Biomedical subjects

R A Reinhardt

Publications and source records attributed to R A Reinhardt.

At least 19 recordsLinked to original sources

PubMed1998

Nicotine and smokeless tobacco effects on gingival and peripheral blood mononuclear cells.

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.

Analysis of Variance↗

PubMed1998

Histology near periodontitis osteoclasts.

Histologic evaluation of periodontal tissues generally has included only areas adjacent to the gingival crevice, without knowledge or quantitation of alveolar crest osteoclastic (periodontitis) activity and infiltrate. The purpose of this study was to use human autopsy material to quantitate collagen and cell types adjacent to presumed periodontitis activity and quiescence, each in the same individual. Thirteen subjects contributed 4 sites each, 2 exhibiting alveolar crest periosteal osteoclasts in resorption lacunae/periodontitis activity (OC/PA) and 2 with no osteoclasts or resorption lacunae/ periodontal quiescence (NOC/PQ). Tissue and cell morphotypes were quantitated by 2 evaluators at 100 intersects in 0.06 mm2 fields progressing from the alveolar crest toward the gingival crevice. Cell morphotypes/tissue components were compared between groups and fields using a general linear model with repeated measures. OC/PA fields adjacent to the alveolar crest contained significantly more intersects with macrophage-like cells (10.7+/-1.1 versus 5.3+/-0.6%, P=0.0003), lymphocytes (4.6+/-1.1 versus 0.7+/-0.2%, P=0.0013), plasma cells (13.3+/-2.7 versus 2.1+/-0.6%, P=0.0004), and less with collagen (48.9+/-3.5 versus 75.0+/-2.0%, P=0.0001) than NOC/PQ fields. Numbers of lymphocytes and plasma cells increased (P=0.0006 and P=0.0002, respectively), and fibroblasts and collagen decreased (P=0.0024 and P=0.0001, respectively) in fields up to 1 mm closer to the gingival crevice. However, apparent osteoclastic activity in periodontitis subjects is associated with a significant inflammatory cell infiltrate, especially macrophages and plasma cells.

Alveolar Bone Loss↗

PubMed1997

Periodontal pathogen-related stimulation indicates unique phenotype of primary cultured human fibroblasts from gingiva and periodontal ligament: implications for oral health disease.

STATEMENT OF PROBLEM: The fibroblast is considered an important cellular component in periodontitis because it is the predominant cell type in periodontal connective tissue. PURPOSE: The purpose of this study was to test whether gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) are heterogeneous in their production of inflammatory mediators associated with bone resorption in response to lipopolysaccharides from the gram-negative bacterium Porphyromonas gingivalis. To test this hypothesis, we (1) compared interleukin-6 production by cultured human PDLF and GF isolated from the same individual when exposed to P. gingivalis lipopolysaccharide; and (2) compared prostaglandin-E2 production by cultured human PDLF and GF isolated from the same individual when exposed to P. gingivalis lipopolysaccharide. MATERIAL AND METHODS: Human periodontal ligament and gingival fibroblasts were cultured from biopsies and exposed to P. gingivalis lipopolysaccharide. Levels of interleukin-6 and prostaglandin-E2 secreted into culture supernatant were measured by enzyme-linked immunosorbent assay and the data analyzed. Gingival fibroblasts secreted similar interleukin-6 and elevated prostaglandin-E2 levels compared with unstimulated cells. Periodontal ligament fibroblasts secreted elevated levels of both mediators compared with unstimulated cells. Secreted levels of interleukin-6 and prostaglandin-E2 by primary gingival and periodontal ligament fibroblast cultures appear to differ when stimulated with a periodontal pathogen-related virulence factor. CONCLUSION: The fibroblast of the periodontal ligament and the fibroblast of the gingiva may represent different phenotypes that play unique roles in tissue responses to implants.

Analysis of Variance↗

PubMed1997

Experimental gingivitis in periodontitis-susceptible subjects.

