Article

The Periodontal Status of Subjects Receiving Non-Steroidal Anti-Inflammatory Drugs

February 1981
Journal of Periodontal Research 16(1):100-8

February 1981
16(1):100-8

DOI:10.1111/j.1600-051X.1980.tb01986.x

Source
PubMed

Authors:

A test group of 22 subjects who had been taking non-steroidal anti-inflammatory drugs for periods in excess of one year were matched with a control group of 22 office workers with reference to age and Plaque Index. It was found that the test group had significantly lower values of Gingival Index and shallower depths of pockets than the control group of subjects. There was a trend also for there to be less loss of attachment in the test group. These results were interpreted as indicating that anti-inflammatory drugs may influence the response of the periodontal tissues to plaque by reducing the prostaglandin concentration in the tissues. The slight decrease in loss of attachment in the test group may also be explained by the reduction in prostaglandin synthesis in the subjects taking anti-inflammatory drugs.

EFFICACY OF DICLOFENAC MOUTHRINSE AS AN ANTI-INFLAMMATORY AGENT FOR THE TREATMENT OF GINGIVITIS 1

Article

Jan 2014

Background: It has been found that topical NSAIDs agents used as anti inflammatory in gingivitis have similar efficacy as compared to the systemic drugs used for the same. Therefore, the aim of the study was to evaluate the efficacy of diclofenac mouthrinse as an anti-inflammatory agent in patients with gingivitis. Materials and Methods: A total of 90 patients were randomly divided in to three groups (30 subjects in each group). Group A-Control group: Scaling and root planning was done on day 1. Group B: Use of 0.074% w/v diclofenac mouth rinse for one month without scaling and root planning. Group C: Scaling and root planning and diclofenac mouth rinse was given for a period of one month thrice daily. Gingival index (score) was recorded at Baseline (Day1), Day 15, Day 30, Day 60. Result: There was a significant decrease in mean gingival index at day 15, day 30 and day 60 in all three groups as compared to the baseline (p=0.001). In group A, there was no significant decrease in mean gingival index at day 60 (p=0.68) but there was a significant decrease in mean gingival index at day 60 in group B (p=0.002) and group C (p=0.027) as compared to day 30. Conclusion: Diclofenac as a topical mouthrinse preceded by scaling and root planning was significantly better anti-inflammatory agent than scaling and root planning alone or diclofenac as a monotherapy in gingivitis.

EFFICACY OF DICLOFENAC MOUTHRINSE AS AN ANTI-INFLAMMATORY AGENT FOR THE TREATMENT OF GINGIVITIS 1

Article

Full-text available

Jan 2014

GINGIVAL TISSUE IL1beta AND PGE2 LEVELS IN PATIENTS WITH CHRONIC PERIODONTITIS AFTER ADDITIONAL THERAPY WITH NON-STEROIDAL ANTI-INFLAMMATORY DRUGS

Article

Full-text available

Dec 2010

Background: The understanding of the pathogenesis of periodontitis makes various progresses in the last decades. Today it is well known that the synthesis of high levels of pro-inflammatory mediators from gingival tissues in response to periodontopathogens results in destruction of soft and hard periodontal tissues and clinical expression of periodontal disease. There is enough evidence that PGE2 and IL-1? are important mediators in the initiation and progression of periodontal disease. Detection of numerous cytokines in high levels in gingival tissues and crevicular fluid may be indicator for activity of periodontitis. The reduction of IL-1? and PGE2 levels after periodontal therapy may be a potential criterion for successful periodontal therapy. The occurrence of increased IL-1? and PGE2 levels in GCF or gingival tissue is able to indicate risk from progression of destruction in specific periodontital site. The current conception of the pathogenesis of periodontitis suggests that additional host modulation approach may inhibit the production of pro-inflammatory mediators in periodontal tissues and may enhance the treatment result. Aim of the study: To evaluate the effectiveness of additional host modulation therapy with NSAID (Aulin � ) in non-surgical therapy of chronic periodontitis by measurement of IL-1? and PGE2 gene expression levels in patient's gingival tissues. Materials and methods: Evaluation of prostaglandin E2 (PGE2) and interleukin-1? (IL-1?) gene expression levels in gingival tissue of chronic periodontitis patients before and after non-surgical periodontal therapy (scaling and root planing) was performed. Prostaglandin E2 (PGE2) and interleukin-1? (IL-1?) gene expression levels in gingival tissue of patients with chronic periodontitis receiving conventional mechanical therapy alone or with additional host modulation therapy with NSAID (Aulin � ) - 100 mg per day were compared. PCR analysis- TagMan RT-PCR for evaluation of gene expression levels of IL-1? and PGE2 in gingival tissue of periodontal patients was applied. Results: Statistically significant differences were found between additional Aulin � therapy group and conventional therapy group. Received correlative coefficient with Spearman analysis was respectively t = -0.72 (p< 0,05) for IL-1? and t = 0.81(p<0,05) for PGE2. The negative values of ddCt in test group reveal lower level of inhibition of gene expression. The comparative analysis of the collected data demonstrates fewer differences between both groups. The deviations in gene expression levels of IL -1? and PGE2 are higher in the patients treated with adjunctive medication with Aulin � . Conclusion: This study confirms the effectiveness of non-surgical therapy in moderate and severe periodontitis. Additional use of non-steroidal anti-inflammatory agent Aulin � results in higher inhibition of the pro-inflammatory cytokines IL-1? and PGE2. This data may be the base for modifying the conventional non-surgical therapy by including anti-inflammatory agents in the treatment of chronic periodontitis.

CORRELATIONS BETWEEN HEALING PARAMETERS AND PGE2 EXPRESSION LEVELS IN NON-SURGICAL THERAPY OF CHRONIC PERIODONTITIS

Article

Full-text available

Nov 2017

Background: The effectiveness and limitations of causal therapy of chronic periodontitis have been thoroughly documented in the literature, and the intensity of the individual destructive host response is taken into consideration, as well. These facts are the basis in research of additional therapeutic approaches to modify tissue response by regulating the amount and activity of pro-inflammatory mediators and those of destruction. Various drugs are being studied to modulate the host's response in chronic periodontitis. The use of non-steroidal anti-inflammatory drugs that inhibit the expression and activity of important mediators has led to positive results. Aim: To assess changes in PGE2 gene expression levels as a result of non-surgical therapy and additional application of a non-steroidal anti-inflammatory agent in chronic periodontitis. Material and methods: Thirty patients with moderate to severe periodontitis without systemic diseases were involved in the study. Clinical and laboratory methods were used to evaluate non-surgical periodontal treatment. Results: The data obtained from the clinical measurements - PD, CAL, BL and BOP shows that no statistically reliable relationship between gene expression of PGE2 and most clinical parameters was found in the control and test groups. Reduction in the values following the therapy was recorded in a lot of patients, but only in the test group (taking NSAIDs) with a pocket depth (PD) ≥5mm a statistically significant, inverse correlation between the PGE2 gene expression levels and changes in the pocket depth was established. Conclusion: Additional therapy with NSAIDs in chronic periodontitis has higher efficacy, manifested by correlation of deep pockets reduction and changes in PGE2 expression.

PERSPECTIVAS DA UTILIZAÇÃO DE ANTIINFLAMATÓRIOS NÃO ESTEROIDAIS NA TERAPIA PERIODONTAL Perspectives on the Use of Nonsteroidal Antiinflammatories on Periodontal Therapy

Article

Full-text available

Jan 2007

New Frontiers on Adjuvants Drug Strategies and Treatments in Periodontitis

Article

Full-text available

Oct 2021
Sci Pharm

Causes of the progression of periodontitis such as an imbalance between the immune response by the host by the release of inflammatory mediators in the response of the oral pathogenic dysbiotic biofilm have been identified. New insights on specific cell signaling pathways that appear during periodontitis have attracted the attention of researchers in the study of new personalised approaches for the treatment of periodontitis. The gold standard of non-surgical therapy of periodontitis involves the removal of supra and subgingival biofilm through professional scaling and root planing (SRP) and oral hygiene instructions. In order to improve periodontal clinical outcomes and overcome the limitations of traditional SRP, additional adjuvants have been developed in recent decades, including local or systemic antibiotics, antiseptics, probiotics, anti-inflammatory and anti-resorptive drugs and host modulation therapies. This review is aimed to update the current and recent evolution of therapies of management of periodontitis based on the adjunctive and target therapies. Moreover, we discuss the advances in host modulation of periodontitis and the impact of targeting epigenetic mechanisms approaches for a personalised therapeutic success in the management of periodontitis. In conclusion, the future goal in periodontology will be to combine and personalise the periodontal treatments to the colonising microbial profile and to the specific response of the individual patient.

