title: Expression of cathepsin K in periodontitis and in gingival fibroblasts.
abstract: OBJECTIVE
  To study non-osteoclastic sources of cathepsin K in periodontitis.
  
  
  METHODS
  Tissue samples were obtained from 10 otherwise healthy periodontitis pati-ents during routine periodontal flap operations and 10 systemically and periodontally healthy individuals who underwent extraction operations for retained third molars. Methods used were immunohistochemistry, image analysis, immunofluorescence double-staining, gingival fibroblast culture, tumour necrosis factor-α (TNF-α) stimulation and Western blotting.
  
  
  RESULTS
  Macrophage-like cells, fibroblast-like cells, vascular endothelial cells and gingival epithelial cells were more intensively stained for cathepsin K and also more frequent in periodontitis than in controls (665 ± 104 vs 258 ± 40 cells mm(-2) , P < 0.01). Some cathepsin K(+) cells in periodontal tissues were CD68(+) , but some were CD68(-) and probably fibroblasts. Indeed, in gingival fibroblast culture, resting fibroblasts released cathepsin K, more 43 kD procathepsin K than 29 kD active cathepsin K. TNF-α increased the release of the activated cathepsin K 4- to 5-fold.
  
  
  CONCLUSIONS
  Results suggest that GCF-cathepsin K is not only osteoclast-derived, but in periodontitis, also other cells contribute to it. GCF-cathepsin K, perhaps together with intracellular, lysosomal collagenolytically active cathepsin K in fibroblasts, macrophages and gingival epithelial cells, can contribute to the loss of attachment and destruction of the periodontal ligament.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, Osmangazi University, Eskisehir, Turkey; Institute of Biomedical Engineering, Bogazici University, Istanbul, Turkey.
authors.forename: A
authors.initials: A
authors.lastname: Beklen
authors.forename: A
authors.initials: A
authors.lastname: Al-Samadi
authors.forename: Y T
authors.initials: YT
authors.lastname: Konttinen
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D056657:Cathepsin K / Q000096:biosynthesis* / Q000494:pharmacology; D005260:Female; D005347:Fibroblasts / Q000201:enzymology* / Q000473:pathology; D005881:Gingiva / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D005891:Gingivitis / Q000201:enzymology* / Q000473:pathology; D006801:Humans; D008264:Macrophages / Q000201:enzymology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000473:pathology; D010513:Periodontal Ligament / Q000187:drug effects; D010514:Periodontal Pocket / Q000473:pathology; D010518:Periodontitis / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D056657:Cathepsin K; D014409:Tumor Necrosis Factor-alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C118659:procathepsin K
keywords: cathepsin K; fibroblasts; periodontitis; tumour necrosis factor-alpha