D. Ricucci et al, JOE 44:3 pp405-413, March 2018
Chronic apical abscess (chronic apical periodontitis) or what those of us who trained at Boston University under the legendary Dr. Herbert Schilder term a lesion of endodontic origin (LEO), is a variation of apical periodontitis caused by a root canal infection that has resulted in an abscess draining to the surface.
The condition is mostly characterized by a periapical radiolucency associated with an intraoral or extraoral sinus tract. A sinus tract is an abnormal pathway which ends in one opening versus a fistula which is an abnormal pathway which connects two spaces, for example, an oral-antral fistula connecting the maxillary sinus to the oral cavity from a non-healing tooth extraction site.
The sinus tract represents a route of drainage of the abscess that follows a path of least resistance through bone, periosteum, and mucosa or skin. The LEO is usually asymptomatic unless the sinus tract becomes clogged.
Histopathologic analysis of LEOs usually reveals a granulomatous lesion containing areas of liquefactive necrosis, disintegrating PMNs and a border of normal macrophages and PMNs. The sinus tract may be completely lined by epithelium but most often only the surface few millimeters are epithelialized with the remainder inflamed connective tissue.
The prevalence of sinus tracts in teeth with apical periodontitis ranges from 8.5% – 18%. They are more common in teeth with large lesions (>5mm) and most frequently open to the oral cavity through the buccal mucosa. Sinus tracts are generally associated with long-standing infectious lesions. Balderhaug et al, found sinus tracts did not develop in monkey molar teeth, open to the oral cavity, until between 100 and 200 days, with epithelial lining associated only with the later stages.
While endodontic infections are usually restricted to the root canal system, in some cases the infection will extend into the periapical tissue and the sinus tract. In fact, most sinus tracts are positive for bacteria. The profile of the bacteria recovered from these sinus tracts mirrors that of infected root canals systems suggesting an intra-radicular infection which had spread and evolved to become a draining extra-radicular infection.
These extra-radicular infections are usually comprised of complex biofilms adhering to the external root surface and floating biofilm masses within the liquefaction areas. The authors of this study set out to look at the morphologic characteristics of intra-radicular and extra-radicular infections in teeth with sinus tracts.
The lesion and apical root segments of 8 untreated teeth and 16 root canal treated teeth with sinus tracts were biopsied during apical surgery. The root canal treated teeth had been previously unresponsive to endodontic treatment. The roots from these teeth were sectioned 3mm coronal to the root tip and the periapical lesion enucleated with the root tip attached. The untreated teeth with lesions attached were obtained through extraction of non-restorable teeth. All specimens were sent for bacteriologic examination.
Histobacteriologic analysis found bacteria in the apical root canal system of all 24 specimens. 22 specimens had bacterial biofilms in the main apical canal. 2 specimens had biofilms only within large lateral canals adjacent to the uncontaminated main canal. In 17 specimens biofilms were found in both the main canals and lateral canal anatomy.
Bacterial biofilms were found on the external root surface of 17 of the specimens and extra-radicular biofilms and planktonic bacteria in all but 4 of the specimens. In most cases, the biofilms were thick and contained several layers of bacterial cells enmeshed in an extracellular matrix. The basic bacterial morphotypes found were cocci, rods, and filaments. There was little difference between the intra-radicular and extra-radicular biofilms though the extra-radicular biofilms were often calcified, not unlike calculus.
There are a number of take-home messages from this study by Ricucci et al on teeth which present with LEOs and sinus tracts:
ABOUT THE AUTHOR
Dr. Howard Bittner, DMD, CAGS