The Effects of Prednisone/Ketoprofen Administration in Association with Amoxicillin Clavulanate Following Periodontal Surgical Therapy in Patients with Severe Chronic Periodontitis

Article

Full-text available

May 2021

Background and Objectives: The aim of this study was to evaluate and compare the effects of two different anti-inflammatory drugs (ketoprofen and prednisone) combined with an antibiotic (amoxicillin + clavulanic acid) and periodontal surgery on dental and periodontal parameters in patients with severe chronic periodontitis. In addition, salivary stress expressed by cortisol levels was assessed. Materials and Methods: An interventional study was performed on 22 periodontal subjects and 19 clinical healthy controls. The patients were divided in four groups, depending on treatment planning, as follows: eight patients received prednisone and antibiotherapy, associated with surgical periodontal therapy; seven patients received ketoprofen and antibiotherapy, associated with surgical periodontal therapy (group II); seven patients received only prednisone. Periodontal healthy patients underwent routine scaling and polishing. Bleeding on probing (BOP), dental mobility and salivary cortisol (ng/mL) were assessed before and after treatment. The means and standard deviations for the salivary cortisol levels (SCLs), dental and periodontal parameters were calculated for all groups using each patient as a unit of analysis. Results: Data analyses showed that the two different anti-inflammatory drugs associated with or without surgical therapy were efficient on inflammation periodontal parameters (BOP, dental mobility). Prednisone treatment alone was associated with a significant decrease of SCLs between pretreatment and post-treatment. Conclusions: In the present study, the effects of either of the anti-inflammatory drugs on inflammation evolution and salivary stress were comparable in patients undergoing antibiotherapy and surgical periodontal therapy.

The use of amnion‐derived cellular cytokine solution for the treatment of gingivitis: A two week safety, dose‐ranging, proof‐of‐principle randomized trial

Article

Full-text available

Feb 2021

Background: A 6-week Phase I clinical trial was performed to primarily evaluate the safety and secondarily determine the preliminary efficacy of a novel biological solution, ST266, comprised of a mixture of cytokines, growth factors, nucleic acids, and lipids secreted by cultured Amnion-derived Multi-potent Progenitor cells on gingival inflammation. Methods: Fifty-four adults with gingivitis/periodontitis were randomly assigned to 1X ST266 or diluted 0.3X ST266 or saline topically applied on facial/lingual gingiva (20μL/tooth). Safety was assessed through oral soft/hard tissue exam, adverse events, and routine laboratory tests. Efficacy was assessed by modified gingival index (MGI), bleeding on probing (BOP), plaque index (PI), pocket depth (PD) and clinical attachment level (CAL). Assessments were performed on Day 0, 8, 12 and 42. ST266 and saline applied daily starting at Day 0 through Day-12 except weekend days. Plasma was analyzed for safety and pro-inflammatory cytokines, interleukin 1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interferon gamma (IFN-γ). Gingival crevicular fluid (GCF) was analyzed for the same cytokines. Subgingival plaque was primarily analyzed by Checkerboard DNA-DNA hybridization. Comparisons with saline were modeled through a generalized estimating equations method adjusting for baseline. Results: No safety concern was found related to ST266. Statistically significant reduction in MGI was noted at Day 42 by 1X ST266 compared with saline (p = 0.044). PD and CAL were reduced by both doses of ST266 at Day 42 (p<0.01) and by 1X ST266 at Day 12 (p<0.05). GCF IL-1β and IL-6 levels were reduced by both doses of ST266 at Day 12 (p<0.05, p<0.01, respectively). IL-6 was also significantly reduced in plasma of both ST266 groups (p<0.05). Significant reductions in red complex bacteria were detected in both ST266 doses. Conclusions: In this "first in human oral cavity" study, topical ST266 was safe and effective in reducing gingival inflammation in 6 weeks. Longitudinal studies with large sample sizes are warranted to assess the therapeutic value of this novel host modulatory compound in the treatment of periodontal diseases. This article is protected by copyright. All rights reserved.

Non-surgical Periodontal Therapy With Adjunctive Topical Metronidazole + Piroxicam Gel Compared With Piroxicam Gel in the Treatment of Chronic Periodontitis

Article

Full-text available

Mar 2019

Cannabinoid type‐2 receptor agonist, inverse agonist, and anandamide regulation of inflammatory responses in IL‐1β stimulated primary human periodontal ligament fibroblasts

Article

Jun 2020

Objective The aim of this study is to understand the role of cannabinoid type 2 receptor (CB2R) during periodontal inflammation and to identify anti‐inflammatory agents for the development of drugs to treat periodontitis (PD). Background Cannabinoid type 2 receptor is found in periodontal tissue at sites of inflammation/infection. Our previous study demonstrated anti‐inflammatory responses in human periodontal ligament fibroblasts (hPDLFs) via CB2R ligands. Methods Anandamide (AEA), HU‐308 (agonist), and SMM‐189 (inverse agonist) were tested for effects on IL‐1β‐stimulated cytokines, chemokines, and angiogenic and vascular markers expressed by hPDLFs using Mesoscale Discovery V‐Plex Kits. Signal transduction pathways (p‐c‐Jun, p‐ERK, p‐p‐38, p‐JNK, p‐CREB, and p‐NF‐kB) were investigated using Cisbio HTRF kits. ACTOne and Tango™ ‐BLA functional assays were used to measure cyclic AMP (cAMP) and β‐arrestin activity. Results IL‐1β stimulated hPDLF production of 18/39 analytes, which were downregulated by the CB2R agonist and the inverse agonist. AEA exhibited pro‐inflammatory and anti‐inflammatory effects. IL‐1β increased phosphoproteins within the first hour except p‐JNK. CB2R ligands attenuated p‐p38 and p‐NFĸB, but a late rise in p‐38 was seen with HU‐308. As p‐ERK levels declined, a significant increase in p‐ERK was observed later in the time course by synthetic CB2R ligands. P‐JNK was significantly affected by SMM‐189 only, while p‐CREB was elevated significantly by CB2R ligands at 180 minutes. HU‐308 affected both cAMP and β‐arrestin pathway. SMM‐189 only stimulated cAMP. Conclusion The findings that CB2R agonist and inverse agonist may potentially regulate inflammation suggest that development of CB2R therapeutics could improve on current treatments for PD and other oral inflammatory pathologies.

Effekte einer mundgesundheitsoptimierten Ernährung auf orale und systemische Entzündungsparameter

