A palato-radicular groove (PRG) is a developmental anomaly primarily found in the maxillary lateral incisors. It is a potential communication path between the root canal and the periodontium that decreases the survival prognosis of the affected tooth, therefore compromising the stability of the dental structure in the oral cavity. The aim of this case report is to present an original technique where a PRG was treated by means of intracanal disinfection, PRG sealing with glass ionomer, replantation with intentional horizontal 180 degree rotation of the tooth, and an aesthetic veneer placed to provide adequate tooth morphology. The clinical and biological benefits of this novel technique are presented and discussed.
Dental Pulp Cavity ; Disinfection ; Glass ; Incisor ; Mouth ; Periodontium ; Prognosis ; Replantation* ; Tooth*

A palato-radicular groove (PRG) is a developmental anomaly primarily found in the maxillary lateral incisors. It is a potential communication path between the root canal and the periodontium that decreases the survival prognosis of the affected tooth, therefore compromising the stability of the dental structure in the oral cavity. The aim of this case report is to present an original technique where a PRG was treated by means of intracanal disinfection, PRG sealing with glass ionomer, replantation with intentional horizontal 180 degree rotation of the tooth, and an aesthetic veneer placed to provide adequate tooth morphology. The clinical and biological benefits of this novel technique are presented and discussed.
Dental Pulp Cavity ; Disinfection ; Glass ; Incisor ; Mouth ; Periodontium ; Prognosis ; Replantation* ; Tooth*

Sarcopenia, defined as decrease in muscle function and mass, is common in patients with moderate to advanced chronic kidney disease (CKD) and is associated with poor clinical outcomes. Muscle mitochondrial dysfunction is proposed as one of the mechanisms underlying sarcopenia. Patients with moderate to advanced CKD have decreased muscle mitochondrial content and oxidative capacity along with suppressed activity of various mitochondrial enzymes such as mitochondrial electron transport chain complexes and pyruvate dehydrogenase, leading to impaired energy production. Other mitochondrial abnormalities found in this population include defective beta-oxidation of fatty acids and mitochondrial DNA mutations. These changes are noticeable from the early stages of CKD and correlate with severity of the disease. Damage induced by uremic toxins, oxidative stress, and systemic inflammation has been implicated in the development of mitochondrial dysfunction in CKD patients. Given that mitochondrial function is an important determinant of physical activity and performance, its modulation is a potential therapeutic target for sarcopenia in patients with kidney disease. Coenzyme Q, nicotinamide, and cardiolipin-targeted peptides have been tested as therapeutic interventions in early studies. Aerobic exercise, a well-established strategy to improve muscle function and mass in healthy adults, is not as effective in patients with advanced kidney disease. This might be due to reduced expression or impaired activation of peroxisome proliferator-activated receptor-gamma coactivator 1α, the master regulator of mitochondrial biogenesis. Further studies are needed to broaden our understanding of the pathogenesis of mitochondrial dysfunction and to develop mitochondrial-targeted therapies for prevention and treatment of sarcopenia in patients with CKD.

Diabetes constitutes a worldwide epidemic that affects all ethnic groups. Cell therapy is one of the best alternatives of treatment, by providing an effective way to regenerate insulin-producing cells lost during the course of the disease, but many issues remain to be solved. Several groups have been working in the development of a protocol capable of differentiating Mesenchymal Stem Cells (MSCs) into physiologically sound Insulin Producing Cells (IPCs). In order to obtain a simple, fast and direct method, we propose in this manuscript the induction of MSCs to express NESTIN in a short time period (2 h), proceeded by incubation in a low glucose induced medium (24 h) and lastly by incubation in a high glucose medium. Samples from cell cultures incubated in high glucose medium from 12 to 168 h were obtained to detect the expression of INSULIN-1, INSULIN -2, PDX-1 and GLUT-2 genes. Induced cells were exposed to a glucose challenge, in order to assess the production of insulin. This method allowed us to obtain cells expressing PDX-1, which resembles a progenitor insulin-producing cell.
Cell Culture Techniques ; Cell- and Tissue-Based Therapy ; Ethnic Groups ; Glucose ; Humans ; Insulin* ; Mesenchymal Stromal Cells* ; Methods ; Nestin*