Clinical risk factors related to failures with zirconia-based restorations: An up to 9-year retrospective study

Objectives

The first objective of this study was to retrospectively evaluate zirconia-based restorations (ZBR). The second was to correlate failures with clinical parameters and to identify and to analyse chipping failures using fractographic analysis.

Methods

147 ZBR (tooth- and implant-supported crowns and fixed partial dentures (FPDs)) were evaluated after a mean observation period of 41.5 ± 31.8 months. Accessorily, zirconia implant abutments (n = 46) were also observed. The technical (USPHS criteria) and the biological outcomes of the ZBR were evaluated. Occlusal risk factors were examined: occlusal relationships, parafunctional habits, and the presence of occlusal nightguard. SEM fractographic analysis was performed using the intra-oral replica technique.

Results

The survival rate of crowns and FPDs was 93.2%, the success rate was 81.63% and the 9-year Kaplan–Meier estimated success rate was 52.66%. The chipping rate was 15% and the framework fracture rate was 2.7%. Most fractographic analyses revealed that veneer fractures originated from occlusal surface roughness. Several parameters were shown to significantly influence veneer fracture: the absence of occlusal nightguard (p = 0.0048), the presence of a ceramic restoration as an antagonist (p = 0.013), the presence of parafunctional activity (p = 0.018), and the presence of implants as support (p = 0.026). The implant abutments success rate was 100%.

Conclusions

The results of the present study confirm that chipping is the first cause of ZBR failure. They also underline the importance of clinical parameters in regards to the explanation of this complex problem. This issue should be considered in future prospective clinical studies.

Clinical significance

Practitioners can reduce chipping failures by taking into account several risk parameters, such as the presence of a ceramic restoration as an antagonist, the presence of parafunctional activity and the presence of implants as support. The use of an occlusal nightguard can also decrease failure rate.     

Hypercapnia modulates cAMP signalling and cystic fibrosis transmembrane conductance regulator‐dependent anion and fluid secretion in airway epithelia

Key points

• Raised arterial blood CO₂ (hypercapnia) is a feature of many lung diseases.
• CO₂ has been shown to act as a cell signalling molecule in human cells, notably by influencing the levels of cell signalling second messengers: cAMP and Ca²⁺.
• Hypercapnia reduced cAMP‐stimulated cystic fibrosis transmembrane conductance regulator‐dependent anion and fluid transport in Calu‐3 cells and primary human airway epithelia but did not affect cAMP‐regulated HCO₃ ⁻ transport via pendrin or Na⁺/HCO₃ ⁻ cotransporters.
• These results further support the role of CO₂ as a cell signalling molecule and suggests CO₂‐induced reductions in airway anion and fluid transport may impair innate defence mechanisms of the lungs.

Abstract

Hypercapnia is clinically defined as an arterial blood partial pressure of CO₂ of above 40 mmHg and is a feature of chronic lung disease. In previous studies we have demonstrated that hypercapnia modulates agonist‐stimulated cAMP levels through effects on transmembrane adenylyl cyclase activity. In the airways, cAMP is known to regulate cystic fibrosis transmembrane conductance regulator (CFTR)‐mediated anion and fluid secretion, which contributes to airway surface liquid homeostasis. The aim of the current work was to investigate if hypercapnia could modulate cAMP‐regulated ion and fluid transport in human airway epithelial cells. We found that acute exposure to hypercapnia significantly reduced forskolin‐stimulated elevations in intracellular cAMP as well as both adenosine‐ and forskolin‐stimulated increases in CFTR‐dependent transepithelial short‐circuit current, in polarised cultures of Calu‐3 human airway cells. This CO₂‐induced reduction in anion secretion was not due to a decrease in HCO₃ ⁻ transport given that neither a change in CFTR‐dependent HCO₃ ⁻ efflux nor Na⁺/HCO₃ ⁻ cotransporter‐dependent HCO₃ ⁻ influx were CO₂‐sensitive. Hypercapnia also reduced the volume of forskolin‐stimulated fluid secretion over 24 h, yet had no effect on the HCO₃ ⁻ content of the secreted fluid. Our data reveal that hypercapnia reduces CFTR‐dependent, electrogenic Cl⁻ and fluid secretion, but not CFTR‐dependent HCO₃ ⁻ secretion, which highlights a differential sensitivity of Cl⁻ and HCO₃ ⁻ transporters to raised CO₂ in Calu‐3 cells. Hypercapnia also reduced forskolin‐stimulated CFTR‐dependent anion secretion in primary human airway epithelia. Based on current models of airways biology, a reduction in fluid secretion, associated with hypercapnia, would be predicted to have important consequences for airways hydration and the innate defence mechanisms of the lungs.     

Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3

Receptors for bone morphogenetic proteins (BMPs), members of the transforming growth factor-beta (TGFbeta) superfamily, are persistently expressed during cardiac development, yet mice lacking type II or type IA BMP receptors die at gastrulation and cannot be used to assess potential later roles in creation of the heart. Here, we used a Cre/lox system for cardiac myocyte-specific deletion of the type IA BMP receptor, ALK3. ALK3 was specifically required at mid-gestation for normal development of the trabeculae, compact myocardium, interventricular septum, and endocardial cushion. Cardiac muscle lacking ALK3 was specifically deficient in expressing TGFbeta2, an established paracrine mediator of cushion morphogenesis. Hence, ALK3 is essential, beyond just the egg cylinder stage, for myocyte-dependent functions and signals in cardiac organogenesis.     

Hepatic and pancreatic involvement in hereditary hemorrhagic telangiectasia: quantitative and qualitative evaluation with 64-section CT in asymptomatic adult patients

Purpose  

To analyse quantitatively and qualitatively asymptomatic hepatic and pancreatic involvement in hereditary haemorrhagic telangiectasia (HHT) using 64-section helical CT.     

Cholangiocarcinoma due to postradiation therapy cholangitis and chronic pancreatitis

There are no reports of cholangiocarcinoma complicating post radiotherapy cholangitis. We report the case of a 40 year old patient who had undergone thoracoabdominal radiotherapy for Hodgkin's disease, 22 years ago. This radiotherapy was complicated, many years later, by chronic pancreatitis and cholangitis. Recurrent angiocholangitis led us to schedule a biliodigestive anastomosis. During surgery, cholangiocarcinoma was discovered. The patient died from his carcinoma some months later.