In addition to the transmission of nerve impulses, there is another, a much slower type of signaling between the nerve endings in peripheral tissues and soma neuron through axonal transport. This process is bidirectional, including both front-and retrograde transportation of various cytochemical alarm agents. It allows transmission of information about the state of the tissue around the nerve endings neuron soma (10). Damage to the nerve endings and other tissue components in the pulp and paper results in the metabolic activation of neurons in the trigeminal ganglion.
In addition to the trauma of the preparation of the
teeth restoration and the subsequent leakage of physical elements, the liberation of the subjects of restoration materials may have a negative influence on the masses. Over the years toxicity of restoration materials considered a primary cause inflammation of the pulp of the tooth and the breakdown of restorative procedures. However, recent studies have shown that toxic components in the restoration materials represent a hazard for the pulp than previously assumed (4).
Although the primary goal of dental treatment procedures elimination of infectious agents in the treatment of caries and periodontal disease and to restore tooth function and aesthetics, these procedures can rarely be carried out without causing harm to the pulp. In the short term, the majority of irritation is experienced. Only after a late stage of the disease and the use of inappropriate procedures that the risk of severe injuries are unavoidable. Long-term formation of scar tissue in the form of reparative dentin, increased fibrosis and intrapulpal mineralization, may omit the pulp defense potential and cause damage in response to new injury (6).
Young people in the pulp chamber is wide,
tooth decay may initiate a proliferative response and lead to what is called the pulp polyp (Fig. 2.25). A prerequisite for this condition is that the roof of the tooth pulp chamber was completely destroyed. Tissue distribution of this expression restorative phase pulpal response, and it became possible thanks to the fact that the process does not occur within a closed system. The pulp of a tooth polyps may become epithelialized on the establishment of contact with gum tissue.
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.
After carious lesions with its bacterial before penetrated the main dentin and progressed in reparative dentin and/or pulp tissue appropriate, mass mobilization inflammatory defense will take place (43, 64) (Fig. 2.22). The most conspicuous feature is the aggregation of neutrophils. Often local abscess grows (Fig. 2.23). Clinically, during the excavation of caries, a drop of pus sometimes it may seem at the exposure site.
Inflammatory changes of tissues, and also the repair of the phenomenon can be seen in the flesh at all stages of active carious lesions. In fact, tissue responses were seen even at very early stages, before any surface collapse, when caries, is reduced to the enamel only (10, 11, 13).
Tooth decay is the main cause of painful events, and inflammatory lesions pulp. In the process of destruction of the tooth, various substances are produced that cause inflammatory affection upon reaching the pulp. The pulp is usually able to tolerate bacterial impact, especially when caries chained to the main dentin. On the contrary, as soon as the reparative dentin or pulp tissue correct, severe inflammatory involvement usually occurs (43, 64)that could jeopardize the continued functioning of the tissues.
Local damage pulp activates the migration of inflammatory cells. After traumas, various substances are exempt from resident cells that invitations neutrophils and mononuclear cells (monocytes and T - and B-lymphocytes) to leave the cardiovascular system. If no or little bacterial involvement in conjunction with the injury, for example. after the preparation of the injury, the infiltration of neutrophils will be limited, and these cells will soon disappear. On the contrary, the bacterial action, for example, along the margins of poorly sealed restoration, neutrophils can accumulate in large quantities and type of the tooth pulp ends of the dentinal tubules (Fig. 2.18). In this position they are likely to contribute to the tooth pulp protection, blocking both the spread of bacterial macromolecules and the penetration of bacterial organisms (4).
Preparation of dentin rotary instruments results instantly increased the tooth pulp blood flow. Activation of peptides containing sensitive nerve arrangements described above, is the mediator of this response (see Main concept 2.2).
In a deep cavity or crown of drugs, the direct effect of moderate heat to the cells of the tooth pulp and vessels extends the tooth pulp blood flow. Excessive heat generation is an inadequate operating procedures and cannot be cancelled, local protective mechanisms, thereby potentially causing serious damage to the tissues. For this reason, it is very important that a proper system of water cooling is in effect when cutting teeth rotary instruments.