Improved access to the bone marrow space by multiple perforations of the alveolar bundle bone after tooth extraction-A case report.

Objectives: The dental alveolus is lined by a thin cortical layer ("bundle bone", "alveolar bone proper", "cribriform plate", "lamina dura"), that can impede access to the bone marrow and its vasculature. During unassisted socket healing, the alveolar bundle bone is gradually resorbed allowing tissue resources from the bone marrow to enter into the socket space. An optimized wound healing process, either during unassisted socket healing or during ridge preservation procedures, with autogenous bone and/or any bone/collagen substitute material, depends at least partly on an adequate vascularization of the socket space.

Micro-CT evaluation of the cortical bone micro-architecture in the anterior and posterior maxilla and the maxillary sinus floor.

Objectives: To perform a within-subject comparison of the cortical bone micro-architecture of the maxillary sinus floor (MSF) to that of the buccal aspect of the anterior and posterior maxilla.

Methods: Micro-CT scans of the buccal aspect of the anterior and posterior maxilla and of the MSF in 14 human anatomical specimens were recorded. Within-subject comparisons were performed for cortical thickness (Ct.

Multiple Perforations of the Sinus Floor During Maxillary Sinus Floor Augmentation to Provide Access to the Bone Marrow Space: A Technical Report.

Introduction: Sinus floor augmentation is a routinely used surgical technique for increasing the bone height/volume of the atrophic posterior maxilla. Optimal integration of the implanted augmentation material within the newly formed bone will-at least partly-depend on adequate vascularization to ensure sufficient recruitment of osteoblast and osteoclast precursor cells.

Methods: The present technical note describes a modification intended to facilitate increased blood inflow into the augmented space.

A root canal filling per se does not have a significant negative effect on the marginal periodontium.

Aim: To evaluate the periodontal status of single-rooted endodontically treated teeth (ET), correcting for patient- and tooth-related factors.

Methods: Clinical parameters (BoP,PD,CAL) of 240 ET and 240 contralateral vital teeth (VT), before and after non-surgical periodontal treatment, were extracted retrospectively from the journals of 175 patients. Possible patient-related (age, gender, smoking status) and tooth-related (interproximal restoration, root canal filling's extent, post, tooth type) confounders were tested.

Periodontopathogens induce expression of CD40L on human platelets via TLR2 and TLR4.

Introduction: The outstanding importance of (soluble) CD40L to cardiovascular disease (CVD) is becoming increasingly apparent as CD40L is an important mediator of thrombotic and inflammatory processes. Platelets are the main source for CD40 ligand, linking platelet stimulatory events to inflammation and adverse adaptive immune responses. Periodontitis represents a chronic dental infection by distinct gram negative bacteria that is associated with an increased risk for CVD.

Decreased phosphorylation of platelet vasodilator-stimulated phosphoprotein in periodontitis--a role of periodontal pathogens.

Introduction: Epidemiological studies indicate an association between periodontitis and cardiovascular disease, but the underlying mechanisms are poorly understood. Vasodilator-stimulated phosphoprotein (VASP) in its phosphorylated form represents a regulator of platelet function and an indicator for the sensitivity of platelets towards physiologically relevant antagonists of platelet function. As platelets and their activation state play a central role in the development of cardiovascular disease, this study aimed to investigate the influence of periodontal disease and periodontal pathogens on intraplatelet VASP-phosphorylation and platelet function.

Periodontopathogens induce soluble P-selectin release by endothelial cells and platelets.

Introduction: Soluble P-selectin plays a pivotal role in inflammation and the development of thrombotic and cardiovascular disease. Accordingly, elevated levels of soluble P-selectin are found in periodontitis and (other forms of) inflammatory diseases. However, the cellular source of soluble P-selectin in periodontitis and the effects of periodontopathogens on P-selectin release are unknown.