Periodontal clinical and microbiological data in desquamative gingivitis patients

Abstract

Objectives: A series of patients affected by desquamative gingivitis (DG) was investigated in order to evaluate relation patterns among clinical parameters relevant to plaque induced periodontitis, periodontal microbiological data and the presence of DG lesions. Patients and methods: Eight oral lichen planus (OLP) and four mucous membrane pemphigoid (MMP) patients were examined. Periodontal measurements (performed at six sites per tooth on all teeth) included probing depth (PD), gingival recession (REC), clinical attachment loss (CAL) and full mouth plaque (FMPS) and bleeding (FMBS) scores; the presence and the exact location (site by site) of DG lesions were carefully recorded. Sub-gingival plaque samples were collected and examined by means of real-time PCR for the quantitative determination of the six most important marker organisms of periodontitis. Statistically significant differences and correlation of studied variables between DG-positive and DG-negative sites were investigated in MMP and OLP cases using Mann–Whitney test (p<0.05) and the Spearman rank correlation coefficient, respectively. Results: OLP gingival lesions do not significantly affect CAL, although the presence of such lesions may reduce REC and increase PD and FMPS. MMP gingival lesions significantly worsened CAL and increased REC and FMPS. In both OLP and MMP cases, no significant difference was found between DG-positive and DG-negative sites as regards the relative percentage of the investigated species on the total bacterial load. Correlations between the presence of DG lesions and clinical parameters (CAL, PD, REC) were not significant (p<0.05). Significant correlations were found for the presence of gingival OLP lesions and Aggregatibacter actinomycetemcomitans (AA) and for the absence of gingival MMP lesions and AA. Conclusions: These findings are not definitive, but highlightthe need for further investigations of periodontal clinical and microbiological aspects of disorders causing DG in order to clarify their potential interference with plaque-related periodontitis.