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Neurovascular events

In addition to the accumulation of neutrophils and immunocompetent cells near the carious lesions, inflammatory reaction also involves extensive neurovascular reactions. These responses consist of branching and sprouting neuropeptide containing nerve endings, increased tooth pulp blood flow, increased vascular permeability and extravasation of fluid and plasma proteins. In the process, severely painful symptoms may be absent (see Chapter 3). Locally increased tissue pressure as a result of vascular leakage can lead to stagnation and local ischemia, thus contributing to the risk of pulpal necrosis.

Earlier assumption that increased tissue of the tooth pulp pressure, as the dominant factor that would compress thin venules in a vicious circle, as a result of a sharp reduction of the tooth pulp blood flow and, perhaps, pulpal necrosis (strangulation theory, is misleading, and was not supported (72). Thus, the clearance of excess fluid and proteins from the blood and lymph vessels (27) in the immediate vicinity of the affected area, as described above, gives the pulp relief and may allow it to survive for a certain period of time.

Summary of changes of tissues in the flesh, as a response to caries can be found in the Core of the concept 2.3.

The basic concept 2.3 changes of Tissues in the pulp and caries

Caries chained to the dentin
  • During him to a pulp, tooth decay destroys the dentin and turns into a mushy mass spread out the cloth contains an abundance of items of bacterial that can provoke inflammatory changes in the flesh.
    But, thanks reactive processes in the dentin (the plasma protein sediments and dentinal sclerosis) and immune reactions pulp, the vital function of tissues rarely threatened so long as tooth decay, is reduced to the primary dentin.
  • Inflammatory participation of surface and medium deep caries in the dentin is usually limited to peripheral parts of the pulp. Inflammatory cells, primarily mononuclear cells (macrophages, plasma cells, and the T - and B-lymphocytes), penetrate into the tissue, but to a limited extent. Traces of repair (e.g.. formation of reparative dentin), often (but not always a prominent feature.
  • Pulps in the teeth of a long and/or the slow progress of caries may show an increase in fibrosis, a reduction of the nervous and vascular supply and intrapulpal salinity, resulting in reduced defense competence.
Direct exposure to
  • Near the bacterial there is accumulation of neutrophils and tissue destruction.
  • In the surrounding areas:
    • immune cell activation and accumulation of macrophages
    • branching and germination of neuropeptide-containing nerve endings,
    • intense cardiovascular activity and localized increased tissue pressure.
Total pulp necrosis can develop after a period of time..
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