PMID- 10029467 OWN - NLM STAT- MEDLINE DCOM- 19990223 LR - 20170214 IS - 0022-0345 (Print) IS - 0022-0345 (Linking) VI - 78 IP - 2 DP - 1999 Feb TI - Production of matrix-degrading enzymes and inhibition of osteoclast-like cell differentiation by fibroblast-like cells from the periodontal ligament of human primary teeth. PG - 681-9 AB - Clinically, the most apparent difference between the primary and permanent dentitions is the physiologic loss of the primary tooth by root resorption. Root resorption is associated with loss of integrity of the periodontal ligament (PDL), followed by recruitment of resorptive cells that remove root structure. We therefore cultured primary dentition PDL fibroblasts (PPDL cells) to investigate in vitro their production of matrix metalloproteinases (MMPs) and tissue inhibitors of MMP (TIMPs), and the effects of soluble factors produced by these cells on osteoclast-like cell differentiation. These studies demonstrate that PPDL cells in vitro have a heterogeneous morphology, and they constitutively synthesize 92-kDa gelatinase, 72-kDa gelatinase, and 53/57-kDa procollagenase as well as TIMP-1, -2, and a third inhibitor of matrix metalloproteinase, as determined by substrate gel zymography and immunoblot analysis. Compared with PDL cells from the permanent dentition, PPDL cells generally produced a greater amount of collagenase but similar amounts of the gelatinases and inhibitors. PPDL cells were treated with pro-inflammatory cytokines to determine their effect on the expression of matrix-degrading enzymes and inhibitors. Interleukin-1alpha and tumor necrosis factor-alpha enhanced the constitutive expression of proteinases but not that of inhibitors in PPDL cells. Conditioned media from PPDL cell lines inhibited the differentiation of osteoclast-like cells in mouse bone marrow cultures. These findings indicate that PPDL cells may modulate the cascade of root resorption both by their regulated production of proteinases and inhibitors and by synthesis of unknown soluble factor(s) that may regulate osteoclast development. FAU - Wu, Y M AU - Wu YM AD - Department of Growth and Development, School of Dentistry, University of California-San Francisco, 94143-0754, USA. FAU - Richards, D W AU - Richards DW FAU - Rowe, D J AU - Rowe DJ LA - eng GR - R03 DE-11183/DE/NIDCR NIH HHS/United States GR - R29 DE-10062/DE/NIDCR NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Dent Res JT - Journal of dental research JID - 0354343 RN - 0 (Culture Media, Conditioned) RN - 0 (Interleukin-1) RN - 0 (Protease Inhibitors) RN - 0 (Tissue Inhibitor of Metalloproteinases) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 3.4.24.- (Metalloendopeptidases) SB - IM MH - Adult MH - Analysis of Variance MH - Animals MH - Cell Differentiation MH - Cell Line MH - Child, Preschool MH - Culture Media, Conditioned MH - Electrophoresis, Polyacrylamide Gel MH - Enzyme Induction/drug effects MH - Extracellular Matrix/enzymology MH - Female MH - Fibroblasts/enzymology MH - Humans MH - Immunoblotting MH - Interleukin-1/pharmacology MH - Male MH - Metalloendopeptidases/antagonists & inhibitors/*biosynthesis MH - Mice MH - Osteoclasts/enzymology MH - Periodontal Ligament/cytology/*enzymology MH - Protease Inhibitors/metabolism MH - Root Resorption/*enzymology MH - Tissue Inhibitor of Metalloproteinases/biosynthesis MH - Tooth, Deciduous/*enzymology MH - Tumor Necrosis Factor-alpha/pharmacology EDAT- 1999/02/24 00:00 MHDA- 1999/02/24 00:01 CRDT- 1999/02/24 00:00 PHST- 1999/02/24 00:00 [pubmed] PHST- 1999/02/24 00:01 [medline] PHST- 1999/02/24 00:00 [entrez] AID - 10.1177/00220345990780020801 [doi] PST - ppublish SO - J Dent Res. 1999 Feb;78(2):681-9. doi: 10.1177/00220345990780020801.