Ameloblastoma of the jaws in children: an evaluation of cases seen in a tertiary hospital in South-Eastern Nigeria

Background: Ameloblastoma is one of the most common benign odontogenic tumours in Nigeria. It is considered uncommon in children. Materials and methods: This is a retrospective study of pediatric patients with histopathological diagnosis of ameloblastoma seen over seven years at the Oral and Maxillofacial Surgery Department of the University of Nigeria Teaching Hospital, Enugu, Nigeria. Relevant information was retrieved from patients’ records and data obtained were analysed using SPSS version 23, the chi-square test was used to compare qualitative variables, a p-value of <0.05 was considered as significant. Results: One hundred and thirty-six cases of ameloblastoma in all age groups were seen within the period. Thirty of the cases met the requirement. The mean age of the patients was 14.4 STD 2.03 (range from 10-17) years. Fourteen (46.7%) patients were male while 16 (53.3%) were female giving a ratio of 1:1.1. The duration of the lesion ranged from 3 months to 72 months (mean 15.07 months). Histologically, the follicular type (n=20, 66.7%) constitute the majority, while the clinical types were solid-multicystic (n=18, 60%) and unicystic (n=12, 40%). Enucleation was the treatment of choice in most (n=18, (60%)) of the patients. Conclusion: Ameloblastoma is relatively uncommon in children, especially those less than ten years of age. The solidmulticystic variety was the predominant type in the children studied. Most patients presented long after the onset of the tumour and enucleation with mechanical curettage produced satisfactory results in these patients. Keywords: Ameloblastoma, odontogenic tumour, children, resection, enucleation. Funding: None declare

Mechanism by which nuclear factor-kappa beta (NF-kB) regulates ovine fetal pulmonary vascular smooth muscle cell proliferation

Platelet activating factor (PAF) modulates ovine fetal pulmonary hemodynamic. PAF acts through its receptors (PAFR) in pulmonary vascular smooth muscle cells (PVSMC) to phosphorylate and induce nuclear translocation of NF-kB p65 leading to PVSMC proliferation. However, the interaction of NF-kB p65 and PAF in the nuclear domain to effect PVSMC cell growth is not clearly defined. We used siRNA-dependent translation initiation arrest to study a mechanism by which NF-kB p65 regulates PAF stimulation of PVSMC proliferation. Our hypotheses are: (a) PAF induces NF-kB p65 DNA binding and (b) NF-kB p65 siRNA attenuates PAF stimulation of PVSMC proliferation. For DNA binding, cells were fed 10 nM PAF with and without PAFR antagonists WEB 2170, CV 3988 or BN 52021 and incubated for 12 h. DNA binding was measured by specific ELISA. For NF-kB p65 siRNA effect, starved cells transfected with the siRNA were incubated for 24 h with and without 10 nM PAF. Cell proliferation was measured by DNA synthesis while expression of NF-kB p65 and PAFR protein was measured by Western blotting. In both studies, the effect of 10% FBS alone was used as the positive control. In general, PAF stimulated DNA binding which was inhibited by PAFR antagonists. siRNAs to NF-kB p65 and PAFR significantly attenuated cell proliferation compared to 10% FBS and PAF effect. Inclusion of PAF in siRNA-treated cells did not reverse inhibitory effect of NF-kB p65 siRNA on DNA synthesis. PAFR expression was inhibited in siRNA-treated cells. These data show that PAF-stimulation of PVSMC proliferation occurs via a PAFR-NF-kB p65 linked pathway