Debridement of the root canal by instrumentation and irrigation is considered the most important single factor in the prevention and treatment of endodontic diseases. In clinical practice, instrumentation of the root canal(s) within the affected tooth is usually the most time consuming and technically demanding element of the treatment. The technical success of the treatment, as judged by the post‐operative radiograph after the root filling, is based on optimized root canal instrumentation. Mounting evidence from epidemiological research is also indicating that the combination of high‐quality coronal restoration and technically satisfactory root canal treatment is associated with the greatest long‐term prognosis. Therefore, it is not surprising that for several decades of endodontic research, a substantial number of articles on instruments and instrumentation have been published in the scientific literature. Although interest in the effects of instrumentation on intracanal infection is not new, it is obvious that during the last few years a renewed focus of interest has appeared on the relationship between instrumentation and infection control in the root canal. The ongoing discussion in international endodontics about one‐appointment therapy in the treatment of apical periodontitis has naturally further motivated the newly emerged research activities. The goal of this review is to gather the relevant and most recent literature and provide an updated analysis of the effect of preparation (instrumentation and irrigation) on the microbial infection in the necrotic root canal.

Apical periodontitis is an inflammatory process in the periradicular tissues caused by microorganisms in the necrotic root canal. Accordingly, to achieve healing of apical periodontitis, the main goal of the treatment must be elimination of the infection and prevention of re‐infection. As shown by recent epidemiological studies in several countries around the world, post‐treatment endodontic disease is a far too common finding. To understand the reasons for survival of resistant bacteria in the filled root canal, it is important to know in detail the interaction between treatment procedures and the root canal flora in primary apical periodontitis. Therefore, in the first half of this review, the focus is placed on control of infection in primary apical periodontitis. This is followed by a detailed description of the resistant root canal microflora and a discussion about the present and future strategies to eliminate even the most resistant microbes in post‐treatment disease.

Internal inflammatory root resorption is a relatively rare resorption that begins in the root canal and destroys surrounding dental hard tissues. Odontoclastic multinuclear cells are responsible for the resorption, which can grow to perforate the root if untreated. The initiating factor in internal root resorption is thought to be trauma or chronic pulpal inflammation, but other etiological factors have also been suggested. Active, expanding resorption requires vital pulp tissue and continuous microbiological irritation, likely from the necrotic coronal part of the root canal. In its classical form, internal root resorption is easy to diagnose. However, in many instances advanced diagnostic methods may be required for a definitive diagnosis. Internal root resorption is usually symptom free, but in cases of perforation, a sinus tract usually forms. The prognosis for treatment of small lesions of internal root resorption is very good. If, however, the tooth structure is greatly weakened and perforation has occurred, the prognosis is poor and tooth extraction must be considered. Sodium hypochlorite, ultrasonic instrumentation and calcium hydroxide are the cornerstones of treatment of internal inflammatory root resorption. Mineral trioxide aggregate is being increasingly used as a root canal filling material, particularly in cases of perforation.

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LC and BF techniques resulted in fewer overfills than TF. Voids were absent in TF fillings, whilst small voids were found in the LC and BF groups.