Thesis

Jan 2019

Maximilian Gärtner

Ziel: Parodontale Erkrankungen scheinen durch Ernährung beeinflusst zu werden. Ziel der klinischen, randomisierten und kontrollierten Studie war es, die Ergebnisse der Pilotstudie (Woelber et al. 2016) zum Einfluss einer mundgesundheitsoptimierten (MGO)-Ernährung auf parodontale Parameter bei einem größeren Probandenkollektiv zu überprüfen. Zusätzlich wurde die Diagnostik um serologische Parameter (CRP, TNFα, IL-6, IL-1ß, Adiponektin, Vitamin D und Fettsäureprofil) erweitert. Methoden: Dreißig Patienten wurden randomisiert und nach Plaquewerten stratifiziert in Experimentalgruppe und Kontrollgruppe aufgeteilt. Die Studie erstreckte sich über acht Wochen. Während des Studienzeitraums durften die Probanden keine Interdentalraumhygiene betreiben. In den ersten zwei Wochen ernährten sich beide Gruppen nach einer gewohnten westlichen Ernährungsweise. Nach einer zweiwöchigen Umstellungsphase stellte die Experimentalgruppe ihre Ernährung für vier Wochen auf eine mundgesundheitsoptimierte Ernährung um. Diese beinhaltete einen weitestgehenden Verzicht einfacher und prozessierter Kohlenhydrate, gesättigter Fett- und Transfettsäuren sowie eine vermehrte Einnahme von nitrathaltigem Gemüse, Omega-3-Fettsäuren, Ballaststoffen, Antioxidantien, pflanzlichem Vitamin C und Vitamin D. Die Kontrollgruppe behielt über die gesamte Studiendauer die westliche Ernährungsweise bei. Während Plaque- und Gingiva-Index mit Ausnahme der Umstellungsphase wöchentlich erhoben wurden, erfolgte die Messung des Parodontalstatus (Sondierungstiefen mit einer drucksensitiven Sonde, Bluten auf Sondieren, Rezessionen) und die serologische Diagnostik nach Woche 2 und Woche 8. Die Messungen wurden verblindet durchgeführt. Ergebnisse: Die Ergebnisse zeigten, dass bei gleicher Abnahme der Plaquewerte (PI: ∆Exp. und ∆Kontrolle: -17,2%) sich die gingivale Entzündung in der Experimentalgruppe signifikant stärker reduzierte (GI: ∆Exp. vs. ∆Kontrolle: -40,8% vs. -19,6%, p=0,0275). Bei den restlichen parodontalen Parametern (ST, BOP, PISA) konnten ebenfalls positive Veränderungen gezeigt werden, jedoch nur teilweise statistisch signifikant. Darüber hinaus zeigte die Experimentalgruppe einen signifikant höheren Anstieg der Vitamin-D-Werte und einen signifikanten Gewichtsverlust. Bezüglich der serologischen Entzündungsmarker konnten keine signifikanten Ergebnisse beobachtet werden. Fazit: Unter Berücksichtigung der Studienlimitationen konnten die Ergebnisse der Pilotstudie bestätigt werden. Die MGO-Ernährung kann gingivale Entzündungen in einem klinisch relevanten Bereich signifikant reduzieren und zudem Gewicht reduzieren, während serologische Entzündungsmarker während dieser Studiendauer nicht betroffen zu sein scheinen.

Effects of Conventional Synthetic Disease-Modifying Antirheumatic Drugs on Response to Periodontal Treatment in Patients with Rheumatoid Arthritis

Article

Full-text available

Aug 2018
BMRI

Rheumatoid arthritis (RA) and periodontitis are common chronic inflammatory diseases and periodontitis is known to be more common and more severe in patients with RA. Based on a paucity of studies about the relationship between common conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and periodontitis, this prospective study aimed to evaluate the adjunctive effect of csDMARDs on response to nonsurgical periodontal treatment in patients with RA. Thirty-two patients with RA (RA group) and 32 systemically healthy patients (control group) with periodontitis were included in this study. The RA group patients were treated with csDMARDs, such as methotrexate, hydroxychloroquine, and sulfasalazine. Conventional nonsurgical periodontal treatment with scaling and root planing was performed in both groups. The extent and severity of periodontitis were evaluated by plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP) at baseline and 4 weeks after periodontal treatment. There was no statistically significant difference of periodontal parameters between the RA and control groups at baseline. Four weeks after scaling and root planing, PD reduction, and CAL gain were higher in the RA group treated with csDMARDs compared to the control group, and the difference was statistically significant ( P = 0.006 and 0.003, respectively). A post hoc analysis of the RA group showed no statistically significant difference on the response to nonsurgical periodontal treatment in multiple csDMARDs therapy and addition of NSAIDs and/or steroids to csDMARDs. In patients with RA, csDMARDs showed beneficial effect on periodontal clinical parameters following the nonsurgical periodontal treatment.

The effect of inflammatory response modulator agents on gingivitis and periodontitis

Article

Full-text available

Sep 2016

Periodontal diseases are infecto-inflammatory diseases. Literature, has tried to elucidate the infections component of gingivitis and periodontitis, for several years. In recent years, much has been discussed about the role of the host response modulators to periodontal therapeutic procedures. The aim of the present literature review was to evaluate the effect of host response modulating agents (anti-inflammatories) on the pathogenesis of gingivitis and periodontitis. A search in the main databases was performed and human and animal studies were selected. The majority of studies was performed in humans and non-steroidal anti-inflammatory drugs in different dosages were used. The results have shown a potential benefit of the non-steroidal anti-inflammatory drugs concerning the microbial challenge. However, this benefit seems not to occur in the long term, thus not supporting it as a periodontal therapeutic approach. Few studies evaluated the effect of steroidal anti-inflammatory drugs on the pathogenesis of periodontal diseases. Moreover, the results in humans and animals are controversial, pointing to a possible deleterious effect of steroidal anti-inflammatory drugs on periodontal structures.

Proinflammatory Cytokines and Periodontal Disease

Article

Full-text available

May 2016

Nada Tawfig Hashim

p>Numerous biological procedures are strictly controlled by cell-cell interactions, which are categorized into two forms: cognate (adhesive) interactions, attained by mutual recognition between membrane-bound cell-surface molecules; and cytokine-mediated interactions [1]. Cytokines (Greek cyto-, cell; and -kinos, movement) are a category of signaling molecules that are used extensively in cellular communication. The responses caused by these substances are diverse and interrelated. Generally, cytokines control growth, mobility and differentiation of lymphocytes, but they also exert a similar effect on other leukocytes and some non-immune cells [2].

Omega-3 fatty acids as an adjunct for periodontal therapy-a review

Article

Full-text available

Jun 2016
CLIN ORAL INVEST

Objectives The aim of this article is to present an overview of omega-3 fatty acids, their anti-inflammatory properties and potential use as an adjunct for periodontal therapy. Materials and methods A general literature search was conducted to provide an overview of omega-3 fatty acids, their metabolism and anti-inflammatory properties. A more specific literature search of PubMed and EMBASE was conducted to identify articles dealing studies investigating the effects of omega-3 fatty acids in the treatment of periodontitis in animals and humans and included cross-sectional, longitudinal and intervention designs. Results To date, there is good emerging evidence that dietary supplementation with fish oil may be of some benefit and this is enhanced if combined with aspirin. All clinical intervention studies to date have been on small sample sizes, and this indicates there is need for larger and more robust clinical trials to verify these initial findings. Conclusions Dietary supplementation with fish oil could be a cost-effective adjunctive therapy to the management of periodontal disease. Clinical relevance The host modulatory properties of omega-3 fatty acids warrant further assessment of their use as an adjunct in the management of periodontitis.

Interleukin-6 receptor inhibitor tocilizumab ameliorates periodontal inflammation in patients with rheumatoid arthritis and periodontitis as well as tumor necrosis factor inhibitors

Article

Full-text available

Dec 2015

Interleukin-6 (IL-6) may play a pathological role in rheumatoid arthritis (RA) and periodontitis. Although the efficacy of medication with IL-6 receptor inhibitor, tocilizumab (TCZ), has been demonstrated in the treatment of RA, very little is known about whether TCZ therapy affects periodontitis. The aim of the present study is to compare periodontal condition in patients with RA and periodontitis before and after TCZ therapy. The study participants consisted of 20 patients with RA and periodontitis who were treated with TCZ and 40 patients with RA and periodontitis who received medication with tumor necrosis factor inhibitor (TNFI). Clinical periodontal and rheumatologic assessments and serum biochemical measurements using enzyme-linked immunosorbent assays were performed at baseline and 3 and 6 months later. TCZ and TNFI therapies significantly reduced periodontal inflammation that was determined by gingival index, bleeding on probing, and probing depth (p < 0.017), although plaque levels were comparable before and after the therapies. Both therapies also significantly decreased disease activity score including 28 joints using C-reactive protein (CRP), number of tender and swollen joints, and serum levels of anti-cyclic citrullinated peptide antibodies, rheumatoid factor, CRP, and matrix metalloproteinase-3 (p < 0.017). Additionally, a significant decrease was observed in periodontal clinical attachment level after TCZ therapy (p < 0.017), but not after TNFI therapy. TCZ therapy significantly decreased serum levels of TNF-α, total immunoglobulin G, and serum amyloid A (p < 0.017), although serum levels of IL-6 and soluble IL-6R were significantly increased (p < 0.017). These results suggest a beneficial effect of TCZ therapy on levels of periodontal inflammation in patients with RA and periodontitis, which might be related to decrease in serum inflammatory mediators.

