120 resultados para agressive periodontitis


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BACKGROUND Findings from animal and human studies have indicated that an oily calcium hydroxide suspension (OCHS) may improve early wound healing in the treatment of periodontitis. Calcium hydroxide as the main component is well known for its antimicrobial activity, however at present the effect of OCHS on the influence of periodontal wound healing/regeneration is still very limited. The purpose of this in vitro study was to investigate the effect of OCHS on periodontopathogenic bacteria as well as on the attachment and proliferation of osteoblasts and periodontal ligament fibroblasts. METHODS Human alveolar osteoblasts (HAO) and periodontal ligament (PDL) fibroblasts were cultured on 3 concentrations of OCHS (2.5, 5 and 7.5 mg). Adhesion and proliferation were counted up to 48 h and mineralization was assayed after 1 and 2 weeks. Furthermore potential growth inhibitory activity on microorganisms associated with periodontal disease (e.g. Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans) as well as the influence of periodontopathogens and OCHS on the HAO and PDL fibroblasts counts were determined. RESULTS More than a 2-fold increase in adherent HAO cells was observed at 4 h following application of OCHS when compared to the control group (p = 0.007 for 2.5 mg). Proliferation of HAO cells at 48 h was stimulated by moderate concentrations (2.5 mg; 5 mg) of OCHS (each p < 0.001), whereas a high concentration (7.5 mg) of OCHS was inhibitory (p = 0.009). Mineralization was observed only for HAO cells treated with OCHS. OCHS did not exert any positive effect on attachment or proliferation of PDL fibroblasts. Although OCHS did not have an antibacterial effect, it did positively influence attachment and proliferation of HAO cells and PDL fibroblasts in the presence of periodontopathogens. CONCLUSIONS The present data suggests that OCHS promotes osteoblast attachment, proliferation and mineralization in a concentration-dependent manner and results are maintained in the presence of periodontal pathogens.

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OBJECTIVES Retrospectively, we assessed the likelihood that peri-implantitis was associated with a history of systemic disease, periodontitis, and smoking habits. METHODS Data on probing pocket depth (PPD), bleeding on probing (BOP), and radiographic bone levels were obtained from individuals with dental implants. Peri-implantitis was defined as described by Sanz & Chapple 2012. Control individuals had healthy conditions or peri-implant mucositis. Information on past history of periodontitis, systemic diseases, and on smoking habits was obtained. RESULTS One hundred and seventy-two individuals had peri-implantitis (mean age: 68.2 years, SD ± 8.7), and 98 individuals (mean age: 44.7 years, SD ± 15.9) had implant health/peri-implant mucositis. The mean difference in bone level at implants between groups was 3.5 mm (SE mean ± 0.4, 95% CI: 2.8, 4.3, P < 0.001). A history of cardiovascular disease was found in 27.3% of individuals with peri-implantitis and in 3.0% of individuals in the implant health/peri-implant mucositis group. When adjusting for age, smoking, and gender, odds ratio (OR) of having peri-implantitis and a history of cardiovascular disease was 8.7 (95% CI: 1.9, 40.3 P < 0.006), and odds ratio of having a history of periodontitis was 4.5 (95% CI 2.1, 9.7, P < 0.001). Smoking or gender did not significantly contribute to the outcome. CONCLUSIONS In relation to a diagnosis of peri-implantitis, a high likelihood of comorbidity was expressed by a history of periodontitis and a history of cardiovascular disease.

