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Amelogenesis imperfecta, hypoplastic type - Dr Sanjana Ravindra
(1) The document discusses amelogenesis imperfecta (AI), which refers to hereditary defects in enamel formation. It describes several classifications of AI based on clinical, radiographic, and histological findings. (2) The main types are hypoplastic (reduced enamel), hypocalcified (soft enamel), and hypomaturation (improperly formed enamel). Clinical features, inheritance patterns, and prevalence are provided for each type. (3) The case report describes a 26-year-old female patient diagnosed with hypoplastic AI based on yellow-brown tooth discoloration and decreased vertical dimension. She was treated with periodontal therapy and full-mouth fixed bridges.
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Amelogenesis imperfecta, hypoplastic type - Dr Sanjana Ravindra
- 1. GOODMORNIN G Dr Sanjana Ravindra Postgraduate Student Oral Medicine and Radiology
- 2. Amelogenesis Imperfecta, HypoplasticType Associated with Some Dental Abnormalities: A Case Report Canger EM, Celenk P, Yenísey M, Odyakmaz SZ. Braz Dent J (2010) 21(2): 170-174. JOURNAL CLUB: 3
- 3. Introduction DEVELOPMENTAL DISTURBANCES an abnormality wherethe pathology starts in the embryonic stage of human life , before the formation of the dentition Orban’s Oral Histology and Embryology, 12th editio
- 4. Introduction DEVELOPMENTAL TOOTH ANOMALIES SIZE • Microdontia •Macrodontia NUMBER • Anodontia • Supernumerary teeth • Pre-deciduous dentition STRUCTURE • AMELOGENESIS IMPERFECTA • Dentinogenesis imperfecta • Dentin dysplasia • Regional odontodysplasia • Dentin hypocalcification SHAPE • Gemination • Twinning • Fusion • Concrescence • Talon cusp • Dilaceration • Dens in dente • Dens evaginatus • Enamel pearl • Globodontia • Mulberry molar • Moon’s molar • Hutchinson incisor • Carabelli cusp • Shovel shaped incisor
- 5. encompasses a complicated group ofconditions that demonstrate developmental alterations in the structure of the enamel in the absence of a systemic disorder. AMELOGENESIS IMPERFECTA AMELOGENES IS ?IMPERFECT A Hereditary enamel dysplasia Hereditary brown enamel Hereditary brown opalescent teeth Shafer’s textbook of Oral Pathology. 6th ed. Elsevier; 2009 www.merriam-webster.comIntroduction
- 6. Case report Canger EM,Celenk P, Yenísey M, Odyakmaz SZ. Amelogenesis Imperfecta, Hypoplastic Type, Associated with Some Dental Abnormalities: A Case Report: Braz Dent J (2010) 21(2): 170-174.
- 7. Case reportBIODATA A 26-year-old female CHIEFCOMPLAINT discoloredteeth MEDICALHISTORY noncontributory. FAMILY HISTORY None had similar problem
- 8. GINGIVA Hyperemic and edematousgingiva. No gingival enlargement ORAL HYGIENE Poor Clinical crown length Adequate Case report
- 9. 17 16 5514 13 52 11 21 22 24 25 26 46 85 44 83 42 41 31 32 73 44 75 36 Clinically short Yellow-brown coloured Loss of contact • CROWNS Decreased – vertical dimension Case report
- 10.
- 11. Periodontal therapy Oral hygieneinstructions, scaling, and root planning. Prosthodontic rehabilitation Full-mouth metal reinforced porcelain fixed bridge restoration Advised and motivated for maintenance of proper oral hygiene & Repeated follow ups 2 WEEKS - NORMAL GINGIVA VERTICAL DIMENSION NORMAL ESTHETIC OR FUNCTIONAL PROBLEMS Case report
- 13.
