Like other connective tissues in the body, the pulp reacts to irritants with inflammation. However, the pulp has certain characteristics that make it unique and that may alter this tissue response – sometimes dramatically. Tumor (swelling) is one of the cardinal signs of inflammation. When the pulp becomes inflamed, anatomical limitations, that is, the hard root canal walls, will preclude an increase in tissue volume. In addition, the pulp almost completely lacks a collateral circulation. These two factors place the pulp at a considerable disadvantage in dealing with edema, necrotic tissue, and foreign material. On the other hand, the pulp is the only connective tissue that has the ability, at least to a certain extent, to protect itself from external irritants by the formation of intratubular and secondary dentin.
In the classic view of pulpal inflammation, immense importance was given to the influence of the anatomical environment on the pulp. It was assumed that with a local inflammation in the pulp there would be an increased blood flow to the inflamed area. The vasodilation and increased capillary pressure and permeability induced by the inflammation would result in an increased filtration from the capillaries into the tissue, which in turn would cause steadily increasing tissue pressure. Gradually, as the pressure outside the vessels rose, the thinwalled vessels were compressed. This would lead to a decrease in blood flow as well as an increase in venous pressure, which in turn would result in increased capillary pressure and a further increase in the filtration from the capillaries to the tissue. Thus, a vicious circle seemed to develop, resulting in a steady increase in tissue pressure. Consequently, since the pulp lacks the possibility of expansion, the final result of the increase in tissue pressure was then thought to be a choking or strangulation of the pulpal vessels at the apical foramen, leading to a stagnation of the blood circulation with resultant ischemia and necrosis.
However, modern research has not supported the strangulation theory. For example, in experiments where the tissue pressure of the pulp is measured, it has been found that a pressure increase in one area of the pulp does not cause a pressure increase in the rest of the pulp. It has also been shown that when local inflammation is induced in the pulp, the tissue pressure increases only in the inflamed area and not in the entire pulp cavity. Experiments with in vivo microscopy have confirmed that an injury in the coronal pulp results in local circulatory disturbances and, if the injury is severe enough, to complete stasis in the vessels in and near the injured area. The circulation in the root pulp, by contrast, is unaffected in these experiments. Experimental studies on the healing of pulpal inflammation have confirmed these findings, and presently there is convincing evidence that even severe inflammatory changes in a limited area of the pulp do not result in a circulatory stoppage in the entire pulp.
Based on these and other studies, a modern theory on the hemodynamics of pulpitis has developed. The pulp normally has a relatively high blood flow which is not significantly influenced by vasodilator substances. Thus, only minor increases in blood flow occur during pulp inflammation, and only locally in the inflamed area. The increase in capillary permeability, therefore, appears to be considerably more important than the increase in blood flow for the inflammatory response in the pulp. Two possibilities exist for the transport of edematous fluids away from an inflamed area in the pulp: 1) lymphatics, and 2) blood vessels in the adjacent uninflamed tissue. Increased drainage into lymphatic vessels from inflamed areas is known to occur in other tissues. In the pulp the lymphatic flow would be further aided by a positive pressure gradient between the inflamed area and the adjacent uninflamed tissue. Because of the positive pressure gradient, transport of fluids will also occur through the tissue itself to adjacent uninflamed tissue which has normal structural characteristics and where no changes in capillary pressure or permeability have occurred. Here there will be a net absorption of fluids from the tissue into the vessels, thus preventing an increase in tissue pressure in the uninflamed areas of the pulp. A generalized edema of the pulp during inflammation, therefore, is prevented by a localized increase in the tissue pressure in the inflamed area, by an increased lymphatic flow, and by a net absorption into the capillaries of the uninflamed tissue adjacent to the inflamed area of the pulp.
Thus, the modern view of the reaction pattern of the pulp is as follows: The pulp reacts to irritants with local inflammation in an area of the tissue that is subjected to the irritants. The inflammatio may remain as a local inflammation for a long time, sometimes for years, if the irritants are mild. If the irritants are removed, for example, if a carious lesion is excavated and a restoration placed in the tooth, the local inflammation may heal. The resistance of the pulp to irritants and its ability for repair are considerable. Still, if the irritants are longlasting and strong enough, the inflammation will spread in the pulp. In most instances the process progresses rather slowly from the periphery where the irritants reach the pulp, toward the central pulp, the root pulp, and the periapical tissues.
