Amelogenesis imperfecta: Four case reports

Department of Oral Medicine and Radiology, Karnavati Tame of Dentistry, Uvarsad, Gandhinagar, Gujarat, India

1 Subdivision of Oral Medication and Radiology, Government Dental College and Hospital, Ahmedabad, Gujarat. India

2 Part of Orthodonture, Karnavati School of Dentistry, Uvarsad, Gandhinagar, Gujarat, India

Address for symmetricalness:Dr. Dhaval N. Mehta, 23, Sunita Fellowship, Beh. C. N. Vidhyalaya, Bhuadharpur Road, Ambawadi, Ahmedabad, Gujarat, India. Email: moc.liamg@08lavahdrd

Copyright. Journal of Scrub Attainment, Biology and Medication

This is an open-access article distributed under the foothold of the Seminal Commons Attribution-Noncommercial-Share Standardized 3.0 Unported, which permits unrestricted use, scattering, and echo in any arbitrate, provided the navigate exercise is decorous cited.

Amelogenesis Imperfecta (AI) represents a pigeonholing of developmental brave, genomic in lineage, which dissemble the structure and clinical appearance of enamel of all or most all the teething in a roughly couple manner. AI is a dangerous difficulty that reduces oral health-related tone of animation and causes about physiological problems. We presented here quadruplet case reports of AI (Hypoplastic and Hypomaturation) which we diagnosed on the pedestal of hellenic clinical and radiographic features.

Keywords:Amelogenesis imperfecta. enamel hypoplasia. hypoplastic odontiasis

Foundation

Amelogenesis imperfecta (AI), a group of contagious diseases touching the enamel in either timber or measuring, is associated with cap malformation and abnormal enamel meanness.[1 ] The prevalence varies from 1:700 to 1:14 000, according to the populations studied.[2 ]

Clinical features of patients with AI bait the role of AI convoluted. AI has been classified on the innovation of clinical, radiographic, and histologic appearance of the enamel desolate and the humor of inheritance of the trait. AI has been categorized as hypoplastic (autosomal dominant/autosomal recessive/x-linked preponderating), hypocalcified (autosomal overabundant/autosomal recessive), hypomaturation types (autosomal recessive/x-linked recessive/autosomal rife) and hypoplastic-hypomaturation quality.[1 ,2 ] Hypoplastic AI represents 60 to 73% of all cases, hypomaturation AI represents 20 to 40%, and hypocalcification AI represents 7%.[3 ]

Hypoplastic mannikin of AI is characterized by slenderize enamel with yellowish-brown color, knockabout or still and shiny, square-shaped crown, insufficiency of nexus ‘between adjacent teeth, matt-up occlusal surfaces of the butt teething due to abrasion, and with/without grooves and/rowdiness. Radiographically, in hypoplastic causa, there is a charge of thin radiopaque grade of enamel with practice radiodensity. Histologically, in hypoplastic cause, defect is in enamel matrix organization.[2 ,4 ,5 ]

Hypocalcified form of AI is the close parkland type and is characterized by figure size and bod of crown, softer enamel which wears calibrate apace and can be outside by a prophylaxis pecker, and causa pigmented-dark chocolate-brown non-white. Radiographically, in hypocalcified manakin, thickness of enamel is normal but radiodensity of enamel is less than that of dentin. Histologically, in hypocalcification type, defects of matrix expression and mineralization is seen.[2 ,4 ,5 ]

Hypomaturation form of AI is characterized by expression oppressiveness of enamel but softer than normal but harder than hypocalcified type and may fling out from the cap, mottled-colored nebulous duster/yellow/brown/snow capped. Radiographically, radiodensity of enamel is standardised thereto of dentin. Histologically, in hypomaturation type, alterations in enamel rod and rod showcase structures had been notable in various studies.[2 ,4 ,5 ]

In hypoplastic-hypomaturation with taurodontism, the enamel is load, mottled yellow to brown, and faveolate. Molar odontiasis marchland taurodontism and betimes teeth ha ve enlarged pulp chambers.[1 ]

Case REPORTS

A 17-year-old male patient presented with a ill of chickenhearted smirch of his teeth since 8 to 9 age. Patient was liberal convinced floor of discolored anterior deciduous odontiasis; yet, recollection and family history was routine. Patient had permanent teething with no missing teeth. All the anterior and arse teeth were abnormal with brown blot; slice attrition toast with arse teeth. Crown of the clinical crowns of swiftness and lower ass odontiasis were reduced. In 11, 14, 21, 22, 24, 34, 42, crudeness were render. Consistence of enamel was hard. Chipping of enamel was not wassail in any teeth [ First ]. Raspberry’s-eye skiagram was taken which showed presence of a tip class of enamel with radiodensity of enamel more dentin [ Convention 2 ]. On the groundwork of clinical and radiographic features, pole diagnosis of hypoplastic AI was made.

Clinical photos showing Amelogenesis Imperfecta (Case www.coseene.net 1 – Case 4)

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