The purpose of this study was to evaluate clinical, microbiological, and gingival crevicular fluid (GCF) profiles in periodontitis-resistant and periodontitis-susceptible subjects during 4 weeks of experimental gingivitis. Experimental groups of similar ages were defined as gingivitis controls (GC; n = 10) and history of rapidly progressive periodontitis (RPP; n = 10), respectively. Prior to baseline, all subjects achieved good plaque control (plaque index (P1I) approximately 0) and gingival health (gingival index (GI) = 0), and had probing depths < or = 4 mm on experimental teeth. For 4 weeks after baseline, oral hygiene around maxillary 2nd premolar and 1st molar teeth was inhibited by a plaque guard. The plaque guard was removed weekly for GCF sampling to determine interleukin (IL)-1 beta and prostaglandin (PG)E2 amounts by ELISAs. In addition, P1I, GI, probing depth, and gingival recession measurements were made. Subgingival plaque darkfield microscopy and DNA probe analysis also were performed. Results indicated that clinical signs of inflammation, microbiological patterns and GCF profiles progressed similarly in both groups. However, plaque accumulated more rapidly in the susceptible subjects. P1I in RPP at 4 weeks was 2.1 +/- 0.1 compared to 1.5 +/- 0.2 in GC, with an incidence of P1I > of 100% versus 50%, respectively (logistic regression; p < 0.0001). Hence, the clinical, microbiological and host factors selected for this study were unrelated to previous susceptibility to periodontitis when evaluated in the experimental gingivitis model. However, the increased rate of plaque accumulation, following thorough plaque removal, in RPP patients suggests a potential factor in disease recurrence in these susceptible subjects.

Adult↗

PubMed1997

HLA-D types and serum IgG responses to Capnocytophaga in diabetes and periodontitis.

Serum IgG responses to the cell envelope proteins (CEPs) from Capnocytophaga sputigena, Capnocytophaga ochracea, and Capnocytophaga gingivalis were examined in periodontally healthy and periodontitis subjects, both with and without type 1 diabetes (n = 60). Serum IgG responses to CEPs were determined by immunoblotting with biotin-goat anti-human IgG and an alkaline phosphatase-streptavidin system. Reactivity was analyzed by transmission densitometry, digitization, and computer manipulation. The patients with diabetes showed significantly (p < 0.01) fewer responses to 14 CEPs (from 81 to 10 kDa) from C. sputigena, 5 CEPs (from 90 to 17 kDa) from C. gingivalis, and the 27-kDa CEP from C. ochracea than in the non-diabetic group. The periodontitis patients showed significantly (p < 0.01) fewer responses to the 25- and 11-kDa CEPs from C. sputigena, the 125- and 17-kDa CEPs from C. gingivalis, and the 42-kDa CEP from C. ochracea than in the periodontally healthy group. HLA-DR4, HLA-DR53, and HLA-DQw3 were associated with periodontitis, while only HLA-DR4 was associated with diabetes (p < 0.02). Significant (p < 0.01) correlations were found between HLA-DR2 and IgG reactivity patterns associated with non-diabetics, and between HLA-DR4 and IgG reactivity patterns associated with diabetic and periodontitis subjects. These results indicate that both type 1 diabetics and periodontitis subjects have a depressed IgG antibody profile to Capnocytophaga, which may account for an increased susceptibility to periodontitis infection. Periodontitis in type 1 diabetes may be related more to the HLA-D type and altered immune function than to the diabetes itself.

Adult↗

PubMed1997

The association between estrogen status and alveolar bone density changes in postmenopausal women with a history of periodontitis.

While numerous studies have demonstrated a relationship between 17-beta-estradiol (E2) deficiencies and skeletal bone loss in postmenopausal females, the influence of E2 deficiency on alveolar bone resorption is poorly understood. The purpose of this study was to examine the association between the estrogen status of postmenopausal women and alveolar bone density changes in a 1-year longitudinal study. Twenty-four postmenopausal women, within 7 years of menopause, were divided into 2 groups, E2-sufficient (n = 10) and E2-deficient (n = 14). Venous blood samples were taken at baseline, 6 months, and 1 year for radioimmunoassay determination of serum E2 levels. At baseline and 1 year, 4 vertical bite-wing radiographs were taken for computer-assisted densitometric image analysis (CADIA). Areas of interest (AOIs) for CADIA were crestal and subcrestal regions of posterior interproximal alveolar bone. Serum E2 levels were significantly higher at all 3 time points in the E2-sufficient subjects (P < 0.002), repeated measures ANOVA). Overall, mean CADIA values (0.30 +/- 0.07 for the E2-sufficient women and -0.44 +/- 0.07 for the E2-deficient women) were statistically different between groups (P < 0.001, repeated measures ANOVA), indicating that the E2-sufficient women displayed a mean net gain in alveolar bone density and the E2-deficient women displayed a mean net loss in alveolar bone density. Furthermore, the E2-sufficient women exhibited a higher frequency of sites demonstrating a gain in alveolar bone density, while the E2-deficient women exhibited a higher frequency of sites demonstrating loss in alveolar bone density. These data suggest that estrogen status may influence alveolar bone density changes as demonstrated with CADIA.

