina lucida. All patients with this major type of EB present syndromic hypoplastic amelogenesis imperfecta (AI), with either a pits and fissures or generalized hypoplastic phenotype. Severe forms of AI are associated with compromised oral health-related quality of life (QoL) mostly due to poor dental aesthetics, dentofacial anomalies, and oral pain. To present the comprehensive dental treatment of a patient with JEB and AI from the age of 20 months until the age of 18 years, including complex orthodontics and digital oral rehabilitation. A male patient with intermediate JEB (homozygous c.3228+1G>A LAMB3 variant) has been under the care of the special care dentistry clinic of the University of Chile since the age of 20 months. His complex dental needs include structural enamel abnormalities in primary and permanent dentition (hypoplastic generalized AI), severe dental crowding with maxillary compression, Class III skeletal pattern, agenesia (#45), and gingivitis. Pediatric dental care included oral hygiene education and preventive strategies (prophylaxis and fluoride applications), maintaining the dentition free of caries. Due to AI, severe tooth sensitivity hindered proper oral hygiene and required early rehabilitation with temporary polycarbonate and metallic crowns. At the age of 16, the patient began orthodontic treatment. A maxillary expansion was performed with two consecutive mini-implant assisted rapid palate expansion (MARPE) bonded to four mini-implants in the palate. After finishing orthodontic treatment metallic multibrackets (duration 19 months), a definitive oral rehabilitation based on digital smile design with feldspathic crowns of all anterior teeth and premolars was performed. Patients with severe generalized hypoplastic syndromic AI associated with JEB benefit from long-term preventive oral care. Complex orthodontic techniques, such as MARPE, and multibrackets can be successfully. Digital smile design provides a definitive oral rehabilitation technique improving oral function, aesthetics, and QoL.
Publicações recentes
ACP4 Variants in Hypoplastic Amelogenesis Imperfecta.
Unique Dental and Craniofacial Manifestations of Hypoplastic Amelogenesis Imperfecta in a Patient With Prune Belly Syndrome: A Rare Case Report.
Intra-familial phenotype variant in hypoplastic amelogenesis imperfecta under a complex genetic component: a family report, whole-exome sequencing, and literature review.
Amelogenesis imperfecta: Analysis of the genetic basis and treatment with a digital workflow: A clinical report.
Full-mouth rehabilitation with lithium disilicate ceramic crowns in hypoplastic amelogenesis imperfecta: a case report and review of literature.
📚 EuropePMC37 artigos no totalmostrando 39
Unique Dental and Craniofacial Manifestations of Hypoplastic Amelogenesis Imperfecta in a Patient With Prune Belly Syndrome: A Rare Case Report.
Case reports in dentistryIntra-familial phenotype variant in hypoplastic amelogenesis imperfecta under a complex genetic component: a family report, whole-exome sequencing, and literature review.
Journal of applied oral science : revista FOBAmelogenesis imperfecta: Analysis of the genetic basis and treatment with a digital workflow: A clinical report.
The Journal of prosthetic dentistryFull-mouth rehabilitation with lithium disilicate ceramic crowns in hypoplastic amelogenesis imperfecta: a case report and review of literature.
BMC oral healthMini-implant assisted palate expansion and digital design in junctional epidermolysis bullosa and amelogenesis imperfecta: Case report.
Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric DentistryGingival proteomics reveals the role of TGF beta and YAP/TAZ signaling in Raine syndrome fibrosis.
Scientific reportsOverexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel.
Frontiers in physiologyRecessive COL17A1 Mutations and a Dominant LAMB3 Mutation Cause Hypoplastic Amelogenesis Imperfecta.
Journal of personalized medicineCase report: Enamel renal syndrome: a case series from sub-Saharan Africa.
Frontiers in oral healthCarbonic anhydrase II deficiency syndrome with amelogenesis imperfecta linked to a homozygous CA2 deletion.
Intractable & rare diseases researchEnamel renal syndrome: A case report with calcifications in pulp, gingivae, dental follicle and kidneys.
Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric DentistryHypoplastic amelogenesis imperfecta, bilateral nephrolithiasis and FGF-23-mediated hypophosphataemia: a triad of FAM20A-related enamel renal syndrome.
BMJ case reportsEnamel defects in Acp4R110C/R110C mice and human ACP4 mutations.
Scientific reportsEnamel and dentin in Enamel renal syndrome: A confocal Raman microscopy view.
Frontiers in physiologyFirst characterization of LTBP3 variants in two Moroccan families with hypoplastic amelogenesis imperfecta.
Archives of oral biologyThe implication of holocytochrome c synthase mutation in Korean familial hypoplastic amelogenesis imperfecta.
Clinical oral investigationsEnamel Renal Syndrome: Protocol for a Scoping Review.