- 14. Introduction Tooth enamelconsists mainly of inorganic material (96%) and oraganic substance and water(4%) Physical properties and physiological function of enamel – directly related to composition, orientation, disposition and morphology of mineral components within tissue During organogenesis, enamel transitions from soft to pliable tissue to its final form- is devoid of protein Final composition is reflection of unique molecular and cellular activities that take place during its genesis Deviation from this pattern lead – AMELOGENESIS IMPERFECTA
- 15. SYNONYMS Hereditary enamel dysplasia Hereditary brown enamel Hereditary brown opalescent teeth
- 16. “AI encompassesa complicated group of conditions that demonstrate developmental alterations in structure of the enamel in the absence of a systemic disorder” “AI represents a group of conditions, genomic in origin, which affect the structure and clinical appearance of the enamel of all or nearly all the teeth in a more or less equal manner, and which may be associated with morphologic or biochemical changes elsewhere in the body” Orphanet Journal of Rare Diseases 2007, 2:17 Definition
- 17. Historical background Spokes in1890, described "brown teeth" with a familial history. In 1907 Turner described some cases of hereditary hypoplasia of teeth in five generations of same family Weinmann & associates in 1945 – introduced term “AMELOGENESIS IMPERFECTA” – it is an ectodermal disturbance, mesodermal components are normal
- 18. ETIOLOGY Dental enamelis a highly mineralised tissue Derived through the synthesis and secretion of proteins Formation of this highly organised and unusual structure is controlled in ameloblasts through interaction of a number of organic matrix molecules
- 19. Development of normalenamel occurs in three stages 1. Formative stage – deposition of organic matrix – Hypoplastic AI 2. Calcification stage – matrix is mineralized –Hypocalcified AI 3. Maturation stage – crystallites enlarge and mature – Hypomaturative AI ETIOLOGY
- 20. Genes and phenotypes Proteins/enzymes forming enamel Type of AI Inheritance 1 Amelogenin Diffuse smooth hypoplastic & hypomaturation X linked 2 Ameloblastin Hypocalcified AD 3 Enamelin Hypoplastic AD, AR 4 Tuftelin hypoplastic AD,AR 5 Kallikrein Hypomaturation AR 6 Matrix metalloproteinase Pigmented hypomaturation AR
- 21. Modes of MendelianInheritance Associated with AI https://www.google.co.in/search?q+phenotype
- 22. CLASSIFICATION Sekar B, DominicAugustine, Murali S. Amelogenesis Imperfecta - A Case Report with Genetic Transmission. IJDA, 2(4), October- December, 2010 395.
- 23.
- 24. BASED ON CLINICAL,MICRORADIOGRAPHIC AND HISTOPATHOLOGICAL FINDINGS BY Darling (1956) Hypoplastic Group 1 – gen pitting Group 2- vertical grooves Group 3- gen hypoplasia Hypocalcified Type 4A- chalky, yellow, brown enamel Type 4B- marked enamel discolouration 7 softness with post eruptive loss of enamel Type 5- gen/ localized discolouration and chipping of enamel
- 25. By Witkop (1957) Hypoplastic Hypocalcification Hypomaturation Pigmented hypomaturation Local hypoplasia
- 26. By Schulze (1970) Type 1hypoplastic Specific features , inheritance 1A Hypoplastic, pitted AD 1B Hypoplastic, local AD 1C Hypoplastic, local AR 1D Hypoplastic, smooth AD 1E Hypoplastic, smooth x-linked D 1F Hypoplastic, rough AD Typw 2 hypomaturation 2A hypomaturation 2B hypomaturation 2C Snow capped teeth, x linked 2D AD Type 3 hypocalcification 3A AD 3B AR Type 4 Hypomaturation- hypoplastic with taurodontismType 4A Hypomaturation- hypoplastic with taurodontism AD Type 4B Hypoplastic- hypomaturation with taurodontism AD Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;200
- 27. Prevalence range from1 in 718 to 1 in 14,000, depending on the population studied. Hypoplastic AI represents 60 – 73% of all cases, Hypomaturation AI represents 20 – 40%, and Hypocalcification AI represents 7% Prevalence
- 28.
- 29.
- 30. Hypoplastic type –autosomal dominant GENERALIZED PITTED • Thin enamel • Open contact • Pinpoint to pinhead pits • Newly erupted teeth: hard with normal yellow-white colour • Staining of teeth- exposure to oral environment- black appearance LOCALIZED PITTED • Linear depression/ large area of hypoplasia • Prominent on buccal surface DIFFUSE SMOOTH • Thin, glossy with smooth surface • ¼ to 1/8 of normal thickness • Yellow color – opaque to translucent brown • Delayed eruption with alveolar resorption DIFFUSE ROUGH Hard with rough granular surface White to yellowish white Thicker enamel at cervical areas https://www.google.co.in/search?q=amelogenesis+hypoplas
- 31. Localized pitted Severe form ofAD Enamel agenesis Yellow colour like normal dentition Surface is rough & granular- ground glass Complete lack of enamel formation Multiple missing teeth https://www.google.co.in/search?q=amelogenesis+hypoplastic Hypoplastic type – autosomal recessive
- 32. Males – Thin, hard,glossy – Like crown preparations, open bite – Opaque white to brown Females – Alternating vertical bands of normal and abnormal enamel https://www.google.co.in/search?q=amelogenesis+hypoplastic Hypoplastic type – x-linked dominant
- 33. Hypoplastic amelogenesis imperfecta, genpitted pattern . Note the numerous pinpoint pits scattered across the surface of the teeth. The enamel between the pits is of normal thickness. hardness. and coloration. Hypoplastic amelogenesis imperfecta, autosomal dominant smooth pattern. Small. yellowish teeth exhibiting hard, glossy enamel with open contact Points and anterior open bite. Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89
- 34.
