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.Th) and porosity (Ct.Po), average pore volume (AvgPo.V), and pore density (Po.Dn). RESULTS: The MSF presented the lowest and the anterior maxilla the highest Ct.Th, while Ct.Po was significantly higher at the MSF compared to the posterior maxilla (p = 0.021). No relevant differences were recorded for AvgPo.V and Po.Dn among regions (p > 0.067). Further, an increased Ct.Th at the MSF was significantly associated with a lower Po.Dn, while a higher Ct.Th and an increased AvgPo.V in the anterior maxilla were associated with a higher Ct.Th and an increased AvgPo.V, respectively, in the posterior maxilla and MSF. Finally, within each region, the AvgPo.V was associated positively with Ct.Po and negatively with Po.Dn. CONCLUSIONS: The cortical bone of the MSF is slightly less thick and slightly more porous compared to the cortical bone at the buccal aspect of the anterior and posterior maxilla. CLINICAL RELEVANCE: During lateral and vertical bone augmentation procedures, the cortical recipient bone is perforated several times to open the bone marrow compartment to facilitate provision of osteoinductive cells and molecules in the augmented space. Whether it is meaningful to approach the MSF in a similar way during MSF augmentation procedures or whether the slightly more porous structure of the MSF observed herein reduces the cortical barrier function already sufficiently has to be assessed in future clinical trials.

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. After preparation of the lateral window and elevation of the Schneiderian membrane, the cortical bone of the sinus floor is perforated several times either by using a piezoelectric device or a microsurgical handpiece with the corresponding tip or bur; these perforations should extend into the trabecular bone. RESULTS AND CONCLUSION: The experiences with this modified technique after 12 patients are presented and discussed. It is expected that by means of this relatively simple technique, increased blood and cell inflow into the augmented space is achieved. This may, in turn, enhance new bone formation and improve the integration of the augmentation material.

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. RESULTS: At baseline, frequency of BoP at an interproximal site at ET versus VT was 70.4% versus 65.0%, respectively. The frequency of teeth with interproximal PD ≥ 5 mm and CAL ≥ 5 mm was 47.9% versus 42.9% and 54.6% versus 49.6% at ET and VT, respectively. Interproximal PD and CAL at ET versus VT were 3.86 versus 3.61 mm and 4.11 versus 3.95 mm. After correcting for tooth-related factors, no significant differences were observed between ET and VT. An improper restoration had a significant (p < 0.001) negative effect on BoP [OR 3.49 (95%CI: 1.95-6.27)], PD [36.81% (95%CI: 18.52-57.92)] and CAL [27.01% (95%CI: 12.67-43.18)]. No significant differences between ET and VT were observed regarding clinical outcome of non-surgical periodontal therapy. CONCLUSIONS: Presence of a root canal filling per se does not have a significant negative influence on the marginal periodontium, when correcting for the quality of the interproximal restoration.

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. This ensures sufficient recruitment of osteoblast and osteoclast precursor cells and facilitates fast bone regeneration and/or uneventful integration of the augmentation material. METHODS: The present technical note describes an easy treatment step after tooth extraction aiming to improve socket healing with or without any ridge preservation procedure, by facilitating an increased blood inflow into the dental alveolus. Specifically, after tooth extraction the alveolar bundle bone is perforated several times - mainly in a palatally/lingually - by a small round bur (diameter < 1 mm) extending into the trabecular bone. RESULTS AND CONCLUSIONS: By means of this relatively simple treatment step, an increased blood inflow into the alveolus is achieved after tooth extraction, which might enhance socket healing and corticalization of the entrance, and in turn result in a lower complication rate (e.g., dry socket), in an enhanced graft incorporation, and/or in a reduced loss of alveolar ridge volume.

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. However, the effects of periodontopathogens on CD40L expression by platelets have not been determined. MATERIAL AND METHODS: Effects of periodontopathogens A. actinomycetemcomitans Y and P. gingivalis on the expression of CD40L were determined and the underlying receptors and pathways were investigated. 26 patients with periodontitis and 19 controls were included in the clinical part of this study. RESULTS: Periodontopathogens directly induce surface expression of CD40L in human platelets. This activation depends on plasma factors like CD14 and involves TLR2 and TLR4 but not FcγRII. Inhibition of PI3K and PLC completely abolishes bacteria-induced surface expression of CD40L. TLR2 and TLR4 agonists, for example, are also able to induce expression and release of CD40L in human platelets. In patients with periodontitis, plasma levels of soluble CD40L are elevated and positivity for P. gingivalis is associated with a statistical significant increase of soluble CD40L. CONCLUSIONS: Our data indicate an involvement of periodontopathogens in increased plasma levels of soluble CD40L in periodontitis and therefore provide a novel link between periodontitis and increased risk for CVD.

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. MATERIAL AND METHODS: Soluble P-selectin was determined in 26 patients with periodontitis and 19 controls. Furthermore, human endothelial cells and platelets were investigated for their ability to elicit soluble and surface P-selectin in response to periodontopathogens A. actinomycetemcomitans Y4 and P. gingivalis. Moreover surface E-selectin and ICAM-1 expression as well as NFκB translocation in response to these bacteria were determined on endothelial cells as well as the formation of platelet-leukocyte complexes. RESULTS: Plasma levels of soluble P-selectin are significantly elevated in periodontitis and correlate with severity of disease and bacterial infection. Stimulation of endothelial cells with periodontopathogens results in rapid surface expression of P-selectin but does not induce NFκB translocation and subsequent de novo synthesis of P-selectin, E-selectin or ICAM-1. In platelets, bacterial stimulation leads to surface expression of P-selectin and fosters the formation of platelet-leukocyte aggregates within minutes. P-selectin is rapidly shed from the surface of platelets and endothelial cells and results in increased levels of soluble P-selectin. CONCLUSIONS: Periodontopathogens are able to directly cause activation of endothelial cells and platelets within minutes. Given that transient periodontitis-associated bacteremia commonly occurs after tooth brushing or chewing, our data suggest that reduction of periodontopathogens might result in potential cardiovascular benefits.

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. MATERIAL AND METHODS: Besides several markers of platelet activation, basal and PGE(1) induced intracellular VASP-phosphorylation were determined in platelets of periodontitis patients (n = 26) and healthy donors (n = 19). Furthermore, platelets from healthy donors were incubated with distinct periodontal pathogens and basal and PGE(1) induced VASP-phosphorylation was determined. RESULTS: Compared to controls, platelets of periodontitis patients showed a significant decrease in basal and PGE(1) induced VASP-phosphorylation. VASP-phosphorylation in platelets from periodontitis patients positive for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis or Tannerella forsythia was significantly decreased compared to patients that were negative for these bacteria. Furthermore, VASP-phosphorylation in platelets isolated from healthy donors was affected by incubation with these periodontal pathogens. CONCLUSIONS: Our results provide evidence that periodontitis interferes with VASP-phosphorylation in human platelets, presumably as a consequence of a direct effect of periodontitis-associated bacteria. Decreased basal and PGE(1) induced VASP-phosphorylation might represent a mechanism responsible for enhanced platelet activation in periodontitis.