A randomized study of open-flap surgery of 32 intrabony defects with and without adjunct bovine bone mineral treatment

Background: Bovine bone mineral (BBM) is extensively used as a filler material in periodontal reconstructive surgery of intrabony defects. Data are mostly available on the combined use of BBM with other biomaterials. The aim of this study is to evaluate healing after open‐flap debridement (OF) of intrabony periodontal defects alone or with adjunct treatment with BBM. Methods: After initial treatment, 32 patients with 32 intrabony periodontal defects participated in the study. Full‐thickness flaps were raised and root surfaces and defects were debrided. Patients were then randomly assigned to treatment groups, either OF alone or combined with defect fill with BBM, and followed in a strict postoperative maintenance care program for 12 months. Results: At 12 months, a mean ± SE gingival recession of 1.1 ± 0.3 mm in OF and 0.9 ± 0.4 mm in BBM occurred. Probing depth reduction was 4.0 ± 0.5 mm in OF and 3.2 ± 0.7 mm in BBM. Gain in clinical attachment level was 2.8 ± 0.6 mm in OF and 2.3 ± 0.8 mm in BBM. Probing bone level was reduced by 2.7 ± 0.7 mm in OF and 1.8 ± 1.1 mm in BBM. None of the above parameters showed significant intergroup differences. In contrast, radiographic defect depth change was significantly greater in BBM (3.4 ± 2.3 mm) than in OF (1.9 ± 1.7 mm). Conclusions: Both treatments resulted in improved periodontal conditions. The adjunctive use of BBM in this study did not enhance the clinical result compared to OF alone.     

Novel KCNQ2 Mutation in a Large Emirati Family With Benign Familial Neonatal Seizures

Mutations in voltage-gated potassium channel Kv7.2 are responsible for benign familial neonatal seizures type 1, a rare monogenic autosomal dominant inherited epilepsy syndrome. We describe a novel mutation (c.1126_1127delA) in exon 9 of KCNQ2, the gene encoding for the Kv7.2 channel, in a large Emirati family with benign familial neonatal seizures type 1. The mutation leads to a frameshift at amino acid position 376, triggering loss of function and haploinsufficiency. Patients with this mutation manifest repeated clonic seizures with normal interictal electroencephalograms and favorable prognoses. Signs occur within the first days of age, lingering well into puberty. KCNQ2 mutation screening, alongside genetic counseling, should be included in diagnostic evaluations of neonatal epileptic patients, potentially sparing the need for unnecessary investigations and treatment. To our knowledge, this report is the first of a KCNQ2 mutation in an Emirati family with benign familial neonatal seizures type 1.