Comparative evaluation of the efficacy of the cyclooxygenase pathway inhibitor and nitric oxide synthase inhibitor in the reduction of alveolar bone loss in ligature induced periodontitis in rats: An experimental study

Article

Full-text available

Mar 2014

Alveolar bone loss is the most striking feature of periodontal disease. The aim of this study was to investigate the effect of a cyclooxygenase (COX) pathway inhibitor and nitric oxide synthase (NOS) inhibitor in the reduction of alveolar bone loss in an experimental periodontal disease (EPD) model. The study was conducted on 60 Wistar rats divided into three groups of 20 rats each and then subjected to a ligature placement around the left maxillary second molars. Group 1 rats were treated with COX inhibitor (diclofenac sodium 10 mg/kg/d), group 2 with NOS inhibitor (aminoguanidine hydrochloride 10 mg/kg/d) and group 3 served as controls, receiving only saline, intraperitoneally 1h before EPD induction and daily until the sacrifice on the 11(th) day. Leukogram was performed before ligation, at 6 h and at the first, seventh and 11(th) days after EPD induction. After sacrifice, all the excised maxillae were subjected to morphometric and histometric analysis to measure the alveolar bone loss. Histopathological analysis was carried out to estimate cell influx, alveolar bone and cementum integrity. Induction of experimental periodontitis in the rat model produced pronounced leucocytosis, which was significantly reduced by the administration of diclofenac sodium and aminoguanidine on the 11(th) day. In morphometric and histometric examinations, both the test drugs significantly (P < 0.05) inhibited the alveolar bone loss as compared with the control group. Both COX inhibitor and NOS inhibitor are equally effective in inhibiting the inflammatory bone resorption in an experimental periodontitis model.

Host Modulation-Promising Direction In Periodontal Therapy

Article

Full-text available

Feb 2014

The primary etiology of the periodontal disease is chronic inflammation due to bacterial infection. It is the host's reaction to the presence of bacteria that mediates tissue destruction .Since the destruction of periodontium is believed to be due to the host response , it is intellectual and logical to consider therapeutic approaches that modulate the host response in addition to antibacterial approaches in periodontal therapy. Improved knowledge of bacterium –host interactions and of the process leading to tissue destruction will help to identify targets for host modulation to reduce periodontitis in selected situations .The objective of this article is to review and update the fundamental scientific concepts of host modulation and to furnish an approach to the main types of therapy used, based on the scientific literature.

What Has Immunology Brought to Periodontal Disease in Recent Years?

Article

Full-text available

Oct 2022
ARCH IMMUNOL THER EX

Recent decades have shed a new light on the pathomechanism of periodontal inflammation. While classic periodontology concentrates on biofilm control, oral hygiene improvement, professional tooth cleaning and surgical correction of damaged periodontal tissues, new aspects of the destruction mechanisms are being raised. Among them, the greatest attention is paid to the influence of host response on the clinical manifestations of the disease. Numerous studies have proved that the shift from gingivitis to periodontitis is not a simple progress of the disease, but an event occurring only in susceptible individuals. Susceptibility may result from appearance of local factors facilitating biofilm accumulation and/or maturation, or from systemic features, among which over-reaction and prolonged agitation of non-specific component of inflammatory response is crucial. The present paper summarizes the association between periodontology and immunology and updates the knowledge accrued mostly in the recent years. After a brief explanation of advances in understanding of the disease aetiology, the most studied and potentially viable immunological markers of periodontal disease are presented. Possible new therapeutic strategies, exploiting knowledge about the nature of host response-immunomodulation and reduction of chronic oxidative stress-are also presented.

Prostaglandins in Bone Resorption

Book

Apr 2020

Periodontal complications of prescription and recreational drugs

Article

Oct 2018

Drug use for both therapeutic and recreational purposes is very widespread in most societies. The range of drugs used, the variations in response to these drugs and other health and behavioral confounders mean that drug use may be an important contributor to individualized periodontal diagnoses. In this narrative review, we review the main reported effects of drugs on the periodontal tissues and periodontal disease processes. Although some of the more common adverse drug reactions on periodontal tissues are well described, in many other cases the evidence for these drug effects is quite limited and based on small case series or isolated reports. Prescription drugs are responsible for a range of effects, including drug-induced gingival overgrowth and increased gingival bleeding, and influence periodontal inflammation and periodontal breakdown. The effects of recreational drugs on the periodontal tissues is less well researched, perhaps for the obvious reason that assembling large cohorts of recreational drug users presents particular challenges. Use of nearly all of these substances is associated with poorer periodontal and dental health, although there is almost certainly a large degree of behavioral confounding in these findings. Overall, further studies of adverse drug reactions on the periodontal tissues are required as this continues to be an important and increasing factor in periodontal health determination. © 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Effect of Flurbiprofen on Alveolar Bone Dynamics during Experimental Periodontitis in Dogs

Article

Feb 1986

Ryoji Kataoka

Alveolar bone loss is the most striking feature of periodotitis in humans and animals. Many chemical mediators have been known to activate osteoclasts, and prostaglandins (PGs) are included in them. Since the levels of PGs increase in inflamed gingiva of humans with periodontitis, PGs would play the main role of alveolar bone destruction in periodontitis. Recently some investigators reported that indomethacin, a potent inhibitor of PG synthesis, reduced the macroscopic bone loss and the number of ostoclasts in some experimental model of periodontitis. But the bone always changes in the architecture by remodeling in which bone formation follows resorption. The inhibitor of PG synthesis may affect not only bone resorption but also formation. In order to understand the change of bone dynamics after administration of such drugs, bone histomorphometry, initiated by Frost et al, is very useful. This study was designed to determine the effect of flurbiprofen, a potent inhibitor of PG synthesis, on alveolar bone loss and the alveolar bone dynamics during experimental periodontitis in dogs by histomorphometry. In both medicated and non-medicated groups, dental floss ligature was placed around the second, third, and fourth premolars of the left jaw during a 32-day experimental period. The second, third and fourth premolars of the right jaw served as control. Evaluation of the dynamics of appositional bone growth was facilitated by subcutaneus administration of calcein and oxytetracycline. Administration began on day 10 of the experimental period with the use of a schedule of 2 days on (calcein), 8 days off, 2 days on (calcein), 8 days off and 2 days on (oxytetracycline). The dosage was about 10 mg/kg/day for calcein and 300 mg/kg/day for oxytetracycline. Medicated group was given daily administration of flurbiprofen (0.2 mg/kg/day) from days 22 to 32. At the end of this experimental period, the dogs were killed. The mandibles were removed and fixed immediately in 70% ethanol, dehydrated and embedded without demineralization in polyester resin. Sections, about 100μm thick, were prepared for histomorphometry. Frontal sections were divided into two segments, shallow side (S) and deep side (D). The alveolar bone surface on shallow and deep segments were further divided into two segments for measuring parameters of bone surface, gingival side (G) and periodontal side (P). The alveolar cortices on shallow and deep segments were further divided into two segments for measuring parameters of internal remodeling, buccal side (Bu) and lingual side (Li). The morphometric measurments were taken at these sites using a computer-based system. The following parameters were measured on alveolar bone surface : the fractional resorption surface (Lr), the active resorption surface ratio (aLr), the number of osteoclasts per 1 mm of active resorption surface (ocNo./arl), the number of osteoclasts (ocNo.), the fractional bone surface with osteoid seam (osLf), and the oxytetracycline single labeled surface ratio (tcLf). The following parameters were measured in alveolar cortex : the number of resorption cavities (Ar), the number of osteons with osteoid seam (osAf), the number of oxytetracycline single labeled osteons (tcAf), the proportion of mineral appositional rate of inflamed to control side (rMo), and the length of circumference of labeled osteon (Sl). The results were as follows : 1. Lr were significantly decreased in gingival side by flurbiprofen. 2. Neither aLr nor ocNo./arl were changed by flurbiprofen. 3. ocNo. were considerably decreased in gingival side by flurbiprofen. 4. Both osLf and tcLf were somewhat increased in gingival side by flurbiprofen. 5. Ar were somewhat decreased by flurbiprofen. 6. osAf were not changed, while tcAf were slightly increased by flurbiprofen. 7. rMo were not changed by flurbiprofen, and Sl were not different between medicated and non-medicated groups. These results (View PDF for the rest of the abstract.)

