CHARACTERIZATION OF MATRIX METALLOPROTEINASE (MMP-8 AND MMP-9) ACTIVITIES IN THE SALIVA AND IN GINGIVAL CREVICULAR FLUID OF CHILDREN WITH DOWNS-SYNDROME

PREVIOUS STUDIES HAVE SHOWN INCREASED susceptibility to periodontal di seases in children with Down's syndrome (DS), The mechanisms involved in the periodontal inflammatory processes in DS are not fully understo od. The present study characterized the periodontal status of 9 non-in stitutionalized DS children 9 to 17 years old (mean 13.6 years) relati ve to their age-matched systemically and periodontally healthy control s, The periodontal status was assessed by visible plaque index (VPI), gingival bleeding index (GBI), and probing depth. We also assessed, by sodium dodecyl sulphate polyacrylamide gel electrophoresis/laser dens itometry and by zymography, the collagenase and gelatinase activities in the gingival crevicular fluid (GCF) and saliva samples collected fr om DS patients and from the controls. Eight of the nine DS children sh owed a periodontium comparable to that seen in healthy controls; begin ning alveolar bone loss was radiographically seen In the DS patient wi th deep periodontal Dockets. The endogenously active collagenase and t otal collagenase activities were slightly higher in GCF of DS children compared to healthy controls. Western blot demonstrated that GCF coll agenase of DS patients was human neutrophil collagenase (MMP-8 or coll agenase-2), which occurred in 75 kDa proMMP-8 and in DS patients, but not in controls, also in 65 kDa active MMP-8 form and occasionally low er 40-50 kDa MMP-8 species. Zymographic analysis revealed the presence of 120 kDa (MMP-9 complexed with neutrophil gelatinase associated lip ocalin or NGAL), 92 kDa (MMP-9) and 72 kDa (MMP-2) gelatinases in DS a nd control GCE Especially in DS GCF MMP-9 occurred in part in 82-85 kD a activated form. Salivary collagenase in DS was high when compared to controls but of the same MMP-8 type as in control saliva. Our finding s suggest that in vivo activated MMP-8 in GCF derived from triggered P MNs and/or cytokine-induced periodontal fibroblasts may reflect period ontal tissue and alveolar bone destruction seen in the early stages of gingivitis/periodontitis associated with Down's syndrome.