We performed tooth extraction and dental treatment in a patient with multiple drug allergies. The patient was a 29-year-old female with a past medical history of anaphylaxis to local anesthesia; she also had multiple drug allergies to antimicrobial agents and anti-inflammatory agents. Treatments were performed under general anesthesia without local anesthesia or anti-inflammatory agents, and were completed without an immediate anaphylatic reaction, although vomiting, abdominal pain, diarrhea, and hoarse voice were noted after transfer from the operation room. Intraoperative and postoperative blood pressure and pulse rate were stable, and the eosinophil count, histamine, and C3, C4, and IgE complement levels were normal before and after treatment. The result suggested that performing tests using allergy indices before and after treatment and performing treatment in expectation of possible anaphylatic reaction enable safe dental treatment in patients with multiple drug allergies.

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The cyclooxygenase (COX) -2-selective nonsteroidal anti-inflammatory drugs (NSAIDs), coxibs are now known to increase cardiovascular risk. As such, rofecoxib has been removed from the U.S. market and sales of valdecoxib have been suspended. The past-generation NSAIDs and phospholipase A₂ (PLA₂) inhibitors are being refocused on as potential anti-inflammatory agents. Presteron, a base drug of the renewed TCPS (tetracycline Presteron) ointment, is an old NSAID having no adverse effects in particular to date. To analyze the anti-inflammatory function of presteron at the cellular level, clonal rat dental pulp cells RDP4-1 were labeled with [³H] -arachidonic acid for 24 h. The cells, pre-incubated with presteron or a counterpart for three minutes, were stimulated with bradykinin or a calcium ionophore: A23187. A23187, as well as bradykinin, induced release of arachidonic acid and its metabolites not from subconfluent cells but only from confluent cells at concentrations around 0.5μM. Presteron at 0.1-0.3μM suppressed the releases in a dose-dependent manner without affecting cell viability, while indomethacin did not. Dexamethasone completely inhibited them. In addition, 0.lμM presteron partly inhibited ovine COX-1 by 10.4%, but it did not inhibit human recombinant COX-2 at all. Thus, presteron inhibits the action of bradykinin, a potent inflammatory mediator, by suppressing Ca²⁺-tdependent cellular PLA₂ (cPLA₂) and/or secretory PLA₂ (sPLA₂), and COX-1, resulting in alleviation of inflammation.

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Actinomycosis is a infectious disease that is characterized by chronic granulomatous and suppurative lesions often caused by Actinomyces israelii. Nowadays, the diagnosis may be difficult because the number of patients with typical symptoms has decreased, and there is a low success rate in culturing the microorganism. In this paper, two cases of osteomyelitis of the mandible caused by infection with Actinomyces are reported. Radiography and CT of these cases revealed bone destruction, and Gram stain of direct smears of pus obtained by extraoral incision showed Gram-positive bacteria with branching filaments.

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