Four-rooted maxillary first molar having C-shaped palatal root canal morphology evaluated using cone-beam computerized tomography: a case report

The aim of this article was to present an endodontically managed maxillary first molar with unusual C-shaped palatal root morphology confirmed by cone-beam computerized tomography (CBCT) images. CBCT axial images showed the presence of C-shaped palatal root canal anatomy with a palatal root bifurcation at the apical third. The evaluation of CBCT images can result in better understanding of root canal anatomy, which enables the clinician to investigate the root canal system and to clean, shape, and obturate it more effectively.     

Clinical and patient-centered outcomes after minimally invasive non-surgical or surgical approaches for the treatment of intrabony defects: a randomized clinical trial

Background: The present study aims to compare the performance of minimally invasive non‐surgical and surgical approaches for the therapy of intrabony defects. Methods: Twenty‐nine patients who presented with intrabony defects were randomly assigned to: 1) a minimally invasive non‐surgical technique (MINST) group, or 2) minimally invasive surgical technique (MIST) group. The chair time of each therapeutic procedure was calculated. The probing depth (PD), position of the gingival margin (PGM) and relative clinical attachment level (RCAL) were evaluated at 3 and 6 months after treatments. The patient perception of discomfort/pain experienced during and after therapy and patient satisfaction regarding treatments were also evaluated. Results: Significant PD reductions, RCAL gains, and no changes in the PGM were obtained at 3 and 6 months in MINST and MIST groups (P <0.05). No differences were observed between groups at any time points (P >0.05). Patient‐oriented outcomes did not demonstrate differences between therapeutic approaches (P >0.05). Significant higher chair times were required in the MIST group than in the MINST group (P <0.05). Conclusions: Minimally invasive non‐surgical and surgical approaches were successfully used for the treatment of intrabony defects and achieved periodontal health in association with negligible morbidity and suitable patient satisfaction. However, non‐surgical therapeutic modality presented an advantage in terms of a reduction of treatment chair time.     

The pathogenesis of periodontal disease: a paradigm shift

Periodontitis is a family of related diseases that differ in etiology, natural history, disease progression and response to therapy, but have a common underlying chain of events, thatareinfluenced by disease modifiers. The clinical manifestations observed are a result of the complex interplay of these factors. The pathogenesis of human periodontitis was placed on a rational footing for the first time by Page & Schroeder in 1976 and the general principles and the overall conclusions reached in that article are still largely acceptable today. Still, an enormous amount has been learned about all aspects of human periodontitis, including its pathogenesis, since 1976. A critical evaluation of the literature regarding the complex relationship between the microbial factor, the host factor and the occurrence of a disease, might be leading us over a surge of a paradigm shift in our understanding the pathogenesis of the disease. It is well acknowledged that while the etiology of periodontitis is bacterial, the pathogenesis is inflammatory. The understanding of regulation of inflammation in periodontitis is far from complete; however, as the understanding of periodontal inflammation increases, the current understanding of the microbiology of periodontitis becomes less clear. While we think we know that bacteria initiate the disease, the role of specific bacteria is still unknown. The current knowledge of the microbiology of periodontitis is based on large cross-sectional and association studies. Periodontitis is seen as the direct consequence of bacterial invasion and is regarded as an infectious disease. It is however, not possible to draw cause and- effect inferences from these studies. One might state that the inflammation precedes the overgrowth of the bacteria. In this scenario, the initiator of the disease might be early, gram-positive colonizers that elicit a profound inflammatory response in the susceptible host. The implication of that paradigm shift outlined above is that periodontitis is an inflammatory disease, and in that case the primary target of pharmacotherapy should be the inflammation, rather than the bacteria. Still, the question to be asked and investigated is whether dampening of the inflammatory response in certain individuals susceptible to periodontitis might prevent development of disease. This is a question yet to be answered.     

Gene expression profiling of mouse condylar cartilage during mastication by means of laser microdissection and cDNA array

Little is known about the mechanisms of mandibular condylar growth. In this study, gene expression in the mandibular condylar cartilage of young post-natal mice was monitored by means of a cDNA microarray, real-time PCR, and laser microdissection before and after the initiation of mastication (newborn, 7 days, 21 days, initiation of mastication, and 35 days). Insulin-like growth factor-1 (IGF-I), transforming-growth-factor-beta-2 (TGFbeta2), and aggrecan mRNAs were clearly expressed at 21 days, while the expression of osteopontin mRNAs was most clear at 35 days. Parathyroid-hormone-related protein (PTHrP), Indian-hedgehog (Ihh), and insulin-like growth factor-2 (IGF-2) mRNAs were clearly expressed during lactation (newborn and 7 days). Heat-shock-protein 84 (HSP-84) and heat-shock-protein 86 (HSP-86) were clearly expressed at 35 days. These results revealed that gene expression changed during mandibular condylar cartilage growth, and that, interestingly, these changes coincided with the initiation of mastication.