A Elevated in early-onset periodontitis 33,34, 241,271 Leukotoxin (1 15 kDa) Elevated in localized early-onset periodontitis and 31, 211, 333 subset of other early-onset periodontitis 110 kDa Elevated in periodontitis patients 118 64 kDa Elevated in early-onset periodontitis 240 Fimbriae Genetic control of immune response 153 37 kDa Activates pro-inflammatorv mediators 323 29 kDa Less frequent in localized early-onset periodontitis, 347 Heat shock proteins (that is, 64 kDa) 147 elevated in early-onset periodontitis ______ Elevated in diseased Patients Outer membrane antigens 40 and 70 kDa Elevated in generalized early-onset periodontitis 340 80, 65, 58, 31 and 20 kDa Antigenic diversity 92 19, 24, 35 and 67 kDa Present in all sera 340 _~ 39, 34, 28 and 16.5 kDa Antigens present on laboratorv and clinical strains 25 58, 48, 28 and 16-18 kDa Major antigens in human antibody response a4 __ 28,38 and 90 kDa 84 17 kDa Present in all sera 84 Elevated in diseased vs. normal subjects -

The ability of stromelysin (SL), fibroblast-type collagenase (FIB-CL) and tissue inhibitor of metalloproteinases (TIMP), to differentiate between healthy, gingivitis and periodontitis sites was investigated. SL and FIB-CL are members of a family of enzymes which are capable of degrading most of the extracellular matrix macromolecules. Extracellular control of these enzymes is performed by TIMP. 40 patients each provided 3 GCF samples from healthy, gingivitis and periodontitis sites. GCF samples were collected by means of sterile paper strips. GCF samples were eluted into 500 microliters of assay buffer and assays for SL, FIB-CL and TIMP were performed by a sandwich ELISA. The mean amounts of SL and TIMP in diseased sites (gingivitis and periodontitis) were significantly higher than the mean amount of these GCF components in healthy sites (MANOVA p values were: 0.006 for SL and 0.001 for TIMP). GCF SL and TIMP differentiated healthy from diseased sites. Both SL and TIMP showed moderate correlation with clinical indices. FIB-CL was detectable in only 20.8% of all sites and did not correlate with disease status.

Post-therapy clinical improvement was associated with a reduction in bacterial prevalence, but statistical significance was only reached at a site level and this microbial reduction was not significant for all organisms. No significant post-therapy effects on the humoral immune response were noted other than a reduced antibody avidity to P. gingivalis and P. intermedia. The lack of a clear pattern in the humoral immune response may reflect a failure of the host response to produce adequate levels of biologically functional antibodies, and complex interactions between the subgingival flora and the host response.

Ninety psoriasis patients, who were either completely cleared of or manifested only a minimal presence of disease signs following 3–4 weeks of twice daily treatment with augmented betamethasone dipropionate (ABD) ointment 0.05%, were enrolled in this multicenter, double-blind, placebo-controlled study. The study was designed to determine if an intermittent pulse dose regimen of ABD ointment could safely and effectively maintain a remission disease status when treatment was applied in three consecutive applications 12 h apart, once a week for a maximum treatment period of 6 months. The disease of 60% of the patients in the active treatment group was successfully controlled for 6 months, while 80% of the placebo-treated patients experienced exacerbation of disease signs. No serious local or systemic treatment-related adverse experiences were reported. ABD ointment 0.05% when applied using the intermittent treatment regimen described here, was shown to be a clinically beneficial and well-tolerated method of long-term (up to 6 months) maintenance therapy for psoriasis patients.

The aim of the present experiment was to study changes in (i) the composition of the inflammatory cell infiltrates and (ii) levels of alpha 2-macroglobulin, lactoferrin and IgG subclasses in gingival crevicular fluid in young and old individuals during 3 weeks of plaque formation. To establish healthy gingival conditions, all subjects received professional tooth cleaning during a 4 week pre-experimental period. The experimental sites included the mesio-palatal, palatal, and disto-palatal surfaces of all teeth present in the 15...25 tooth region. At baseline (day 0) assessments of plaque and gingivitis, microbial sampling and gingival fluid assessment were performed and one gingival biopsy harvested from each subject. Following the baseline examination, the participants abolished mechanical tooth cleaning measures in the palatal and approximal surfaces of 15...25. The clinical examination and the gingival fluid measurement were repeated on days 7, 14 and 21 of no oral hygiene. The microbiological sampling and the biopsy procedure were repeated on days 7 and 21. The gingival crevicular fluid samples harvested from the old individuals had higher levels of alpha 2-macroglobulin and IgG3 compared to young subjects. The immunohistochemical analyses of the biopsies demonstrated that the gingival lesion representing the old individuals harbored a higher proportion of B-cells and a lower density of PMN cells compared to the infiltrate in the young group of subjects. It is suggested that differences exist in the inflammatory response to de novo plaque formation in young and old individuals.