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Systemic antibiotics in conjunction with scaling and root planing (SRP), can offer an additional benefit over SRP alone in the treatment of periodontitis, in terms of clinical attachment loss (CAL) and pocket depth change, and reduced risk of additional CAL loss. However, antibiotics are not innocuous drugs. Their use should be justified on the basis of a clearly established need and should not be substituted for adequate local treatment. The aim of this review is to discuss the rationale, proper selection, dosage and duration for antibiotic therapy so as to optimize the usefulness of drug therapy.
INTRODUCTION During the past two decades, dentists and microbiologists have embraced periodontal antibiotic therapy as a powerful adjunct to conventional mechanical debridement for therapeutic management of the periodontal diseases,[,] as the evidence for bacterial specificity in periodontitis has accumulated and strengthened. Antibiotics, are defined as naturally occurring or synthetic organic substances that, in low concentrations, inhibit or kill selective microorganisms.[] The concept of antibiotic periodontal therapy centers upon the pathogenic microbiota, the patient, and the drug.[] There are numerous antibiotics that could be employed to treat periodontal infections, but it is often unclear which antibiotic would provide the greatest benefit to a patient with a specific periodontal infection, with minimal adverse effects. The discussion below concerns with the rationale, proper selection, dosage and duration for antibiotic therapy so as to optimize the usefulness of drug therapy. Drug factors: This includes the specific properties of antibiotics like spectrum of activity (narrow/broad), type of activity (bactericidal/bacteristatic), sensitivity of the organism (Minimal inhibitory concentration values), relative toxicity, pharmacokinetic profile, route of administration, evidence of clinical efficacy and cost of the drug. The microbial composition of subgingival plaque varies considerably from patient to patient. The description of the Gram stain reaction and the anaerobic requirement of the infectious periodontal microbiota provided the first guidelines for selection of antimicrobial therapy.
1849 Elizabeth Blackwell is awarded a medical degree from Geneva Medical College in Geneva, New York, becoming the first modern female doctor of medicine. 'I'm a first-time mom,' Carranza says, 'and the child- care staff has helped teach me how to handle new developments in my daughter's life. Cesar Carranza is a family medicine doctor in Chicago, Illinois and is affiliated with Norwegian American Hospital. He received his medical degree from National.
Delineation of the type of periodontal infection (exogenous/endogenous) may be important in selecting a proper strategy for antimicrobial therapy in periodontics.[] Two critical factors should be specifically considered in selecting a systemic antibiotic in periodontal therapy:[] Gingival fluid concentration and Minimum inhibitory concentration (MIC). The 90% minimum inhibitory concentration (MIC 90) is an in vitro determination of the concentration that will inhibit growth of 90% of the bacterial strains of a species that are tested. Antimicrobial activity can be defined as a relationship between C GCF and MIC 90 100 (C GCF/MIC 90) = antimicrobial activity expressed as a percentage for each antibiotic and each organism. Antibiotics that can achieve 90% inhibition of growth of an organism appear on the 100% line. The most effective antibiotics for treatment of a particular periodontal pathogen are those that equal or exceed the 100% value. Periodontal diseases in which antibiotics can be used: •.
Exhibits high antimicrobial activity at levels that occur in GCF for all periodontal pathogens except E. Corrodens, S. Sputigena and Peptostreptococcus, inhibits the growth of the gram positive facultative anaerobes.[] Studies indicate that more than 60% of adult periodontitis patients sampled harboured periodontal plaque that exhibited β-lactamase activity. For this reason, administration of β-lactamase sensitive penicillins, including amoxicillin alone, is not generally recommended and, in some cases, may accelerate periodontal destruction.
Amoxicillin-Clavulanate (Augmentin) - The generally accepted strategy is to administer amoxicillin with an inhibitor of beta-lactamase such as clavulanic acid. Beta-lactamase-producing strains are generally sensitive to this preparation. Augmentin may be useful in the management of patients with refractory or localized aggressive periodontitis patients. In guided tissue regeneration, systemic amoxicillin-clavulanic acid therapy has been used to suppress periodontal pathogens and increase the gain of clinical attachment.[].
There are many different antibiotic protocols but few well designed, randomized controlled trials that test the efficacy of these protocols. Periodontal infections may be considered as mixed infections, in which a variety of aerobic, microaerophilic, and anaerobic bacteria, both gram negative and gram positive, sensitive to different drugs are involved. Therefore, it seems better to use more than one antibiotic to cover all the periodontal pathogens in some clinical situations. Combination of antibiotics may help[] •. SEQUENTIAL SYSTEMIC ANTIBIOTICS Antibiotics that are bacteriostatic (e.g., tetracycline) generally require rapidly dividing microorganisms to be effective.