Anti-inflammatory Activity of Cannabinoid Receptor 2 Ligands in Primary hPDL Fibroblasts

Article

Dec 2017
ARCH ORAL BIOL

Objectives: Approximately 65 million adults in the US have periodontitis, causing tooth loss and decreased quality of life. Cannabinoids modulate immune responses, and endocannabinoids are prevalent during oral cavity inflammation. Targets for intervention in periodontal inflammation are cannabinoid type 1 and 2 receptors (CB1R, CB2R), particularly CB2R because its levels increase during inflammation. We previously demonstrated that SMM-189 (CB2R inverse agonist) decreased pro-inflammatory cytokine production in primary microglial cells. The hypothesis of this study was that cannabinoids anandamide (AEA), HU-308 (CB2R selective agonist), and SMM-189 decrease pro-inflammatory IL-6 and MCP-1 production by primary human periodontal ligament fibroblasts (hPDLFs) stimulated with P. gingivalis LPS, TNF-α, or IL-1β. Design: Cytotoxic effects of cannabinoid compounds (10-4-10-6.5 M), LPS (1-1000 ng/ml), TNFα (10 ng/ml) and IL-1β (1 ng/ml) were assessed by measuring effects on cellular dehydrogenase activity. IL-6 and MCP-1 production were measured using Mesoscale Discovery (MSD) Human Pro-Inflammatory IL-6 and MSD Human Chemokine MCP-1 kits and analyzed using MSD Sector 2400 machine. Results: EC50 values for AEA, SMM-189, and HU-308 were 16 μM, 13 μM, and 7.3 μM respectively. LPS (1 μg/ml), TNF-α (10 ng/ml), and IL-1β (1 ng/ml) increased IL-6 and MCP-1 production, which were inhibited by AEA, SMM-189, and HU-308. AEA alone significantly increased IL-6, but not MCP-1 levels, but the other cannabinoids alone had no effect. Conclusion: The effective inhibition of LPS, TNF-α, IL-1β stimulated IL-6 and MCP-1 production by CB2R ligands in hPDLFs suggests that targeting the endocannabinoid system may lead to development of novel drugs for periodontal therapy, aiding strategies to improve oral health.

Host modulation therapy with anti-inflammatory agents

Article

Nov 2017

Philip M Preshaw

Host modulation therapy refers to a treatment concept in which drug therapies are used as an adjunct to conventional periodontal treatment to ameliorate destructive aspects of the host inflammatory response. This strategy is not new in the treatment of periodontitis. Previously, nonsteroidal anti-inflammatory drugs have been investigated in this regard, with evidence of reductions in alveolar bone resorption when these drugs are used for prolonged periods of time. However, the risk of significant unwanted effects precludes the use of both nonselective nonsteroidal anti-inflammatory drugs and the selective cyclooxygenase-2 inhibitors as adjunctive treatments for periodontitis. Currently, the only available adjunctive host response modulator that is licensed for the treatment of periodontitis is subantimicrobial dose doxycycline, which functions as an inhibitor of matrix metalloproteinases. Although clinical benefits have been shown in carefully conducted randomized controlled trials, the efficacy of subantimicrobial dose doxycycline in routine clinical practice has yet to be determined. Anti-cytokine therapies have been developed for use in the treatment of rheumatoid arthritis, the pathogenesis of which bears many similarities to that of periodontitis; however, the significant risk of unwanted effects (as well as cost and lack of human trials in the treatment of periodontal diseases) precludes the use of any of the currently available anti-cytokine therapies in the treatment of periodontitis. The identification of pro-resolving lipid mediators as well as small molecule biologicals that influence inflammatory responses offers the best potential, at the present time, for the development of novel host response modulators in periodontal therapy, but much research remains to be done to confirm safety and efficacy.

Evaluation of correlation between periodontitis and rheumatoid arthritis in an Indian population

Article

Jan 2010

Background and Objective: Considering the hypothesis that generated a link between joint diseases and periodontitis many centuries back, and the renewed interest lately in association between periodontitis and specifically rheumatoid arthritis, this study was undertaken in an Indian population. A correlation was done between the degree of periodontal disease in subjects with rheumatoid arthritis (RA) and non rheumatoid arthritis (NRA). Materials and Methods: The study comprised of 202 subjects, who were divided into rheumatoid arthritis and non rheumatoid arthritis groups of 101 subjects each. The periodontal status was evaluated through an inclusion criteria by evaluating the probing pocket depth (PPD), clinical attachment loss (CAL), bleeding scores and plaque scores. The degree of periodontal disease was compared to the severity of rheumatoid arthritis. Results: There was no statistically significant prevalence and severity of periodontal disease in the RA and NRA groups. Interpretation and Conclusion: Thus, as per this study, RA is not a risk indicator for periodontal disease, as both these diseases were not associated significantly in the Indian population.

Tooth Movement

Article

Oct 1991

Zeev Davidovitch

This article reviews the evolution of concepts regarding the biological foundation of force-induced tooth movement. Nineteenth century hypotheses proposed two mechanisms: application of pressure and tension to the periodontal ligament (PDL), and bending of the alveolar bone. Histologic investigations in the early and middle years of the 20th century revealed that both phenomena actually occur concomitantly, and that cells, as well as extracellular components of the PDL and alveolar bone, participate in the response to applied mechanical forces, which ultimately results in remodeling activities. Experiments with isolated cells in culture demonstrated that shape distortion might lead to cellular activation, either by opening plasma membrane ion channels, or by crystallizing cytoskeletal filaments. Mechanical distortion of collagenous matrices, mineralized or non-mineralized, may, on the other hand, evoke the development of bioelectric phenomena (stress-generated potentials and streaming potentials) that are capable of stimulating cells by altering the electric charge on their membrane or their fluid envelope. In intact animals, mechanical perturbations on the order of about 1 min/d are apparently sufficient to cause profound osteogenic responses, perhaps due to matrix proteoglycan-related "strain memory". Enzymatically isolated human PDL cells respond biochemically to mechanical and chemical signals. The latter include endocrines, autocrines, and paracrines. Histochemical and immunohistochemical studies showed that during the early places of tooth movement, PDL fluids are shifted, and cells and matrix are distorted. Vasoactive neurotransmitters are released from periodontal nerve terminals, causing leukocytes to migrate out of adjacent capillaries. Cytokines and growth factors are secreted by these cells, stimulating PDL cells and alveolar bone lining cells to remodel their related matrices. This remodeling activity facilitates movement of teeth into areas in which bone had been resorbed. This emerging information suggests that in the living mammal, many cell types are involved in the biological response to applied mechanical stress to teeth, and thereby to bone. Essentially, cells of the nervous, immune, and endocrine systems become involved in the activation and response of PDL and alveolar bone cells to applied stresses. This fact implies that research in the area of the biological response to force application to teeth should be sufficiently broad to include explorations of possible associations between physical, cellular, and molecular phenomena. The goals of this investigative field should continue to expound on fundamental principles, particularly on extrapolating new findings to the clinical environment, where millions of patients are subjected annually to applications of mechanical forces to their teeth for long periods of time in an effort to improve their position in the oral cavity. Recently developed research tools such as cell culture techniques and immunologic probes, are the best hope for enhancing this development.

Evaluation of periodontal status and analysis of relationship between periodontal clinical parameters and selected standard inflammatory parameters in patients with coronary heart disease and chronic periodontitis

Article

Mar 2011

Introduction: Chronic periodontitis and coronary heart disease are prevalent in general population. Recently, periodontitis has been recognized as an independent risk factor of a cardiovascular episode. Aim of the study: To evaluate periodontal status and analyse the relationship between periodontal clinical parameters and selected inflammatoryparameters in patients with coronary heart disease and chronic periodontitis. Material and methods: The study involved 57 individuals: group 1 - 19 subjects with chronic periodontitis and diagnosed CHD (n=19); group 2 - 18 subjects with periodontitis without CHD (n=18); group C - 20 healthy controls (n=20). Clinical periodontal parameters and selected inflammatoryparameters were evaluated. All the patients from group 1 were chronically treated with acetylsalicylic acid and most were on statins. Results: No statistically significant differencesconcerning standard inflammatoryparameters (leucocytosis, fibrinogen, CRP) between study groups were observed. Conclusions: Smaller activity of periodontal inflammation in patients with coronary disease suggests the influenceofprolongedacetylsalicylicacidtreatment on the inflammatoryprocess. Assessment of inflammatory process activity with theuse of classic parameters did not reveal any differences between studied groups.

