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![Factors producing injury to ameloblasts:
• Nutritional deficiency [vitamin A,C,D]
• Exanthematous diseases
[eg: measles, chicken pox, scarlet fever]
• Congenital syphilis
• Hypocalcemia
• Birth injury, prematurity, Rh hemolytic disease
• Local infection or trauma
• Ingestion of chemicals (fluoride)
• Idiopathic causes](https://image.slidesharecdn.com/developmentaldisturbancesinstructureofteeth-190607092218/75/Developmental-disturbances-in-structure-of-teeth-4-2048.jpg)
![Due to nutritional deficiency and Exanthematous fevers:
In Earlier studies ricketes was the major cause
• At present
vitamin A and C are also causes
produce enamel hypoplasia due to interference in
metabolic function of ameloblasts
result in pitting and pits tend to stain
• Central and lateral incisors, cuspids and first molars are
frequently involved [ primary teeth to appear]](https://image.slidesharecdn.com/developmentaldisturbancesinstructureofteeth-190607092218/75/Developmental-disturbances-in-structure-of-teeth-5-2048.jpg)
![Due to congenital syphilis
• Involves max and mand central incisors and first molars
• Anterior tooth affected are called “HUTCHINSON’S
TEETH”
• Molars referred as “MULBERRY MOLARS” [moon
molars, Fournier's molars]](https://image.slidesharecdn.com/developmentaldisturbancesinstructureofteeth-190607092218/75/Developmental-disturbances-in-structure-of-teeth-6-2048.jpg)
![Due to hypocalcemia
Tetany - Due to decreased level of calcium in blood [ fall
as low as 6 – 8 mg/100ml]
Most common – vitamin D deficiency and parathyroid
deficiency
• Causes Pitting](https://image.slidesharecdn.com/developmentaldisturbancesinstructureofteeth-190607092218/75/Developmental-disturbances-in-structure-of-teeth-9-2048.jpg)
![Due to local infections or trauma:
• Single tooth is involved [permanent max incisors or
max or mand premolars]
• Degree of hypoplasia ranging from mild, brownish
discoloration of enamel to severe pitting and
irregularity of tooth surface.
• Single tooth referred as “TURNER’S TEETH” condition -
>> TURNER’S HYPOPLASIA](https://image.slidesharecdn.com/developmentaldisturbancesinstructureofteeth-190607092218/75/Developmental-disturbances-in-structure-of-teeth-11-2048.jpg)
Uploaded byDr. Santhu Sadasivan
Developmental disturbances in structure of teeth
This document discusses enamel defects including hereditary enamel dysplasia and enamel hypoplasia. It describes the three stages of enamel development and factors that can disrupt this process such as nutritional deficiencies, infections, trauma, and genetic conditions. Specific enamel defects are defined including pitted enamel hypoplasia and enamel discoloration seen in conditions like congenital syphilis and fluorosis. Classification systems for hereditary enamel dysplasia and clinical, radiographic, and genetic features are also summarized.
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Enamel development consists of three stages: formative (organic matrix deposition), calcification (mineralization), and maturation (crystallite enlargement).
Enamel defects can arise from hereditary or environmental factors affecting tooth formation, influenced by factors like nutritional deficiencies, congenital syphilis, or trauma.
Conditions like Turner’s Hypoplasia and mottled enamel from fluoride exposure lead to discoloration, pitting, and structural defects in teeth.
Hereditary enamel dysplasia impacts both dentitions with a prevalence of 1 in 700-4000 and relates to mutations in enamel genes affecting the structure. Amelogenesis imperfecta classified into 4 types based on clinical and genetic criteria. Each type shows distinct enamel characteristics regarding thickness and quality.
Radiographic examination shows thin or absent enamel with poor mineralization, while histological findings reveal disturbances in ameloblast development.
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Developmental disturbances in structure of teeth
- 1.