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BACKGROUND Limited data exist on the longitudinal crestal bone changes around teeth compared with implants in partially edentulous patients. This study sought to compare the 10-year radiographic crestal bone changes (bone level [BL]) around teeth and implants in periodontally compromised (PCPs) and periodontally healthy (PHPs) patients. METHODS A total of 120 patients were evaluated for the radiographic crestal BL around dental implants and adjacent teeth at time of implant crown insertion and at the 10-year follow-up. Sixty patients had a previous history of periodontitis (PCPs), and the remaining 60 were PHPs. In each category (PCP and PHP), two different implant systems were used. The mean BL change at the implant and at the adjacent tooth at the interproximal area was calculated by subtracting the radiographic crestal BL at the time of crown cementation from the radiographic crestal BL at the 10-year follow-up. RESULTS At 10 years after therapy, the survival rate ranged from 80% to 95% for subgroups for implants, whereas it was 100% for the adjacent teeth. In all eight different patient categories evaluated, teeth demonstrated a significantly more stable radiographic BL compared with adjacent dental implants (teeth BL, 0.44 ± 0.23 mm; implant BL, 2.28 ± 0.72 mm; P <0.05). Radiographic BL changes around teeth seemed not to be influenced by the presence or absence of advanced bone loss (≥3 mm) at the adjacent implants. CONCLUSIONS Natural teeth yielded better long-term results with respect to survival rate and marginal BL changes compared with dental implants. Moreover, these findings also extend to teeth with an initial reduced periodontal attachment level, provided adequate periodontal treatment and maintenance are performed. As a consequence, the decision of tooth extraction attributable to periodontal reasons in favor of a dental implant should be carefully considered in partially edentulous patients.

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Periodontitis is a chronic inflammatory disease of the periodontium, which is caused by pathogenic bacteria in combination with other risk factors. The bacteria induce an immunoinflammatory host response, which can lead to irreversible matrix degradation and bone resorption. Periodontitis can be successfully treated. To achieve regenerative periodontal healing, bioactive molecules, such as enamel matrix derivative (EMD), are applied during periodontal surgery. Recently, it has been shown that obesity is associated with periodontitis and compromised healing after periodontal therapy. The mechanisms underlying these associations are not well understood so far, but adipokines may be a pathomechanistic link. Adipokines are bioactive molecules that are secreted by the adipose tissue, and that regulate insulin sensitivity and energy expenditure, but also inflammatory and healing processes. It has also been demonstrated that visfatin and leptin increase the synthesis of proinflammatory and proteolytic molecules, whereas adiponectin downregulates the production of such mediators in periodontal cells. In addition, visfatin and leptin counteract the beneficial effects of EMD, whereas adiponectin enhances the actions of EMD on periodontal cells. Since visfatin and leptin levels are increased and adiponectin levels are reduced in obesity, these adipokines could be a pathomechanistic link whereby obesity and obesity-related diseases enhance the risk for periodontitis and compromised periodontal healing. Recent studies have also revealed that adipokines, such as visfatin, leptin and adiponectin, are produced in periodontal cells and regulated by periodontopathogenic bacteria. Therefore, adipokines may also represent a mechanism whereby periodontal infections can impact on systemic diseases.

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BACKGROUND Information on the microbiota in peri-implantitis is limited. We hypothesized that neither gender nor a history of periodontitis/smoking or the microbiota at implants differ by implant status. MATERIALS AND METHODS Baseline microbiological samples collected at one implant in each of 166 participants with peri-implantitis and from 47 individuals with a healthy implant were collected and analyzed by DNA-DNA checkerboard hybridization (78 species). Clinical and radiographic data defined implant status. RESULTS Nineteen bacterial species were found at higher counts from implants with peri-implantitis including Aggregatibacter actinomycetemcomitans, Campylobacter gracilis, Campylobacter rectus, Campylobacter showae, Helicobacter pylori, Haemophilus influenzae, Porphyromonas gingivalis, Staphylococcus aureus, Staphylococcus anaerobius, Streptococcus intermedius, Streptococcus mitis, Tannerella forsythia, Treponema denticola, and Treponema socranskii (p < .001). Receiver operating characteristic curve analysis identified T. forsythia, P. gingivalis, T. socranskii, Staph. aureus, Staph. anaerobius, Strep. intermedius, and Strep. mitis in peri-implantitis comprising 30% of the total microbiota. When adjusted for gender (not significant [NS]), smoking status (NS), older age (p = .003), periodontitis history (p < .01), and T. forsythia (likelihood ratio 3.6, 95% confidence interval 1.4, 9.1, p = .007) were associated with peri-implantitis. CONCLUSION A cluster of bacteria including T. forsythia and Staph. aureus are associated with peri-implantitis.

