Quantitative assessment of apoptotic and proliferative gingival keratinocytes in oral and sulcular epithelium in patients with gingivitis and periodontitis.

BACKGROUND: Periodontal disease is caused by a chronic infection inducing an inflammatory reaction that leads to a breakdown of tooth-supporting tissue. The maintenance of an equilibrium between the host defence and microorganisms in the sulcus is essential to preserve health. All multicellular organisms have mechanisms for killing their own cells, and use physiological cell death for defence, development, homeostasis and ageing. Apoptosis and proliferation are very important phenomena in regulating this and a disturbance is often associated with disease e.g. cancer, AIDS, Alzheimer's disease, rheumatoid arthritis. OBJECTIVE: The aim of this study was to determine whether the number of apoptotic and proliferative gingival keratinocytes differed between patients with gingivitis and those with periodontitis. MATERIAL AND METHODS: The distribution of neutrophil elastase, PCNA/cyclin, DNA fragmentation (apoptosis) and p53 was determined with immunocytochemical techniques. We used paraffin-embedded sections from gingival biopsies and did quantitative analyses. RESULTS AND CONCLUSION: These showed that 5-12% of the keratinocytes in the basal layers of the epithelium proliferated in the two groups. Fewer apoptotic cells were seen in the oral epithelium than in the sulcus in all subjects in both groups. Only in the most apical part of the sulcus, close to the junctional epithelium, did the number of apoptotic keratinocytes exceed the proliferative ones in patients with periodontitis.

Immunolocalization of interleukin-8 and proliferating cell nuclear antigen in gingival keratinocytes in patients with periodontitis.

The aim of this study was to investigate the relation between local expression of IL-8 and the localization of neutrophilic granulocytes, using CD16 as a marker of neutrophils. We also investigated the correlation between IL-8 and epithelial proliferation using proliferating cell nuclear antigen (PCNA) as a marker of proliferation. The distribution of IL-8, CD16 and PCNA/cyclin was determined by immunocytochemical techniques. We used cryostat-cut sections from gingival biopsies harvested from 5 subjects with and 5 subjects without periodontitis. Our histological examination demonstrated that the localization of neutrophilic granulocytes in gingival tissue from patients with periodontitis did not correlate with the expression of IL-8. In all tissue sections from patients and controls, the inflammatory cells accumulated near the pocket epithelium and only a few leukocytes deviated from this pattern. In the patient group, keratinocytes not belonging to the pocket or junctional epithelium expressed IL-8 without any evidence of a chemoattractant effect on neutrophils. The marker of proliferation, PCNA/cyclin, was expressed in keratinocytes in the basal cell layer. The expression was less pronounced in the control group. Our finding that IL-8 was expressed in proliferating cells suggests that IL-8 may have a role in keratinocyte proliferation.