A study of inter- and intra-examiner reliability of pocket depth and attachment level.

Factors affecting inter- and intra-examiner variability for probing pocket depth and periodontal attachment level were studied on a sample of 20 patients, each given six full-month examinations, two by each of 3 examiners. The major determinant of both dimensions of variability was the degree of periodontal destruction, measured as either pocket depth or level of attachment: the greater the degree of destruction, the greater the disagreements within and between examiners. Differences in variability were generally minor between sites on anterior and sites on posterior teeth, between midsites and proximal sites, and between sites on the facial and sites on the lingual surface. When differences were found between the average variances for different kinds of sites, they may have been due to corresponding differences between the average depths, and not to any inherently greater difficulty in measuring one kind of site than another.

Persistence of staphylococcal cell-wall components in inflammatory sites may be due to the modulation by sulphated polyelectrolytes of autolytic wall enzymes: a working hypothesis.

The interaction of leucocytes with Staphylococcus aureus results in killing of the bacterial cells, but large portions of the bacterial cell walls persist apparently phagocytic cells for long periods. The mechanisms of biodegradation of staphylococci by leucocyte factors have shown that degradation of cell walls in vitro may be the result of the activation, by leucocyte kationic proteins, of the bacterial autolytic wall enzymes that are responsible for degrading the cell walls from within. This process is markedly inhibited by sulphated polysaccharides like dextran sulphate, by heparin, or by polyanetholesulfonate (liquoid). These anionic polyelectrolytes have also been shown to inhibit the lysis of staphylococci treated with bacteriolytic concentrations of penicillin G. Staphylococci injected intraarticularly into the knee joint of rats underwent massive plasmolysis, but structures compatible with cell walls (peptidoglycan) persisted within macrophages in the inflammatory sites, for long periods. It is postulated that the inability of leucocytes to degrade staphylococcal cell-wall components may be the result of the interference, by anionic polyelectrolytes likely to accumulate in the inflammatory sites, with the activation of the autolytic systems. Alternatively, anionic polyelectrolytes may coat the bacterial cells and interfere with the binding of the autolytic enzymes with their corresponding substrates.