- 35. Thickness of enamel Normal-hypoplasia( middle 3rd of labial surface) Consistency of enamel Soft – lost after eruption- scrapped with instrument Colour of enamel Newly erupted teeth- dull lustreless opaque, white, honey coloured or yellowish orange or brown Significance : Exposed dentin- hypersensitive anterior opn bite Rapid calculus formation Hypocalcified type – aD & AR Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89
- 36. Dentition exhibiting diffuse yellow-browndiscoloration . Note numerous teeth with loss of coronal enamel except for the cervical portion. Hypocalcified type – aD & AR Extensive loss of coronal enamel and the similar density of enamel and dentin. Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89
- 37. Autosomal dominant Xlinked recessiveAutosomal recessive Hypomaturative type
- 38. Commonly in males Bothin primary and permanent dentition Primary teeth: ground glass opaque white appearance Permanent teeth :mottled yellow white, may be darkened with absorption of stains Tight contact point Enamel approaches normal thickness. Point of explorer can be forced into enamel Hypomaturative type – autosomal dominant
- 39. Both in primaryand permanent dentition Enamel has milky to shiny, agar brown deeply stained on contact with exogenous agents Normal thickness. Chips away around restoration Forms large amount of calculus which may contain pigment forming agents Teeth may resorb within alveolus https://www.google.co.in/search?q=amelogenesis+hypomaturativ Hypomaturative type – autosomal recessive
- 40. Snow capped Zone of white opaque enamel on incisal and occlusal surface (1/4 to 1/3 of the surface) Looks like fluorosis Anteriors, premolars/molars Both dentitions https://www.google.co.in/search?q=snow+capped Hypomaturative type – x linked recessive
- 41. Predominant defect– enamel hypomaturation Enamel appears – mottled yellow-white to yellow brown Pits are seen frequently on buccal surface of teeth Radiographically – enamel appears similar to dentin Large pulp chambers may be seen in single rooted teeth in addition to varying degrees of taurodontism Hypomaturation- hypoplastic with taurodontism – Autosomal dominant https://www.google.co.in/search?q=amelogenesis+hypomatu+tauro
- 42. Predominant defect –enamel hypoplasia in which enamel is thin but also hypomature Radiographically- Similar to hypomaturation-hypoplastic variant, except decrease in thickness of enamel https://www.google.co.in/search?q=amelogenesis+hypomatu+tauro Hypoplastic - hypomaturation with taurodontism – Autosomal dominant
- 43. Radiographic features Squarish typeof crown being devoid of the normal mesial and distal contours Normal enamel cap is missing and in its place a thin and opaque layer of enamel Low or absent cusps, with serrations of varying sharpness Lack of contrast between enamel and dentin Obliteration of pulp chamber Loss of contour Enamel Pulp chamber https://www.google.co.in/search?q=amelogenesis+tauro
- 44. TYPE CLINICAL APPEARANCE ENAMEL THICKNESS HYPOPLASTIC (TYPE I) Crownssize : small to normal, lack proxmal contacts, color varies from normal to opaque white – yellow brown Varies from thin and smooth to normal thickness with grooves, furrows and/or pits HYPOMATURATIO N (TYPE II) Varies from creamy opaque to marked yellow/brown, surface of teeth soft and rough, dental sensitivity and open bite common Normal thickness with enamel that often chips and abrades easily around restoration HYPOCALCIFIE D (TYPE III) Opaque white to yellow-brown, soft rough enamel surface, dental sensitivity and open bite common, heavy calculus formation common Normal thickness with enamel that often chips and abrades easily HYPOMATURATIO N/ HYPOPLASIA/ TAURODONTISM (TYPE IV) White/Yellow- Brown mottled, teeth can appear small and lack proximal contact Reduced, hypomineralized areas and pits RADIOGRAPHIC APPEARANCE INHERITANCE Enamel has normal to slightly reduced contrast/ thin Autosomal dominant, recessive, or X- linked Enamel has contrast similar to or > than dentin, unerupted crowns have normal morphology Autosomal dominant, recessive, or X- linked Enamel has contrast similar to or < dentin, unerupted crowns have normal morphology Autosomal dominant, recessive Enamel contrast normal to slightly > dentin, large pulp chambers Autosomal dominant Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89
