Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry.
In this study, we investigated the synthetic and proliferative activity of infiltrating mononuclear cells in sections of granulation tissue from periodontitis lesions in both adult periodontitis (AP) and early onset periodontitis (EOP) patients. We also investigated the role of apoptosis in the remodelling of the inflamed tissue. We utilised a Ki-67 antigen specific antibody and a histone messenger RNA (mRNA) probe to detect cells undergoing cell division in the sections. Oligonucleotide probes for 28S ribosomal RNA and for the detection of poly A mRNA were utilised to detect cells with synthetic capacity. Apoptosis was determined using terminal transferase labelling of fragmented DNA with Biotin labelled dUTP. Biopsies of granulation tissue were obtained from 9 AP patients, from 10 EOP patients and for comparative purposes, biopsies of gingival tissue from 4 patients with AP. There were no differences regarding the relative proportions of cells with synthetic capacity or in the numbers of dividing cells in the periodontitis tissue sections. However, we observed an increase in the number of dividing cells in the AP granulation tissues compared to the AP gingival sections and that these cells were predominantly fibroblast like in appearance. Apoptotic cells consisted mainly of connective tissue cells; mainly fibroblasts with few if any leukocytes being apoptotic other than polymorphonuclear leukocytes. Only a few cyto-phagocytic macrophages were ever observed in the gingival and granulation tissues. We conclude that the turnover of infiltrating leukocytes in inflamed periodontal tissue is low, that they probably arrive at this site by recruitment from distant lymph nodes, and that neither cell division nor programmed cell death significantly alter the numbers of inflammatory cells. On the other hand, fibroblast apoptosis and cell division occur within the periodontium as these are typical processes in the normal turnover and remodelling of these tissues.
Koulouri
O
O
Periodontology Unit, Glasgow Dental Hospital and School, Scotland, UK.
Lappin
D F
DF
Radvar
M
M
Kinane
D F
DF
D000328:Adult; D010520:Aggressive Periodontitis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017209:Apoptosis; D002455:Cell Division; D053938:DNA Fragmentation; D005347:Fibroblasts / Q000378:metabolism; D006097:Granulation Tissue / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D019394:Ki-67 Antigen / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008875:Middle Aged; D015345:Oligonucleotide Probes; D010518:Periodontitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis; D012339:RNA, Ribosomal, 28S / Q000032:analysis
D019394:Ki-67 Antigen; D015345:Oligonucleotide Probes; D012333:RNA, Messenger; D012339:RNA, Ribosomal, 28S