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Increased intracellular levels of lysosomal β‐glucuronidase in peripheral blood PMNs from humans with rapidly progressive periodontitis
Author(s) -
Pippin D. J.,
Cobb C. M.,
Feil P.
Publication year - 1995
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1995.tb01251.x
Subject(s) - degranulation , pathogenesis , intracellular , immunology , granulopoiesis , peripheral blood , medicine , peripheral , glucuronidase , granulocyte , periodontitis , endocrinology , chemistry , enzyme , biology , haematopoiesis , biochemistry , microbiology and biotechnology , receptor , stem cell
Release of potent lysosomal enzymes by degranulation of polymorphonuclear leukocytes (PMNs) in host gingiva may contribute significantly to tissue destruction and the pathogenesis of periodontal disease. A pilot study established that peripheral blood PMNs from humans with rapidly progressive periodontitis (RPP) contained significantly increased amounts of intracellular lysosomal β ‐glucuronidase as compared to healthy controls. This investigation gained insight into the question: are the increased levels of β ‐glucuronidase in persons with RPP an a priori genetically determined PMN characteristic, or a reactive phenomenon induced by the periodontal disease process during granulopoiesis? Twelve healthy controls and twelve otherwise healthy individuals with RPP participated in a repeated measures design of T 0 (initial, baseline), T 1 (four weeks after disease control therapy), and T 2 (two months later). At each visit clinical indices (GI, pocket depths, GCF flow, plaque index) were performed and peripheral blood obtained. PMNs were isolated and suspended as 5×10 6 cells in 2.0 ml of HBSS. PMN suspensions were tested for total intracellular β ‐glucuronidase, degranulation induced by 1×10 −6 M and 5×10 −7 M FMLP challenges, and unchallenged for non‐specific enzyme release. PMNs from individuals with RPP contained significantly higher absolute amounts of β‐glucuronidase and released greater absolute amounts at FMLP challenge at T 0 , T 1 , and T 2 compared to controls. No relationship was found between any of the clinical indices and β ‐glucuronidase levels and no pattern was discovered relating to the repeated measures over time. We conclude that RPP peripheral blood PMNs contain elevated levels of β ‐glucuronidase that are not induced by the periodontal disease process.