No abstract

Apical disease etiopathogenesisA periapical pathogenic infection exhibits complex microbial ecologies. There is a predominance of obligate anaerobic bacteria in the necrotic pulp, and a close correlation with black-pigmented anaerobic rods in acute periapical inflammation [1]. Many endodontopathic black-pigmented species such as P. gingivalis, P. nigrescens, and P. intermedia have been observed in extra-radicular lesions [2] and strong correlations have been observed with the species P. endodontalis, S. sputigena, and Peptostreptococcus micros [3]. In contrast, there is negative or no correlation with Canocytophaga ochraces, Veillonella parvula and other endodontopathic species [3]. Some patients have apical lesions and defective root canal treatments which are detected by routine exams or have been asymptomatic for years. There have been many varying hypotheses on the etiopathogenesis of apical pathosis that include both bacterial and host factors [2]. It is not clear, however, how a stable apical pathosis becomes unstable. For example, how do bacteria that have established a permanent residence in necrotic teeth and voided root canal fillings with microbial presence become unstable? As well, how do asymptomatic teeth with apical lesions become unstable?Besides the various species of bacteria that are pathognomonic of acute periapical infections another major factor, the contribution of viral infection, should also be considered [4]. In particular, the herpesvirus, with its cycle of inactivation and activation may explain the episodic nature of periapical disease. Ferreira et al showed in two separate studies that exudative samples from acute apical abscesses most often contained human herpesvirus-8 (HHV8; 48% and 54.5% of samples) [5,6]. Guilherme et al found that saliva samples from patients with root canals contained HHV-8 in 84% of successful root canals, and 89% of failing root canals [7]. The Epstein-Barr virus (EBV) was found in 72.5% of apical periodontal