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BACKGROUND Although regenerative treatment options are available, periodontal regeneration is still regarded as insufficient and unpredictable. AIM This review article provides scientific background information on the animated 3D film Cell-to-Cell Communication - Periodontal Regeneration. RESULTS Periodontal regeneration is understood as a recapitulation of embryonic mechanisms. Therefore, a thorough understanding of cellular and molecular mechanisms regulating normal tooth root development is imperative to improve existing and develop new periodontal regenerative therapies. However, compared to tooth crown and earlier stages of tooth development, much less is known about the development of the tooth root. The formation of root cementum is considered the critical element in periodontal regeneration. Therefore, much research in recent years has focused on the origin and differentiation of cementoblasts. Evidence is accumulating that the Hertwig's epithelial root sheath (HERS) has a pivotal role in root formation and cementogenesis. Traditionally, ectomesenchymal cells in the dental follicle were thought to differentiate into cementoblasts. According to an alternative theory, however, cementoblasts originate from the HERS. What happens when the periodontal attachment system is traumatically compromised? Minor mechanical insults to the periodontium may spontaneously heal, and the tissues can structurally and functionally be restored. But what happens to the periodontium in case of periodontitis, an infectious disease, after periodontal treatment? A non-regenerative treatment of periodontitis normally results in periodontal repair (i.e., the formation of a long junctional epithelium) rather than regeneration. Thus, a regenerative treatment is indicated to restore the original architecture and function of the periodontium. Guided tissue regeneration or enamel matrix proteins are such regenerative therapies, but further improvement is required. As remnants of HERS persist as epithelial cell rests of Malassez in the periodontal ligament, these epithelial cells are regarded as a stem cell niche that can give rise to new cementoblasts. Enamel matrix proteins and members of the transforming growth factor beta (TGF-ß) superfamily have been implicated in cementoblast differentiation. CONCLUSION A better knowledge of cell-to-cell communication leading to cementoblast differentiation may be used to develop improved regenerative therapies to reconstitute periodontal tissues that were lost due to periodontitis.

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Comparative genomics of virulent Tannerella forsythia ATCC 43037 and a close health-associated relative, Tannerella BU063, revealed, in the latter, the absence of an entire array of genes encoding putative secretory proteases that possess a nearly identical C-terminal domain (CTD) that ends with a -Lys-Leu-Ile-Lys-Lys motif. This observation suggests that these proteins, referred to as KLIKK proteases, may function as virulence factors. Re-sequencing of the loci of the KLIKK proteases found only six genes grouped in two clusters. All six genes were expressed by T. forsythia in routine culture conditions, although at different levels. More importantly, a transcript of each gene was detected in gingival crevicular fluid (GCF) from periodontitis sites infected with T. forsythia indicating that the proteases are expressed in vivo. In each protein, a protease domain was flanked by a unique N-terminal profragment and a C-terminal extension ending with the CTD. Partially purified recombinant proteases showed variable levels of proteolytic activity in zymography gels and toward protein substrates, including collagen, gelatin, elastin, and casein. Taken together, these results indicate that the pathogenic strain of T. forsythia secretes active proteases capable of degrading an array of host proteins, which likely represents an important pathogenic feature of this bacterium.

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OBJECTIVES To characterize the physical characteristics of a new low abrasive erythritol powder (EPAP) and to evaluate its influence on the clinical and microbiologic parameters over a period of 6 months in patients undergoing supportive periodontal therapy (SPT). METHOD AND MATERIALS Prior to the clinical application, the particle size and abrasion level of EPAP were compared to glycine air-polishing powder (GPAP) ex vivo. Subsequently, 40 chronic periodontitis patients previously enrolled in SPT were randomly assigned into two groups for the treatment with subgingival EPAP or repeated scaling and root planing (SRP). At baseline (BL), bleeding on probing positive (BOP+) sites with probing pocket depth (PPD) of ≥ 4 mm but no detectable calculus were defined as study sites. During SPT, these sites were either treated by EPAP or SRP at BL, 3, and 6 months (3M, 6M). When indicated, additional SRP was provided. Plaque Index, BOP, PPD, clinical attachment level (CAL), and subgingival plaque were evaluated at BL and 6M. RESULTS EPAP yielded lower abrasiveness and smaller particle sizes when compared to GPAP. In 38 patients completing the study, EPAP and SRP resulted in significant reductions of BOP% (EPAP, 40.45%; SRP, 42.53%), PPD (EPAP, -0.67; SRP, -0.68), and increase of CAL (EPAP, 0.48; SRP, 0.61) while at 6M no statistically significant between-group differences were observed (P > .05). Microbiologic evaluation revealed minor shifts in the composition of the subgingival biofilm without influence on periodontopathogenic bacteria. CONCLUSION The subgingival use of EPAP by means of an air-polishing device may be considered safe and may lead to comparable clinical and microbiologic outcomes to those obtained with SRP. CLINICAL RELEVANCE The subgingival use of EPAP appears to represent a promising modality for the removal of subgingival biofilm during SPT.