- 45. Histopathological examination Verythin enamel, voids within enamel & composed of laminations of irregularly arranged enamel prisms Enamel-dentin junction, show some exaggerated scalloping. Areas of homogeneous aprismatic enamel or fused indistinct prisms, with “a reduction in distance between enamel rod incremental lines” https://www.google.co.in/search?q=amelogenesis+slides
- 46. Syndromes associated Amelogenesi simperfect with taurodontism Trichodentoo sseous syndrome Tricho-dento-osseous syndrome. Dentition exhibiting diffuse enamel hypop lasia and hypomaturat ion. At birth, the patient exhibit kinky "steel wool" hair texture with time, the hair gets straightened. Taurodontism of the first molar and the enamel. which is thin and similar in density to the dentin. Neville BW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89
- 47. Cone rod dystrophy Kohlschutter-Tonzsyndrome Usher syndrome Other syndromes
- 48. Non enamel anomaliesseen in Amelogenesis Imperfecta Delayed tooth eruption Congenitally missing teeth Anterior open bite Taurodontism Pulpal calcification Root and crown resorption Hypercementosis Root malformations Malocclusion Gingivitis
- 49. Diagnosis Clinical diagnosis Cheesy consistencyof enamel with loss of enamel Radiographic diagnosis Missing enamel cap with low or absent cusp
- 50. Differential diagnosis Dental fluorosisDentinogenesis imperfecta
- 51.
- 52. Reason for choosingthis article Developmental disorder presents with severe dental anomalies. Its important to diagnose the condition as early as possible to balance the decision for early intervention and long-term survival of the restorations. Also consider the social implications for these patients and intervene to relieve their suffering. Thus, this article is an attempt to improve the clinician’s knowledge about the clinical & radiographic diagnosis as well as intervention required for such a condition.
- 53.
- 54. 1. www.merriam-webster.com 2. NevilleBW, Douglass DD, Allen CM, Bouquot JE. Abnormalities of teeth. In: Oral and Maxillofacial Pathology. 2nd ed.. Pennsylvania:Elsevier;2004. 89-94. 3. Regezi J, Sciubba JJ. Oral Pathology- Clinical Pathologic Correlations. 3rd ed. WB Saunders Company; 1999. 4. Rajendran R, Sivapathasundaram. Shafer’s textbook of Oral Pathology. 6th ed. India: Elsevier; 2009. 5. Kumar GS. Orban’s Oral histology and embryology. 12th ed. Elsevier; 2009. 6. White SC, Pharaoh MJ editors. Normal Radiographic Anatomy. In: Oral Radiology- Principles and Interpretation 5th edition. St.Louis (US): Mosby/Elsevier; 2004. 7. Bailleul-Forestier I, Molla M, Verloes A, Berdal A. The genetic basis of inherited anomalies of the teeth. Part 1: clinical and molecular aspects of non-syndromic dental disorders. Eur J Med Genet 2008;51:273-291. 8. Mehta DN, Shah J, Thakkar B. Amelogenesis imperfecta: Four case reports. J Nat Sc Biol Med 2013;4:462- 5. 9. Seow WK. Dental development in amelogenesis imperfecta: a controlled study. Pediatr Dent 1995;17:26-30. 10. Gökçe K, Canpolat C, Özel E. Restoring function and esthetics in a patient with amelogenesis imperfecta: a case report. J Contemp Dent Pract 2007;8:90-101. 11. Siadat H, Alikashi M, Mirfazaelian A. Rehabilitation of a patient with amelogenesis imperfect using all- ceramic crowns: a clinical report. J Prosthet Dent 2007;98:85-88. 12. Toksavul S, Ulusoy M, Türkün M, Kümbüloğlu Ö. Amelogenesis imperfecta: the multidisciplinary approach: a case report. Quintessence Int 2004;35:11-14.
