Antibiotics are important adjuncts in the treatment of infectious diseases, including
periodontitis. The most severe criticisms to the indiscriminate use of these drugs
are their side effects and, especially, the development of bacterial resistance. The
knowledge of the biological mechanisms involved with the antibiotic usage would help
the medical and dental communities to overcome these two problems. Therefore, the aim
of this manuscript was to review the mechanisms of action of the antibiotics most
commonly used in the periodontal treatment (i.e. penicillin, tetracycline, macrolide
and metronidazole) and the main mechanisms of bacterial resistance to these drugs.
Antimicrobial resistance can be classified into three groups: intrinsic, mutational
and acquired. Penicillin, tetracycline and erythromycin are broad-spectrum drugs,
effective against gram-positive and gram-negative microorganisms. Bacterial
resistance to penicillin may occur due to diminished permeability of the bacterial
cell to the antibiotic; alteration of the penicillin-binding proteins, or production
of β-lactamases. However, a very small proportion of the subgingival microbiota is
resistant to penicillins. Bacteria become resistant to tetracyclines or macrolides by
limiting their access to the cell, by altering the ribosome in order to prevent
effective binding of the drug, or by producing tetracycline/macrolide-inactivating
enzymes. Periodontal pathogens may become resistant to these drugs. Finally,
metronidazole can be considered a prodrug in the sense that it requires metabolic
activation by strict anaerobe microorganisms. Acquired resistance to this drug has
rarely been reported. Due to these low rates of resistance and to its high activity
against the gram-negative anaerobic bacterial species, metronidazole is a promising
drug for treating periodontal infections.