The CIELab and CIEDE2000 coverage error (ΔE* and ΔE', respectively) of basic shades of different gingival shade guides and gingiva-colored restorative dental materials (n = 5) was calculated as compared to a previously compiled database on healthy human gingiva. Data were analyzed using analysis of variance with Tukey-Kramer multiple-comparison test (P < .05). A 50:50% acceptability threshold of 4.6 for ΔE* and 4.1 for ΔE' was used to interpret the results. ΔE* / ΔE' ranged from 4.4/3.5 to 8.6/6.9. The majority of gingival shade guides and gingiva-colored restorative materials exhibited statistically significant coverage errors above the 50:50% acceptability threshold and uneven shade distribution.

Background: Although retrograde peri‐implantitis (RPI) is not a common sequela of dental implant surgery, its prevalence has been reported in the literature to be 0.26%. Incidence of RPI is reported to increase to 7.8% when teeth adjacent to the implant site have a previous history of root canal therapy, and it is correlated with distance between implant and adjacent tooth and/or with time from endodontic treatment of adjacent tooth to implant placement. Minimum 2 mm space between implant and adjacent tooth is needed to decrease incidence of apical RPI, with minimum 4 weeks between completion of endodontic treatment and actual implant placement. The purpose of this study is to compile all available treatment modalities and to provide a decision tree as a general guide for clinicians to aid in diagnosis and treatment of RPI. Methods: Literature search was performed for articles published in English on the topic of RPI. Articles selected were case reports with study populations ranging from 1 to 32 patients. Any case report or clinical trial that attempted to treat or rescue an implant diagnosed with RPI was included. Results: Predominant diagnostic presentation of a lesion was presence of sinus tract at buccal or facial abscess of apical portion of implant, and subsequent periapical radiographs taken demonstrated a radiolucent lesion. On the basis of case reports analyzed, RPI was diagnosed between 1 week and 4 years after implant placement. Twelve of 20 studies reported that RPI lesions were diagnosed within 6 months after implant placement. A step‐by‐step decision tree is provided to allow clinicians to triage and properly manage cases of RPI on the basis of recommendations and successful treatments provided in analyzed case reports. It is divided between symptomatic and asymptomatic implants and adjacent teeth with vital and necrotic pulps. Conclusions: Most common etiology of apical RPI is endodontic infection from neighboring teeth, which was diagnosed within 6 months after implant placement. Most common findings, radiographically and clinically, are lesions around implant apex and sinus tract. A small number of implants did not improve with treatment. Decision tree provides a path to diagnose and treat lesions to facilitate their management. Further studies are needed to focus on histologic data around periapical microbiota to establish specific etiology and differential diagnoses compared with marginal peri‐implantitis and other implant‐related conditions.

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Aim To investigate (1) the cytotoxic potential of the brown precipitate (BP) formed with sodium hypochlorite (NaOCl) and chlorhexidine gluconate (CHX), using both a small animal model of Caenorhabditis elegans (C. elegans) and cultured human gingival fibroblasts; and (2) the chemical composition of BP using Time‐of‐Flight Secondary Ion Mass Spectrometry (ToF‐SIMS). Methodology Brown precipitate was obtained by mixing equal volumes of 6% NaOCl and 2% CHX and separating the BP from clear supernatant by centrifugation. The brown precipitate was weighed and solubilized in dimethyl sulfoxide for cytotoxicity experiments. The cytotoxic effect of BP was assessed using C. elegans larvae and primary immortalized human gingival fibroblasts‐hTERT (hTERT‐hNOF) cells. Various dilutions of BP (25 ng/µL–150 ng/µL), supernatant (0.15% v/v), NaOCl (1:100–1:1000 dilutions of 6% NaOCl) or CHX (1:500–1:1000 dilutions of 2% CHX) along with vehicle control (0.5% v/v ethanol and 0.15% v/v DMSO) or untreated control (growth medium) were tested on C. elegans larvae and hTERT‐hNOF cells. Viability was assessed in C. elegans larvae using stereomicroscopy and in hTERT‐hNOF cells using dehydrogenase‐based colorimetric assay. ToF‐SIMS was used to assess the chemical composition of BP in comparison with CHX and para‐chloroaniline (PCA). The C. elegans and cell line data were analysed using Log‐Rank test and Student's t‐test, respectively (p < .05). Results BP‐75 ng/µL and BP‐150 ng/µL were significantly more toxic to C. elegans larvae than the untreated, vehicle, supernatant or CHX treatment groups (p < .0001). Similarly, in hTERT‐hNOF cells, BP‐50 ng/µL, BP‐75 ng/µL and BP‐150 ng/µL induced significant cytotoxicity within 2 h compared with untreated, vehicle, supernatant and CHX treatments (p < .05). ToF‐SIMS analysis of BP revealed ion composition characteristic of both CHX and the carcinogen PCA. Conclusions Brown precipitate was toxic in both C. elegans larvae and hTERT‐hNOF cells. The ToF‐SIMS analysis of BP revealed ions characteristic of CHX and PCA that could account for the toxicities observed in C. elegans larvae and human gingival fibroblasts. Because of the insoluble and toxic nature of BP, consecutive use of CHX and NaOCl irrigants should be avoided in root canal treatment.

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