Alveolar Bone Loss↗

PubMed1996

Gingival fluid tetracycline release from bioerodible gels.

Intracrevicular antimicrobial therapy is consistent with the site-specific nature of periodontitis. Considerable research has focused on the use of nonresorbable fibers. However, a bioerodible system is desirable. The purpose of this study was to assess tetracycline release and safety following a single application of a syringable 35% tetracycline hydrochloride in a lactic-glycolic acid gel. 31 generally healthy adult volunteers (mean age = 59 years) were enrolled in and completed this randomized, double-blind eight day study. 2, 6-10 mm non-adjacent interproximal pockets that bled on pocket probing were chosen as experimental sites in each subject. I experimental site and the surrounding gingival crevice received small particle size tetracycline in gel while the other site received larger particle size tetracycline in gel. Gingival crevicular fluid (GCF) was collected prior to treatment and 15 min, 1, 2, 3, 4 and 8 days post-treatment. GCF tetracyline concentrations were determined by agar diffusion bioassay and GCF volume measurements. 61% and 71% of sites had > or = 100 micrograms/ml tetracycline 3 days following application of large (mean concentration = 430 +/- 92 micrograms/ml) and small particle gels (mean concentration = 418 +/- 70 micrograms/ml), respectively. 37% and 55% of sites had measurable tetracycline 8 days after placement of large (mean concentration = 86 +/- 31 micrograms/ml) and small particle gels (mean concentration = 293 +/- 79 micrograms/ml), respectively. The most common adverse event was "bitter taste" (10% of subjects). Based upon the reduction in probing depths and % of sites bleeding on probing at 8 days relative to pretreatment, and the absence of any serious adverse events, it is concluded that these bioerodible gels are safe, and since the bacteriostatic range for most putative periodontopathogens is in the 2-10 micrograms/ml range, the tetracycline levels observed at days 3 and 8 likely represent significant antimicrobial efficacy.

Adult↗

PubMed1996

Nicotine effects on PGE2 and IL-1 beta release by LPS-treated human monocytes.

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.

Adult↗

PubMed1995

Purification and characterization of Porphyromonas gingivalis outer membrane antigens.

Porphyromonas gingivalis is strongly associated with periodontal disease. Significant titres of specific IgG antibodies to P. gingivalis can be found in healthy individuals and those with periodontitis. In this study, 22 outer membrane antigens ranging from 15.5 to 107.6 kDa were recognized by sera from persons with periodontitis and controls. Serum from individuals with periodontitis showed a significantly higher IgG response to a 31.4-kDa antigen (p < 0.05); serum from those with gingivitis demonstrated a significantly higher response to a 15.5-kDa antigen (p < 0.05). The response to the 15.5-kDa antigen might represent a protective immune response while that to the 31.4-kDa could serve as a marker for disease susceptibility. These two antigens were purified to homogeneity and their N-terminal amino acid sequences determined. The sequences did not correspond to any previously described P. gingivalis antigens. The role of these two antigens in the pathogenesis of periodontal disease remains to be determined.

Adult↗

PubMed1995

Response to intracrevicular controlled delivery of 25% tetracycline from poly(lactide/glycolide) film strips in SPT patients.

Controlled local delivery of antibiotics has been shown to reduce periodontopathic micro-organisms with minimal side-effects. Clinical studies in our laboratory have shown that 25% tetracycline HCl delivered from poly(D,L-lactide/glycolide) film strips (25 TTC-PLGA) released therapeutic concentrations of tetracycline for 10 days. The present pilot study compared the intracrevicular delivery of 25% tetracycline HCl incorporated in these biodegradable film strips to scaling and root planing (SRP) in 10 adult periodontitis patients, who in spite of therapy and regular supportive periodontal treatment (SPT), continued to possess 5 bleeding periodontal pockets at least 5 mm deep. Sites were randomly selected to receive the following treatments: (1) 25 TTC-PLGA, (2) control strips without TTC (PLGA), (3) SRP, and (4) untreated control. Film-strip retention was augmented with a suture/cement technique, followed by strip removal after 2 weeks. Clinical parameters and subgingival bacterial morphotypes (darkfield analysis) were evaluated over time (0, 2.4, 8, 12, 26 weeks). Results indicated that, compared to baseline, 25 TTC-PLGA film strips caused significant (p < or = 0.01): (1) probing depth reduction for 26 weeks, (2) a clinical attachment level gain for 12 weeks, (3) lower %s of spirochetes for 4 weeks and motile rods for 8 weeks (p < or = 0.05), and (4) an accompanying increase in cocci for 4 weeks. In the scaled and root planed sites, probing depth was the only finding that demonstrated a significant change from baseline (p < or = 0.01). Controls and PLGA showed isolated reductions in probing depth and % of motile organisms. From these findings, applications of intracrevicular 25 TTC-PLGA, when compared to scaling and root planing, appears to have an enhanced antibacterial effect and a similar clinical effect in SPT patients. The results of this study indicate further investigation of 25 TTC-PLGA film strips should be undertaken using more subjects and sophisticated microbiological and clinical measurements.

