Predicting Agenesis of the Mandibular Second Premolar from Adjacent Teeth

Early diagnosis of agenesis of the mandibular second premolar (P2) enhances management of the dental arch in the growing child. The aim of this study was to explore the relationship in the development of the mandibular first molar (M1) and first premolar (P1) at early stages of P2 (second premolar). Specifically, we ask if the likelihood of P2 agenesis can be predicted from adjacent developing teeth. We selected archived dental panoramic radiographs with P2 at crown formation stages (N = 212) and calculated the likelihood of P2 at initial mineralisation stage 'Ci' given the tooth stage of adjacent teeth. Our results show that the probability of observing mandibular P2 at initial mineralisation stage 'Ci' decreased as both the adjacent P1 and M1 matured. The modal stage at P2 'Ci' was P1 'Coc' (cusp outline complete) and M1 'Crc' (crown complete). Initial mineralisation of P2 was observed up to P1 'Crc' and M1 stage 'R½' (root half). The chance of observing P2 at least 'Coc' (coalescence of cusps) was considerably greater prior to these threshold stages compared to later stages of P1 and M1. These findings suggest that P2 is highly unlikely to develop if P1 is beyond 'Crc' and M1 is beyond 'R½'

Aluminum enhances inflammation and decreases mucosal healing in experimental colitis in mice

The increasing incidence of inflammatory bowel diseases (IBDs) in developing countries has highlighted the critical role of environmental pollutants as causative factors in their pathophysiology. Despite its ubiquity and immune toxicity, the impact of aluminum in the gut is not known. This study aimed to evaluate the effects of environmentally relevant intoxication with aluminum in murine models of colitis and to explore the underlying mechanisms. Oral administration of aluminum worsened intestinal inflammation in mice with 2,4,6-trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis and chronic colitis in interleukin 10-negative (IL10(-/-)) mice. Aluminum increased the intensity and duration of macroscopic and histologic inflammation, colonic myeloperoxidase activity, inflammatory cytokines expression, and decreased the epithelial cell renewal compared with control animals. Under basal conditions, aluminum impaired intestinal barrier function. In vitro, aluminum induced granuloma formation and synergized with lipopolysaccharide to stimulate inflammatory cytokines expression by epithelial cells. Deleterious effects of aluminum on intestinal inflammation and mucosal repair strongly suggest that aluminum might be an environmental IBD risk factor.Mucosal Immunology advance online publication, 16 October 2013; doi:10.1038/mi.2013.78