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Biomedical subjects

S Offenbacher

Publications and source records attributed to S Offenbacher.

At least 55 records · Page 3Linked to original sources
PubMed1998

Potential pathogenic mechanisms of periodontitis associated pregnancy complications.

During normal pregnancy, maternal hormones and locally acting cytokines play a key role in regulating the onset of labor, cervical ripening, uterine contraction, and delivery. Maternal infections during pregnancy have been demonstrated to perturb this normal cytokine and hormone-regulated gestation, sometimes resulting in preterm labor, preterm premature rupture of membranes, and preterm low birth weight (PLBW), i.e., < 2,500 g and < 37 weeks of gestation. Our research focus has been to determine whether periodontal infections can provide sufficient challenge to the mother to trigger PLBW. New experiments from 48 case-control subjects have measured gingival crevicular fluid (GCF) levels of PGE(2) and IL-1-beta to determine whether mediator levels were related to current pregnancy outcome. In addition, the levels of 4 periodontal pathogens were measured by using microbe-specific DNA probes. Results indicate that GCF-PGE(2) levels are significantly higher in PLBW mothers, as compared with normal birth weight (NBW) controls (131.4 +/- 21.8 vs. 62.6 +/- 10.3 [mean +/- SE ng/mL], respectively, at P = 0.02). Furthermore, within primiparous PLBW mothers, there was a significant inverse association between birth weight (as well as gestational age) and GCF-PGE(2) levels at P = 0.023. These data suggest a dose-response relationship for increasing GCF-PGE(2) as a marker of current periodontal disease activity and decreasing birth weight. Microbial data indicate that 4 organisms associated with mature plaque and progressing periodontitis--bacteroides forsythus, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Treponema denticola--were detected at higher levels in PLBW mothers, as compared to NBW controls. These data suggest that biochemical measures of maternal periodontal status and oral microbial burden are associated with current PLBW.

Aggregatibacter actinomycetemcomitans↗
PubMed1998

PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression.

Diabetes mellitus is a systemic disease that affects more than 12 million people in the United States and represents a risk factor for periodontitis with odds ratios of 2.1 to 3.0. New data support the concept that in diabetes-associated periodontitis, the altered host inflammatory response plays a critical role. We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. First, we found that there was an unexpected high level of GCF mediators among the IDDM subjects, even in the gingivitis and mild periodontitis patients. Furthermore, the GCF and monocytic mediator responses were obviously bimodal in distribution with respect to periodontal status. Gingivitis patients and mild periodontitis patients represented one low response group, and the moderate and severe periodontitis subjects the high response group. Accordingly, these 4 periodontal subgroups were pooled to form 2 main groups for analyses--group A (AAP Types I-II) and group B (AAP Types III-IV). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta when compared to non-diabetic controls with similar periodontal status. Within the diabetic group, the GCF levels of these inflammatory mediators were almost 2-fold higher in group B subjects when compared to diabetics from group A. Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. Insulin-dependent diabetic patients with gingivitis or mild periodontitis (group A) and moderate to severe periodontitis (group B) have abnormal monocytic inflammatory secretion in response to LPS challenge from Porphyromonas gingivalis (P. gingivalis) as compared to non-diabetic periodontal patients. Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. This upregulated monocytic trait is thought to exist independently of the presence of severe periodontal disease since, in non-diabetic patients with adult periodontitis, Gram-negative bacterial infections alone are not sufficient to elicit a systemic hyperresponsive monocytic trait. Between group A and group B diabetics, there was no significant difference in metabolic control as expressed by mean level of glycosylated hemoglobin (HbA1c). In conclusion, our data suggest that diabetic patients have exaggerated inflammatory responses when compared to non-diabetic controls. Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). Thus, we suggest that insulin-dependent diabetes mellitus is a significant risk factor for more severe periodontal disease because, as compared to non-diabetics, diabetic subjects react with an abnormally high degree of inflammation to an equivalent bacterial burden.

