The present study examined the effect of applying a pulsed electromagnetic field (PEMF) on bone formation around a rough-surfaced dental implant. A dental implant was inserted into the femur of Japanese white rabbits bilaterally. A PEMF with a pulse width of 25 microseconds and a pulse frequency of 100 Hz was applied. PEMF stimulation was applied for 4 h or 8 h per day, at a magnetic intensity of 0.2 mT, 0.3 mT or 0.8 mT. The animals were sacrificed 1, 2 or 4 weeks after implantation. After staining the resin sections with 2% basic fuchsin and 0.1% methylene blue, newly formed bone around the implant on tissue sections was evaluated by computer image analysis. The bone contact ratios of the PEMF-treated femurs were significantly larger than those of the control groups. Both the bone contact ratio and bone area ratio of the 0.2 mT- and 0.3 mT-treated femurs were significantly larger than the respective value of the 0.8 mT-treated femurs (P < 0.001). No significant difference in bone contact ratio or bone area ratio was observed whether PEMF was applied for 4 h/day or 8 h/day. Although a significantly greater amount of bone had formed around the implant of the 2-week treated femurs than the 1-week treated femurs, no significant difference was observed between the 2-week and 4-week treated femurs. These results suggest that PEMF stimulation may be useful for promoting bone formation around rough-surfaced dental implants. It is important to select the proper magnetic intensity, duration per day, and length of treatment.

We herein present a rare case of acquired methemoglobinemia associated with alkaptonuria. Alkaptonuria is a congenital error of metabolism caused by the deficiency of homogentisic acid oxidase, which subsequently results in the accumulation of homogentisic acid (HGA) in body tissues. As renal dysfunction progresses, the level of HGA excretion in the urine decreases and the blood concentration of HGA increases. HGA oxidizes oxyhemoglobin to methemoglobin, which can induce multiple organ failure accompanied by tissue hypoxia, intravascular hemolysis and metabolic acidosis. The mortality of this disease is high when alkaptonuria is associated with the presence of methemoglobinemia; therefore, treatment should be carefully planned in such cases.

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