Adult↗

PubMed1995

Antibody responses of Porphyromonas gingivalis infected gingivitis and periodontitis subjects.

UNLABELLED: Porphyromonas gingivalis demonstrates a strong association with adult periodontitis although some individuals with the infection do not experience attachment loss. Therefore differences in the immune response to this organism may be of importance to the outcome of the disease. OBJECTIVE: The aim of this study was to determine whether P. gingivalis positive subjects with and without periodontal breakdown, reacted differently to P. gingivalis antigens as assessed by the pattern of serum antibody reactivity. MATERIALS AND METHODS: Two highly defined groups of subjects were chosen for this study. Both demonstrated P. gingivalis in their plaque and both had responded to P. gingivalis as shown by the presence of serum antibodies. The two groups differed only in their apparent clinical susceptibility to periodontal breakdown. Western blots of P. gingivalis membrane antigens were probed with sera from the two groups to determine their reactivity to specific antigens. RESULTS: Analysis of the immunoblots showed that there were no differences in either the total numbers of bands, or bands recognized by the majority of subjects in the gingivitis and adult periodontitis groups. There were however, four bands recognized by the majority of the gingivitis group and not by the majority of the adult periodontitis group, there being a significant difference (P = 0.03) in the recognition of the 91.4-kDa antigen band. A further five antigens of lower molecular weight were seen by the majority of the adult periodontitis group and not by the majority of the gingivitis group. When sera were tested against purified P. gingivalis LPS, the results indicated that the five antigens seen by the majority of the adult periodontitis group had molecular weights which were in the range exhibited by the LPS antigens. CONCLUSION: These results suggest that gingivitis and adult periodontitis subjects with P. gingivalis infection, may recognize different P. gingivalis antigens.

Adult↗

PubMed1995

The effects of smokeless tobacco on clinical parameters of inflammation and gingival crevicular fluid prostaglandin E2, interleukin-1 alpha, and interleukin-1 beta.

The purpose of this study was to examine the effect of smokeless tobacco (ST) on gingival inflammation as assessed clinically and biochemically by gingival crevicular fluid (GCF) levels of PGE2, IL-1 alpha, and IL-1 beta. These parameters were compared in ST users (n = 12) and control, non-tobacco using subjects (n = 8) matched for plaque and probing depth levels. Both GI and GCF PGE2 concentration were significantly (P < 0.05) elevated at ST placement sites compared to sites in control subjects. A short-term longitudinal trial spanning 7 days also was undertaken within ST users (n = 18) to study the dynamics of gingival inflammation when ST is moved to a new site. At day 0 habitual ST placement sites exhibited a significantly (P < 0.05) higher GI compared to non-tobacco placement sites. Following transfer of ST to a new placement site, 48 hour GI scores were increased (P < 0.05) at this region. Although GCF parameters were not significantly altered, over 80% of the subjects developed dramatic inflammatory reactions in the alveolar mucosa, ranging from erythema to ulceration, at the new site of placement. This observation of a more severe response in alveolar mucosa compared to gingiva may be related to the physical location of ST or differences in tissue characteristics.

Adult↗

PubMed1995

IgG antibody subclass response to Porphyromonas gingivalis outer membrane antigens in gingivitis and adult periodontitis.