A case of patient with multi-joint pain received with steroid and agents that affect bone mineral homeostasis during supportive periodontal therapy

Article

Jan 2014

Drugs, medications and periodontal disease

Article

Oct 2014

This paper reviews the effects that drugs may have on the gingival and periodontal tissues. Drug-induced gingival overgrowth has been recognised for over 70 years but is becoming a more prevalent occurrence with wider use of antihypertensive and immunosuppressant drugs. The anti-inflammatory steroids, non-steroidal drugs and anti-TNF-α agents might all be expected to exert a dampening effect on chronic periodontitis although the evidence is somewhat equivocal and none of these drugs has emerged as potentially valuable adjuncts to treat periodontal disease. Desquamative gingivitis is a clinical appearance of aggressive gingival inflammation with which a number of drugs have been associated and the oral contraceptives have also been implicated in the development of gingival inflammation. Patients who are prescribed bisphosphonates and anti-platelet drugs are at risk of serious side effects following more invasive dental procedures including extractions and surgical treatments although timely, conventional management of periodontal disease may be undertaken to reduce periodontal inflammation, prevent disease progression and ultimately the need for extractions.

Systemic medication and the inflammatory cascade

Article

Feb 2014
PERIODONTOL 2000

Periodontal disease is caused by inflammatory processes initiated by the presence of a biofilm. The management of this disease process is largely achieved by disrupting the biofilm to allow regression of inflammation and healing. As our patients are living for longer they are likely to have been exposed to systemic medications that aim to reduce inflammation. These drugs have been shown to decrease inflammation within the periodontal tissues despite not being a primary function of their use. This paper aims to review the relative effects of common systemic medications on the periodontal tissues by analyzing their modes of action and discussing current research and the implications for periodontal treatment.

Effectiveness of additional therapy with NSAID (Aulin) on distribution of shallow and deep periodontal pockets in patients with chronic periodontitis (Pilot study)

Article

Full-text available

Mar 2010

Introduction: Currently accepted understanding about the role of the host inflammatory response in the progression of destructive periodontal diseases is the basis of therapeutic approaches with NSAIDs. Reduced levels of IL-1 and PGE2 in crevicular fluid and gingival tissues are measured in patients with adjunctive host modulation therapy in comparison with conventional mechanical therapy alone in numerous studies. The healing in patients with this additional therapy demonstrates successful elimination of gingival inflammation with pocket depth reduction and attachment level improvement. Aim: To investigate the effectiveness of additional host modulation therapy with NSAID (Aulin) in patients with chronic periodontitis. Material and methods: The study involves 14 adult patients suffering moderate to advanced periodontitis, instructed for strict daily plaque control (including personal hygiene involving interdental brushes and dental floss) and antimicrobial mouth rinsing with 0.2% chlorhexidine (Corsodyl) and is treated with scaling and root planning. On the 5th day of the treatment the patients are put on adjunctive systemic administration of NSAID (Aulin) for 14 days, twice daily x100 mg. The efficiency of the therapy is measured at its 6th week with the same clinical parameters - PD, CAL, HI, and PBI. Results: The results of the treatment depict significant shift in the distribution of shallow and deep periodontal pockets. The shallow pockets (1-3mm) in the initial status of the patients are 23.8% from all measured pockets and at the end of the applied treatment this number rises up to 75.7%. The initial level of the deep periodontal pockets (≥5mm) is 9.8% and decreases to 0.5% after treatment. The quantity of pockets with moderate depth (3- 5mm) decreases from 66.5% to 38.7% at the end of the evaluated treatment. Conclusion: Within the limits of this pilot study we may conclude that the additional host modulation therapy

Binary regulation of interleukin(IL)-6 production by EP 1 and EP 2 /EP 4 subtypes of PGE 2 receptors in IL1β-stimulated human gingival fibroblasts

Article

Feb 2002
J PERIODONTAL RES

Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions.

Assessment of the efficacy of a nonsteroidal anti-inflammatory drug, NaprosynR, in the treatment of gingivitis

Article

Jul 1990
J PERIODONTAL RES

A double-blind, placebo-controlled trial was conducted to determine the effects of the nonsteroidal anti-inflammatory drug Naprosyn® (naproxen) on gingival inflammation. The enrollment of 114 patients provided 102 patients valid for efficacy evaluation, each having a mean gingival index (GI) score of 1.5 or greater at test-teeth sites. Patients were given oral Naprosyn 500 mg b.i.d. or placebo for 30 days. At 28 d, full-mouth prophylaxis was performed. Gingival index, modified sulcular bleeding index (SBI), and plaque index (PI) scores were taken at baseline, at 28 d, and at 30 d. When the 28-d index measurements were compared to baseline, the drug had no significant effect on plaque index scores or gingival inflammation. Statistically, Naprosyn enhanced the resolution of gingival inflammation following removal of microbial plaque. Thus, although this drug does not suppress the inflammation-inducing properties of plaque, Naprosyn may enhance recovery following plaque removal.

Cyclooxygenase2Dependent Prostaglandin Production by Peripheral Blood Monocytes Stimulated With Lipopolysaccharides Isolated From Periodontopathogenic Bacteria

Article

Oct 2000

Prostaglandin E2 (PGE2) plays important roles in the pathogenesis of periodontal disease. Recent studies have revealed the existence of 2 isozymes of cyclooxygenase (COX), called COX-1 and COX-2. The purpose of the present study was to investigate the contribution of COX-1 and COX-2 to PGE2 production by human peripheral blood monocytes that are stimulated with lipopolysaccharides (LPS) from periodontopathogenic bacteria. LPS were isolated from Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) and Porphyromonas gingivalis (P. gingivalis) by the phenol-water method. Peripheral blood monocytes were stimulated with LPS for the indicated periods, and the levels of PGE2 or interleukin (IL)-1 beta in the culture media were measured by enzyme-linked immunosorbent assay. Expression of COX-1 and -2 proteins was studied by immunocytochemical staining, and COX-2 mRNA expression was examined by Northern blot analysis. Peripheral blood monocytes stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS produced PGE2 in a time- and dose-dependent manner. Indomethacin, a non-selective COX-1/COX-2 inhibitor, and NS-398, a specific COX-2 inhibitor, completely inhibited PGE2 production. Immunocytochemical staining of COX-1 and COX-2 proteins showed that expression of COX-2 protein was increased in monocytes that were stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS, compared with that in unstimulated monocytes, whereas expression of COX-1 protein was not altered. Northern blot analysis showed that monocytes stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS expressed COX-2 mRNA, while COX-2 mRNA was not detectable in unstimulated cells. Treatment of A. actinomycetemcomitans-LPS-stimulated monocytes with NS-398 induced a significant increase of IL-1 beta production to the same extent as treatment with indomethacin. These results suggest that COX-2 is induced in monocytes stimulated with LPS derived from A. actinomycetemcomitans and P. gingivalis and that the COX-2 is primarily responsible for PGE2 production. COX-2 may be pivotal in PGE2 production in periodontal lesions and may be involved in inflammatory responses.

The effect of long-term aspirin intake on the outcome of non-surgical periodontal therapy in smokers: A double-blind, randomized pilot study

Article

Apr 2013
J PERIODONTAL RES

Objective: The objective of this parallel, double-blind, randomized pilot study was to determine the effect of a daily dose of 325 mg of aspirin (ASA) on the clinical outcomes of scaling and root planing in a selected group of adult smokers. Background: The response to periodontal therapy is inferior among smokers compared to non-smokers. Long-term intake of ASA has been shown to exert a positive impact on reducing both the prevalence and severity of periodontitis, among high-risk groups of subjects such as heavy smokers and diabetics. It is reasonable to assume that systemic administration of ASA in conjunction with reduction of the bacterial load by scaling and root planing may improve and prolong the benefits of periodontal therapy. To date, only few prospective interventional clinical studies have specifically addressed the periodontal needs of smokers. Methods: The study includes 24 smokers. The following clinical parameters were measured preoperatively and at 3, 6, 9 and 12 mo postoperatively: (i) gingival index; (ii) plaque index; (iii) probing depth; (iii) probing attachment level; (iv) gingival recession; and (v) bleeding scores. Study subjects received scaling and root planing over several visits and were randomly assigned into two equal groups; a control group (C), which received a placebo and a test group (T), which took a daily dose of 325 mg ASA. No additional therapy was provided over the 1 year observation period. Results: There were more statistically significant differences (p < 0.05; one- tailed) between pretest and posttest scores in the T group than in the C group. Mean percent increase in sites with probing depth 1-3 mm (T: 8.78; C: 7.21); mean percent reduction in sites with probing depth 4-6 mm (T: -7.25; C: -5.09 not statistically significant, NS); mean percent reduction in sites with probing depth ≥ 7 mm (T: -1.42; C: -02.09); mean percent reduction in sites with probing attachment level 3-4 mm (T: -3.63; C: 0.48 NS); mean percent reduction in sites with bleeding on probing (T: -12.37; C: -2.59 NS) (p < 0.05, NS). Conclusions: Daily intake of 325 mg of ASA following scaling and root planing improved treatment outcomes in smokers, without an increase in gingival bleeding tendency. ASA promoted a higher incidence of shallow pockets and more gain in attachment level.

