Healing of Periapical Lesions - The Body's Response To Microbial Invasion

The Body's Response To Microbial Invasion

In response to tissue injury, neutrophils leave the circulatory system in great numbers and gather at the site of tissue injury. They are drawn to the site by chemotaxis, following a concentration gradient of chemotactic molecules until they reach the site of greatest concentration: the site of injury and microbial presence. Once there, the antimicrobial action of superoxide and hydrogen peroxide, derived from the metabolic processes of the neutrophils, act to combat the microbial invasion. While primarily mobilized to kill the invading microorganisms, the neutrophils actually cause a significant amount of host tissue damage as well. Although the neutrophils themselves rarely remain alive for more than a few days, the excessive accumulation of dead neutrophils and the enzymes they released is a major cause of tissue breakdown in the acute phases of apical periodontitis.

Soon after inflammation has been initiated, macrophages enter the scene and, if not controlled by the initial ambush of neutrophils and their tactics, the microbial invasion is faced with a second strike consisting of these leukocytes, along with lymphocytes. Together, the cells of this second strike compose the bulk of the apical periodontitis lesion and serve an important role in the subsequent chronic phase of inflammation of apical periodontitis, as they can live for many months. Some researchers posit that it must not be macrophages that are involved, as they could not appropriately discriminate between the varied array of opsonized entities as necessary, and that, in reality, the properties ascribed to the macrophage in the initiation phase of the inflammatory response actually belong to the lymphatic dendritic cell. It is unclear, however, if the latter is a distinct population of cells or if it is merely a particularly specialized strain of macrophage.

When infections such as these occur elsewhere in the body, the host defense system, able to travel the body via the circulatory system, is, more often than not, capable of appropriately gaining access to the site of infection in order to mount a proper and successful retaliation. Dental pulp, which is a richly vascularized and innervated tissue, is enclosed by tissues, such as dentin, which are incapable of expanding. It has terminal blood flow and possesses only small-gauge circulatory access at the apical foramen. All of these characteristics severely constrain the defensive capacity of the pulp tissue when faced with the different aggressions to which it may be subjected. As a result, necrotic tissue located within the pulp chamber and canals provide nutrients for pathogenic bacteria to grow and form a periapical lesion; the infected tooth serves as a biochemically and physiologically ideal location for bacterial growth and maturation, and, in essence, acts as a refuge from which bacterial reinforcements can mobilize to the periapical lesion. It is this concept that serves as the basis for conventional endodontic therapy; both chemical and mechanical debridement procedures are essential in effectively disrupting and removing the microbial ecosystem that is associated with the disease process. Thus, whenever a pulp is removed and the canal treated and filled in a manner that is compatible with or favorable to a physiologic reaction, we may expect a satisfactory percentage of endodontic success.