Porphyromonas gingivalis is an important oral pathogen with a strong association with adult periodontitis. Significant titers of specific IgG antibodies to P. gingivalis can be found in the sera of both gingivitis and periodontitis patients. Since IgG subclasses have different biological characteristics, the present study dealt with the serum IgG subclass response to outer membrane antigens of P. gingivalis. Western blot analysis of P. gingivalis outer membrane was carried out using 20 adult periodontitis and 20 age- and sex-matched gingivitis patients. Antibodies in sera of both adult periodontitis and gingivitis patients recognized 38 antigen bands, ranging in molecular mass from 11.1 to 161 kDa. IgG2 was the predominant antibody subclass response in both patient groups in terms of the numbers of outer membrane antigens recognized, followed by IgG3, IgG1, and IgG4. More antigens in all IgG subclasses except IgG4 were recognized in adult periodontitis cases. Of the 23 antigens identified by IgG2 antibodies, 9 were recognized predominantly in adult periodontitis and 3 in the gingivitis group. In the IgG1 subclass, 4 antigens were recognized predominantly in the adult periodontitis group while only 1 antigen was recognized significantly more in the gingivitis group. The IgG3 response identified 14 antigens ranging in molecular mass from 11.1 to 61.2 kDa in both groups. Ten antigens were recognized significantly by the adult periodontitis group. The lowest response was seen by IgG4 antibodies, with only 3 antigens of molecular mass 61.2, 52.3, and 38.8 kDa recognized, the latter two significantly in the adult periodontitis group.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Bacterial↗

PubMed1994

Prostaglandin E (PGE) and interleukin-1 beta (IL-1 beta) levels in gingival crevicular fluid during human orthodontic tooth movement.

The purpose of this study was to examine gingival crevicular fluid (GCF) levels of two potent bone resorbing mediators, prostaglandin E (PGE) and interleukin-1 beta (IL-1 beta), during human orthodontic tooth movement. The study included 10 patients, each having one treatment tooth undergoing orthodontic movement and a contralateral control tooth. The GCF was sampled at control sites and treatment (compression) sites before activation and a 1, 24, 48, and 168 hours. Prevention of plaque-induced inflammation allowed this study to focus on the dynamics of mechanically stimulated PGE and IL-1 beta GCF levels. The PGE and IL-1 beta levels were determined with radioimmunoassay. At 1 and 24 hours, mean GCF IL-1 beta levels were significantly elevated at treatment teeth (8.9 +/- 2.0 and 19.2 +/- 6.0 pg, respectively) compared with control teeth (2.0 +/- 1.1 pg, p = 0.0049, and 2.9 +/- 1.0 pg, p = 0.0209, respectively). The GCF levels of PGE for the treatment teeth were significantly higher at 24 and 48 hours (108.9 +/- 11.9 and 97.9 +/- 7.3 pg) than the control teeth (61.8 +/- 7.2 pg, p = 0.0071, and 70.8 +/- 7.4 pg, p = 0.0021, respectively). The GCF levels of PGE and IL-1 beta remained at baseline levels throughout the study for the control teeth, whereas significant elevations from baseline in GCF IL-1 beta (24 hours) and PGE levels (24 and 48 hours) were observed over time in the treatment teeth (p < or = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Gingival fluid IL-1 beta and IL-6 levels in menopause.

Menopause and oophorectomy without estrogen therapy (ED) have been associated with increased production of bone-active cytokines by peripheral blood mononuclear cells. The current study extended evaluation to gingival crevicular fluid (GCF) levels of interleukin (IL)-1 beta and IL-6 in such subjects compared to premenopausal and postmenopausal estrogen-treated females (ES). 13 ED and 13 ES Caucasians with a history of moderate-severe adult periodontitis provided GCF from 1-3 clinically identical sites each (5-6 mm probing depth, 5-7 mm clinical attachment loss, bleeding on probing). 30 s GCF samples were obtained and evaluated for IL-1 beta and IL-6 levels using two-site enzyme-linked immunosorbent assays (ELISAs). The frequency of GCF IL-1 beta-positive subjects was elevated in ED versus ES (92% versus 23%; p < 0.0004, chi 2 analysis). IL-6 was detected more frequently in ED subjects (23% versus 8%; not significant); however, the frequency of IL-6 detection was low in both groups due to short sampling times. These data support the concept that clinical conditions causing low estrogen environments allow increased local production of the bone-active cytokine IL-1 beta, and perhaps IL-6.

Adult↗

PubMed1994

Histological evaluation of interleukin-1 beta and collagen in gingival tissue from untreated adult periodontitis.