Heightened immune response to autocitrullinated Porphyromonas gingivalis peptidylarginine deiminase: A potential mechanism for breaching immunologic tolerance in rheumatoid arthritis

Article

Full-text available

Mar 2013
ANN RHEUM DIS

Background Rheumatoid arthritis (RA) is characterised by autoimmunity to citrullinated proteins, and there is increasing epidemiologic evidence linking Porphyromonas gingivalis to RA. P gingivalis is apparently unique among periodontal pathogens in possessing a citrullinating enzyme, peptidylarginine deiminase (PPAD) with the potential to generate antigens driving the autoimmune response. Objectives To examine the immune response to PPAD in patients with RA, individuals with periodontitis (PD) and controls (without arthritis), confirm PPAD autocitrullination and identify the modified arginine residues. Methods PPAD and an inactivated mutant (C351A) were cloned and expressed and autocitrullination of both examined by immunoblotting and mass spectrometry. ELISAs using PPAD, C351A and another P gingivalis protein arginine gingipain (RgpB) were developed and antibody reactivities examined in patients with RA (n=80), individuals with PD (n=44) and controls (n=82). Results Recombinant PPAD was a potent citrullinating enzyme. Antibodies to PPAD, but not to Rgp, were elevated in the RA sera (median 122 U/ml) compared with controls (median 70 U/ml; p<0.05) and PD (median 60 U/ml; p<0.01). Specificity of the anti-peptidyl citrullinated PPAD response was confirmed by the reaction of RA sera with multiple epitopes tested with synthetic citrullinated peptides spanning the PPAD molecule. The elevated antibody response to PPAD was abolished in RA sera if the C351A mutant was used on ELISA. Conclusions The peptidyl citrulline-specific immune response to PPAD supports the hypothesis that, as a bacterial protein, it might break tolerance in RA, and could be a target for therapy.

Levels of prostaglandin E2, thromboxane, and prostacyclin in periodontal tissues

Article

Jun 2006
J PERIODONTAL RES

Prostaglandin E2 (PGE2), thromboxane A2 (TXA2), and prostacyclin (PGI2) are naturally occurring metabolites of arachidonic acid which have been associated with inflammation. To assess the relative importance of these mediators in periodontal diseases, the levels of all three were measured by radioimmunoassay in human tissues removed during surgery. TXA2 and PGI2 were determined as their stable hydrolysis products thromboxane B2 (TXB2) and 6-keto-prostaglandin F1α (6-K-PGF1α), respectively. Tissues from periodontal pockets were separated into superficial (n = 8) and deep (n = 22) samples. Noninflamed gingival samples (n = 3) were taken from distal wedges with no clinical evidence of periodontal disease. Most of the samples taken from deep sites (73%) had measurable PGE2 with a mean level of 122 pg/mg. Half of these samples also had measurable TXB2 which correlated positively with levels of PGE2. Half of the superficial gingival samples had detectable levels of PGE2, and none had detectable TXB2. 6-K-PGF1α was found in virtually all samples but at somewhat lower levels in noninflamed tissue. Neither PGE2 nor TXB2 were detected in noninflamed samples.

Gingival and periodontal health in systemic lupus erythematosus

Article

May 2006
COMMUNITY DENT ORAL

Abstract – This study compared the periodontal health of patients with SLE with that of healthy controls. Patients with systemic lupus erythematosus had significantly lower periodontal probing depths compared with healthy controls. It is possible that systemic drugs such as corticosteroids and NSAIDS may be responsible for these reduced probing depths but this study did not reveal a statistically significant effect of drugs. There is thus no evidence for a predisposition to increased periodontal disease in SLE.

The effect of a systemically administered non-steroidal anti-inflammatory drug (Flurbiprofen) on experimental gingivitis in humans

Article

Dec 2005
J CLIN PERIODONTOL

Non-steroidal anti-inflammatory drugs reduce the acute inflammatory reaction and alveolar bone loss of experimental periodontitis in dogs by mechanisms thought to be associated with the inhibition of prostaglandin synthesis. 25 healthy volunteers abstained from tooth cleaning for 21 days. Experimental gingivitis developed in all subjects. On day 21, the subjects were divided into 3 treatment groups; oral flurbiprofen (100 mg/day) + toothbrushing (A), placebo + toothbrushing (B) and oral flurbiprofen (100 mg/day) only (C). Treatment continued for 6 days. Plaque indices (PI), gingival indices (GI) and probing pocket depths (PPD) were recorded at 6 points on each of 6 maxillary teeth on days 1, 22, 23, 24 and 27. Crevicular fluid flow (CFF) was quantified with a Periotron on days 1. 22 and 27 in groups A and B, and on days 1 and 27 in group C. There were no changes in PPD throughout the study. A reduction of GI occurred between days 22 and 27 for all treatment groups. CFF was also reduced between days 22 and 27 in groups A and B. The differences between the 3 treatments were very small. It is concluded that systemic flurbiprofen (100 mg/day) can reduce the signs of an experimental gingivitis over 6 days. This effect may be seen when the drug is used alone and as an adjunct to toothbrushing.

Relationship between gingival inflammation and painfulness of periodontal probing

Article

Dec 2005
J CLIN PERIODONTOL

Abstract The relationship of gingival inflammation to the pain associated with periodontal probing was assessed at baseline (B), and 1 month (1M) and 3 months (3M) later in 46 subjects. At each of the 3 sessions, clinical measures of gingival inflammation included an observational gingival index and bleeding score. In addition, periodontal probings of all existing teeth was performed with a constant force probe (25 g). Following completion of the probing at each session, subjects rated the global painfulness of the probing using a visual analog scale for pain. Results of this study showed that judged painfulness of probing was related to clinical inflammation (bleeding score) at baseline and 1 month and suggest that the degree of periodontal inflammation is related to the pain and discomfort associated with periodontal probing.

Mechanisms of alveolar bone destruction in periodontitis

Article

Feb 2007
PERIODONTOL 2000

The effects of a typical-action nonsteroidal anti-inflammatory drug on ligature-induced periodontal disease in the squirrel monkey

Article

Feb 1986
J CLIN PERIODONTOL

Abstract Prostaglandins are believed to be important mediators of periodontal inflammation and bone resorption. The purpose of the present blind study was to quantify clinically and histologically the effects of a topically applied non-steroidal prostaglandin synthetase inhibitor, namely a substituted oxazolopyridine derivative (SOPD), on ligature-induced periodontal disease in the squirrel monkey. For a period of 14 days, one group of ligated animals received 2 daily topical applications of the SOPD. A group receiving systemically administered indomethacin served as a positive control while a group receiving only topically applied vehicle served as a negative control. Results indicate that throughout the 14-day period of the study, the SOPD significantly inhibited gingival inflammation and loss of attachment as compared to either the placebo or indomethacin groups. Both indomethacin and the SOPD significantly inhibited bone resorption.

