Esthetic implant solutions in the periodontally compromised anterior region. Expanding the indications for immediate implant placement with the socket rebuilding technique (SRT).

Recent literature has shown that tooth extraction in the esthetic zone is followed by enormous amounts of ridge reduction caused by bone and soft tissue remodeling. The clinical implication of this, among other factors that warrant discussion, is the limitations regarding immediate implant placement in the esthetic zone. On the other hand, staged approaches - even those combined with alveolar ridge preservation techniques and/or alveolar ridge reconstruction - do not always show predictable results, so that esthetic compromises are quite common. Only under optimal conditions do the current literature and common consensus reports support the use of immediate implant placement to preserve the natural esthetic architecture of the former periodontal structures that had surrounded the extracted tooth. Absolutely mandatory, among other factors, are a sufficient bony compartment and an adequate soft tissue volume. The present article outlines a clinical methodology to reestablish the missing prerequisites for the immediate placement of implants, even in periodontally compromised and severely reduced situations, combining different approaches reasonably approved by the literature. Thus, the so-called socket rebuilding technique (SRT) is presented in this article to ensure esthetic results under challenging periodontal conditions.

Association Between Genetic Risk for Type 2 Diabetes and Structural Brain Connectivity in Major Depressive Disorder.

BACKGROUND: Major depressive disorder (MDD) and type 2 diabetes mellitus (T2D) are known to share clinical comorbidity and to have genetic overlap. Besides their shared genetics, both diseases seem to be associated with alterations in brain structural connectivity and impaired cognitive performance, but little is known about the mechanisms by which genetic risk of T2D might affect brain structure and function and if they do, how these effects could contribute to the disease course of MDD. METHODS: This study explores the association of polygenic risk for T2D with structural brain connectome topology and cognitive performance in 434 nondiabetic patients with MDD and 539 healthy control subjects. RESULTS: Polygenic risk score for T2D across MDD patients and healthy control subjects was found to be associated with reduced global fractional anisotropy, a marker of white matter microstructure, an effect found to be predominantly present in MDD-related fronto-temporo-parietal connections. A mediation analysis further suggests that this fractional anisotropy variation may mediate the association between polygenic risk score and cognitive performance. CONCLUSIONS: Our findings provide preliminary evidence of a polygenic risk for T2D to be linked to brain structural connectivity and cognition in patients with MDD and healthy control subjects, even in the absence of a direct T2D diagnosis. This suggests an effect of T2D genetic risk on white matter integrity, which may mediate an association of genetic risk for diabetes and cognitive impairments.