Black stain is characterized as a dark line or an incomplete coalescence of dark dots localized on the cervical third of the tooth. Over the last century, the etiology of black stain has been the subject of much debate. Most of the studies concerning this issue were conducted in pediatric population. According to the reviewed articles published between 2001 and 2014, the prevalence of black stain varies from 2.4% to 18% with equal sex distribution. The majority of the authors confirm the correlation between the presence of black stain and lower caries experience. The microflora of this deposit is dominated byActinomycesspp. and has lower cariogenic potential than nondiscolored dental plaque. Iron/copper and sulfur complexes are thought to be responsible for the dark color. In patients with black stain saliva has higher calcium concentrations and higher buffering capacity. Factors such as dietary habits, socioeconomic status, and iron supplementation may be contributing to the formation of black stain.

Objective: To analyze the influence of the length of temporary intraoral skeletal anchorage devices (TISAD/TAD) on their long-term stability in the mandible in a homogenous group of patients. Materials and Methods: A group of generally healthy patients of the same gender (female) and with a statistically insignificant age difference (20–29 years) highly homogenous with respect to known factors affecting the success rate of TISAD/TAD was evaluated. One type of TISAD/TAD was applied (6- or 8-mm long). Each patient received both 6- and 8-mm-long TISAD/TAD in randomly selected mandibular quadrants: left or right. The long-term success rate of TISAD/TAD was analyzed. Results: The 8-mm orthodontic mini-screw implants were significantly more stable than the 6-mm ones in the analyzed group. Conclusion: The length of the TISAD/TAD may be one of the factors that can affect the long-term success rate in the mandibles of 20- to 29-year-old women.

Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI-resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be involved in CML progression and TKI-resistance and warrant further study.