Adult↗
PubMed1998

Adjunctive use of a subgingival controlled-release chlorhexidine chip reduces probing depth and improves attachment level compared with scaling and root planing alone.

The present studies evaluated the efficacy of a controlled-release biodegradable chlorhexidine (CHX) (2.5 mg) chip when used as an adjunct to scaling and root planing on reducing probing depth (PD) and improving clinical attachment level (CAL) in adult periodontitis. Two double-blind, randomized, placebo-controlled multi-center clinical trials (5 centers each) were conducted; pooled data are reported from all 10 centers (447 patients). At baseline, following 1 hour of scaling and root planing (SRP) in patients free of supragingival calculus, the chip was placed in target sites with PD 5 to 8 mm which bled on probing. Chip placement was repeated at 3 and/or 6 months if PD remained > or = 5 mm. Study sites in active chip subjects received either CHX chip plus SRP or SRP alone (to maintain study blind). Sites in placebo chip subjects received either placebo chip plus SRP or SRP alone. Examinations were performed at baseline; 7 days; 6 weeks; and 3, 6, and 9 months. At 9 months significant reductions from baseline favoring the chlorhexidine chip compared with both control treatments were observed with respect to PD (chlorhexidine chip plus SRP, 0.95 +/- 0.05 mm; SRP alone, 0.65 +/- 0.05 mm, P < 0.001; placebo chip plus SRP, 0.69 +/- 0.05 mm, P < 0.001) and CAL (chlorhexidine chip plus SRP, 0.75 +/- 0.06 mm; SRP alone, 0.58 +/- 0.06 mm, P < 0.05; placebo chip plus SRP, 0.55 +/- 0.06 mm, P < 0.05). The proportion of patients who evidenced a PD reduction from baseline of 2 mm or more at 9 months was significantly greater in the chlorhexidine chip group (19%) compared with SRP controls (8%) (P < 0.05). Adverse effects were minor and transient toothache, including pain, tenderness, aching, throbbing, soreness, discomfort, or sensitivity was the only adverse effect that was higher in the chlorhexidine group as compared to placebo (P = 0.042). These data demonstrate that the adjunctive use of the chlorhexidine chip results in a significant reduction of PD when compared with both SRP alone or the adjunctive use of a placebo chip. These multi-center randomized control trials suggest that the chlorhexidine chip is a safe and effective adjunctive chemotherapy for the treatment of adult periodontitis.

Adult↗
PubMed1998

A clinical study of bacterial contamination of chlorhexidine-coated filaments of an interdental brush.

The purpose of this study was to assess the effectiveness of a chlorhexidine coating on the nylon filaments of an interdental brush in reducing bacterial contamination from actual clinical usage. In addition, the residual antimicrobial capacity of the coating over time from clinical exposure was studied. The same type of interdental brush, one with chlorhexidine-coated nylon filaments (antibacterial) and one with uncoated (control) nylon filaments was used with 20 subjects who were participating in a periodontal maintenance program. All subjects had more than four interproximal spaces large enough to accommodate the interdental brush at the start of the study. The subjects served as their own controls in this cross-over design. They used their brushes daily for one and two weeks, respectively. After the last use, each brush was kept in a controlled environment (20-22 degrees C, 65% relative humidity) for 24 hours for air drying. It was found that antimicrobial activity was detected on the chlorhexidine-coated filaments, even after one or two weeks of storage. The mean residual antimicrobial activity of the test filaments at one week was significantly higher than that found on the filaments after two weeks. The mean number of bacteria attached to the antimicrobial filaments were significantly fewer than those on uncoated, control filaments at both one week and two weeks of usage. These results suggest that chlorhexidine-coated filaments on an interdental brush can significantly reduce bacterial contamination and retain this antimicrobial activity for up to two weeks of use.

Adult↗
PubMed1997

Eicosanoids in periodontal diseases: potential for systemic involvement.

