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. Antibiotic treatment of periodontitis aims at eradicating or controlling specific pathogens. Prime candidates for antibiotic therapy are patients with recently diagnosed active periodontitis or a history of recurrent disease who fail to stabilize following mechanical/surgical therapy. Since a variety of microbes with differing antimicrobial susceptibility profiles may cause periodontitis, selection of antimicrobial agents should be based on proper microbial diagnosis and sensitivity testing, as well as consideration of the patient's medical status. The risk of treating chemotherapeutically solely on the basis of clinical features, radiographic findings or a limited microbiological analysis, is failure to control the pathogens or overgrowth of new pathogens. A review of published papers reveals that appropriate systemic antibiotic therapy may enhance healing in patients with recent or high risk of periodontal breakdown. Systemic antibiotic therapy seems more predictable than topical administration in eradicating periodontal pathogens from deep periodontal pockets. Several promising antimicrobial agents for periodontitis treatment need testing in placebo‐controlled, double‐blind, randomized clinical trials.

The subgingival occurrence of yeasts and species of Enterobacteriacae and Pseudomonas was studied in 500 adults with severe periodontitis. All subjects had sites non‐responding or “refractory” to conventional periodontal therapy. Most subjects had received one or more courses of broad‐spectrum systemic antibiotics. Subgingival microbial samples were collected with paper points and transported in VMGA III. The bacterial samples were plated on enriched brucella blood agar and incubated anaerobically, and on TSBV, TBC, and Sabouraud agar, which were incubated in 10% CO2. Yeasts were speciated using the API 20C micro‐method system and the germ tube test (for Candida albicans). Enteric organism's and pseudomonads were speciated with the API 20E kit system. Yeasts, enteric rods and pseudomonads were subjected to antibiotic susceptibility testing. The occurrence of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, and Bacteroides intermedium was also determined in the patients studied. In the 500 periodontitis patients, yeasts were detected in 84 (16.8%), enteric rods or pseudo‐monads in 51 (10.2%), and both yeasts and enterics or pseudomonads in 6 (1.2%). Candida albicans comprised 83.3% of the isolated yeasts. Enterobacteriaceae averaged 21–39% of the cultivable flora in culture‐positive cases, with Enterobacter cloacae, Enterobacter agglomerans, Proteus mirabilis, Klebsietta pneumonias, and Klebsiella oxytoca being the most frequent species. Pseudomonas aeruginosa was isolated from 10 patients, averaging 23.4% of the cultivable subgingival flora. All Candida isolates, and 86–95% of the enteric rods and pseudomonads, were resistant to 1 μg/ml of tetracycline, penicillin G, and erythromycin. In patients positive for yeasts, enteric rods or pseudomonads, A. actinomycetemcomitans was isolated from about one‐fifth, B. intermedius from about one‐third, and B. gingivalis from 5% of the individuals. The present findings suggest that yeasts or enteric rods or pseudomonads occur in the subgingival flora of about one‐third of “refractory” adult periodontitis patients. We caution against using antibiotics without prior microbiological screening in treating this patient group.

Patients with CP in the United States frequently yielded subgingival periodontal pathogens resistant in vitro to therapeutic concentrations of antibiotics commonly used in clinical periodontal practice. The wide variability found in periodontal pathogen antibiotic-resistance patterns should concern clinicians empirically selecting antibiotic treatment regimens for patients with CP.