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Background Outcome studies of nonsurgical root canal treatment (NSRCT) in permanent teeth of children are scarce. This study investigated survival and assessed the variables associated with failure of endodontically treated teeth (ETT) in 6- to 18-year-olds. Methods Records of subjects who received NSRCT at age 6–18 years at Boston University between 2007 and 2015 were assessed for the occurrence of untoward events. Kaplan–Meier survival curves were used to investigate the survival of ETT in the total sample. Adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) were estimated. Results The analysis included 341 patients (424 ETT). Kaplan–Meier survival curves differed according to age at treatment (log-rank P = 0.026), with survival being the lowest among the youngest age group. The estimated 5-year survival probability was 80% for 15- to 18-year-olds, 64.8% for 12- to 14-year-olds and 46.4% for 6- to 11-year-olds. Compared to age at treatment of 15–18 years, age at treatment of 6–11 years (aHR: 2.19, 95% CI 1.02–4.67) and 12–14 years (aHR: 2.02, 95% CI 1.15–3.55) was associated with an increased risk of ETT failure. In the total study sample, the estimated cumulative survival probability was 93.3% at 12 months, 88.0% at 24 months, 76.2% at 36 months, 71.0% at 48 months, and 69.1% at 60 months. Conclusions In children, ETT are more likely to survive when NSRCTs are performed at an older age.

Introduction Cracked teeth are a common clinical finding; however, their presence renders diagnosis and prognosis unreliable. The purpose of this research was to assess the correlations of multiple factors on the prognosis of cracked teeth that had undergone endodontic treatment. Methods A total of 3680 patients who received endodontic treatment by an advanced postdoctoral education program in endodontics with follow-up records of at least 1 year were assessed. From this sample, 62 patients met the inclusion criteria and were included in the final analysis. The factors being evaluated included demographics, clinical symptoms and signs, radiographic findings, and restoration type. Statistical analysis was then completed using the chi-square and Fisher exact tests. Results The mean follow-up period was 23.3 months, with an overall tooth success rate of 75.8%. The success rates differed significantly when the patient had an existing preoperative periapical lesion, lacked a proper permanent restoration on the treated tooth, or had a post placed after root canal treatment. Data analysis showed that restoring the tooth after endodontic treatment was the single most important factor for prognosis. In fact, the endodontically treated teeth with definitive full-coverage restorations had a 2-year success rate of 93.6%. Conclusion Full-coverage restorations should be considered an important part of the treatment plan for cracked teeth treated endodontically.

Similar to other disciplines of advanced dentistry, a clinician may encounter complications or unforeseen circumstances during endodontic therapy. Every clinician performing endodontic procedures would have experienced a range of outcomes ranging from a case well done to an unfavorable prognosis related to a procedural accident. Examples of complications during the root canal procedure include ledge formation, separated instruments, and over-instrumentation. However, fear of procedural accidents should not deter a practitioner from performing root canal treatment. An experienced clinician uses knowledge, clinical skill and acumen, experience, and awareness of his or her own limitations to minimize these accidents.

Bacteria or their products may cause chronic inflammation and subsequent bone loss. This inflammation and bone loss may be associated with significant morbidity in chronic otitis media, periodontitis, endodontic lesions, and loosening of orthopedic implants caused by lipopolysaccharide (LPS)-contaminated implant particles. Currently, it is not clear how bacteria or endotoxin-induced bone resorption occurs and what cell types are involved. Here we report thatPorphyromonas gingivalis, a periodontal pathogen, andEscherichia coliLPS induce osteoclastic cell formation from murine leukocytes in the absence of osteoblasts. In contrast, stimulation with parathyroid hormone had no effect. These multinucleated, tartrate-resistant acid phosphatase-positive cells were positive for receptor activator of NF-κB (RANK), the receptor for osteoprotegerin ligand (OPGL), also known as RANK ligand (RANKL). Blocking antibodies demonstrated that their formation was dependent upon expression of OPGL and, to a lesser extent, on tumor necrosis factor alpha. Mononuclear cells represented a significant source of OPGL production. In vivo,P. gingivalisinjection stimulated OPGL expression in both mononuclear leukocytes and osteoblastic cells. Thus, these findings describe a pathway by which bacteria could enhance osteolysis independently of osteoblasts and suggest that the mix of cells that participate in inflammatory and physiologic bone resorption may be different. This may give insight into new targets of therapeutic intervention.