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AIMS Over the past decades, the placement of dental implants has become a routine procedure in the oral rehabilitation of fully and partially edentulous patients. However, the number of patients/implants affected by peri-implant diseases is increasing. As there are--in contrast to periodontitis--at present no established and predictable concepts for the treatment of peri-implantitis, primary prevention is of key importance. The management of peri-implant mucositis is considered as a preventive measure for the onset of peri-implantitis. Therefore, the remit of this working group was to assess the prevalence of peri-implant diseases, as well as risks for peri-implant mucositis and to evaluate measures for the management of peri-implant mucositis. METHODS Discussions were informed by four systematic reviews on the current epidemiology of peri-implant diseases, on potential risks contributing to the development of peri-implant mucositis, and on the effect of patient and of professionally administered measures to manage peri-implant mucositis. This consensus report is based on the outcomes of these systematic reviews and on the expert opinion of the participants. RESULTS Key findings included: (i) meta-analysis estimated a weighted mean prevalence for peri-implant mucositis of 43% (CI: 32-54%) and for peri-implantitis of 22% (CI: 14-30%); (ii) bleeding on probing is considered as key clinical measure to distinguish between peri-implant health and disease; (iii) lack of regular supportive therapy in patients with peri-implant mucositis was associated with increased risk for onset of peri-implantitis; (iv) whereas plaque accumulation has been established as aetiological factor, smoking was identified as modifiable patient-related and excess cement as local risk indicator for the development of peri-implant mucositis; (v) patient-administered mechanical plaque control (with manual or powered toothbrushes) has been shown to be an effective preventive measure; (vi) professional intervention comprising oral hygiene instructions and mechanical debridement revealed a reduction in clinical signs of inflammation; (vii) adjunctive measures (antiseptics, local and systemic antibiotics, air-abrasive devices) were not found to improve the efficacy of professionally administered plaque removal in reducing clinical signs of inflammation. CONCLUSIONS Consensus was reached on recommendations for patients with dental implants and oral health care professionals with regard to the efficacy of measures to manage peri-implant mucositis. It was particularly emphasized that implant placement and prosthetic reconstructions need to allow proper personal cleaning, diagnosis by probing and professional plaque removal.

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BACKGROUND The purpose of this clinical study was to assess the prevalence of acidic oral mucosal lesions and periodontal conditions in patients suffering from erosive esophageal reflux disease (ERD) compared with non erosive esophageal reflux disease (NERD) patients, both treated with long term proton pump inhibitors (PPI). METHODS Seventy-one patients with diagnosed GERD were studied: i.e. 29 ERD and 42 NERD patients. Thorough visual examination of the oral mucosa and a periodontal evaluation was performed. The primary outcome was defined as a statistically significant difference, between the two groups, in the presence of acidic lesions of the oral mucosa and specific periodontal parameters. RESULTS This study failed to demonstrate statistically significant differences between ERD and NERD patients with respect to the prevalence of oral mucosal lesions. However, significantly more ERD patients suffered from severe periodontitis (CAL ≥ 5 mm) as compared to NERD patients. Accordingly, it may be assumed that PPI-use had no adverse effects on the prevalence of acidic oral mucosal lesions and on periodontal destruction. CONCLUSIONS Within the limitations of this study it may be concluded that ERD and NERD patients need separate evaluation with respect to periodontal destruction. Moreover, long term PPI medication had no adverse clinical impact on acidic oral mucosal lesions and periodontal destruction. Further studies are necessary to elucidate the role of reflux in the periodontal destruction of ERD individuals.

