J Clin Periodontol

AIM: To assess whether periodontal treatment can lead to clinical, glycaemic control and quality of life improvements in metabolically unbalanced diabetic patients (type 1 or type 2) diagnosed with periodontitis. METHODS: In this open-labelled randomized controlled trial, diabetic subjects (n = 91) were given "immediate" or "delayed" periodontal treatment (full-mouth non-surgical scaling and root planing, systemic antibiotics, and oral health instructions). The main outcome was the effect on glycated haemoglobin (HbA1C ) and fructosamine levels. The General Oral Health Assessment Index and the SF-36 index were used to assess quality of life (QoL). RESULTS: Periodontal health significantly improved after periodontal treatment (p < 0.001). Periodontal treatment seemed to be safe but had no significant effects on glycaemic control based on HbA1C (adjusted mean difference with a 95% confidence interval (aMD) of 0.04 [-0.16;0.24]) and fructosamine levels (aMD 5.0 [-10.2;20.2]). There was no obvious evidence of improvement in general QoL after periodontal treatment. However, there was significant improvement in oral health-related QoL (aMD 7.0 [2.4;11.6], p = 0.003). CONCLUSION: Although periodontal treatment showed no clinical effect on glycaemic control in this trial, important data were provided to support periodontal care among diabetic patients. Periodontal treatment is safe and improves oral health-related QoL in patients living with diabetes. ISRCTN15334496

Ph+/VE-cadherin+ identifies a stem cell–like population of acute lymphoblastic leukemia sustained by bone marrow niche cells

Although leukemic stem cells (LSCs) show a symbiotic relationship with bone marrow microenvironmental niches, the mechanism by which the marrow microenvironment contributes to self-renewal and proliferation of LSCs remains elusive. In the present study, we identified a unique subpopulation of Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia (ALL) cells coexpressing markers of endothelial cells (including VE-cadherin, PECAM-1, and Flk-1) and committed B-lineage progenitors. After long-term coculture with bone marrow stromal cells, tumor cells formed hematopoietic colonies and cords, expressed early stem- cell markers, and showed endothelial sprouting. Gene expression profiles of LSCs were altered in the presence of stromal cell contact. Stromal cell contact promoted leukemic cell VE-cadherin expression, stabilized β-catenin, and up-regulated Bcr-abl fusion gene expression. Our study indicates that these specific tumor cells are uniquely positioned to respond to microenvironment-derived self-renewing and proliferative cues. Ph+/VE-cadherin+ tumor subpopulation circumvents the requirement of exogenous Wnt signaling for self-renewal through stromal cell support of leukemic cell VE-cadherin expression and up-regulated Bcr-abl tyrosine kinase activity. These data suggest that strategies targeting signals in the marrow microenvironment that amplify the Bcr-abl/VE-cadherin/β-catenin axis may have utility in sensitizing drug-resistant leukemic stem cells