Interleukin-1 beta (IL-1 beta) may be related to the pathological processes associated with periodontitis, primarily due to its ability to induce collagenase, increase neutrophil chemotaxis, and stimulate bone resorption. This study was designed to histologically quantitate IL-1 beta positive cells from various histologic fields in untreated gingivitis/early periodontitis (G/EP) versus moderate/severe periodontitis (M/SP) gingival tissues, and associate these with collagen loss. Two gingival biopsies from 8 patients were collected, one from a G/EP site and one from a M/SP site. Mouse monoclonal antibodies in combination with an avidin-biotin-peroxidase system were used to stain for IL-1 beta, while the van Gieson method was used to stain for collagen in serial sections. Collagen loss in G/EP (35%) and M/SP (52%) fields was consistent with gingivitis and periodontitis, respectively. IL-1 beta positive cells in combined coronal/sulcular (Co/Su) and apical/sulcular (Ap/Su) fields (nearest the bacterial insult) were significantly more numerous compared to combined coronal/middle (Co/Mi) and apical/middle (Ap/Mi) fields (p < 0.05). While numbers and percentages of IL-1 beta positive cells were generally higher in M/SP biopsies, differences were not significant. Further, there was no correlation between the number of IL-1 beta positive cells and percent collagen loss. However, a significant correlation between IL-1 beta positive cells and corresponding gingival crevicular fluid IL-1 beta concentrations was noted (r = 0.65, p = 0.01). Through the use of immunohistochemistry, this study demonstrated that the presence of IL-1 beta + cells does not appear to have a direct association with collagen loss.

Adult↗

PubMed1994

Prostaglandin E2 and interleukin-1 levels in smokeless tobacco-induced oral mucosal lesions.

Inflammatory mediators released as a result of smokeless tobacco (ST)-induced irritation may play a role in the development of oral mucosal lesions at habitual tobacco placement sites in ST users. The present study examined levels of interleukin-1 (IL-1) and prostaglandin E2 (PGE2) in ST-induced mucosal lesions and compared these to mediator levels in clinically normal mucosa. Soft tissue biopsies were obtained from white mucosal lesions at habitual placement sites and normal alveolar mucosal tissue at non-placement sites in 18 ST users. Fifteen non-tobacco using subjects also provided normal alveolar mucosal biopsies. IL-1 and PGE2 were recovered from the specimens, and mediator levels were determined by enzyme immunoassay. Prostaglandin E2 levels (pg/mg) were lower in both regions in the ST subjects, but values did not vary significantly between the regions with 2.77 +/- 0.72 and 2.86 +/- 0.99 at placement and non-placement sites, respectively, in ST users and 7.31 +/- 3.84 in non-tobacco users. Both IL-1 alpha and IL-1 beta (pg/mg) were significantly (p < 0.01) elevated in ST lesions (IL-1 alpha = 25.56 +/- 4.00; IL-1 beta = 7.76 +/- 1.68) compared to either non-placement sites in ST users (IL-1 alpha = 14.64 +/- 2.65; IL-1 beta = 1.63 +/- 0.72) or non-tobacco users (IL-1 alpha = 12.84 +/- 2.60; IL-1 beta = 2.04 +/- 0.75). In view of IL-1's role in keratinocyte proliferation and its inflammatory effects, this cytokine may contribute to mucosal and gingival alterations observed in ST users.

Adult↗

PubMed1994

Smokeless tobacco effects on monocyte secretion of PGE2 and IL-1 beta.

The use of smokeless tobacco (ST) products is associated with mucosal lesions, gingival recession, and attachment loss at the site of tobacco placement. Monocytes/macrophages are primary producers of PGE2 and IL-1 beta, inflammatory mediators which are thought to play a role in the destruction of the periodontium. The purpose of this study was to determine the effect of ST alone and in combination with a major stimulator of inflammation, bacterial lipopolysaccharide (LPS), on monocyte secretion of these mediators. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy donors who were non-ST users. PBM were incubated for 24 hours in RPMI 1640 containing various concentrations of ST (0%, 0.005%, 0.01%, 1%) with or without 10 micrograms/ml LPS (Porphyromonas gingivalis LPS or Escherichia coli LPS). Of the ST preparations, only 1% ST resulted in PBM mediator secretion (7.7 +/- 2.0 ng/ml for PGE2 and 1.3 +/- 0.2 ng/ml for IL-1 beta) above that of control (unstimulated) cultures. Furthermore, the combination of 1% ST and LPS resulted in a potentiation of PGE2 release (5-fold for E. coli LPS + 1% ST and 10-fold for P. gingivalis LPS + 1% ST; P < 0.0001, one-way ANOVA) relative to the LPS preparations alone. In contrast, PBM IL-1 beta release decreased more than 2-fold upon E. coli LPS and 1% ST exposure, relative to treatment with E. coli LPS alone (P < 0.0001, one-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