Kara, Demir, Tezel, Zihni removed. After resolution of the periodontal infection (a period of seven weeks), the patient was placed on an individually tailored maintenance care program including continuous evaluation of the occurrence and the risk of disease progression. However, after a week, bleeding, edema and dark red discoloration on the marginal areas of gingiva developed again (Figure 3). Further medical tests were carried out to look for searching an underlying systemic disease and its impact on the etiology of the disease. Because of the results were in normal limits, we suspected acute streptococcal infection. Although acute streptococcal infection was suspected because of the clinical features of the patient, for being sure bacterial sample was obtained by scraping the surfaces of the gingival lesions with a sterile chip and the anaerobic-culture technique were used to identify the bacteria. Cultures of the gingival samples grew streptococcus pyogenes and a few other microorganisms. To prevent antibiotic resistance development with chemotherapeutic agents in the treatment of aggressive periodontitis, we decided to use an alternative treatment primarily, which was based on the microorganism’s growth characteristics. The acidic oral pH required for growing of the Streptococcus species was tried to change and the optimal oral pH in normal values was kept. For this purpose, an antacid chewing tablet (Rennie 680mg, Roche, Turkey), which includes calcium and magnesium carbonate, was offered two times a day for a week. To determine the effectiveness of this medication, normal whole saliva pH and whole saliva pH after using the Figure 3. Clinical view of anterior region of the oral cavity after the treatment for aggressive periodontitis showing acute streptococcal gingivitis. October 2007 - Vol.1 antacid were measured (Inolab pH meter level 2, Wissenschafllich Technische, Germany) (Figure 4). This normal value was picked up of the same patient in different moments. At the end of this additional treatment, oral health was obtained (Figure 5). DISCuSSION In a revised classification system for periodontal diseases, AP was redefined to comprise a complex entity of microbial alterations and cellular dysfunctions that differentiate the underlying molecular mechanisms from chronic periodontal disease.8 The aggressive nature of this disease process is due in part to A. actinomycetemcomitans, which is regarded as the key etiological agent based on studies reporting a frequency rate of nearly 90% in periodontal lesions.9 There is a consensus about the method and application of the treatment for AP. Once AP has been diagnosed, a comprehensive periodontal treatment plan must be developed. The treatment of periodontal diseases is divided into four phases: systemic, hygienic, corrective and maintenance / supportive therapy. As treatment progresses through the four phases, the dentist uses both surgical and non-surgical therapy to remove biofilm created by the bacterial pathogens; this procedure is in agreement with good medical practice because the bacterial load should be reduced as much as possible prior to the use of antibiotics. The adjunctive systemic use of antimicrobials along 1st sample: Without any intervention. 2nd sample: 5 minutes after oral antiacid administration. 3rd sample: 30 minutes after oral antiacid administration. 4th sample: 60 minutes after oral antiacid administration. 5th sample: 6 hours after oral antiacid administration. 6th sample: 6.5 hours after oral antiacid administration. 7th sample: After using the antacid two times a day for one week. Figure 4. PH values of normal and with antacid administration saliva samples. 253 European Journal of Dentistry