The potential application of gingival crevicular fluid (GCF) levels of prostaglandin E2 (PGE2) for predicting periodontal disease severity and reflecting disease activity has been described by several investigators. The potential application of GCF levels of PGE2 for predicting amniotic fluid levels of PGE2, and thereby estimating risk of preterm low birth weight, has not been explored until recently. The fact that intraamniotic levels of many inflammatory mediators, such as prostaglandin E2, increase during pregnancy and peak at delivery suggests that these mechanisms play an important role in normal physiologic parturition. There is increasing evidence to suggest that the presence of a subclinical endogenous Gram-negative infection of periodontal disease may present a systemic challenge sufficient to initiate the onset of premature labor, either as a source of lipopolysaccharide (LPS, endotoxin) and/or through stimulation of secondary inflammatory mediators such as PGE2 and interleukin 1 beta (IL-1 beta). This pilot investigation determines associations among the levels of PGE2 in gingival crevicular fluid, within serum, and within amniotic fluid of 18 women who were undergoing routine amniocentesis during early midtrimester, in an attempt to reveal new baseline data regarding the relationship between periodontal inflammatory mediators and intraamniotic mediators during normal parturition. Full-mouth periodontal examinations were performed and samples of GCF, serum and amniotic fluid were collected from each subject for the quantitative assessment of PGE2 by radioimmunoassay (RIA). Results of a pairwise regression analysis model reveal that PGE2 levels within the GCF are positively associated with intraamniotic PGE2 levels at the P = 0.018 level of significance. Thus, gingival crevicular levels of PGE2 may be used to provide an indirect estimate of the amniotic fluid levels of PGE2.

Amniotic Fluid↗
PubMed1997

Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases.

The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. Diabetics were divided into group A (gingivitis or mild periodontal disease) and group B (moderate to severe periodontal disease). In addition, 17 non-diabetic individuals with various degrees of periodontal disease served as control patients. Diabetics as a group had a significantly higher monocytic TNF alpha production in response to increasing Porphyromonas gingivalis A 7436 lipopolysaccharide concentrations (0, 0.003, 0.03, 0.3 and 3.0 micrograms/ml) as compared to non-diabetic patients with gingivitis or adult periodontitis (p < 0.05). A significant difference in the dose response was also noted in the level of TNF alpha secreted as a function of P. gingivalis LPS concentrations between group A and B diabetics, as determined by two-way repeated measurements ANOVA (p < 0.05). Furthermore, there was no significant difference in the mean HbA1C between the two diabetic groups, and the TNF alpha level was not significantly associated with the HbA1C level within diabetic patients. These data suggest that the diabetic state results in an upregulated monocytic TNF alpha secretion phenotype (4.6-fold increase) which, in the presence of Gram-negative bacterial challenge, is associated with a more severe periodontal disease expression. In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients.

Adult↗
PubMed1997

Meta-analysis of the effect of systemic metronidazole as an adjunct to scaling and root planing for adult periodontitis.

The purpose of this meta-analysis was to provide a quantitative overview of clinical trials assessing the use of systemic metronidazole (S-MET) as an adjunct to scaling and root planning (S&RP) in the treatment of adult periodontitis. Eight clinical trials were chosen based upon a priori selection criteria, and two outcomes, "reduction in probing pocket depth" (PD) and "gain in clinical attachment level" (CAL), were analyzed. Results for each outcome were stratified by initial PD 1-3 mm, 4-6 mm, or > or = 7 mm and length of follow-up 4-6 wk, 9-13 wk, or 14-26 wk. S-MET in conjunction with S&RP was superior to S&RP alone in reducing PD where initial PD was 4-6 mm and follow-up was 9-13 wk (0.43 mm; 99% CI 0.12, 0.73). No significant advantage was observed for S-MET for reducing PD where initial PD was less than 4 mm or follow-up was longer than 13 wk. S-MET in conjunction with S&RP was superior to S&RP alone in reducing CAL where initial PD was 4-6 mm and follow-up was 4-6 wk (0.29; 99% CI 0.01, 0.58) and where follow-up was 9-13 wk (weighted mean difference 0.32; 99% CI 0.03, 0.61). Significant heterogeneity of effect was not seen for PD or Cal at any level of initial PD or length of follow-up. No significant dose-response relationship was observed. This meta-analysis was limited due to diversity of data presentation and the small number of trials in each stratum. These results suggest that S-MET in conjunction with S&RP may offer a benefit over S&RP alone in the treatment of adult periodontitis patients in managing pockets of 4 mm or greater, but the additional benefit was not evident if initial PD was less than 4 mm or follow-up was beyond 13 wk.

