Apical periodontitis: a very prevalent problem.

Apical periodontitis, an inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp space of teeth and is a remarkably widespread problem.1 The prevalence of apical periodontitis increases with age: by 50 years of age, 1 in 2 individuals will experience the disease.2 In individuals over 60 years old, the prevalence of apical periodontitis rises to 62%. 2 The clinical management of apical periodontitis involves infection control by root canal treatment, which is the only viable alternative to the unsatisfactory option of tooth loss. On the basis of an average number of 2.2 root fillings per adult,3 it can be estimated from census data that there are 25 million root filled teeth in Australia and more than 420 million root filled teeth in the US. In the year 1990, an estimated 14 million root canal treatments were performed in the US alone.4 The magnitude of the problem does not seem to have been fully appreciated, and therefore apical periodontitis has not attracted the attention deserved by such a common disease. Another reason that apical periodontitis may not have received a greater degree of interest is that the success rate of treatment has generally been regarded as high, of the order of 87%. 2 This figure applies to endodontic treatment done in specialist practice where a higher expertise is likely to result in a better technical standard of treatment, whereas the success rate in general practice is of the order of 72%. 2 However, when the failure rate is measured relative to the prevalence of root canal treatment, the full dimension of the problem becomes apparent. When a conservative failure rate of 13% for root canal treatment in the average population is assumed, it can be estimated that there are 3.3 million failed root canal treatments in Australia and 54 million in the US; taking the greater failure rate for treatment in general practice, the figures could be as high as 7 million and 117 million, respectively. When these numbers are multiplied by the cost of endodontic retreatment and crown or restoration replacement, the cumulative economic impact is in the order of billions of dollars. In recent years there has been a trend toward focusing on the technical aspects of mechanical instrumentation of the root canal as a measure of success of endodontic treatment. Although the mechanical elements of treatment undoubtedly deserve attention, a critical evaluation of relevant factors involved in the etiology of endodontic failure is more likely to yield meaningful information and, ultimately, rational treatment solutions. Sound clinical treatment must be based on a clear understanding of the causative factors in the disease process, so that intelligent and logical solutions can be applied to address the problem. For apical periodontitis, the essential role of microbial infection is well recognized as the critical etiological factor. Therefore, endodontic treatment is fundamentally the clinical management of a microbiological problem. It is logical, then, that the principal treatment objective is elimination of bacteria and exclusion of further infection from the root canal. A clean, infection-free canal can best be accomplished by mechanical instrumentation in the presence of antibacterial irrigation followed by an antimicrobial intracanal dressing, which should in most cases provide predictable elimination of bacteria. Although the method of root filling with guttapercha was first described more than 135 years ago,5 it is astonishing that relatively modest progress has been made in defining the relative contribution of the root filling in the overall antimicrobial approach to root canal treatment. The idea that fluids percolating into an empty “dead” space might break down and be the cause of apical periodontitis originated as early as the 1930s,6 but vestiges of the concept linger to the present day despite evidence demonstrating the fallacy of the idea.7,8 The hypothesis that the “dead” space was a prime cause of apical periodontitis was propagated further during the mid-1950s and 1960s when the “Washington study,” taken together with an o oo ORAL SURGERY ORAL MEDICINE