Waleed R. El-Beialy

The aim of this study was to evaluate the effectiveness of maintaining the periosteal attachment of the facial and palatal cortical plates on crestal bone loss that occurs at the margin of dental implants placed immediately in split anterior maxillary alveolar ridges. This was a prospective randomized comparative clinical trial. The study population included 22 patients with edentulous anterior maxillary alveolar ridges who presented for treatment during the period March 2012 to September 2013. The selected patients were divided randomly into two equal groups. All patients underwent a maxillary ridge splitting technique; a total of 43 implants were placed immediately. A full thickness mucoperiosteal flap was performed in the control group patients, while a split thickness mucosal flap was done in the study group patients. Assessments included measurements of the linear changes in the marginal bone surrounding the implants immediately postoperative and after 6 months. Measurements were taken from cross-sectional and longitudinal cone beam computed tomography images using special software. The partial thickness flap used in the study group decreased the percentage of bone loss by 9.5% for the labial bone plate, 7.9% for the palatal bone plate, and 3.5% for the mesiodistal bone plate.

Proteomic and genomic studies commonly involve the assessment of mRNA levels using reverse transcription-polymerase chain reaction (PCR) and real-time quantitative PCR. An internal standard RNA is fundamentally analyzed along with the investigated mRNA to document the specificity of the effect(s) on mRNA and to correct for inter-sample variations. In our studies implementing estrogen treatments on different cell lines, we initially used glyceraldehyde-3-phosphate dehydrogenase (G3PDH) as an internal standard. However, the results of PCR amplification demonstrated that 17β-estradiol enhanced the expression of the G3PDH gene, rendering it impossible to use G3PDH as an unbiased comparative control.

Modulation of the physiologically influential Na(+),K(+)-ATPase is a complex process involving a wide variety of factors. To determine the possible effects of the protein tyrosine phosphatase (PTP) inhibitors dephostatin and Et-3,4-dephostatin on human and pig, renal cells and enzymatic extracts, we treated our samples (15 min-24 h) with those PTP inhibitors (0-100 microM). PTP inhibitors were found to possess a concentration-dependent inhibition of Na(+),K(+)-ATPase activity in both human and pig samples. The inhibition was similarly demonstrated on all cellular, microsomal fraction and purified Na(+),K(+)-ATPase levels. Despite rigorous activity recovery attempts, the PTP inhibitors' effects were sustained on Na(+),K(+)-ATPase activity. Western blotting experiments revealed the expression of both alpha(1)- and beta(1)-subunits in both human and pig tissues. alpha(1)-Subunits possessed higher tyrosine phosphorylation levels with higher concentrations of PTP inhibitors. Meanwhile, serine/threonine residues of both alpha(1)- and beta(1)-subunits demonstrated diminished phosphorylation levels upon dephostatin treatment. Accordingly, we provide evidence that Na(+),K(+)-ATPase can be regulated through tyrosine phosphorylation of primarily their alpha(1)-subunits, using PTP inhibitors.

We investigated the possible roles of estrogen on plasma membrane Ca(2+)-ATPase (PMCA) in human fibroblast-like synovial cells (HFLS) and mouse macrophage-like cells (RAW 264.7). Western blots revealed the expression of PMCA 2 and 4 in both cells. In vitro treatments with 17beta-estradiol for 24 hours resulted in a concentration dependent decrease in PMCA expression. Moreover, Ca(2+)-ATPase specific activity was similarly decreased with estrogen treatments. However, treatments for 1 hour in the presence or absence of cycloheximide demonstrated non-significant effects. These results suggest that estrogen has a modulatory role on Ca(2+) homeostasis through decreasing PMCA expression and abating their activity.

Several epidemiological studies have reported that temporomandibular disorder is more prevalent in women, which suggests the involvement of sex hormones, such as estrogen, in the pathogenesis of this disease. PCR amplification and Western blotting were employed to target the expression of estrogen receptors (ERs) in human fibroblast-like synovial and ATDC5 cells. The effect of estrogen was investigated through the expression of RANKL, osteoprotegerin (OPG), M-CSF/CSF-1 and c-fms. We showed expression of M-CSF/ CSF-1 and c-fms, with time-dependent increase in both after the addition of estrogen. Based on previous studies reporting that M-CSF/CSF-1 regulates the proliferation and differentiation of hemopoietic progenitor cells into mature macrophages, we put forward a new hypothesis based on the increased inflammation and tendency of females to suffer more from temporomandibular disorder (TMD) in the presence of external exacerbating factors. Detection of RANKL and OPG in ATDC5 and expression of both in HFLS was confirmed with complete disappearance of the RANKL band, and marked increase in the expression of OPG after 1 h from the addition of estrogen.

Temporomandibular disorder (TMD), a progressive disease entity, and osteoarthrosis preferentially affect females, denoting a possible role of estrogen. Using RAW 264.7 cells, the expression of estrogen receptors (ERs) alpha and beta and the consequent effect of estrogen was investigated. We present the novel detection of ER beta expression in RAW 264.7 cells. Furthermore, we innovatively demonstrated the increase in expression of both ER alpha and beta, as well as RANK and c-fms, with estrogen treatment. However, a decrease in expression of c-fms, RANK and ER beta, and nearly no change in the expression of ER alpha were experienced upon further increase in estrogen concentrations. These findings lead us to hypothesize a new mechanism of inflammation in TMD.