Adult↗
PubMed1997

A study of attachment loss patterns in survivor teeth at 18 months, 36 months and 5 years in community-dwelling older adults.

Most of our knowledge regarding the natural history of periodontitis in adults has come from clinical studies of dental patients. However, it is known that dental patients usually are not representative of what actually happens in the population. This paper presents population-based attachment loss trends in survivor teeth to address the following issues; 1) whether attachment loss during 1 period in time is associated with higher risk for attachment loss at a subsequent period in the same subject; 2) whether sites in survivor teeth with deeper periodontal pockets at baseline are more likely to experience future attachment loss; and 3) whether the effect of regular use of dentists' services on attachment loss are demonstrated in a community-dwelling population. In 1988, the University of North Carolina School of Dentistry initiated the Piedmont 65+ Dental Study, which was designed to elicit 800 dentate respondents in the 5-county area who were examined again at 18, 36 and 60 months. Our findings indicated that, for the 3 time periods investigated, attachment loss during the first period was not related to the incidence of attachment loss at a subsequent period for most people. However, for people who experience multiple episodes, the second episode was likely to immediately follow the first episode. This pattern did not occur at the site level where no site experienced more than 2 successive episodes, and a previous episode did not put a site at higher risk for a subsequent episode. Our data also indicated that both baseline pocket depth and irregular dental visits were positively associated with the proportion of sites that demonstrated break-down over the next 5 yr.

Aged↗
PubMed1997

A 5-year study of attachment loss in community-dwelling older adults: incidence density.

This is the second of three papers that present trends in attachment loss and tooth loss over a 5-yr period in a population of community-dwelling elderly black and whites. The first paper in this series showed that in addition to subject attrition during the 5 yr of the study, teeth also were lost. This loss of subjects and teeth resulted in trends that were not always consistent over time, because people were lost from the study and teeth with more active and advanced periodontal disease were more likely to be lost. In these instances, the incidence density (time-to-event) analytic strategy is useful. Incidence density is the average rate of occurrence for a fixed follow-up period. In 1988, the University of North Carolina School of Dentistry initiated the Piedmont 65+ Dental Study, which was designed to elicit 800 dentate respondents in the 5-county area who were examined again at 18, 36 and 60 months. Our findings indicated that for every 1000 sites followed for 1 yr in this population, 20.6 sites will experience attachment loss of 3+mm. Incidence densities varied greatly by subgroup, indicating that certain characteristics predispose sites for attachment loss. A multivariate logistic regression model indicated that people who are smokers, Porphyromonas gingivalis positive, have 5 or more missing teeth, are not high school graduates, and have not had a dental visit in the last 5 yr are at higher risk of attachment loss. Posterior teeth and mesiobuccal sites are at higher risk. We conclude that incidence density analyses are useful for longitudinal periodontal data and we illustrate the use of incidence density rates to plan clinical trials.

Aged↗
PubMed1997

A 5-year study of attachment loss and tooth loss in community-dwelling older adults.