Successive necrosis of the tissue in the direction of the apical foramen then takes place.
Pathogenesis of Pulpitis
Inflammation in the pulp develops in the same manner as in other tissues. The cellular phase is dominated at first by neutrophilic leukocytes; lymphocytes, macrophages, and plasma cells appear later. The last cell types, however, dominate the histological picture during sustained pulp inflammation, giving it the character of a chronic inflammation.
Thus, following the vascular phase of the inflammatory reaction, which in the pulp is characterized by a rather slight increase in blood flow, dilation and increased permeability of the capillaries, and accumulation of fluids in the tissue, the neutrophilic leukocytes are attracted to the area by chemotaxis. They pass through intercellular gaps in the vessel walls and accumulate in the tissue, where they function as phagocytes. If at this time the irritants can be removed, there is a considerable potential for repair. If not, probably more neutrophilic leukocytes will arrive on the scene. These cells have a life span of only a few hours and will soon start to break down, releasing toxic cellular components and proteolytic enzymes which may destroy cells, fibers, and ground substance in the inflamed area of the pulp. If the tissue destruction is severe enough, it may be recognized clinically as a drop of pus when the pulp chamber is opened. If the leukocytic breakdown occurs slowly, encapsuled abscesses can form and may be seen microscopically. This encapsulation of the destroyed tissue may for a time delay further tissue destruction. Sometimes even calcification of the abscess membrane is seen. It is not known whether or not pulpal repair may occur at this stage of the inflammatory process.
Gradually, the scene is no longer dominated by neutrophilic leukocytes, but by lymphocytes that have come to the inflamed area, left the capillaries, and aggregated in the tissue. The inflammation is now no longer acute, but chronic, and in addition to the lymphocytes, macrophages and plasma cells will typically be seen in the inflamed area. Both B lymphocytes and T lymphocytes have been recognized in the pulp, representing the humoral and cell-mediated systems of immunity. Invasion of the pulp tissue by antigenic products may be inhibited by the complexing of these products with antibodies and the formation of antigen–antibody complexes which in turn are phagocytized and digested, especially by macrophages. However, lymphocytes may also have a destructive effect on the pulp tissue, either through direct cytotoxic activity or through biologically active and destructive cytokines. Macrophages can lead to tissue destruction as well through the production of cytokines, collagenase, and other products. Thus, the immune response may inflict further damage to an already injured pulp. This again may result in an increased chemotactic activity and attraction of neutrophilic leukocytes. An acute inflammatory reaction may then be superimposed on the chronic inflammation. This is a rather common occurrence in inflamed pulps, although in many instances an acute episode will be caused by new external irritants reaching the pulp tissue.
Pulpal inflammation is, therefore, a dynamic process. Various stages of the inflammatory process can often be observed in different areas of the same pulp. A typical observation would be necrosis of the tissue in the area where the inflammation started. The tissue subjacent to this area may be inflamed, dominated by the cells typical of a chronic inflammation. Also, in this area one or more encapsulated microabscesses may be seen. Apical to the inflamed area, noninflamed pulp tissue will be present. Without treatment, the inflammation (and later the necrosis) will gradually spread in an apical direction until the entire pulp becomes necrotic. A total pulpitis in the sense that the entire pulp is infiltrated by inflammatory cells does not seem to occur.
A rare variation in the development of pulp inflammation is the formation of a pulp polyp. Under particularly favorable circumstances, the successive breakdown of the pulp can stop temporarily when a carious attack or a traumatic injury has resulted in an opening of the pulp cavity. Instead of becoming necrotic, the pulp tissue may start to proliferate. A proliferating pulpitis or a pulp polyp then develops. On the surface the pulp polyp normally has a necrotic layer, but in some instances it becomes epithelialized. However, the epithelial lining does not give the protection seen in the gingiva. It is infiltrated with inflammatory cells, is ulcerated, and bleeds easily when touched. Occasionally a pulp polyp may reach the gingiva, and a tissue bridge between the gingiva and the pulp is established. A pulp polyp may last for a relatively long time, but the end result will always be total tissue breakdown as described above.