Eighty‐two periodontal patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous resection surgery (FO) which were randomly assigned to various quadrants in the dentition. Therapy was performed in 3 phases: non‐surgical, surgical, and supportive periodontal treatment (SPT) ≤ 7 years. Clinical data consisted of probing depth (PD), clinical attachment level (CAL), gingival recession (REC), bleeding on probing (BOP), suppuration (SUP), and supragingival plaque (PL). Because of the necessity to exit many CS treated sites due to breakdown, data for CS were reported only up to 2 years. All therapies produced mean PD reduction with FO > MW > RP > CS following the surgical phase for all probing depth severities. By the end of year 2 there were no differences between the therapies in the 1 to 4 mm sites. There were no differences in PD reduction between MW and RP treated sites by the end of year 3 in the 5 to 6 mm sites and by the end of year 5 in the ≥ 7 mm sites. FO produced greater PD reduction in ≥ 5 mm sites through year 7 of SPT. Following the surgical phase, FO produced a mean CAL loss and CS and RP produced a slight gain in 1–4 mm sites. RP and MW produced a greater gain of CAL than CS and FO following the surgical phase in 5 to 6 mm sites, but the magnitude of difference decreased during SPT. Similar CAL gains were produced by RP, MW, and FO in sites ≥ 7 mm. These gains were greater than that produced by CS and were sustained during SPT. Recession was produced with FO > MW > RP > CS. This relationship was maintained throughout SPT. The prevalences of BOP, SUP, and PL were greatly reduced throughout the study and were comparable between sites treated by RP, MW, and FO while the CS sites had more BOP and SUP. J Periodontol 1996;67:93–102.

Eighty-two patients were treated in a split mouth design with coronal scaling (CS), root planing (RP), modified Widman surgery (MW), and flap with osseous surgery (FO) which were randomly assigned to the various quadrants in the dentition. Following phase I and phase II therapy, the patients received supportive periodontal treatment (SPT) at 3-month intervals for up to 7 years. Clinical attachment level (CAL) was determined initially, post-phase I, post-phase II and prior to each SPT appointment. If a site lost > or = 3 mm of CAL from its baseline, it was classified as a breakdown site. Baselines were the initial exam for sites treated by CS and 10 weeks post-phase II for sites treated by RP, MW, and FO. Data were grouped by probing depth (PD) severity at the initial exam and at post-phase II. The breakdown for CS sites was assessed separately from RP, MW, and FO sites because of different baselines and retreatment protocols. Sites treated by CS had a higher incidence of breakdown than the other therapies through year 1 of SPT. The breakdown incidences/year for RP and MW sites were similar and greater than for FO sites in 1 to 4 mm and 5 to 6 mm PD categories. Breakdown incidence of RP sites was greater than MW sites which was greater than FO sites initially > or = 7 mm. Differences in incidence of breakdown between therapies after recategorizing data by post-phase II PD were the same as above, except no difference was present between RP and MW sites > or = 7 mm. Breakdown incidences were greater in increasing PD severities regardless of when they were categorized. There was no further loss of CAL one year after retreatment in 88% of sites. Patients with higher breakdown incidences tended to be smokers at the initial exam.

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking-related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone-resorbing factors, PGE2 and IL-1 beta. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non-smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 ng/ml, 1 microgram/ml, 10 micrograms/ml and 100 micrograms/ml) with or without 10 micrograms/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE2 and IL-1 beta by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE2 and IL-1 beta above that of unstimulated cultures. However, PGE2 release was potentiated 1.7-fold by the combination of P. gingivalis LPS and 10 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.05, one-way ANOVA). Prostaglandin E2 release also was potentiated 3.5-fold by P. gingivalis LPS and 100 micrograms/ml nicotine relative to P. gingivalis LPS alone (p < 0.00001, one-way ANOVA) and 3.1-fold by E. coli LPS and 100 micrograms/ml nicotine relative to E. coli LPS alone (p < 0.00001, one-way ANOVA). IL-1 beta secretion was lower for either LPS plus 100 micrograms/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS-mediated monocyte secretion of PGE2 by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.

The purpose of this study was to compare, using cell blot analysis, the association of gingival tissue mononuclear cells (GTMC) isolated from lesions displaying histories of early-onset periodontitis (EOP; typically B-lymphocyte dominated) and gingivitis (typically T-lymphocyte dominated) with the B-cell stimulating cytokine, interleukin (IL)-4, and the T-cell stimulating cytokine, IL-2. Eleven EOP patients and 11 age- and gender-similar gingivitis control (GC) subjects participated. Gingival tissue adjacent to the alveolar crest normally removed during surgery was digested in collagenase-containing media and GTMC were isolated by density gradient centrifugation. Cells were separated into four aliquots. One was left unstimulated; the remainder were stimulated for 2 hours with Porphyromonas gingivalis outer membrane protein, mitogen Concanavalin A, or common antigen tetanus toxoid. Cells then were centrifuged onto transfer membranes and incubated in RPMI 1640 media for 6 hours to allow absorption of secreted cytokine. Membranes were treated with monoclonal anti-IL-2 or anti-IL-4, followed by a biotin-conjugated second layer, streptavidin-alkaline phosphatase and nitro blue tetrazolium/5-bromo-4-chloro-indolyl-phosphate (NBT/BCIP) color development. A higher percentage of GTMC from EOP patients were IL-2+ when stimulated with P. gingivalis compared with GTMC from GC patients (20 +/- 2% vs. 12 +/- 2%, P < 0.003). A higher percentage of non-stimulated GTMC from EOP patients produced IL-4 than from GC (22 +/- 4% vs. 6 +/- 3%, P < 0.00007), as well as when stimulated with P. gingivalis (22 +/- 3% vs. 13 +/- 2%, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 microl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 microg/ml nicotine, 1 microg/ml Porphyromonas gingivalis LPS, or 1 microg/ml P. gingivalis LPS and either 100 microg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1beta. Treatments were compared by repeated measures ANOVA. 100 microg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 microg/ml nicotine and 1% ST, however, had no effect on IL-1beta secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+ 100 microg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 microg/ml nicotine significantly downregulated IL-1beta secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.