The present investigation was carried out to study the prevalence and clinical appearance of destructive periodontal disease in a school population of 15to 16-year old adolescents in Amsterdam. In addition the prevalence of Actinobacillus actinomycetemcomitans was studied in those subjects showing attachment loss. Attachment loss was diagnosed in 230 of the 4565 subjects participating which is about 5% of the population studied. Within this population males were more frequently affected than females (P = 0.008). Extensive periodontal destruction was found in 16 subjects (0.3%). In this group a female/ male ratio was found of 1.3:1. As a result of the epidemiological survey, 105 subjects with attachment loss volunteered for further investigation. The results showed that presence of plaque, redness and swelling of the gingiva, and bleeding on probing were general phenomena. In addition, the bleeding/plaque ratio, as determined for each subject at sites without attachment loss, increased with the severity of periodontal disease as expressed by the number of sites with attachment loss (P = 0.0038) as well as by the amount of destruction at these sites (P = 0.002). A. actinomycetemcomitans could be identified in 18 of the 105 subjects with attachment loss. Analysis showed that A. actinomycetemcomitans was more frequently isolated in subjects with moderate to severe periodontal breakdown than in subjects with mild breakdown (P < 0.02). When estimating the percentage of juvenile Periodontitis patients on the basis of the classically accepted criteria, it seems likely that between 0.1% to 0.2% of the population in Amsterdam is suffering from this disease entity. (J Periodontol 1989;60:604-610.)
Cystatins are physiological inhibitors of cysteine proteinases and widely distributed in human tissues and fluids including saliva. Cystatins S, SA, SN, and D are only found in glandular saliva and tear fluid whereas cystatin C has been detected in all tested biological fluids. Previous studies demonstrated that total cystatin activity and cystatin C concentration were highest in whole and parotid saliva of periodontitis patients compared to healthy subjects suggesting a response of the salivary glands to an inflammatory condition of the oral cavity. Based on these results we studied a possible change in the concentration of cystatin S, cystatin C, albumin, IgA, amylase activity, and cystatin activity in whole and parotid saliva of 20 periodontitis patients as a consequence of periodontal treatment. Saliva samples were quantified for cystatins S and C, albumin, and IgA by enzyme‐linked immunosorbent assay. Amylase was determined in an activity assay and total cystatin activity was measured towards papain. The clinical condition of the subjects improved significantly after 6 months of periodontal therapy whereas biochemical analyses of whole and parotid saliva indicated that significant changes in salivary protein composition occurred only in whole saliva. Total cystatin activity (P < 0.05) and cystatin C concentration (P < 0.05) of whole saliva samples collected after periodontal treatment decreased to normal healthy control values. Further, concentrations of cystatin S were unchanged during the periodontal treatment process. These results suggest that other sources of cystatins than the parotid gland; i.e., other salivary glands or crevicular fluid, are involved in the decrease of total cystatin activity in whole saliva after periodontal treatment. J Periodontol 1996;67:205–212.
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. It can be hypothesized that the subgingival presence of A. actinomycetemcomitans in non‐LJP patients is not predictive for a poor response to initial treatment. Therefore, recognition and treatment of A. actinomycetemcomitans associated periodontitis, if diagnosed in an early stage, may be possible to treat with conventional mechanical periodontal treatment. It remains to be determined if the presence of A. actinomycetemcomitans in these patients is a risk factor for further breakdown. J Periodontol 1993;64:40–47.
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