Apical periodontitis is typically the body's defense response to the threat of microbial invasion from the root canal.Lopez-Marcos, JF. Aetiology, classification and pathogenesis of pulp and periapical disease, Med Oral Patol Oral Cir Bucal 2004 9:Suppl pages 58-62, 52-7. Primary among the members of the host defense mechanism is the polymorphonuclear leukocyte, otherwise known as the neutrophil. The task of the neutrophil is to locate and destroy microbes that intrude into the body – anywhere in the body – and they represent the hallmark of acute inflammation.Nair, PNR: Pathobiology of the Periapex. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 465.

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.Raven, PH, Johnson, GB. Biology, 5th Edition. Boston: McGraw-Hill Companies, 1999. page 1072.

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.Ross, MH, Histology: A Text and Atlas, 3rd Edition. Philadelphia: Lippincott, Williams and Wilkins, 1995. page 339.

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.Ross, MH, Histology: A Text and Atlas, 3rd Edition. Philadelphia: Lippincott, Williams and Wilkins, 1995. page 315. 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.Lopez-Marcos, JF. Aetiology, classification and pathogenesis of pulp and periapical disease, Med Oral Patol Oral Cir Bucal 2004, 9:Suppl, 58-62, 52-7.Castellucci, A, Blumenkranz, U: Periapical Disease. In Castellucci, A, editor: Endodontics, Volume 1, Las Vegas: Las Vegas Institute, page 160. As a result, necrotic tissue located within the pulp chamber and canals provide nutrients for pathogenic bacteria to grow and form a periapical lesion;Fidel, RAS. Complicated crown fracture: a case report, Braz Dent J 2006 17:1 pages 83-86. 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.Baumgarten, JC, Hutter, JW: Endodontic Microbiology and Treatment of Infections. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 501. 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.Blayney, JR: JADA 15:1217-1221, 1928, quoted by Lovdahl, PE, Gutmann, JL: Problems in Nonsurgical Root Canal Retreatment. In Gutmann, JL, editor: Problem Solving in Endodontics, 3rd Edition. St. Louis: Mosby, Inc. 1997, page 157.

Breakthrough in bacteriology

In 1890, W.D. Miller, considered the father of oral microbiology, was the first to associate pulpal disease with the presence of bacteria.Sgan-Cohen, H.D. Oral hygiene: history and future recommendations. Int J Dent Hyg 2005 3:2 pages 54–58. This was confirmed by Kakehashi, who, in 1965, proved that bacteria were the cause of pulpal and periradicular disease in studies using animal models; pulpal exposures were initiated in both normal and germ-free rats, and while no pathologic changes were exhibited in the mouths of the germ-free rats, introduction of the normal oral microbial flora produced pulpal necrosis and led to periradicular lesion formation in the normal rats.Kakehashi, S. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol 1965 Sep 20 pages 340-349. The germ-free rats healed regardless of the severity of pulpal exposure, demonstrating that the presence or absence of bacteria was the determinant for pulpal and periapical disease.

Moreover, it has since been discovered that endodontic infections are polymicrobial. In fact, the bacteria present within endodontic infections are thoroughly similar to the bacteria that are involved in periodontal disease. It has also been shown that certain enzymes produced by bacteria are detrimental to the host, and can work in concert with the destructive capability of the enzymes released by dying neutrophils. Recent studies have revealed that the gene for collagenases could be detected in stains of Porphyromonas gingivalis, one of the many endodontic infective agents that are also involved in periodontal disease.Baumgarten, JC, Hutter, JW: Endodontic Microbiology and Treatment of Infections. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 505.

Additionally, it has been proven that a positive correlation exists between the number of bacteria in an infected root canal and the size of the resultant periradicular radiolucency.Baumgarten, JC, Hutter, JW: Endodontic Microbiology and Treatment of Infections. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 503.

In attempting to resolve a periapical lesion of endodontic origin, it is essential to be conscious of these principles in order to effectively combat the infection. Without proper consideration for the causes, the pulpal and periapical infection cannot be suitably treated, for effective patient management requires the correct diagnosis and removal of the cause of the infection of endodontic origin to correct the associated periapical lesion. Because periapical disease is almost inevitably preceded by pulp disease, proper chemomechanical debridement of the infected root canals, together with incision and drainage of associated periradicular swellings, will usually allow for rapid improvement in patient signs and symptoms.Baumgarten, JC, Hutter, JW: Endodontic Microbiology and Treatment of Infections. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 511. The same end can be accomplished by extracting the involved tooth.

Source of infection Although periapical changes will be in response to pulpal changes the majority of the time, it is still important to determine the disease process sequence. When the disease process is of pulpal origin, the pulpal infection and necrosis may drain not only through the apical foramen, but also through an accessory canal, which may present radiographically as a periradicular or furcation radiolucency. This may further lead to furcal involvement through loss of clinical attachment and alveolar bone. A cursory clinical examination and radiographic analysis can easily lead the clinician off the right course and pulpal involvement might be overlooked when the tooth is asymptomatic. Similarly, a periodontal abscess may very well appear to be pulpal in origin, when in fact it is not. Notwithstanding the tissue of origin, though, when it is determined that there is a pulpal involvement to the periodontal lesion, the endodontic infection should be controlled prior to beginning definitive management of the periodontal lesion, especially when regenerative or bone grafting techniques are planned.Novak, J: Classification of Diseases and Conditions Affecting the Periodontium. In Newman, MG, editor: Carranza’s Clinical Periodontology, 9th Edition. Philadelphia: W.B. Saunders Company, 2002. page 71.

Focusing on proper procedure To achieve healing of the periapical lesion, one must obtain and maintain a decontaminated root canal system. System is to be emphasized, because the root canal system does not merely consist of tapering cone-shaped canals from orifice to apex, but rather, can and often is an intricate labyrinth of canals that diverge and weave to form an elaborate web of anastomosing passages.Gutmann, JL, Witherspoon DE: Obturation of the Cleaned and Shaped Root Canal System. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. pages 296, 332 and 349. It is precisely because of this reality that “it is important to appreciate that files produce shape, but it is essential to understand that irrigants clean [the] root canal system.Ruddle, CJ: Cleaning and Shaping the Root Canal System. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 235. Copious amounts of sodium hypochlorite are necessary to utterly dissolve all remnants of pulp tissue as well as completely destroy all microorganisms.Ruddle, CJ: Cleaning and Shaping the Root Canal System. In Cohen, S. Burns, RC, editors: Pathways of the Pulp, 8th Edition. St. Louis: Mosby, Inc. 2002. page 258. The tooth stability does not undergo major changes after surgery comparated with the initial value which was determined before establishing any kind of treatment.(webpage has a translation button)(webpage has a translation button)

Conventional therapy