They do not function well if a bactericidal antibiotic (e. Kumki Tamil Mp3 Songs Download Free. g., amoxicillin or metronidazole) is given concurrently. When both types of drug are required, they are best given serially, not in combination, to avoid unfavourable interaction yet derive the benefit of both.[] In one such study, six patients with recurrent progressive periodontitis were given the usual adult dosage of doxycycline for 4 days followed by amoxicillin with clavulanate for 5 days. Five similar patients were given doxycycline alone for 10 days. After 25 weeks, patients receiving the sequential combination had significantly greater pocket depth reduction than those receiving doxycycline alone.[] In another study, all patients with recurrent periodontitis received regular bimonthly scaling and sequential dose of doxycycline and metronidazole. In the combined antibiotic group, 9% were observed to have recurrent periodontitis, whereas 42% of the placebo group showed signs of recurrent disease. Although these differences appear statistically significant, by 7 months after metronidazole, no difference in microbiota between groups could be detected.[]. COMBINATION THERAPY A combination of metronidazole and amoxicillin (MA) has shown to be an effective antibiotic regime to combat Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis-associated periodontal infections.[] One important clinical finding in a study by Winkel et al.,[] was the observation that patients with subgingival P.
Gingivalis at baseline who were treated with metronidazole+amoxicillin showed approximately half the number of >5 mm pockets after therapy compared with P. Gingivalis positive patients treated with placebo. Guerreo et al.[] used a comparable treatment protocol in patients with aggressive periodontitis and showed significantly better improvement of all periodontal parameters in the antibiotic treated patients compared to placebo treated subjects 6 months post-treatment. These studies have revealed that, in chronic as well as in aggressive periodontitis, the antibiotics result in better resolution of the periodontal inflammation, better probing depths, and attachment loss reduction. Metronidazole and clindamycin appear to be more efficient in eradicating the anaerobic periodontopathic bacteria than doxycycline or mechanical therapy alone.[] Metronidazole ciprofloxacin combination is effective against A. Metronidazole targets obligate anaerobes, and ciprofloxacin targets facultative anaerobes. This is a powerful combination against mixed infections.
Studies of this drug combination in the treatment of refractory periodontitis have documented marked clinical improvement.[]. SUMMARY It has been established that systemic antibiotics can significantly enhance the effects of mechanical periodontal therapy in conjunction with measures that improve the oral hygiene. Clinical studies of systemic antibiotic therapy in adult periodontitis, refractory periodontitis, aggressive periodontitis patients have been given in. As suggested by Herrera et al.[] and Haffajee et al.[] the mean “gain” in attachment of 0.3-0.4 mm may appear small, but it was based on change throughout the mouth including sites with shallow probing depths whose post-therapy improvement would be expected to be modest. As a bench mark, periodontitis subjects monitored after treatment and on supportive periodontal therapy for about 12 years only experienced an average annual full mouth mean attachment loss of 0.042 mm (normal susceptibility subjects) to 0.067 mm (high susceptibility subjects).[] Thus, attachment level “gain” of 0.3 mm would be equivalent to reversing 4-7 years of disease progression in a treated and maintained population.[]. Clinical studies of systemic antibiotic therapies in adult periodontitis patients with recent disease activity prior to antibiotic therapy[] All the antibiotics used in periodontal therapy, inhibit growth of the major periodontal pathogens P.
Gingivalis, C. Rectus and Capnocytophaga. In direct contrast, none are particularly effective in the inhibition of E. Corrodens (minocycline and doxycycline being best).
Minocycline appears to be the most effective antibiotic, which achieves levels that should be completely inhibitory (antibiotic activity = 600%) to most of the periodontal pathogens but may inhibit the growth of beneficial species as well.[] Amoxicillin appears almost as effective as minocycline. Tetracycline, the most commonly used antibiotic, but appears to be a relatively poor choice for A. Actinomycetemcomitans infections, for which it has been used most commonly. Erythromycin appears to be a poor choice for any pathogenic oral infection.
Metronidazole is uniquely effective in treating Selenomonassputigena and Peptostreptococcus infections and equal to minocycline in treating Fusobacterium infections. CONCLUSION Periodontal infections can involve a variety of pathogens with different antimicrobial sensitivities and resistance patterns. In periodontal infections, tissue barriers and biofilms should be removed, by mechanical debridement prior to or with antibiotics. The periodontal disease status and the antimicrobial regimen must be determined carefully to succeed with antimicrobial periodontal therapy.
Unless antimicrobial agents against periodontal disease are used intelligently, we may soon face a new breed of oral microorganisms with heightened defenses that will ensure the survival of the species, allows for greater pathogenicity and transfer genetic material coding for increased virulence and antibiotic resistance to other oral and nonoral microorganisms.
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