- 2. Development of enamelhas three major stages: formative stage deposition of organic matrix. Calcification stage matrix mineralization Maturation stage crystallites enlarge and mature
- 3. An incomplete ordefective formation of the organic enamel matrix of teeth Types: Hereditary type • Both deciduous and permanent dentitions involved • Only enamel is affected Environmental factors • Either dentition or single tooth affected • Both enamel and dentin are affected
- 4. Factors producing injuryto ameloblasts: • Nutritional deficiency [vitamin A,C,D] • Exanthematous diseases [eg: measles, chicken pox, scarlet fever] • Congenital syphilis • Hypocalcemia • Birth injury, prematurity, Rh hemolytic disease • Local infection or trauma • Ingestion of chemicals (fluoride) • Idiopathic causes
- 5. Due to nutritionaldeficiency and Exanthematous fevers: In Earlier studies ricketes was the major cause • At present vitamin A and C are also causes produce enamel hypoplasia due to interference in metabolic function of ameloblasts result in pitting and pits tend to stain • Central and lateral incisors, cuspids and first molars are frequently involved [ primary teeth to appear]
- 6. Due to congenitalsyphilis • Involves max and mand central incisors and first molars • Anterior tooth affected are called “HUTCHINSON’S TEETH” • Molars referred as “MULBERRY MOLARS” [moon molars, Fournier's molars]
- 7. Upper central incisor– screw driver shaped tapering absence of central tubercle or calcification center Crowns of 1st molars irregular shaped enamel arranged in agglomerate mass
- 8. Hutchinson’s Incisor characteristic ofcongenital syphilis incisors are peg-shaped or screwdriver-shaped widely spaced notched at the end with a crescent-shaped deformity
- 9. Due to hypocalcemia Tetany- Due to decreased level of calcium in blood [ fall as low as 6 – 8 mg/100ml] Most common – vitamin D deficiency and parathyroid deficiency • Causes Pitting
- 10. Due to birthinjuries: • Present in deciduous teeth and first permanent molars • Disturbance produced in enamel and dentin • Caused due to trauma or change of environment at the time of birth • Rh hump: Staining of teeth in Rh hemolytic diseased children- deposition of blood pigment in enamel & dentin- green, brown or bluish hue.( ring-like defect)
- 11. Due to localinfections or trauma: • Single tooth is involved [permanent max incisors or max or mand premolars] • Degree of hypoplasia ranging from mild, brownish discoloration of enamel to severe pitting and irregularity of tooth surface. • Single tooth referred as “TURNER’S TEETH” condition - >> TURNER’S HYPOPLASIA
- 12. Due to fluoride: mottled enamel First described by GV Black and Frederick. As a result of fluoride in water supply Maximum allowable level of fluoride :1 ppm The severity of the mottling increases with an increasing amount of fluoride in the water. Pathogenesis Higher levels of fluoride, there is interference with the calcification process of the matrix.
- 13. C/F: white fleckingor spotting on the surface. mild changes manifested by white opaque areas. moderate and severe changes showing pitting and brownish staining of the surface and corroded appearance of the teeth & may show a tendency for wear and fracture.
- 15. A I Hereditary Enamel Dysplasia Hereditary Brown Enamel Hereditary Brown Opalescent Teeth
- 16. It isa hereditary disorder affecting enamel formation in both deciduous & permanent dentitions. prevalence is 1 in 700 to 4000 with slight male predilection. Genes related to A I Mutations in the AMELX, ENAM, and MMP20 genes causes malfunction of the proteins in the enamel: ameloblastin, enamelin, tuftelin and amelogenin.
- 17. Based on clinical,histological & genetic criteria-Witkop & Sauk Type I : Hypoplastic I A Pitted, AD I B Local, AD I C Local, AR I D Smooth, AD I E Smooth, X-linked dominant I F Rough, AD I G Enamel agenesis ,AR Type II : Hypomaturation II A Diffuse Pigmented, AR II B Diffuse , X-Linked recessive II C Snow-capped teeth, X-linked Type III : Hypocalcified III A Diffuse AD III B Diffuse AR Type IV : Combination Type IV A Hypomaturation- hypoplastic with taurodontism,AD IV B Hypoplastic- hypomaturation with taurodontism,AD
- 18. AD Pinpoint or pin head sized pits are scattered across the surface of the teeth. Pits arranged in rows or columns. Buccal surface affected more severely.
- 19. Pin point/pin head sized pits in rows. Linear depression or area of hypoplasia. Middle third of buccal surface. Incisal or occlusal unaffected. All teeth or some teeth affected Primary or both dentitions
- 20. Thin, hard,glossy Looks like crown preparations- open bite. Opaque white to brown. X-linked dominant – Type I E Similar features in males Alternating vertical bands of normal and abnormal enamel seen in females.
- 21. Thin, hard,rough Tapering of occlusal and incisal surfaces. Open contact & open bite. Type I G (Enamel Agenesis) No enamel Yellow teeth Tapering
- 22. Defect inthe maturation of crystal structure. Teeth normal in shape. Mottled opaque white- brown- yellow discoloration Softer than normal- Tend to chip from underlying dentin. Snow capped – zone of white opaque enamel on incisal and occlusal surface.
- 23. No significantmineralization. Enamel soft and easily lost. Colour yellowish brown to orange on eruption but later becomes stained brown to black.
- 24. H/P: Hypoplastic- disturbancein differentiation of ameloblasts defects in matrix formation. Hypomaturation – alterations in enamel rod and rod sheath structures. Hypocalcification – defects of matrix structure and mineral deposition.
- 25. Radiographic features: Theenamel may appear totally absent or as very thin layer. It appears to have same approximate radiodensity as that of dentin.