Search

Aim The aim of the present study was to test the presumptive therapeutic effect of chlorhexidine digluconate in a population with untreated gingivitis and presence of abundant calculus. SETTING AND STUDY DESIGN: Sixty subjects (approximately mean age of 23.4) were recruited from a knitting factory in the Province of Guangdong, People's Republic of China. By applying a double-blind clinical trial design the participants were divided into two groups (Test and Control) and matched according to their mean GI scores. The Test group (n = 20) was assigned to two daily mouthrinses for 6 days per week using 0.12% chlorhexidine digluconate (Peridex). The Control group (n = 40) rinsed twice daily with a placebo solution. All the rinsings were supervised and timed for 45 s. No attempt was made to influence the oral hygiene habits of the participants. Prior to and after 3 months of the supervised rinsing, plaque was scored using the Plaque Index system (PII), and gingivitis was assessed using the criteria of the Gingival Index system (GI). Calculus was scored according to the Calculus Surface Severity Index system (CSSI), and stain was also graded by the Discoloration Index system (DI). Results After 3 months, the Test group (n = 13) showed significant reduction in mean PII, GI and percentage of gingival bleeding (GB%), while significant increases in mean DI were observed. The improvement in gingival health was observed at all regions with marked reduction in mean GI (from GI = 1.40 to 1.08) and GB% reduction by 24-52%. The proportion of GI = 2 was also reduced significantly from 50-36%. The Control group (n = 23) also showed a decrease in mean PII but significant increases in the mean GI and GB%. Intergroup comparison showed statistically significant differences between mean GI, percentage of gingival bleeding (GB%) and mean DI for the test and control groups after 3 months of supervised rinsing. However, there were no significant intergroup differences for mean PII. Conclusion In conclusion, there was a significant effect of chlorhexidine on gingivitis, although the effect may be too limited to assure prognostic benefits in the prevention of future disease progression.

Periodontitis may be viewed as an infectious disease with a number of specific characteristics. Pathogens of the subgingival microbiota can interact with host tissues even without direct tissue penetration. Hence, antimicrobial agents must be available at a sufficiently high concentration not only within the periodontal tissues, but also outside, in the environment of the periodontal pocket. The subgingival microbiota accumulate on the root surface to form an adherent layer of plaque with the characteristics of a biofilm. Several mechanisms, such as diffusion barriers, and selective inactivation of agents lead to an increased resistance of bacteria in biofilms. Mechanical supragingival plaque control is indispensable to prevent the re-emergence of periodontal pathogens and the re-establishment of a biofilm in treated sites. Since specific features have important implications for the use of antimicrobial agents in periodontal therapy, extrapolations from experiences made in the therapy of other infections are only partially valid. The ultimate evidence for the efficacy of systemic or local chemotherapy must be obtained from treatment studies in humans with adequate follow-up.

The purpose of this review was to evaluate the evidence supporting the hypothesis that viral infection plays a role in the development of periodontitis. An involvement in periodontal diseases has been suspected specifically for human immunodeficiency virus (HIV) and herpes viruses. An association has been demonstrated between HIV infection and some distinct forms of periodontal infection, i.e. necrotizing lesions. Furthermore, reports of increased prevalence and severity of chronic periodontitis in HIV-positive subjects suggests that HIV infection predispose to chronic periodontitis. Several studies, most of them from the same research group, have demonstrated an association of herpesviruses with periodontal disease. Viral DNA have been detected in gingival tissue, gingival cervicular fluid (GCF) and subgingival plaque from periodontaly diseased sites. In addition markers of herpesviral activation have been demonstrated in the GCF from periodontal lesions. Active human cytomegalovirus (HCMV) replication in periodontal sites may suggest that HCMV re-activation triggers periodontal disease activity. Concerns regarding sampling, methods and interpretation cast doubts on the role of viruses as causes of periodontal disease.