- 55. 13. Santos MCLG,Line SRP. The genetics of amelogenesis imperfecta: a review of the literature. J Appl Oral Sci 2005;13:212-217. 14. Begum N, Bhandarkar GP, Kini R, Naik V, Rashmi K, D Souza LC. Amelogenesis Imperfecta: A Series of Case Report.Int J Adv Health Sci 2015;2(1):17-21. 15. Crawford PJM, Aldred M, Bloch-Zupan A. Amelogenesis imperfecta. Orphanet J Rare Dis 2007;2:17-27. 16. Poulsen S, Gjqrup H, Haubek D, Haukali G, Hintze H, Lqvschall H, et al.. Amelogenesis imperfecta - a systematic literature review of associated dental and oro-facial abnormalities and their impact on patients. Acta Odontol Scand 2008;66:193-199. 17. Nigam P, Singh VP, Prasad KD, Tak J. Amelogenesis Imperfecta: A Case Report and Review of Literature. Int J Sci Stud 2015;2(10):146-149. 18. Jan C.-C. Hu Yong-Hee P, Hazzazzi AC, Simmer JP. Enamel Formation and Amelogenesis Imperfecta. Cells Tissues Organs 2007;186:78–85. 19. Sunil RP, Agarwal A. Hypoplastic amelogenesis imperfecta. Journal of Dental Sciences & Oral Rehabilitation. 2008. 20. Chhaparwal Y, Jhawar A, Lele A, Rathi S. Case Report on hypoplastic amelogenesis imperfecta with multiple impacted teeth. Journal of Dental and Medical Sciences. 2279-0861.Volume 13, Issue 5 Ver. V. (May. 2014), PP 79-82. 21. Chengappa, Murali.R, Sivagami.N. Rehabilitation of Mutilated Natural Dentition associated with Amelogenesis Imperfecta – A Case Report. INT J OF DENTAL CLINICS 2010:2(4): 77-79. 22. Sekar B, Dominic Augustine, Murali S. Amelogenesis Imperfecta - A Case Report with Genetic Transmission. IJDA, 2(4), October-December, 2010 395.
Editor's Notes
- #4 The Primary & Permanent Dentition are subject to considerable variation in the number , Size & Form of teeth and the structure of the dental tissues
- #5 is a hereditary disorder that expresses a group of conditions that cause developmental alterations in the structure of enamel.
- #8 A 26-year-old female patient presented with a chief complaint of discolored teeth. Medical history was noncontributory. Extraoral examination did not reveal any relevant findings. No other family member had the same dental problem.
- #9 The patient’s oral hygiene was poor and she presented hyperemic and edematous gingiva. Bleeding on probing scores of the teeth was determined as one. There was no gingival enlargement around the teeth, so the clinical crown lengths were adequate.
- #10 Twenty-three teeth were erupted. Six of them were primary teeth and 17 were permanent teeth. Tooth crowns were clinically short and featured yellow-brown colored surfaces. Tissue loss affected all teeth. There was loss of contact between the teeth. Vertical dimension of the face was also decreased. There was no anterior open bite
- #11 Panoramic radiograph of the patient revealing the presence of 6 over-retained primary teeth and 15 totally impacted permanent teeth (18, 17, 15, 23, 27, 28, 38, 37, 35, 33, 43, 44, 45, 47, 48). Pulpal calcifications are seen in all teeth congenital absence of maxillary right lateral tooth is clearly visible. B = Full-mouth periapical radiographs of the maxilla and mandible. The density of dentin is not differentiated from enamel. The loss of contact between the teeth can be easily detected. the enamel layers of all teeth giving an appearance similar to that observe after mechanical preparation. Pulp chambers had normal size and shape except for 26 There were stones in the crown pulps and the radicular pulps were obliterated. In addition, external resorption was noted on the crowns of both impacted 2nd permanent molars. The lamina duras were normal. The crowns of mandibular left central incisors and lateral incisors became close to each other and the roots were separated from each other
- #12 The initial stage periodontal therapy consisted of oral hygiene instructions, scaling, and root planning. Two weeks later, the gingival edema was resolved and hyperemic appearance of gingiva turned to normal. Also bleeding on probing was normal. After radiographic examination of crown/root ratio, root number and morphology of the present teeth, construction of full-mouth metal reinforced porcelain fixed bridge restoration was planned. The occlusal vertical dimension was 3 mm lower than normal. First of all, a splint, made of self cured hard acrylic, was constructed to increase the vertical dimension. The adaptation of the temporomandibular joints and masticatory muscles was carefully observed periodically during 4 months and, after this period, the patient tolerated well her new vertical dimension. The supporting teeth were prepared 1 mm axially, occlusally and incisally to provide sufficient space for denture (Fig. 3a). Impressions were obtained by putty and light viscosity of addition silicon material (Elite putty & Light; Zhermack, Rovigo, Italy). After metal framework and porcelain trail stage, and the glasure stage, fixed partial dentures were cemented with polycarboxilate cement (Adhesor Carbofine; Spofa Dental, Hungary) (Fig. 4). The patient received instructions on cleansing of the subpontic and interproximal areas, and was re-examined after 1 week. Follow-up visits were scheduled at 3 months and then at 6 months. No esthetic or functional problems were seen after the follow
- #13 Intraoral clinical appearance after the completion of the restorative treatment. A = View of completed maxillary restorations. B = View of completed mandibular restorations. C = Post-treatment view of the teeth in maximum intercuspation.