Tooth loss is a widely recognized endpoint measure for the effects of periodontal diseases and the impact of periodontal therapy. In fact, traditional clinical measures of periodontal status often are considered to be surrogate endpoints in that they are assumed to be related to tooth loss. However, the strength of the relationship between attachment loss and tooth loss in a representative population of untreated subjects has not been studied extensively. The purpose of this paper is to present the trends in attachment loss over a 5-yr period in a population of community-dwelling elderly blacks and whites. Specifically, this paper presents attachment loss trends both at the person and tooth level to address the following issues; 1) whether teeth that experience attachment loss during 1 time period are more likely to be lost at the next time period; and 2) given similar levels of attachment loss, why are some people more likely to lose teeth? In 1988, the University of North Carolina School of Dentistry initiated the Piedmont 65+ Dental Study, which was designed to elicit 800 dentate respondents in the 5-country area who were examined again at 18, 36 and 60 months. Our findings indicated that teeth with poorer attachment level at baseline had a higher probability of being lost during the next 5 yr and teeth that experienced attachment loss during a time period were more likely to be lost during the next time period than teeth without additional attachment loss. In addition, it appears that there are person-level characteristics associated with increasing tendency towards tooth loss in people with similar periodontal status, a finding that may clarify the relationship between attachment loss and tooth loss.

Activities of Daily Living↗
PubMed1997

The design and implementation of trials of host modulation agents.

Over the last two decades it has become more evident that although oral microorganisms are essential agents of periodontal pathogenesis, interpatient variability in the host response is a major determinant of the expression of periodontal disease extent and severity. Data from animal models and human studies have identified many of the components of the host inflammatory response which serve as critical mediators of clinical inflammation, attachment loss, and bone resorption. Studies suggest that certain pharmacologic agents, which act at a molecular level to block specific inflammatory mediators, appear to attenuate disease progression. These promising findings herald a new era in periodontal medicine. Anti-infective therapies may soon be supplemented with anti-inflammatory pharmacological agents. However, there are many unanswered issues regarding formulation design, clinical application, potential indication claims, and clinical study design. Furthermore, current considerations of fundamental mechanisms of pathogenesis, as well as new data from epidemiologic studies emphasizing the multifactorial nature of disease, are changing the underlying assumptions which have served to guide our design of anti-infective drug trials over the last two decades. There are new questions regarding appropriate outcome measurements which are to be reconsidered. For example, the measurement of a change in periodontal disease status, either during progression or in response to therapy, is fundamentally unidimensional and may be only mildly informative when one considers that the disease is multifactorial by nature. Using an example from intensive care medicine, pathophysiologic studies of septic shock have demonstrated that the microbial dose and the host inflammatory mediator response are far better predictors of patient morbidity and mortality than any combination of clinical signs associated with clinical shock. Clinical trials of anti-cytokine and anti-inflammatory drugs to treat shock are now designed and conducted taking strategic advantage of this knowledge by including measurements of microbial dose and host response. It appears prudent that the design and implementation of clinical trials of host modulation agents also benefit from our current insights into pathogenesis and not represent a template-driven adaptation of historical, anti-infective clinical trial protocols.

Anti-Infective Agents↗
PubMed1997

A phase I/II clinical trial to evaluate a combination of recombinant human platelet-derived growth factor-BB and recombinant human insulin-like growth factor-I in patients with periodontal disease.

