Myeloid-related protein (MRP)8/14 (calprotectin) and its subunits MRP8 and MRP14 in plaque-induced early gingival inflammation.

BACKGROUND

The inflammatory myeloid-related protein, MRP8/14, also called calprotectin, and its subunits MRP8 and MRP14 have been detected and identified recently in gingival crevicular fluid (GCF). It has been suggested that the type and phase of inflammation can be discriminated on the basis of differences in the expression of calprotectin and its subunits, released during activation and/or death of granulocytes and monocytes. The purpose of this study was to quantify calprotectin and its subunits (MRPs) simultaneously in the GCF during the initial phase of experimentally induced gingivitis, and to examine their inter- and intra-individual variations.

MATERIAL AND METHODS

Fifteen healthy non-smoking subjects, aged 18-30, were involved in this study. An initial hygiene phase (days -11 to 0) was followed by 10 days of undisturbed plaque accumulation. At days -11, -3, 0, 10, 11, clinical parameters were recorded and GCF samples collected with Durapore strips from 12 sites in each subject. Quantitative analyses of total proteins, MRP8/14, MRP14 and MRP8 were performed by ELISA procedures.

RESULTS

During the experimental phase with no oral hygiene (days 0-10), the clinical parameters Plaque Index, Gingival Index (GI) and bleeding on probing increased as expected, confirming that plaque accumulation leads to gingival inflammation. Levels of the MRPs were individually variable. They increased with plaque accumulation in one-half of the subjects, and decreased in the other subjects. The levels of MRP8/14 and MRP14 at subject recruitment (day -11) could predict a significant part of the GI at day 10. Only minute amounts of the subunits MRP8 and MRP14 were detected in comparison with the complex MRP8/14 throughout the experiment. Considerable variations were noted among sites within subjects.

CONCLUSION

The expression of calprotectin in the early phase of experimental gingivitis is variable between subjects, and two groups of subjects can be differentiated according to their response patterns. Clinical parameters at the very first visit (day -11) seemed to be different in the two response groups. The results of the present investigation indicate that the inflammatory response to plaque accumulation depends on the initial status of the subjects, which may not be leveled out by the introduction of perfect oral hygiene. Whether these patterns reflect a different susceptibility to periodontal diseases remains to be determined.