- #15 Hereditary dental anomaly- deciduous & permanent dentition
- #19 AI is caused by mutations in genes that control amelogenesis and follows inheritance patterns of autosomal-dominant, autosomal recessive or X- linked modes of transmission.3 - 5, 8, 12, 14 There are also patients for whom a family history cannot be identified but where a mutation is present. 2, 5, 6, 8, 12, 13 The inheritance pattern of X-linked disorders dictates that male to male transmission cannot occur. Conversely, all female offsprings of the affected male must be affected. Affected females have a 50% of passing on the trait to the offspring of either sex. 1, 9 Mutations in the amelogenin gene (AMELX) cause X-linked amelogenesis imperfecta, while mutations in the enamelin gene (ENAM) cause autosomal-inherited forms of amelogenesis imperfecta. Recent reports involve kallikrein-4 (KLK4), MMP-20 and DLX3 genes in the etiologies of some cases.
- #20 The format ion of enamel is a mul tistep process, and problems may ar ise in anyone of the steps . In general. the development of enamel can be divided into three maj or stages:
- #22 A phenotype (from Greek phainein, meaning "to show", and typos, meaning "type") is the composite of an organism's observable characteristics or traits, such as its morphology, development, biochemical or physiological propertie and behavior
- #29 Other dental features associated with AI include quantitative and qualitative enamel deficiency, pulpal calcifications, taurodontism and root malformations, impaction of permanent teeth, progressive root and crown resorption, congenitally missing teeth and anterior and posterior open bite occlusion.3
- #30 Inadequate deposition of enamel matrix
- #32 As the name implies. enamel agenesis demonstrates A total lack of enamel formation
- #35 Enamel matrix is formed normally but without significant mineralization
- #38 Defect in maturation of enamel crystal structure
- #45 Radiographic characteristics- reduced contrast between enamel and dentine
- #46 Histopathological view showing no enamel at the incisal edge area The histopathologic alterations present in amelogenesis imperfec ta are not evident in routine prepa ration s. Because decalci ficati on of the teeth is necessar y before processing to allow sectioning of paraffin -embedded specimens. all the enamel is lost. To examine the enamel structu re of altered teeth, grou nd sections of nondecalcilied specimens are prepared. The alte rat ions discovered are highly diverse and vary with each cli nical ty pe of amelogenesis imperfecta
- #47 Some authors suggest that hypomaturation-hypoplastic amelogenesis imperfccta may represent par tia l expression of the trlcho-d cnto-o sseous syndrome. More recently, the genemutatio n respo nsib le for trlcho-dentoosseous syndrome has been isolated and shown not to be present in cases of hypomaturation-hypoplastic amelogenesis irnperfecta . If only dental changes are seen in the absence of hair or bone cha nges, either in the in dividual or wit hin the family, the diag nosis of amelogenesis lmperfecta appears appropriate.
- #48 AR occurance of hypoplastic/hypomineralized AI ocular symptoms include photophobia, reduced central vision with a gradual loss of night vision Cns degenerative disorder with convulsions dementia epilepsy characteristic yellow teeth that are consistent with hypocalcified AI Genetically inherited disorder characterized by progressive hearing loss n retinitis pigmentation also reported to of having thin enamel that resemble hypoplastic AI
- #51 DF:occurs due to excessive intake of fluoride during formative stafe. history of exposure, does not chip off, no open contact gingiva normal DI: color may vary from blue to brownish violet to yellowish brown Scalloping at DEJ is absent. shape and size of crown and root are relatively normal density , obliteration of pulp chamber presence of periapical radiolucency without pulpal involvement
- #52 Gingival Health Management in AI Treatment of Dental Malocclusions Depends on severity; Problems include aesthetics, sensitivity, vertical dimension, caries, open bite, delayed eruption and impaction Where enamel is very thin, full coverage needed as soon as possible Less severe cases, aesthetics are main consideration. Full crowns or facial veneers