Mechanical Periodontal Treatment Research Articles

Microbiological and Clinical Monitoring of Non‐Localized Juvenile Periodontitis in Young Adults: A Report of 11 Cases

It has been shown that patients with localized juvenile periodontitis (LJP) often harbor Actinobacillus actinomycetemcomitans in the subgingival area. However, little is known of the oral microflora in non-LJP juvenile periodontitis patients with less extensive disease. The purpose of this study was to describe the microflora and clinical parameters of young adults with minor to moderate periodontitis during treatment for a period of 1 year. Eleven patients 15 to 16 years of age were studied. All of them had 4 to 8 mm loss of attachment at minimally one site, but the typical clinical description of localized juvenile periodontitis was an exclusion criterion in this study. Microbiological examination of the deepest periodontal pocket and of the tongue revealed that 6 patients harbored Actinobacillus actinomycetemcomitans and 5 harbored Porphyromonas gingivalis. Almost all subjects showed relatively high proportions of Prevotella intermedia, Campylobacter rectus, motile organisms, and spirochetes. On the basis of clinical and microbiological parameters the 11 patients could be assigned to 1 of 2 groups. Six cases had moderate periodontal breakdown with loss of attachment at 7 to 44 sites. All harbored A. actinomycetemcomitans and 5 of them P. gingivalis. These 6 cases responded relatively well to initial treatment despite the continued presence of A. actinomycetemcomitans. The other group consisted of 5 cases with relatively minor periodontal breakdown; i.e, 1 or 2 sites with 4 to 6 mm loss of attachment. Neither A. actinomycetemcomitans nor P. gingivalis was detected in the deepest pocket of these patients. All 5 responded well to initial treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Microbiological and clinical results of metronidazole plus amoxicillin therapy in Actinobacillus actinomycetemcomitans-associated periodontitis.

We report on the microbiological and clinical effects of mechanical debridement in combination with metronidazole plus amoxicillin therapy in 118 patients with Actinobacillus actinomycetemcomitans-associated periodontitis. Patients were categorized into 3 groups: 28 had localized periodontitis; 50 had generalized periodontitis, and 40 had refractory periodontitis. After initial treatment and metronidazole plus amoxicillin therapy 114 of 118 (96.6%) patients had no detectable A. actinomycetemcomitans. Significant reduction in pocket probing depth and gain of clinical attachment were achieved in almost all patients. Four patients were still positive for A. actinomycetemcomitans after therapy. Metronidazole resistance (MIC greater than 25 micrograms/ml) was observed in 2 of 4 strains from these patients. Patients still positive for A. actinomycetemcomitans or Porphyromonas gingivalis showed a significant higher bleeding tendency after therapy. It was concluded that mechanical periodontal treatment in combination with the metronidazole plus amoxicillin therapy is effective for subgingival suppression of A. actinomycetemcomitans in patients with severe periodontitis.

Ultrastructural observations on bacterial invasion in cementum and radicular dentin of periodontally diseased human teeth.

In this study the bacterial invasion in root cementum and radicular dentin of periodontally diseased, caries-free human teeth was examined. In addition, structural changes in these tissues, which could be related to the bacterial invasion, were reported. Twenty-one caries-free human teeth with extensive periodontal attachment loss were studied by light and scanning electron microscopy. At the base of the gingival pocket, bacteria were found in the spaces between remnants of Sharpey's fibers and their point of insertion in the cementum. In teeth that had been scaled and root planed, most of the root cementum had been removed. Bacterial invasion was found in the remaining root cementum. The invasion seemed to start as a localized process, often involving only one bacterium. In other areas bacteria were present in lacunar defects in the cementum. These lacunae extended into the radicular dentin. In 11 teeth bacteria had invaded the dentinal tubules. Most bacteria were located in the outer 300 microns of the dentinal tubules, although occasionally they were found in deeper parts. In two of the nontreated teeth, bacteria were detected on the pulpal wall. No correlation was found between the presence of bacterial invasion and the absence of radicular cementum. No bacteria were found in the portion of the root located apically to the epithelial attachment. These data are in agreement with our results from cultural studies of the bacterial flora in these structures. It was also demonstrated that in spite of meticulous scaling and root planning and personal oral hygiene, bacterial plaque remained present on radicular surfaces. Both the invaded dentinal tubules and the lacunae could act as bacterial reservoirs from which recolonization of treated root surfaces occurs. From these reservoirs bacteria could also induce pulpal pathoses. Since these bacterial reservoirs are not eliminated by conventional mechanical periodontal treatment, it seems appropriate to combine mechanical periodontal therapy with the use of chemotherapeutic agents.