The primary objective of this study was to assess the safety of recombinant human (rh) platelet-derived growth factor-BB (PDGF-BB) and (rh) insulin-like growth factor-I (IGF-I) when applied to periodontal osseous defects in humans; a secondary objective was to begin to accrue data on the therapeutic dose of these growth factors (GFs) required to stimulate periodontal regeneration. Thirty-eight human subjects possessing bilateral osseous periodontal lesions were assigned to one of two treatment groups in a split-mouth design. Following full-thickness flap reflection, test sites received local application of the therapeutic drug delivered in coded syringes by a "masked" investigator. Two dose levels were tested, 50 micrograms/ml each of rhPDGF-BB and rhIGF-I in a gel vehicle (LD-PDGF/IGF-I) and 150 micrograms/ml each of rhPDGF-BB and rhIGF-I plus vehicle (HD-PDGF/IGF-I). Control treatment consisted of either conventional periodontal flap surgery or surgery plus vehicle. Safety analyses included physical examination, hematology, serum chemistry, urinalysis, antibody titers, and radiographic evaluation of bony changes. The primary therapeutic assessment was bone fill measured at re-entry 6 to 9 months after treatment. No local or systemic safety issues were found as a result of GF administration. No patients developed antibodies to the rhGF proteins. In subjects treated with LD-PDGF/IGF-I, there were no enhancements in periodontal regeneration compared to controls. However, in patients treated with HD-PDGF/IGF-I, statistically significant increases in alveolar bone formation were noted as measured by surgical re-entry 9 months following drug delivery (P < 0.05). This corresponded to an increase of 2.08 mm of new vertical bone height and 42.3% osseous defect fill in the HD-PDGF/IGF-I subjects versus only 0.75 mm and 18.5% gains in new bone height and osseous fill, respectively, in the controls. Furcation lesions, although limited in number, responded most favorably to treatment, with 2.8 mm horizontal osseous fill. The results from this study suggest that the local application of rhPDGF-BB and rhIGF-I to periodontal lesions is safe at the dose levels studied. LD-PDGF/IGF-I did not elicit increased defect fill compared to the control; however, HD-PDGF/IGF-I resulted in a significant promotion in bone regeneration. Additional studies are warranted to more fully characterize the effects of PDGF/IGF-I on periodontal regeneration in humans.

Administration, Topical↗
PubMed1997

Inflammatory mediator response as a potential risk marker for periodontal diseases in insulin-dependent diabetes mellitus patients.

The gingival crevicular fluid (GCF) and monocytic secretion of prostaglandin E2 (PGE2) and interleukin 1 beta (IL-1 beta) were measured in a group of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 systemically healthy individuals. Diabetics were divided into Group A (gingivitis or mild periodontal disease) and Group B (moderate or severe periodontal disease). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta as compared to non-diabetic controls who were matched with regard to periodontal disease severity (P < 0.00001 and P = 0.0005, respectively). Within the diabetic population, the GCF levels of these inflammatory mediators were almost 2-fold higher in Group B as compared to Group A (P = 0.01, P = 0.006, respectively for GCF-PGE2 and IL-1 beta). Furthermore, diabetics as a group had a significantly higher monocytic PGE2 and IL-1 beta production in response to various concentrations of both Escherichia coli and Prophyromonas gingivalis lipopolysaccharide (LPS) as compared to non-diabetic patients with adult periodontitis (P = 0.0001). LPS dose-response curves demonstrated that monocytes from Group B diabetics produced approximately 3 times more PGE2 than Group A monocytes; however, there was no significant difference in monocytic IL-1 beta secretion within the IDDM patients. The levels of GCF or monocytic mediators did not correlate with age, race, or glycosylated hemoglobin (HbA1C) levels. Our data suggest that the high GCF and monocytic secretion of PGE2 and IL-1 beta in IDDM patients may be a consequence of a systemic response trait and that the presence of Gram-negative infections such as periodontal diseases may interact synergistically to yield high local levels of these mediators and a more severe periodontal condition.

Adult↗
PubMed1997

Nonsteroidal anti-inflammatory drugs as adjuncts in the management of periodontal diseases and peri-implantitis.

For the past three decades, prostaglandin E2 and other arachidonic acid metabolites have been recognized as important proinflammatory mediators in bone resorption and various forms of periodontal disease. Nonsteroidal anti-inflammatory drugs are chemical compounds that selectively inhibit the synthesis of metabolites of the cyclooxygenase pathway, thereby blocking the production of prostaglandins, thromboxane, and prostacyclin. Inhibiting prostaglandin E2 synthesis with nonsteroidal anti-inflammatory drugs has been unequivocally shown in both animal and human studies to be of primary therapeutic efficacy. Recent lines of nonsteroidal anti-inflammatory drugs research have focused on the development of daily topical administration forms such as gels, toothpastes, and rinses. Furthermore, new studies have implicated prostaglandin E2 in the peri-implantitis process, opening the possibility to manage failing implants with topical nonsteroidal anti-inflammatory drug delivery systems.

Administration, Topical↗