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Mercury (Hg) is widely used in the dental working environment, exposing dental practitioners and assistants to potentially toxic Hg vapors. Concentrations of Hg in vapor and in particulate matter (PM10) were measured in the Dental Simulation Laboratory (DSL) and in the Dental Clinic (DC) at the School of Dentistry, University of Puerto Rico. PM10 samples were collected over a 36-h period and Hg vapor was collected for eight-hour periods. PM10 mass was determined gravimetically and Hg (bound to PM10 and vapor) was extracted and analyzed by atomic absorption. Indoor levels of PM10 in the DSL ranged from 9.2 to 41.6 microg/m3 and 35.0 to 68.2 microg/m3 in the DC. Levels of particle-bound Hg ranged from 0.1 to 1.2 microg/m3 and in vapor 1.1 to 3.3mg/m3 at the DSL; the DC levels ranged from <0.01 to 0.2 microg/m3 for particle bound Hg and 13.6 to 102.7 microg/m3 in vapor. PM10 concentrations were below Indoor Air Quality suggested limits for total dust (100 microg/m3). Levels of mercury bound to PM10 were low; however, mercury vapor was several times higher than the suggested OSHA (permissible exposure limit–100 microg/m3) in the DSL.

Apical periodontitis is produced in the majority of cases by intraradicular infection. Treatment consists in the elimination of the infectious agents by endodontia. Even when carrying out a correct cleansing and filling of canals, it is possible that periapical periodontitis will persist in the form of an asymptomatic radiolucency, giving rise to the post-endodontic periapical lesion.

The clinical manifestations of contact allergic dermatitis to dental materials are not uniform. This study was performed to detect the frequent allergens in the dental series associated with contact dermatitis and to define the causal relationship between the different allergens and the relevant clinical presentations. Between the years 2000 and 2004, 134 patients, aged 20-80 years, were patch tested. 121 patients were included in the study. The most frequent oral manifestations were cheilitis and perioral dermatitis (25.6%), burning mouth (15.7%), lichenoid reaction (14.0%), and orofacial granulomatosis (10.7%). 18 (14.9%) patients were dental personnel, all of whom suffered from hand dermatitis. The common allergens detected included goldsodiumthiosulphate (14.0%), nickel sulfate (13.2%), mercury (9.9%), palladium chloride (7.4%), cobalt chloride (5.0%), and 2-hydroxyethyl methacrylate (5.8%). Positive reactions to metals were frequent in all the different clinical variants, and no specific association between a specific clinical presentation and a particular allergen was found. Allergy to mercury was not a significant factor contributing to the pathogenesis of oral lichenoid reactions. However, a strong association with contact allergy to mercury in dental fillings was found in 2 patients with orofacial granulomatosis.

Apical periodontitis is a chronic inflammatory disorder of periradicular tissues caused by aetiological agents of endodontic origin. Persistent apical periodontitis occurs when root canal treatment of apical periodontitis has not adequately eliminated intraradicular infection. Problems that lead to persistent apical periodontitis include: inadequate aseptic control, poor access cavity design, missed canals, inadequate instrumentation, debridement and leaking temporary or permanent restorations. Even when the most stringent procedures are followed, apical periodontitis may still persist as asymptomatic radiolucencies, because of the complexity of the root canal system formed by the main and accessory canals, their ramifications and anastomoses where residual infection can persist. Further, there are extraradicular factors — located within the inflamed periapical tissue — that can interfere with post-treatment healing of apical periodontitis. The causes of apical periodontitis persisting after root canal treatment have not been well characterized. During the 1990s, a series of investigations have shown that there are six biological factors that lead to asymptomatic radiolucencies persisting after root canal treatment. These are: (i) intraradicular infection persisting in the complex apical root canal system; (ii) extraradicular infection, generally in the form of periapical actinomycosis; (iii) extruded root canal filling or other exogenous materials that cause a foreign body reaction; (iv) accumulation of endogenous cholesterol crystals that irritate periapical tissues; (v) true cystic lesions, and (vi) scar tissue healing of the lesion. This article provides a comprehensive overview of the causative factors of non-resolving periapical lesions that are seen as asymptomatic radiolucencies post-treatment.