JMIR research protocolsGhrelin hormone might have a potential role in amelogenesis.
International journal of clinical practiceA novel ENAM mutation causes hypoplastic amelogenesis imperfecta.
Oral diseasesA novel homozygous SLC13A5 whole-gene deletion generated by Alu/Alu-mediated rearrangement in an Iraqi family with epileptic encephalopathy.
American journal of medical genetics. Part AA Novel De Novo SP6 Mutation Causes Severe Hypoplastic Amelogenesis Imperfecta.
GenesAmelogenesis imperfecta with Class III malocclusion, reduced crown size and decreased OVD: A multi-disciplinary management and a 5-year follow-up.
Clinical case reportsHypoplastic amelogenesis imperfecta: Diagnosis approch.
La Tunisie medicaleAMBN mutations causing hypoplastic amelogenesis imperfecta and Ambn knockout-NLS-lacZ knockin mice exhibiting failed amelogenesis and Ambn tissue-specificity.
Molecular genetics & genomic medicineDental caries and hypoplastic amelogenesis imperfecta: Clinical, structural, biochemical and molecular approaches.
Microbial pathogenesisEnamel renal syndrome: A novel homozygous FAM20A founder mutation in 5 new Brazilian families.
European journal of medical geneticsCandidate gene sequencing reveals mutations causing hypoplastic amelogenesis imperfecta.
Clinical oral investigationsAn Interdisciplinary Approach for Hypoplastic Amelogenesis Imperfecta: A Case Report.
The open dentistry journalMineral features of connective dental hard tissues in hypoplastic amelogenesis imperfecta.
Oral diseasesDefects in the acid phosphatase ACPT cause recessive hypoplastic amelogenesis imperfecta.
European journal of human genetics : EJHGA novel AMELX mutation causes hypoplastic amelogenesis imperfecta.
Archives of oral biologyRecessive Mutations in ACPT, Encoding Testicular Acid Phosphatase, Cause Hypoplastic Amelogenesis Imperfecta.
American journal of human geneticsAbrogation of epithelial BMP2 and BMP4 causes Amelogenesis Imperfecta by reducing MMP20 and KLK4 expression.
Scientific reportsA rare association--amelogenesis imperfecta, platispondyly and bicytopenia: a case report.
Journal of medical case reportsMissense Mutation in Fam83H Gene in Iranian Patients with Amelogenesis Imperfecta.
Iranian journal of public healthVariability of systemic and oro-dental phenotype in two families with non-lethal Raine syndrome with FAM20C mutations.
BMC medical geneticsNovel FAM20A mutation causes autosomal recessive amelogenesis imperfecta.
Archives of oral biologyNovel ENAM and LAMB3 mutations in Chinese families with hypoplastic amelogenesis imperfecta.
PloS oneMutations in the latent TGF-beta binding protein 3 (LTBP3) gene cause brachyolmia with amelogenesis imperfecta.
Human molecular geneticsAssociações
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Doença com base genética
Um médico geneticista pode ajudar no diagnóstico de Amelogênese imperfeita, tipo hipoplástica e no aconselhamento genético da família.
Doenças relacionadas
Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico
Perguntas frequentes
O que as famílias mais perguntam sobre esta doença — cada resposta com a fonte de onde saiu
Não há cura definitiva catalogada para esta condição de origem genética. O manejo odontológico atua na proteção, prevenção de cáries e reabilitação protética dos dentes afetados.
Referências
Fontes citadas no texto, publicações do grafo e bases de dados usadas neste verbete
5 fontes citadas no texto · 6 publicações do grafo RarasNet (PubMed) · 5 bases de dados. Títulos, periódicos e PMIDs vêm direto da fonte, sem intermediação de IA.
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Citar este verbete
Raras. (2026). Amelogênese imperfeita, tipo hipoplástica. Em Raras — Enciclopédia de Doenças Raras do Brasil. https://raras.org/doenca/amelogenese-imperfeita-tipo-hipoplastica
Formato APA. Conteúdo sob CC BY 4.0 — reuso livre com atribuição.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
Amelogênese imperfeita, tipo hipoplástica
📋 Origem dos dados
Esta página agrega dados de fontes públicas e oficiais. Dados sobre cobertura no SUS (PCDT, CEAF) são verificados ativamente por agente proativo (ver badge no infobox). Demais dados têm atribuição de fonte + data da última sincronização — clique para abrir o original.
- Doença rara (ontologia)
- fonte: Orphanet
- Identificador unificado
- fonte: MONDO
- Codificação WHO/SUS
- fonte: WHO ICD-10 / DATASUS
- CID-11 (futuro)
- fonte: WHO ICD-11
- NIH/GARD
- fonte: GARD (NIH)
- Indexação biomédica
- fonte: MeSH (NLM)
- Dado público estruturado
- fonte: Wikidata