Retreatability of three calcium silicate-containing sealers and one epoxy resin-based root canal sealer with four different root canal instruments

This study characterized the interactions of mineral trioxide aggregate with a synthetic tissue fluid composed of a neutral phosphate buffer saline solution and root canal dentin in extracted human teeth using inductively coupled plasma-atomic emission spectroscopy, scanning electron microscopy, energy dispersive X-ray analysis, and X-ray diffraction. Mineral trioxide aggregate exposed to synthetic tissue fluid at 37 degrees C released its metallic constituents and produced precipitates with a composition and structure similar to that of hydroxyapatite [Ca10(PO4)6(OH)2-HA]. Endodontically prepared teeth filled with mineral trioxide aggregate and stored in synthetic tissue fluid at 37 degrees C for 2 months produced at the dentin wall an adherent interfacial layer that resembled hydroxyapatite in composition. The authors conclude that Ca, the dominant ion released from mineral trioxide aggregate, reacts with phosphates in synthetic tissue fluid, yielding hydroxyapatite. The dentin-mineral trioxide aggregate interfacial layer results from a similar reaction. The sealing ability, biocompatibility, and dentinogenic activity of mineral trioxide aggregate is attributed to these physicochemical reactions.

Mineral trioxide aggregate (MTA) has been shown to be bioactive because of its ability to produce biologically compatible carbonated apatite. This study analyzed the interaction of MTA and white Portland cement with dentin after immersion in phosphate-buffered saline (PBS). Dentin disks with standardized cavities were filled with ProRoot MTA, MTA Branco, MTA BIO, white Portland cement + 20% bismuth oxide (PC1), or PC1 + 10% of calcium chloride (PC2) and immersed in 15 mL of PBS for 2 months. The precipitates were weighed and analyzed by scanning electron microscopy (SEM) and x-ray diffraction. The calcium ion release and pH of the solutions were monitored at 5, 15, 25, and 35 days. The samples were processed for SEM observations. Data were analyzed by using analysis of variance or Kruskall-Wallis tests. Our findings revealed the presence of amorphous calcium phosphate precipitates with different morphologies. The apatite formed by the cement-PBS system was deposited within collagen fibrils, promoting controlled mineral nucleation on dentin, observed as the formation of an interfacial layer with tag-like structures. All the cements tested were bioactive. The cements release some of their components in PBS, triggering the initial precipitation of amorphous calcium phosphates, which act as precursors during the formation of carbonated apatite. This spontaneous precipitation promotes a biomineralization process that leads to the formation of an interfacial layer with tag-like structures at the cement-dentin interface.

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.