Preclinical Paediatrics · MU Sofia

31. Anomalies in tooth structure. Dental dysplasia - risk factors, pathogenesis and classification.

Explains dental dysplasia as defects in hard tooth tissue caused by disturbances at different stages of dentition, then sets out risk factors grouped as genetic, general (in utero and childhood) and local (after birth). Covers pathogenesis through impaired ameloblast function, with separate mechanisms for hypoplasia, hypomineralisation and hyperpigmentation, plus a short note on how dysplasia is inherited. Ends with a classification into hereditary, congenital and acquired forms, including Turner's dental dysplasia and fluorosis, with two diagrams on aetiology and pathogenesis.

Inside: 2 sections · 2 labelled pictures · 15 flashcards · 4 min

Topic 31 of 40 in the MU Sofia syllabus for Preclinical Paediatrics (Dental Medicine, Year 3). The free AceMed note covers it in 2 sections, about 592 words (4 min of reading), with 15 flashcards.

In this note

  1. ANOMALIES IN TOOTH STRUCTURE. DENTAL DYSPLASIA- RISK FACTORS, PATHOGENESIS AND CLASSIFICATION
  2. RELATIONSHIP BETWEEN AETIOLOGY AND PATHOGENESIS OF DENTAL DYSPLASIA

ANOMALIES IN TOOTH STRUCTURE. DENTAL DYSPLASIA- RISK FACTORS, PATHOGENESIS AND CLASSIFICATION

DENTAL DYSPLASIA: defects that occur in the structure of hard tooth substances as result of disturbances occurring at different stages of dentition

Ameloblasts function can be compromised dye to the quality of synthesized and secreted proteins and amount of secreted matrix.

RISK FACTORS:

Classified into:

  • Genetic Factors
  • General Factors (or endogenous)
  • Local Factors (or exogenous)

GENETIC FACTORS

  • This is defective genetic information encoded for the function of cells that make up tooth structures
  • Inherited defects affect all teeth e.g. generalised hereditary dysplasia

GENERAL FACTORS (OR ENDOGENEOUS)

  • These act during foetal development and childhood. Factors acting in utero are:
  • Improper nutrition of pregnant women
  • Infectious diseases
  • Chronic diseases
  • Early and late toxicosis of pregnancy
  • Endogenous factors in childhood induce acquired dysplasia. These factors are:
  • Haemophytic disease of newborn
  • Hypotrophy
  • Dyspepsia
  • Hypovitaminosis
  • Rickets
  • Frequent Infections
  • Chronic Diseases

LOCAL FACTORS (OR EXOGENOUS)

  • Local factors that act after the birth of child. Only affects single teeth, hence act locally
  • Local factors include:
  • Chronic complication of untreated caries in a primary tooth affecting permanent dentition
  • Trauma of primary tooth
  • Local action of radiation
  • Causes acquired dysplasia only in permanent dentition

PATHOGENESIS

MECHANISM of development of hypoplasia is through the impairment of function of ameloblasts

  • Affects the quality of synthesized and secreted proteins
  • Affects the amount of secreted matrix

Impairment of ameloblasts can occur through multiple different ways:

  • Defects in the genetic information
  • Rubella (during first three months of pregnancy) directly injures them
  • In premature infants where the building cells are damaged
  • Congenital allergies through inadequate Ca content in blood, increased acidity, impaired water and mineral metabolism
  • Rickets disturbs the entire metabolism, mainly Ca/P
  • Toxic dyspepsia leads to loss of water, salts, Ca, K and Mg meaning building cells are damaged
  • When [F] is taken in toxic doses, it damages the ameloblasts

MECHANISMS for occurrence of hypomineralization are:

  • In the disturbed function of ameloblasts, defective matrix does not provide the current mineralization. For example, due to:
  • Genetic diseases, chronic toxic effect of fluoride, congenital lues and nephrotic syndrome
  • Relatively properly formed matrix can add factors that disturb the required amount of minerals. For example, due to:
  • Toxicosis of pregnancy, hypoparathyroidism, hypopituitarism, frequent conditions of increased temperature, coeliac disease

MECHANISMS for development of hyperpigmentations are:

  • Pigments of disease processes can penetrate among the matrix currently under construction
  • They form complexes with apatite crystals

Types of Pigments are:

  • Haemolytic anaemia- circulation of blood pigments

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