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Intrabony periodontal defects are a frequent complication of periodontitis and, if left untreated, may negatively affect long-term tooth prognosis. The optimal outcome of treatment in intrabony defects is considered to be the absence of bleeding on probing, the presence of shallow pockets associated with periodontal regeneration (i.e. formation of new root cementum with functionally orientated inserting periodontal ligament fibers connected to new alveolar bone) and no soft-tissue recession. A plethora of different surgical techniques, often including implantation of various types of bone graft and/or bone substitutes, root surface demineralization, guided tissue regeneration, growth and differentiation factors, enamel matrix proteins or various combinations thereof, have been employed to achieve periodontal regeneration. Despite positive observations in animal models and successful outcomes reported for many of the available regenerative techniques and materials in patients, including histologic reports, robust information on the degree to which reported clinical improvements reflect true periodontal regeneration does not exist. Thus, the aim of this review was to summarize, in a systematic manner, the available histologic evidence on the effect of reconstructive periodontal surgery using various types of biomaterials to enhance periodontal wound healing/regeneration in human intrabony defects. In addition, the inherent problems associated with performing human histologic studies and in interpreting the results, as well as certain ethical considerations, are discussed. The results of the present systematic review indicate that periodontal regeneration in human intrabony defects can be achieved to a variable extent using a range of methods and materials. Periodontal regeneration has been observed following the use of a variety of bone grafts and substitutes, guided tissue regeneration, biological factors and combinations thereof. Combination approaches appear to provide the best outcomes, whilst implantation of alloplastic material alone demonstrated limited, to no, periodontal regeneration.

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Recent reports focusing on virulence factors of periodontal pathogens implicated proteinases as major determinants of remarkable pathogenicity of these species, with special emphasis on their capacity to modulate complement activity. In particular, bacteria-mediated cleavage of C5 and subsequent release of C5a seems to be an important phenomenon in the manipulation of the local inflammatory response in periodontitis. In this study, we present mirolysin, a novel metalloproteinase secreted by Tannerella forsythia, a well-recognized pathogen strongly associated with periodontitis. Mirolysin exhibited a strong effect on all complement pathways. It inhibited the classical and lectin complement pathways due to efficient degradation of mannose-binding lectin, ficolin-2, ficolin-3, and C4, whereas inhibition of the alternative pathway was caused by degradation of C5. This specificity toward complement largely resembled the activity of a previously characterized metalloproteinase of T. forsythia, karilysin. Interestingly, mirolysin released the biologically active C5a peptide in human plasma and induced migration of neutrophils. Importantly, we demonstrated that combination of mirolysin with karilysin, as well as a cysteine proteinase of another periodontal pathogen, Prevotella intermedia, resulted in a strong synergistic effect on complement. Furthermore, mutant strains of T. forsythia, devoid of either mirolysin or karilysin, showed diminished survival in human serum, providing further evidence for the synergistic inactivation of complement by these metalloproteinases. Taken together, our findings on interactions of mirolysin with complement significantly add to the understanding of immune evasion strategies of T. forsythia and expand the knowledge on molecular mechanisms driving pathogenic events in the infected periodontium.

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OBJECTIVE To determine the microbiota at implants and adjacent teeth 10 years after placement of implants with a sandblasted and acid-etched surface. MATERIAL AND METHODS Plaque samples obtained from the deepest sites of 504 implants and of 493 adjacent teeth were analyzed for certain bacterial species associated with periodontitis, for staphylococci, for aerobic gram-negative rods, and for yeasts using nucleic acid-based methods. RESULTS Species known to be associated with periodontitis were detectable at 6.2-78.4% of the implants. Significantly higher counts at implants in comparison with teeth were assessed for Tannerella forsythia, Parvimonas micra, Fusobacterium nucleatum/necrophorum, and Campylobacter rectus. Higher counts of periodontopathogenic species were detectable at implants of current smokers than at those of non-smokers. In addition, those species were found in higher quantities at implants of subjects with periodontitis. The prevalence of Prevotella intermedia, Treponema denticola, C. rectus, and moreover of Staphylococcus warneri might be associated with peri-implant inflammation. Selected staphylococcal species (not Staphylococcus aureus), aerobic gram-negative rods, and yeasts were frequently detected, but with the exception of S. warneri, they did not show any association with periodontal or peri-implant diseases. CONCLUSIONS Smoking and periodontal disease are risk factors for colonization of periodontopathic bacteria at implants. Those bacterial species may play a potential role in peri-implant inflammation. The role of S. warneri needs further validation.

