The Function and Reliability of the Orogranulocytic Migratory Rate as a Measure of Oral Health

Abstract

The phenomenon of leukopedesis in gingival and periodontal tissues was measured by counting the number of orogranulocytes migrating into the mouth during repeated intervals of 30 seconds. Measurements were carried out with a computerized electronic cell grading system and classified as a nonsubjective laboratory routine for indexing oral inflammation. For orogranulocytic migratory rate (OMR) readings above 1.2 X 10,/30 sec, a minimum of three determinations is required for reliability. Single readings suffice for OMR's below 0.5 X 106/30 sec, which indicates that the system is suitable for mass screening purposes.Polymorphonuclear granulocytes become extravascular after penetrating the walls of capillaries, venules, and lymphatic vessels. Through this process of leukopedesis, a constant number of polymorphonuclear granulocytes is maintained throughout the tissues. The epithelial attachment and the tissues forming the gingival crevice appear to be the only tissues in the human mouth that provide the pathway for extravascular polymorphonuclear granulocytes to continue their migration into the mucus that covers all free surfaces of the oral cavity (Fig 1).The rate at which the granulocytes emerge into the mucus is proportional to the rate of leukopedesis. In the presence of an infiammatory reaction in the periodontal tissues, the rate of leukopedesis is increased and leads not only to the formation of a cellular infiltrate but also to an increase in the rate of granulocytic migration. Living polymorphonuclear granulocytes in the oral mucus have been designated "orogranulocytes" (OGC's). The mucus, which is elab-

Analysis of saliva for periodontal diagnosis

“…Klinkhammer et al (1968) standardized collection and counting of leukocytes in saliva and developed the orogranulocytic migratory rate (OMR). The OMR was found to be correlated with gingival index (Klinkhammer & Zimmerman 1969). In an experimental gingivitis model, the number of granulocytes in saliva increased before the appearance of clinical gingivitis (Friedman & Klinkhammer 1971, Skougaard et al 1969.…”

Novel rinse assay for the quantification of oral neutrophils and the monitoring of chronic periodontal disease

“…Earlier studies, which utilized time‐consuming serial rinses and counting techniques, found similar correlations (12,18). It has been previously shown that the rate at which oral neutrophils migrate into the oral cavity increases in the presence of inflammation (10) and that oral neutrophil counts positively correlate with both increasing pocket depth and the gingival index (11,12). Interestingly, Raeste & Aura (13) found that the leukocyte count in the first rinse of the OMR series also reflects the severity of periodontal disease.…”

Short-Chain Carboxylic-Acid-Stimulated, PMN-Mediated Gingival Inflammation

“…This histological evidence unequivocally demonstrated an increase in polymorphonuclear leukocyte emigration into the gingiva as the first histological indication of a gingival inflammatory response. As later demonstrated by Klinkhamer and Zimmerman (1969) and later by Golub et al (1981), this response can occur within minutes to hours, rather than the days to weeks it normally takes to identify the clinical signs.…”

“…These results may, in part, explain the apparent association between gingival inflammation and periodontal disease. These results may also, in part, explain the absence of a predictive relationship between gingival inflammation and subsequent periodontal disease progression (Lang et al, 1990 A re-assessment of these subjective measures began slowly with the observation that oral leukocyte numbers increase concurrently with gingival inflammation (Klinkhamer and Zimmerman, 1969). The pioneering histological characterization and classification of the gingival inflammatory response solidified this hypothesis (Page and Schroeder, 1976).…”

“…The effects are dose-and acid-dependent in the mM range, with butyric > propionic > acetic > lactic acid. In addition, SCCA were found to inhibit periodontal ligament fibroblast adhesion (Eftimiadi et al, 1993 (Klinkhamer and Zimmerman, 1969;Golub et al, 1981) or SCCA . Normal neutrophil apoptosis is prevented by stimulation with a number of chemoattractants, cytokines, and butyrate (for review, see Liles and Klebanoff, 1995;Savill and Haslett, 1995;Stringer et al, 1996).…”