31 - Anomalies in Tooth Structure + Dental Dysplasia Flashcards

1
Q

What are the main structure anomalies?

A

Hypoplasia
Hypo-mineralisation
Hypo-Maturation
Hyper-Pigmentation

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2
Q

What is Hypoplasia

A

Its a defect due to enamel deficiency.
Causes: problems during enamel matrix formation, nutritional factors + fluorosis
Results in an abnormal thickness + shape of enamel

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3
Q

What is Hypo-Mineralisation?

A

It is a disturbance during enamel matrix mineralisation, which results in soft + poorly mineralised enamel.
The shape and thickness is normal

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4
Q

What is Hypo-Maturation?

A

This is a disturbance in enamel maturation.

It results in enamel that is clinically identical to Hypo-mineralised enamel

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5
Q

What is Hyper-Pigmentation?

A

Permanent pathological colouration from postponed pigments in tooth structure.
It CANNOT be removed with external cleaning

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6
Q

What are the main diseases that cause tooth anomalies?

A
Hereditary Dysplasia
Congenital Dysplasia
Acquired Dysplasia 
Amelogenesis imperfecta
Icterus Gravis Neonatorum 
Turner's Teeth
Fluorosis
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7
Q

What is Hereditary Dysplasia?

A
This can affect both dentitions and can cause:
Hypo-Mineralisation
Hypo-Maturation
Hypoplasia 
This also includes genetic risk factors
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8
Q

What is Congenital Dysplasia

A

This mainly affects the primary teeth.
Causes:
Hypoplasia - via malnutrition of pregnant women in 2nd trimester, occurs in early toxicosis of pregnancy

Hypo-Mineralisation - via malnutrition of pregnant women, late toxicosis of pregnancy + rubella, corticosteroid treatment, and in premature infants

Hyper-Pigmentation - occurs after porphyria or taking tetracyclines

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9
Q

What is Acquired Dysplasia?

A

This is developed by 3 types of factors:
Exogenous, Endogenous + Local
They affect permanent dentition as they develop after birth and can be all 4 structural defects

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10
Q

ADs - Endogenous factors in childhood

A
Hemolytic disease of the newborn
hypotrophy 
dyspepsia 
hypovitaminosis 
rickets
frequent infections
chronic diseases
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11
Q

ADs - Exogenous Factors

A

These are local factors acting after the birth of the child

They affect single teeth + only where they are acting factors locally

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12
Q

ADs - Local Factors

A
A chronic complication of untreated caries in a primary tooth affects permanent dentition.
Trauma of primary tooth
Local action of radiation
Affect individual teeth
Dysplasias are asymmetric
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13
Q

Mechanism of Development of Hypoplasia

A

Impairs the functions of ameloblasts:

  • Affects the quality of the synthesised + secreted proteins
  • Affects the amount of secreted matrix
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14
Q

Ways of impairment of the Ameloblasts

A

Defect in genetic information

Rubella in 1st trimester of pregnancy - directly injures ameloblasts

In premature infants - building cells are damaged

Congenital Allergies - inadequate Calcium (Ca) content in blood, increased acidity, impaired water + mineral metabolism

Rickets - disturbs entire metabolism - Mainly Ca/P

Toxic dyspepsia - loss of water, salts, Ca, K, Mg - building cells are damaged

When fluoride is taken in toxic doses, it damages the ameloblasts

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15
Q

Mechanisms for hypomineralisation

A

In the disturbed function of ameloblasts, a defective matrix that does not provide the correct mineralisation

They can act as factors disturbing the required amount of minerals at relatively properly formed matrix

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16
Q

Examples of Disturbed function of ameloblasts

A

Genetic Diseases

Chronic toxic effect of fluorine

Native Lues:
Nephrotic Syndrome
Hypoproteinaemia 
Dysproteinaemia 
Hypophosphatemia 

Acidosis

17
Q

Examples of Relatively Properly Formed matrix

A

Pregnancy Toxicosis

Hypoparathyroidism

Hypopituitarism

Common Temperature Conditions: Celiac Disease

18
Q

Mechanisms for development of Hyperpigmentation’s

A

Pigments from the disease enter the developing matrix + form complex compounds of apatite structure

19
Q

Types Of Pigments

A

Haemolytic Anaemia - Circulation of blood pigments

Tetracycline Molecules - Enters placenta + forms calcium orthophosphate complex in matrix
-In UV radiation it oxidises + turns brown

Cardiovascular Drugs - Stain teeth w/blood pigments

20
Q

Mechanisms of Inheritance of a Dental dysplasia

A

Genetic information
Gene
Dominant + Recessive Genes

21
Q

Genetic Information

A

Type + function of cells is determined by info encoded in the DNA
RNA molecule is derived from a DNA matrix - determines protein synthesis in the cell
Transcription factors determine which genes may occur via production of RNA
These are hereditary mechanisms, any genetic defect can be traced to the pedigree

22
Q

Gene

A

An entire portion of DNA required for synthesis of a functional polypeptide molecule

23
Q

Dominant Gene

A

A gene that expresses a phenotype in a single dose

24
Q

Recessive Gene

A

Gene that expresses a phenotype in a double dose

25
Q

Classification of Dental Dysplasias

A

Hereditary DD
Congenital DD
Acquired DD

26
Q

Hereditary DD

A

Amelogenesis imperfecta hereditarya

  • Hypoplasia
  • Hypomineralisation
  • Hypomaturation

Dentinogenesis imperfecta Hereditarya
-Loss of enamel, dentin becomes brown/blue

Odontogenesis imperfecta herediatrya

27
Q

Congenital DD

A

Hypoplasia
Hypomineralisation
Pigmentation

28
Q

Acquired DD

A

Hypoplasia
Hypomineralisation
Hypomaturation
Pigmentation

Turner’s DD

  • Post icterus neonatorum
  • Post Rachit
  • Post dyspepsia
  • Post hypovitaminosis
  • Post infectious diseases
  • Post general diseases
  • Post tetracyclines
  • Fluorosis