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OBJECTIVES To assess a selection of host-derived biomarkers in peri-implant sulcus fluid (PISF) and gingival crevicular fluid (GCF) from adjacent teeth 10 years following implant placement. MATERIAL AND METHODS Peri-implant sulcus fluid and GCF samples obtained from the deepest sites of 504 implants and 493 adjacent teeth were analysed for levels of interleukin (IL)-1β, matrix metalloproteinase (MMP)-3, MMP-8, MMP-1, and MMP-1 bound to tissue inhibitor of MMP (TIMP)-1 (MMP-1/TIMP-1) by enzyme-linked immunosorbent assay (ELISA) technique. RESULTS Overall, MMP-8 was detected in 90% of the sites. In more than 50% of the sites, IL-1β was identified while in 30% of the sites MMP-1, MMP-1/TIMP-1 and MMP-3 were found over the detection level. Increased biomarkers levels from PISF and GCF were positively correlated (r = 0.375-0.702; P < 0.001). However, no qualitative and quantitative differences were found between PISF and GCF. The levels of MMP-1 were negatively correlated with those of MMP-1/TIMP-1 at implants (r = -0.644; P < 0.001). Median MMP-1 levels at implants were high (5.17 pg/site) in subjects with severe chronic periodontitis and low in patients with mild-to-moderate chronic periodontitis (0 pg/site; P = 0.026) or gingivitis (0 pg/site; P = 0.034). Levels of IL-1β were found to be different in GCF according to the periodontal conditions (P = 0.001) with the highest level found in mild-to-moderate periodontitis (6.2 pg/site). Clinical attachment levels at implants demonstrated an inverse correlation with MMP-1/TIMP-1 (r = -0.147; P = 0.001). CONCLUSIONS Increased levels of MMP-8 and IL-1β in PISF or GCF may be associated with inflammation around teeth and implants while lower levels of MMP-1/TIMP-1 may be an indicator of disease progression around implants.

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INTRODUCTION Apical surgery is an important treatment option for teeth with post-treatment periodontitis. Although apical surgery involves root-end resection, no morphometric data are yet available about root-end resection and its impact on the root-to-crown ratio (RCR). The present study assessed the length of apicectomy and calculated the loss of root length and changes of RCR after apical surgery. METHODS In a prospective clinical study, cone-beam computed tomography scans were taken preoperatively and postoperatively. From these images, the crown and root lengths of 61 roots (54 teeth in 47 patients) were measured before and after apical surgery. Data were collected relative to the cementoenamel junction (CEJ) as well as to the crestal bone level (CBL). One observer took all measurements twice (to calculate the intraobserver variability), and the means were used for further analysis. The following parameters were assessed for all treated teeth as well as for specific tooth groups: length of root-end resection and percentage change of root length, preoperative and postoperative RCRs, and percentage change of RCR after apical surgery. RESULTS The mean length of root-end resection was 3.58 ± 1.43 mm (relative to the CBL). This amounted to a loss of 33.2% of clinical and 26% of anatomic root length. There was an overall significant difference between the tooth groups (P < .05). There was also a statistically significant difference comparing mandibular and maxillary teeth (P < .05), but not for incisors/canines versus premolars/molars (P = .125). The mean preoperative and postoperative RCRs (relative to CEJ) were 1.83 and 1.35, respectively (P < .001). With regard to the CBL reference, the mean preoperative and postoperative RCRs were 1.08 and 0.71 (CBL), respectively (P < .001). The calculated changes of RCR after apical surgery were 24.8% relative to CEJ and 33.3% relative to CBL (P < .001). Across the different tooth groups, the mean RCR was not significantly different (P = .244 for CEJ and 0.114 for CBL). CONCLUSIONS This CBCT-based study demonstrated that the RCR is significantly changed after root-end resection in apical surgery irrespective of the clinical (CBL) or anatomic (CEJ) reference levels. The lowest, and thus clinically most critical, postoperative RCR was observed in maxillary incisors. Future clinical studies need to show the impact of resection length and RCR changes on the outcome of apical surgery.