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Aetiology of apical periodontitis

Apical periodontitis, as a rule, affect the teeth containing necrotic pulp tissue, and traditional texts of communication between not vital pulp tissue, what?stagnation` body fluids, and periapical inflammation. Such hollow tubes theory is considered necrotic pulp channels as a space in which tissue fluids from periapex will flow into the country and to communicate with the dead tissue to form irritant cocktail, whose subsequent percolation back across the apical hole will cause periapical breakdown. the first proposal is that the drugs, except for invalid host tissues can be involved in the periapical irritation really came much earlier than when Miller (1890) found a microorganism in necrotic masses. Sampling, culture and identification methods were pretty raw, and it was many decades before the scientific and microbiological methods have managed to establish a clear causal link between bacterial infection and disease in the pulp and periapex.

Some key and surprisingly the last stages include:

  • opening Kakehashi et al.
    in 1965, in a sterile animals, pulp tissue could prevent the broad impact of mouth for many months without any side effects. Pulp tissue remained healthy and reparative calcific barriers often were laid despite the clash hair and food products in open wounds. On the contrary, the mass of a normal animal, whose mouths contained microorganisms predictable died after exposure to mouth, with the development of periapical inflammation and bone loss;
  • careful microbiological studies Sundqvist (1976) on the teeth of a man weakened by injuries, which showed that the teeth with necrotic infected pulp channel content developed apical periodontitis, while teeth with necrotic masses, but not suitable microflora remained in the periapical health; and
  • the Primate of the study Moller et al. (1981), in which the pulps were mechanical products, either under aseptic conditions, or allowing infected saliva to enter. Only on animals, in which microorganisms were allowed to enter in developed apical periodontitis. Teeth sterile necrotic masses had no detectable periapical lesions.
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