title: Quantitative assessment of apoptotic and proliferative gingival keratinocytes in oral and sulcular epithelium in patients with gingivitis and periodontitis.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Periodontology, Center for Oral Biology, Karolinska Institutet, Huddinge, Sweden. Frederik.Jarnberg@ofa.ki.se
authors.forename: F
authors.initials: F
authors.lastname: Jarnbring
authors.forename: E
authors.initials: E
authors.lastname: Somogyi
authors.forename: J
authors.initials: J
authors.lastname: Dalton
authors.forename: A
authors.initials: A
authors.lastname: Gustafsson
authors.forename: B
authors.initials: B
authors.lastname: Klinge
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D017209:Apoptosis; D002455:Cell Division; D016213:Cyclins / Q000032:analysis; D005260:Female; D005881:Gingiva / Q000473:pathology*; D005891:Gingivitis / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D015603:Keratinocytes / Q000473:pathology*; D019272:Leukocyte Elastase / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000473:pathology*; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D018709:Statistics, Nonparametric; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D016213:Cyclins; D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53; D019272:Leukocyte Elastase