Cemento-osseous dysplasia is a benign fibro-osseous lesion of the tooth-bearing region of the jaws with a periodontal ligament origin. It appears predominantly in Black and Asian middle-aged females. Its importance is that it could mimic a periapical lesion in the early, translucent stage. In this report a rare case of familial cemento-osseous dysplasia is presented: a 50-years old Caucasian woman with labial paraesthesia and radiological translucency around the roots of the mandibular incisors and the first molar teeth. The lesion around the first molar was diagnosed as periapical granuloma and a root canal treatment was carried out. The diagnosis of florid cemento-osseous dysplasia and the treatment plan based on two- and three-dimensional radiographic examinations were certified histologically after surgical removal of the lesion. We screened the family members - including the patient’s mother, daughter and son - and identified a periapical version of cemento-osseous dysplasia in the daughter. Our case highlights the difficulties of differential diagnosis of cemento-osseous dysplasia and other periapical pathologies. The inconsistencies in the present classification of cemento-osseous dysplasia are also discussed with a proposal for a different classification based on new aspects that would be very helpful in setting up a correct treatment plan.

Background: Pravastatin, a known inducer of endothelial nitric-oxide synthase (eNOS) was demonstrated in human placenta, however the exact mechanism of it’s action is not fully understood. Since placental NO (nitric oxide) synthesis is of primary importance in the regulation of placental blood flow, we aimed to clarify the effects of pravastatin on healthy (n = 6) and preeclamptic (n = 6) placentas (Caucasian participants).Methods: The eNOS activity of human placental microsomes was determined by the conversion rate of C14 L-arginine into C14 L-citrulline with or without pravastatin and Geldanamycin. Phosphorylation of eNOS (Ser1177) was investigated by Western blot. Microsomal arginine uptake was measured by a rapid filtration method.Results: Pravastatin significantly increased total eNOS activity in healthy (28%,p<0.05) and preeclamptic placentas (32%,p<0.05) using 1 mM Ca²⁺promoting the dissociation of a eNOS from it’s inhibitor caveolin. Pravastatin and Geldanamycin (Hsp90 inhibitor) cotreatment increased microsomal eNOS activity. Pravastatin treatment had no significant effects on Ser1177 phosphorylation of eNOS in either healthy or preeclamptic placentas. Pravastatin induced arginine uptake of placental microsomes in both healthy (38%,p < 0.05) and preeclamptic pregnancies (34%,p < 0.05).Conclusions: This study provides a novel mechanism of pravastatin action on placental NO metabolism. Pravastatin induces the placental microsomal arginine uptake leading to the rapid activation of eNOS independently of Ser1177 phosphorylation. These new findings may contribute to better understanding of preeclampsia and may also have a clinical relevance.

Cytochrome c is a member of the respiratory chain of the mitochondria. Non-membrane-bound (free) cytochrome c can be reduced by gluthatione as well as ascorbic acid. We investigated the effect of pH, Ca²⁺, Mg²⁺and anionic phospholipids on the reduction of cytochrome c by glutathione.The reduction of cytochrome c by thiols was measured using photometry. Mitochondrial oxygen consumption was detected by use of oxygen electrode. Glutathione does not reduce cytochrome c at pH = 7.0 in the absence of Ca²⁺and Mg²⁺. The reduction of cytochrome c by glutathione is inhibited by anionic lipids, especially cardiolipin. The typical conditions of apoptosis—elevated pH, Ca²⁺level and Mg²⁺—increases the reduction of cytochrome c. Glutathione (5 mM) causes increased mitochondrial O₂consumption at pH = 8.0, in the presence of ADP either 1 mM Mg²⁺or 1 mM Ca²⁺. Our results suggest that membrane bound cyt c does not oxidize glutathione. Free (not membrane bound) cytochrome c can oxidize glutathione. In mitochondria, O₂is depleted only in the presence of ADP, so the O₂depletion observed in the presence of glutathione can be related to the respiratory chain. Decreased glutathione levels play a role in apoptosis. Therefore, membrane unbound cyt c can contribute to apoptosis by oxidation of glutathione.

Our research group developed a novel nano-pitted (NP) TiO₂ surface on grade 2 titanium that showed good mechanical, osteogenic, and antibacterial properties; however, it showed weak hydrophilicity. Our objective was to develop a surface treatment method to enhance the hydrophilicity of the NP TiO₂ surface without the destruction of the nano-topography. The effects of dilute and concentrated orthophosphoric (H₃PO₄) and nitric acids were investigated on wettability using contact angle measurement. Optical profilometry and atomic force microscopy were used for surface roughness measurement. The chemical composition of the TiO₂ surface and the oxidation state of Ti was investigated using X-ray photoelectron spectroscopy. The ccH₃PO₄ treatment significantly increased the wettability of the NP TiO₂ surfaces (30°) compared to the untreated control (88°). The quantity of the absorbed phosphorus significantly increased following ccH₃PO₄ treatment compared to the control and caused the oxidation state of titanium to decrease (Ti⁴⁺ → Ti³⁺). Owing to its simplicity and robustness the presented surface treatment method may be utilized in the industrial-scale manufacturing of titanium implants.