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Quintessence Publishing: Journals: QI
Quintessence International

Edited by Eli Eliav

ISSN 0033-6572 (print) • ISSN 1936-7163 (online)

July/August 2011
Volume 42 , Issue 7

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Altered Functional Activity Patterns Of Fibroblasts Related To Periodontitis By Systemic Plasminogen Deficiency (Ligneous Periodontitis)

Idil Kurtulus, DDS, PhD, Dr/Batool Kazmi, MSc, PhD, Dr/Mark P. Lewis, BSc, PhD, Prof Dr/Seyhun Solakoglu, MD, PhD, Prof Dr/Volker Schuster, MD, PhD, Prof Dr/Crispian Scully, MD, PhD, Prof Dr/Aslan Gökbuget, DDS, PhD, Prof Dr/Gerhard Wahl, DDS, PhD, Prof Dr

Pages: 601–609
PMID: 21716989

We report one case of ligneous periodontitis, which is a clinical sign of hypoplasmino-genemia. It appears as massive, painless ulcerated gingival enlargements and alveolar bone destruction in the affected area. The course of the disease is progressive and typically ends with early loss of teeth. At present, no efficient treatment option seems to be available. To investigate the cause of the rapid bone destruction in this disease, gingival tissue specimens were taken from one patient and a healthy control patient to compare the function of fibroblastic cells. Our results showed that diseased fibroblasts (1) reorganized collagen lattices more rapidly than normal cells, (2) demonstrated a greater overall production of pro and active matrix metalloproteinase-2 (MMP-2) and increased activation of this protease, and (3) showed a more active phenotype than healthy fibroblastic cells. From these preliminary results, there seems to be increased MMP-2 production and activation, which might be one compensatory (but insufficient) mechanism for the decreased (plasmin-dependent) pericellular fibrinolysis in plasminogen-deficient patients. Further studies on this subject should evaluate the exact pathomechanism of plasminogen on this enzymatic bone and connective tissue destruction. (Quintessence Int 2011;42:601–609)

Key words: hypoplasminogenemia, ligneous conjunctivitis, ligneous periodontitis, pseudomembranous lesions, treatment options, type I plasminogen deficiency

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