[Fluoridation and parodontosis].
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The findings of a cytologic study of the gingival fluid in patients with gingivitis and periodontitis have revealed differences in the cellular composition of the gingival fluid in normal subjects and patients with gingivitis and periodontitis. This recommends such studies for the diagnosis of inflammatory diseases of the periodontium and for the differential diagnosis between gingivitis and periodontitis.
Though gingivitis has a prevalence of close to 100 per cent in many populations, most forms of the 'disease' are self-limiting and reversible: tooth support and function are not compromised so the public health importance of the condition is questionable. Periodontitis occurs in a number of different clinical forms which may have quite different aetiological factors and--perhaps more importantly--host predispositions. Collectively, however, these diseases result in only a minority (approximately 5-20 per cent) of most populations which have been adequately surveyed having destructive periodontitis of a 'clinically significant' degree, i.e. with pockets over 6 mm, attachment loss over 4 mm or teeth requiring extraction because of their periodontal condition alone. Indeed, current evidence shows the reasons for tooth loss, though complex, to be primarily related to caries and its sequelae (both infective and iatrogenic). Indeed, in populations without access to dental health care services most people keep most of their teeth for most of their lives. Destructive periodontitis, therefore, is not the public health problem it was until recently assumed to be. Nevertheless, a prevalence of 5-20 per cent constitutes an endemic disorder of very significant proportion. The ability to identify such individuals in advance would be a major breakthrough, as would methods for detecting the intraoral sites of those individuals susceptible to breakdown, or undergoing a phase of active and destructive periodontitis. The former may be approached by genetic and general health screening, plus measurement of immune status to relevant microbial virulence factors; the latter by microbiological, biochemical and immunological screening of oral fluids--notably gingival crevicular fluid samples on a site specific basis.
Samples of gingival crevicular fluid (GCF) were harvested from sites manifesting features characteristic of active disease including inflammation, periodontal attachment loss, and radiographic signs of alveolar bone destruction in untreated patients with advanced periodontitis. The presence and concentrations of interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) were measured using ELISAs specific for these cytokine molecules. IL-1 alpha and/or IL-1 beta were identified in the GCF of 15 of 15 patients having untreated periodontitis. Ninety percent (71 of 79) of the sites tested contained measureable amounts of IL-1, with IL-1 beta as the more frequently occurring form. IL-1 alpha levels ranged from 0.23 nM to 13.9 nM in the GCFs. IL-1 beta levels were between 0.04 nM and 5.28 nM. Marked reductions of total IL-1 levels were observed following effective treatment. Both forms of IL-1 messenger RNA (mRNA) were detected in 17 of 17 gingival tissue samples from 6 patients. These results demonstrate that IL-1 is produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 may serve as a marker of periodontal tissue destruction.
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In order to determine the molecular-size distribution of gingival proteoglycans (PGs) and glycosaminoglycans (GAGs) both in periodontal health and disease states, gingival tissues were obtained from patients with early onset periodontitis (EOP) and adult periodontitis (AP) and also from periodontally healthy subjects. Gel filtration chromatography of gingival PGs revealed different profiles for periodontally diseased and healthy gingiva. Healthy gingiva was mainly composed of high-molecular size proteins and PGs, while diseased gingival tissue presented a decrease in high-molecular size PG forms and a shift towards low-molecular size proteins and PGs. This indicates the degradation of PG macromolecules during periodontal disease activity. Furthermore, this shift towards low-molecular size forms was more intense in EOP patients when compared to AP patients. Gel filtration of gingival GAGs also demonstrated depolymerization of GAGs, with low-molecular size GAGs being more intense in periodontally diseased gingiva, while healthy gingival GAGs profile was mainly composed of high-molecular size GAGs. Similar to the profile of gingival PGs, low-molecular size gingival GAGs were more prominent in gingival tissue from patients with EOP. These findings suggest that both PGs and GAGs, essential components of the extracellular matrix (ECM), are depolymerized during periodontal disease activity, which is more prominent in EOP. Since the basic feature of periodontal disease is matrix degradation, ECM components, more specifically PGs and GAGs, are likely to provide valuable information for a better understanding of periodontal disease activity.
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