Endodontic infections and systemic health – where should we go?

Abstract

Listen

Translate article

About 100 years ago, the endodontic focal infection theory claimed that bacteria remaining after root canal treatment could be the cause of systemic conditions, such as arthritis and kidney or heart diseases. The spread of this theory resulted in an era when teeth were extracted instead of being treated endodontically. Indeed, extractions were not only meant to treat these systemic diseases but also even act as a prophylactic measure to reduce the risk of developing them. The research advocating the focal infection theory was criticized at the time of the original publications, and very soon studies with much better designs were published to discredit the concept. Ancient past? Times gone and forgotten? Maybe not. ‘Mausoleums of gold’ may have been replaced with more modern restorative materials, but – despite all the bells and whistles of modern endodontics – we still have to accept that in many, maybe most, infected cases microbes are still left behind and persistent or recurrent apical disease can and does occur. Indeed, the advent of cone beam computed tomography (CBCT) has made us realize that conventional diagnostic methods appear to underestimate the prevalence of apical lesions associated with root-filled teeth. The decision whether to retreat asymptomatic, functioning teeth is not always an easy one. A tooth that may seem to a dentist as a clear treatment case can be just fine for the patient, and we have to judge carefully whether the benefits of further treatment outweigh the risks. Apical periodontitis is a defensive inflammatory reaction aiming to restrain infection within the root canal system. Whether we should consider apical periodontitis as a ‘disease’ at all is (luckily for me!) beside the point here. However, the question whether the apically detected inflammation is a threat to systemic health has again been raised, and this is a question the endodontic community needs to react to. It has been proposed that periodontitis is linked to a number of systemic conditions – cardiovascular disease, diabetes, rheumatoid arthritis, renal diseases, low birthweight, Alzheimer's disease, Parkinson's disease, even erectile dysfunction – on the basis of systemic inflammation. However, most studies show association, and opinions of the cause-effect relationship and the effect of periodontal treatment on the disease risk still differ dramatically. Nevertheless, the possibility of oral infections as an independent risk for systemic health has caused much interest (and worry) among dentists, other health professionals and the general population. If periodontal inflammation, especially severe periodontitis, can be demonstrated to be a causative or contributing factor to any or many systemic diseases, the question still remains if apical periodontitis has similar effects, and if it does, how, to whom and when? Should we be concerned about small persistent lesions only detected with CBCT, or only be concerned about large and/or multiple lesions? These questions remain unanswered. The European Society of Endodontology (ESE) has recognized the need for high-quality evidence to answer these questions. The first action was to organize an ESE Research Meeting with the topic ‘The relationship between apical periodontitis and general health’ in October 2014. Even though the general consensus of the meeting was that the level of evidence in general was low, we do know something! In this issue of International Endodontic Journal, some of the lecturers of that meeting share their expertise, addressing the questions such as the relationship between apical periodontitis and cardiovascular disease or diabetes, as well as potential virulence mechanisms of some endodontic microbes that might contribute to the persisting disease. These articles will help the clinician to take into account some of the systemic health concerns and to make more informed decisions while considering the treatment options for endodontically diseased teeth. Personally, I do not think that we should consider every root-filled tooth with slightly widened apical periodontal ligament as a failure and cause of concern to systemic health. At the same time, we should not dismiss the possibility that persistent periapical inflammation in an asymptomatic functioning tooth could be a more serious threat than expected. Just recently, the ESE has taken a leading role in the search for more evidence and launched a grant programme to specifically support high-quality studies examining the role of endodontic and systemic diseases. For the future of our discipline, the evidence may be crucial. If we cannot find the evidence, one way or another, the focal infection theory could resurface, and once more be based on low-level evidence and opinions rather than facts.