Host and bacterial adhesion.

Bacterial adhesion is an important step in tissue colonization and depends extensively on the surface properties of a bacterial cell. For many microorganisms the prerequisite for host body occupancy is a break in tissue continuity. The next step is ongoing tissue destruction by products of bacterial metabolism: microbial enzymes and toxins. This happens, for example, in the initial phase of periodontitis. The mechanisms of adhesion are related to the specific structures present on the bacterial cell surface. This article summarizes recent data about bacterial attachment to host cells.

T-cell interactions with extracellular matrix proteins in periodontal disease.

Lymphoid cell infiltration of periodontal tissues undergoing pathological destruction suggests a functional interdependence between connective tissue proteins such as collagen, fibronectin and elastin and mononuclear cells, mainly T lymphocytes. The aim of the study was to assess T lymphocyte proliferation after stimulation by mAb OKT3 and then costimulation by ECM (extracellular matrix) proteins, as well as T-cell adhesion to connective tissue proteins in patients with adult periodontitis, early-onset periodontitis, chronic gingivitis and experimental gingivitis. Controls included patients with clinically healthy periodontium. Statistical analysis of results showed a significantly decreased level of T lymphocyte proliferation in response to costimulating action of ECM proteins among patients with adult periodontitis as compared to the control group. Reactivity of T-cells was much higher in experimental gingivitis than in adult periodontitis, and significantly lower in chronic gingivitis than in controls. In addition, T-cell interaction with ECM proteins was abnormal in early-onset periodontitis patients, but was not statistically significant.

[Microflora of periodontal pockets in advanced periodontitis]. / Mikroflora kieszonek dziaslowych w zaawansowanym zapaleniu przyzebia.

The aim of study was the evaluation of periodontal pockets microflora in patients with advanced periodontitis. From each subject 16-20 samples were taken using paper points. Pooled sample after 60 s. mixing was serially diluted in reduced BHI. For total cell counts and for the isolation of black pigmented anaerobes Brucella agar supplemented with 5% sheep blood, hemin, menadione, with and without Kanamycin-Vancomycin mixture and BM agar plates were used. For isolation of A. actinomycetemcomitans TSBV agar plates were used. Cultures were incubated in anaerobic chamber at 37 degrees C for 7 days and TSBV agar plates in an atmosphere of 95% air-5% CO2 at 37 degrees C for 5 days. Microorganisms were identified by Gram staining, colony morphology, fluorescence in UV-light, haemagglutination of 3% sheep erythrocytes, fermentation of sugars, production of indole, urease (API 20A), specific enzymes (Rapid ID 32A). Twenty seven subjects with clinically recognized periodontitis were examined. Microorganisms important in periodontitis were isolated from periodontal pockets of almost all examined subjects. The number of bacteria obtained from the sample of one patient ranged from 1 x 10(4) CFU/ml to 3,6 x 10(6) CFU/ml. Porphyromonas gingivalis was identified in the samples taken from 17 patients, Prevotella intermedia-19, Actinobacillus actinomycetemcomitans -11, Fusobacterium nucleatum-9, Peptostreptococcus spp.-22.