During the past decade, extensive microbiologic, immunologic, and morphologic research studies have shown that any colonization of tooth surfaces by pathogenic bacteria – even transient or superficial colonization – triggers both humoral and cellular host defense responses, regardless of whether the bacterial challenge is incipient (acute) or progressive (chronic).
The breakdown of the complex host defense mechanism is usually temporary, but it destroys the host organism’s system of equilibrium, resulting in a disease process. From the endodontic perspective, this biologic equilibrium primarily concerns the balance between calcium and phosphate ion exchange during the continuous process of demineralization and remineralization of enamel and exposed dentin. As long as a disease process is reversible, as in the case of initial dental caries, the concepts of “progression” and “remission” exist. Clinical evidence of caries indicates that the acidogenic plaque bacteria are demineralizing more enamel than can be remineralized. In this sense, dental caries is rather a chronic destructive process. Irreversible forms of caries may develop during the superficial stage, with no prospect of remission.
As the carious lesion starts progressing from the enamel into the dentin, an inflammatory pulpal reaction is initiated. Histologically, neutrophilic granulocytes, lymphocytes, and macrophages begin to appear within the odontoblastic layer. The odontoblastic processes get embedded in a layer of sclerosed dentin, usually with initial formation of peritubular dentin followed by mineralization of the odontoblastic processes (Frank and Voegel, 1980).
The odontoblastic processes in the upper layers of carious dentin exhibit splayed ends, with membranous fragments within the lumen of the tubule. In this area, there are also large numbers of bacteria (Yamada et al., 1983). If a superficial carious lesion is chronic in nature, in addition to the shrinking odontoblastic border, a small amount of reparative dentin formation will be seen.
Arrested caries in the middle of the dentin (caries media) is characterized by reparative dentin formation, shrinkage of the odontoblastic layer, and cellular infiltration. In the case of active caries, there is massive inflammatory cell infiltration in addition to the damage to the odontoblastic layer.
If the pulp is exposed by the carious process, an electron photomicrograph will show a large number of dead and necrotic cells within the pulpal tissues. Adjacent to the foci of necrosis will be lymphocytes, plasma cells, and macrophages. Polymorphonuclear leukocytes predominate near the site of exposure, some of which are intact and others partially destroyed, with their organelles scattered in the extracellular matrix.
Micro-organisms are found within the neutrophilic granulocytes and macrophages. The endothelial cells of the vascular elements are also damaged, and leukocytes are released from vessels.
If the carious process results in deep dentinal cavities, inflammation of endodontium occurs within a week, the odontoblastic layer is destroyed and the pulp is infiltrated by neutrophilic granulocytes. Bacteria, necrosis, and cellular destruction occur and reparative (secondary) dentin formation is limited. The injection of a bacterial extract into an open pulp chamber elicits local abscess formation with resorption of bone, cement, and dentin (Stabholz and Sela, 1983).
As bacteria penetrate into the dentinal tubules, neutrophilic granulocytes within the pulp migrate toward the orifices of the tubules and engage the bacteria. This process releases lysosomal enzymes and leads to destruction of the pulpal tissues. During the course of the subsequent phagocytosis of the destroyed tissues by polymorphonuclear or mononuclear phagocytes, the cell debris disintegrates, leading to the release of more lysosomal enzymes and further tissue destruction and chemotactic attraction of additional inflammatory cells.
The toxic substances that lead to enhancement of the inflammatory reaction include bacteria, their metabolic by-products, their breakdown products, and finally also the breakdown products of the affected dentin. At this point of the process, a “vicious circle” ensues, manifested by an irreversible pulpitis (Langeland, 1981). Pulp regions near to the necrotic areas are filled with neutrophilic granulocytes that phagocytize the bacteria. This process leads ultimately to the dissolution of entire segments of the pulpal tissue and proceeds in an apical direction (Lin et al., 1984).
It is important to note, however, that the histologic picture of acute inflammation with a preponderance of acute inflammatory cells does not imply that all clinical symptoms of acute inflammation will be present. In cases of deep caries (caries profunda), Langeland (1981) established that of 224 teeth with partial pulpal necrosis and severe inflammation, 81 were not associated with clinical pain. Furthermore, Langeland did not find any correlation between the depth of the carious lesion and the occurrence of pain.
It has also been observed that irreversible pulpitis with pulpal necrosis is often accompanied by swelling of the apical periodontal ligament space. The cause for this early periapical reaction appears to be penetration of toxins through intact radicular pulpal tissues. Gram-negative bacteria with external membranes that release endotoxin can elicit a complement reaction. The activation of complement causes release of biologically active peptides, resulting in an increase in vascular permeability and aggregation of neutrophilic granulocytes and macrophages.
Enzymes released during phagocytosis can lead to osseous tissue destruction (Pitts et al., 1982).