INCREASED INTRACELLULAR LEVELS OF LYSOSOMAL BETA-GLUCURONIDASE IN PERIPHERAL-BLOOD PMNS FROM HUMANS WITH RAPIDLY PROGRESSIVE PERIODONTITIS

Release of potent lysosomal enzymes by degranulation of polymorphonucl ear leukocytes (PMNs) in host gingiva may contribute significantly to tissue destruction and the pathogenesis of periodontal disease. A pilo t study established that peripheral blood PMNs from humans with rapidl y progressive periodontitis (RPP) contained significantly increased am ounts of intracellular lysosomal beta-glucuronidase as compared to hea lthy controls. This investigation gained insight into the question: ar e the increased levels of beta-glucuronidase in persons with RPP an a priori genetically determined PMN characteristic, or a reactive phenom enon 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, basel ine), T-1 (four weeks after disease control therapy), and T-2 (two mon ths later). At each visit clinical indices (GI, pocket depths, GCF flo w plaque index) were performed and peripheral blood obtained. PMNs wer e isolated and suspended as 5x10(6) cells in 2.0 ml of HBSS. PMN suspe nsions were tested for total intracellular beta-glucuronidase, degranu lation induced by 1x10(-6) M and 5x10(-7) M FMLP challenges, and uncha llenged for non-specific enzyme release. PMNs from individuals with RP P contained significantly higher absolute amounts of beta-glucuronidas e 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 o f the clinical indices and beta-glucuronidase levels and no pattern wa s discovered relating to the repeated measures over time. We conclude that RPP peripheral blood PMNs contain elevated levels of beta-glucuro nidase that are not induced by the periodontal disease process.