Effects of antibiotics on the developing enamel in neonatal mice.

PURPOSE: Identifying factors causing Molar-Incisor Hypomineralization (MIH) is an ongoing challenge. Preterm infants, routinely treated with antibiotics in cases of suspected sepsis, are more commonly affected by dental developmental defects. This study aimed to investigate the effects of gentamycin and ampicillin on the developing enamel in neonatal CD-1 mice in vivo. METHODS: Neonatal mice were randomized into a study (n = 36) and a control (n = 35) group. Antibiotics were injected intravenously for 4 days. All mice were sacrificed after 15-18 days. Micro-CT was used to analyse the mineral density (MD) of the enamel and the proportion of the enamel object volume (vol%) in first molars and incisors. RESULTS: We demonstrated a significantly lower vol% enamel in the maxillary (30.9% vs. 32.7%; p = 0.004) and mandibular (32.5% vs. 34.6%; p = 0.015) molars in the study group than in the controls. The incisors were divided into segments upon analysis. We demonstrated both lower vol% and lower MD of the enamel in most segments in treated individuals compared to controls (p < 0.05). CONCLUSION: The reduced MD and vol% in the molars and incisors are likely to have been caused by the antibiotics given during tooth development. The presented analysis of teeth in neonatal mice with micro-CT could be a valid model for further research on dental developmental defects.

Canines are affected in 16-year-olds with molar-incisor hypomineralisation (MIH): an epidemiological study based on the Tromsø study: "Fit Futures".

AIM: This was to determine the prevalence, distribution of affected teeth and severity of MIH in adolescents from Northern Norway. METHODS: It was part of a cross-sectional health survey Fit Futures including 16-year-olds from two neighbouring municipalities, Tromsø and Balsfjord. RESULTS: The prevalence of MIH was 13.9% (110 of 794). The maxillary first permanent molars (FPMs) were 1.6 times more frequently affected than in the mandible (P < 0.001). The FPMs on the right side were 1.2 times more often affected than the FPMs on the left side (P = 0.038). The maxillary incisors were 2.5 times more often affected than the incisors in the mandible (P < 0.001). The proportions of participants whose canines and incisors were involved were 22.8 and 41.8%, respectively. Altogether 201 FPMs were affected; 54.0% of these had opacities only, 24.3% had posteruptive breakdown (PEB), 18.8% had atypical restorations, and 3.0% had been extracted due to MIH. The buccal surfaces were most often affected in FPMs. More severe lesions were found in the mandibular FPMs compared with the maxillary FPMs (P = 0.002). In the lower canines, only opacities were recorded, while in the upper jaw 13.0% of the affected canines showed PEBs. The distribution of MIH in the dentition was not symmetrical. CONCLUSION: The prevalence of MIH (13.9%) in the study population of 16-year-olds from Northern Norway is consistent with previous Scandinavian reports. The distribution pattern shows that one participant in four with MIH had at least one affected canine. Further studies are needed to describe the localisation of defects on the enamel surface and to relate these findings to enamel thickness and the duration of amelogenesis.

Insulin-associated modulation of neuroendocrine counterregulation, hypoglycemia perception, and cerebral function in insulin-dependent diabetes mellitus: evidence for an intrinsic effect of insulin on the central nervous system.

Evidence for an intrinsic effect of insulin on the central nervous system is accumulating. To test the hypothesis that insulin per se may modulate neuroendocrine counterregulation, hypoglycemia perception, and cerebral function in insulin-dependent diabetes mellitus, we examined 27 patients without any sign of classical autonomic neuropathy or evidence of so-called hypoglycemia unawareness. We used the hyperinsulinemic (0.67 vs. 2.00 mU/kg.min), stepped hypoglycemic (5.6/3.5/2.4/2.0 mmol/L) clamp technique to assess the patient's awareness of and response to equivalent hypoglycemic stimuli under different degrees of physiological hyperinsulinemia (approximately 270 vs. approximately 810 pmol/L) after an overnight euglycemic clamp (5.6 mmol/L). Simultaneously, the patient's cerebral function was assessed from his electrophysiological activity and neuropsychological skills. Higher degrees of physiological hyperinsulinemia caused enhanced neuroendocrine response (adrenaline, P < 0.05; noradrenaline, P < 0.03; GH, P < 0.02; beta-endorphin, P < 0.03; ACTH, P = 0.12; cortisol, P = 0.06; PRL, P = 0.08) and symptom awareness (total symptoms, P < 0.04; autonomic symptoms, P < 0.02; neuroglycopenia symptoms, P < 0.05; sweating, P < 0.05; heart pounding, P < 0.02; trembling, P < 0.01; lack of concentration, P < 0.02) to occur. Deteriorations of electrophysiological activity (middle latency auditory-evoked potentials, P < 0.04; Pa peak latencies, P < 0.05; Pa-V interpeak latencies, P = 0.08) and neuropsychological skills (Stroop test, P < 0.05; trail making, P = 0.12) were more pronounced the higher the insulin level, but at similar blood glucose concentrations. We conclude that insulin-associated modulation of neuroendocrine counterregulation, hypoglycemia perception, and cerebral function may occur in insulin-dependent diabetes mellitus, which indicates an intrinsic effect of insulin on the human brain.