We evaluated the clinical utility of Telithromycin, a novel ketolide oral antibiotic, in the treatment of acute dental infections by comparing it with treatments with cefdinir or cefcapene-pivoxil, which are Cefem antibiotics. In addition, we surveyed patients by questionnaire on their impressions of the therapeutic effects of these antibiotics. Telithromycin was administered to 24 patients at a dose of 600 mg once a day for 3 days and cefdinir or cefcapene-pivoxil was administered to 20 patients at a dose of 300 mg three times a day over an equivalent 3-day period or 5-day period. The clinical efficacy rate was determined according to the standard established by Japanese Society of Oral Therapeutics and Pharmacology, during a period of up to 7 days after the administration. The clinical efficacy rate in the Telithromycin group and Cefem antibiotics group was 91% and 90%, respectively. The questionnaire survey showed that an improvement of rational symptoms up to 7 days after the administration was seen by 90% or more of patients in both groups. This research showed the advantage of the Telithromycin dose regimen as compared to treatment with Cefem antibiotics. We found that Telithromycin with its advantage of a convenient single dose a day was as effective as treatment with Cefem antibiotics. We therefore conclude that Telithromycin has an important potential for the treatment of acute dental infections.

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In Na, K-ATPase reaction, Na⁺ is indispensable to the formation of phosphointermediate, and K⁺ promotes dephosphorylation of phosphointermediate. It is known that Li⁺, Rb⁺, and Cs⁺, which are homologs of K⁺ and NH₄⁺, have a similar action to that of K⁺, but the details are not well understood. In the current study we examined the effects of the homologs of K⁺ and NH₄⁺ on Na, K-ATPase reaction and hydrolysis of p-nirophenyl phosphate (p-NPP), a partial reaction of Na, K-ATPase, using Na, K-ATPase purified from rabbit brains. In addition, since some previous reports suggested that inhibition of Na, K-ATPase activity by cisplatin may be the cause of renal failure, we examined the effects of cisplatin on the Na, K-ATPase activity which was dependent on the homologs of K⁺ and NH₄⁺.
The homologs of K⁺ and NH₄⁺ promoted ATPase activity in the presence of Na⁺ and Mg²⁺, and the order of the promoting effect and the affinity was K⁺> NH₄⁺ = Cs⁺= Rb⁺ > Li⁺. As no additive promotion of ATPase activity was observed by the addition of any of these ions in the presence of K⁺, the effects of these ions were thought to be similar to that of K⁺.
All the ions except Li⁺ activated hydrolysis of p-NPP as partial reaction of Na, K-ATPase. On the other hand, Li⁺ showed a promoting effect, as Na⁺ does, on ATPase activity in the absence of K⁺, whereas other homologs of K⁺ and NH₄⁺ did not. Cisplatin inhibited ATPase activity irrespective of the presence of K⁺, or homologs of K⁺ or NH₄⁺. Furthermore, cisplatin inhibited p-NPP hydrolysis activated by the homologs of K⁺ or NH₄⁺ and ATPase activity activated by Na⁺ or Li⁺.
These findings suggest that all the homologs of K⁺ and NH₄⁺ have an action on Na, K-ATPase activity, similar to that of K⁺, and only Li⁺ has both Na⁺- and K⁺- like effects, and that cisplatin inhibits ATPase and p-NPPase activities activated by the homologs of K⁺ and NH₄⁺.

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Cefditoren (CDTR) concentrations in human serum, gingiva, mandibular bone, and dental follicle following a single oral administration of cefditoren pivoxil (CDTR-PI) (200 mg) were studied. The mean concentrations in serum, gingiva, mandibular bone, and dental follicles peaked at identical times, 2 hours after administration, and were 1.89μg/mL, 0.76, 0.38, and 0.77μg/g, respectively. The mean concentration ratios of gingiva/serum, mandibular bone serum, and dental follicles/serum at the peak time were 0.43, 0.21, and 0.41, respectively. Most of the CDTR concentrations in gingiva, mandibular bone, and dental follicles exceeded the MIC for 80% of clinically isolated strains of oral streptococci. Thus, CDTR-PI may be a valuable antimicrobial agent for the treatment of odontogenic infection.

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