A multidisciplinary approach to the diagnosis and treatment of early-onset periodontitis: a case report.

BACKGROUND: The diagnosis and treatment of early-onset forms of periodontitis (EOP) represent a major challenge to periodontists. In this case report, we describe a multidisciplinary approach for the treatment of a patient with severe generalized juvenile periodontitis (GJP). Our approach incorporates clinical laboratory evaluation with conventional concepts of periodontal pathogenesis and therapeutics to diagnose and effectively treat EOP. METHODS: The 17-year-old female patient presented with clinical and radiographic evidence of severe attachment loss. Microbiological testing showed the presence of known periodontal pathogens including Actinobacillus actinomycetemcomitans, Prevotella intermedia, and Porphyromonas gingivalis. Routine immunological tests did not reveal any of the functional defects thought to play a role in the pathogenesis of EOP After initiation of therapy, which consisted of scaling and root planing, supplemented with administration of systemic antibiotics, a reduction in probing depth and gain in clinical attachment could be demonstrated. Microbiological testing was used to monitor the composition of the periodontal microbiota and to adjust antimicrobial therapy accordingly. RESULTS: Using a non-surgical approach to treatment, except for 2 root amputations performed without flap reflection, we have been able to stabilize this patient's periodontal condition over the course of a 2-year follow-up period. CONCLUSIONS: This treatment strategy provides an efficacious alternative to more aggressive forms of therapy and should therefore be considered for the treatment of patients with severe EOP.

Generalized aggressive periodontitis in a prepubertal patient: a case report.

A 10-year-old boy presented with generalized gingival inflammation, extensive alveolar bone loss, and tooth mobility. Clinical and radiographic examination supplemented by microbiologic investigation led to a diagnosis of classically termed prepubertal periodontitis (now known as generalized aggressive periodontitis). Other than severe periodontitis, the child was systemically healthy. Neither unusual infections nor abnormalities in neutrophil functions were detected. Microbiologic examinations by culture revealed the presence of the periodontal pathogen Actinobacillus actinomycetemcomitans. Treatment consisted of extraction of mobile teeth, supragingival and subgingival debridement, subgingival curettage, and root planing combined with a 1-week prescription of a combination of metronidazole and amoxicillin. Scanning electron microscopy of extracted teeth revealed hypoplastic and aplastic cementum at the periodontally exposed and intact surfaces. Clinical and microbiologic follow-up was continued over a 1-year period. No periodontal lesions have been detected, and A actinomycetemcomitans could not be isolated from the subgingival areas of the remaining teeth at the end of the first year. Since A actinomycetemcomitans was the main pathogen present in the subgingival microflora of the patient, it might play a key role in the etiology of prepubertal periodontitis.

In vitro antimicrobial susceptibility of different serotypes of Actinobacillus actinomycetemcomitans.

In vitro susceptibility of Actinobacillus actinomycetemcomitans (A.a.) serotypes to selected antimicrobial agents was investigated by the agar dilution method on supplemented Mueller-Hinton test medium. Eighty-three A.a. strains, 80 recent isolates from 40 periodontally healthy or diseased subjects, and three type strains were included in the study. Serotype a represented 20, serotype b 32, serotype c 17, and serotype e 7 and nontypable 4 of the tested strains. The most effective drugs against all A.a. serotypes in vitro were cefaclor, cefuroxime, tetracycline hydrochloride, doxycycline, trimethoprim-sulfamethoxazole (cotrimoxazole), and ciprofloxacin, which inhibited 100% of the strains at 4.0 micrograms/ml, 4.0 micrograms/ml, 1.0 microgram/ml, 2.0 micrograms/ml, 0.06 microgram/ml, and 0.015 microgram/ml, respectively. Serotypes a and e were more susceptible to cefaclor and cefuroxime than were serotypes b and c; 100% of the first two groups were inhibited at 2.0 micrograms/ml and 1.0 microgram/ml. Ampicillin inhibited 92% of the tested strains at 1.0 microgram/ml. Serotype b was always susceptible to ampicillin. Metronidazole exhibited the best activity against serotype a strains. The lowest minimal inhibitory concentration values for benzylpenicillin, ampicillin, erythromycin, doxycycline, and metronidazole were encountered among serotype b isolates. The results of the present study indicate minor differences in the in vitro antimicrobial susceptibility patterns of different A.a. serotypes, except to metronidazole. Also, the new oral cephalosporins and cotrimoxazole, rare antimicrobial agents in periodontology, showed promising efficacy against all A.a. strains.