Serum from Postmenopausal Women Directs Differentiation of Human Clonal Osteoprogenitor Cells from an Osteoblastic toward an Adipocytic Phenotype

Article

Full-text available

Apr 2007

A consistent observation in osteoporosis is bone volume reduction accompanied by increased marrow adipose tissue. No single cause linking the two phenomena has yet been identified. In a human progenitor cell clone (hOP 7) derived from bone marrow, however, we have demonstrated that rabbit serum can direct differentiation away from an osteoblast lineage to one of adipocytes. We now report on whether human serum has a similar effect. Serum was collected from 10 pre- and 10 postmenopausal women and from the 10 postmenopausal women before and following 6-week hormone replacement therapy (HRT). hOP 7 cells were cultured with the various sera, and after 7-14 days adipocytogenesis was determined by oil red O staining and lipoprotein lipase (LPL) and glycerol 3-phosphate dehydrogenase (G3PDH) expression. Incubation with 10% premenopausal serum led to labeling of 10.9% of cells (P<0.05) with oil red O, whereas application of 10% postmenopausal serum led to a much larger effect, 43.5% labeling (P<0.001 with respect to premenopausal serum). Oil red O positivity was accompanied by loss of type I collagen expression and increased LPL and G3PDH expression. HRT did not reverse the adipocytogenic effect of postmenopausal serum. In conclusion, serum from postmenopausal women contains factors that steer hOP 7 bone progenitor cells toward an adipocytic phenotype, irrespective of HRT. The study suggests a role for serum factors in the development of fatty marrow in postmenopausal osteoporosis.

Effects of NSAID on beagle crevicular cyclooxygenase metabolites periodontal bone loss

Article

Jun 1992

This investigation focuses on the changes in the concentrations of cyclooxygenase (CO) products present within the crevicular fluid in naturally-progressing periodontitis in the beagle and the effects of various non-steroidal anti-inflammatory drugs (NSAIDs) on these metabolite levels and disease progression. Six groups of 5-6 beagles with periodontitis were followed for 6 months to determine the pretreatment rate of radiographic bone loss. At baseline, groups of animals were placed on soft chow to promote disease progression. Groups were treated with either placebo, three different formulations of systemic ibuprofen, systemic naproxen or topical flurbiprofen. During the 6-month treatment phase, crevicular fluid (CF) samples and radiographs were taken at regular intervals. Radioimmunoassay of CF samples from untreated animals demonstrated a steady increase in prostaglandin E2 (PGE2) over baseline values. At 1 month, CF-PGE2 levels increased 2-fold over baseline and, by 6 months, had reached a 5- to 6-fold elevation. Crevicular fluid thromboxane B2 (CF-TxB2) levels rapidly reached a 4- to 5-fold peak over baseline at 1 month and subsequently dropped to a 2-fold elevation for the remainder of the study. The rate of bone loss (BLOSS) in untreated animals increased 38% during the 6-month period, as compared to baseline pretreatment BLOSS rates. Overall, there was a significant depression in the CF levels of both PGE2 and TxB2 in all NSAID-treated groups. All NSAID treatments significantly retarded BLOSS, ranging from 21.0-36.9% of the control BLOSS rate. Furthermore, CO activation represents a major regulatory step in bone destruction and may thereby serve as an important site for pharmacological modulation.

Tooth Movement

Article

Full-text available

Feb 1991

Ze'ev Davidovitch

Arachidonic acid, prostaglandin E2 and leukotriene C4 levels in gingiva and submandibular salivary glands of rats fed diets containing n−3 fatty acids

Article

Dec 1991

The effect of dietary n-3 fatty acids on prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) levels in rat salivary glands and gingiva was examined in two separate nutritional studies. In the first set of experiments, two groups of male weanling Sprague-Dawley rats were fed semipurified diets containing 10% corn oil (control group) or 10% menhaden oil (experimental group). Rats were killed after 8 wk on the diets; the fatty acid composition of total phospholipids and the concentrations of PGE2 and its precursor, arachidonic acid, were measured in gingiva and submandibular salivary glands (SMSG). Dietary n-3 fatty acids were incorporated into the tissue phospholipids. Arachidonic acid levels were reduced by 56% in gingiva and SMSG of rats fed menhaden oil compared with the control rats fed the diet containing corn oil. The concentrations of PGE2 in SMSG and gingiva of rats fed the diet containing menhaden oil were reduced by 74% and 83%, respectively. In a subsequent nutritional study, we tested whether the diet-induced reduction in tissue arachidonic acid levels would also result in a corresponding decrease in LTC4 production. Three groups of rats were fed diets containing 5% corn oil (group 1), 4% ethyl ester concentrate of n-3 fatty acids plus 1% corn oil (group 2), or 5% ethyl ester concentrate of n-3 fatty acids (group 3). After 6 wk of feeding, gingiva and SMSG were analyzed for arachidonic acid content and in vitro production of LTC4.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of the NSAID piroxicam, topically administered, on the development of gingivitis in Beagle dogs

Article

Jun 1991

A single-blind investigation was designed to study the effects of piroxicam in preventing gingival inflammation and plaque formation in beagle dogs. Twelve 1-year-old beagles were brought to optimum oral hygiene and gingival health. Thereafter, they were fed a moist plaque-promoting diet and were divided into three groups. The first group received daily administration of 1.0 ml placebo gel (methylcellulose) painted on the teeth. The second group received 1.0 ml of gel containing 2 mg/ml piroxicam and the third group received 1.0 ml liquid containing 2 mg/ml of piroxicam. Placebo and test solutions were applied daily, and dogs were examined biweekly for evaluation of plaque accumulation, gingival inflammation, bleeding upon gentle probing and tooth staining. Data were analyzed using the Krushkal-Wallis test. Over the treatment period, plaque accumulation was substantial in all three groups and was not significantly different between the three groups. By week 2, the gingival index in the piroxicam-treated dogs was significantly lower than that of the placebo-treated group and remained so throughout the study, with the exception of wk 6 and 12 in the topical gel-treated group. Mean percent bleeding sites were also significantly less in the piroxicam-treated groups than in the control dogs. Staining of the teeth increased for all groups over the 16-wk treatment period. These data indicate that piroxicam can significantly inhibit the development of gingival inflammation in beagle dogs.

Role of interleukin-1 and prostaglandin in vitro bone resorption induced by Actinobacillus actinomycetemcomitans lipopolysaccharide

Article

Jun 1991

Lipopolysaccharide (Y4 LPS) isolated from Actinobacillus actinomycetemcomitans strain Y4 induced bone resorption in BALB/c mouse calvaria organ culture. The calcium release from LPS-low responsive C3H/HeJ mouse calvaria by Y4 LPS was very low. Indomethacin almost completely inhibited prostaglandin E2 (PGE2) production by Y4 LPS-stimulated BALB/c mouse calvaria, but did not suppress interleukin-1 (IL-1) release from the calvaria, and partially suppressed the bone resorption. Dexamethasone strongly inhibited the PGE2 and IL-1 production by Y4 LPS-stimulated BALB/c mouse calvaria, as well as Y4 LPS-induced bone resorption. Dexamethasone inhibited expression of membrane IL-1 on osteoblastic cells stimulated with Y4 LPS, but indomethacin did not. Furthermore, anti-IL-1 serum partially suppressed the calcium release from Y4 LPS-stimulated BALB/c mouse calvaria. These results suggest that both PGE2 and IL-1 participate in Y4 LPS-induced bone resorption in vitro.

Use of digital radiography to demonstrate the potential of Naproxen as an adjunct in the treatment of rapidly progressive periodontitis

Article

Oct 1991

The effect of the non-steroidal anti-inflammatory drug, naproxen, in reducing periodontal disease activity was assessed in 15 patients with rapidly progressive periodontitis. All patients in this double-blind study were treated with scaling and root planing. Thereafter, 7 patients receiving 500 mg naproxen b.i.d. for 3 months, and 8 patients received placebo. Disease activity was assessed in three ways. First, alveolar bone height was determined using standardized radiography. Second, alterations in alveolar bone metabolism were assessed using 99m-Tc-methylene diphosphonate uptake prior to dosing and 3 months later. Finally, bone loss or gain was detected using digital subtraction radiography. In this study, conventional subtraction images were processed to isolate the area of change and superimpose the change on the original radiograph. This allowed determination of both the direction and location of osseous changes. There was significantly less bone loss as determined by analysis of bone height during the 3-month study in the naproxen-treated patients when compared to the placebo-treated patients (p less than 0.001). Radiopharmaceutical uptake was significantly reduced in the alveolar bone in patients receiving naproxen (p less than 0.03), whereas no significant change was observed in the placebo-treated patients. Furthermore, the subtraction radiographs showed a significant increase in the proportion of teeth demonstrating bone gain in the naproxen-treated group. These findings indicate that naproxen may be a useful adjunct to scaling and root planing in patients with rapidly progressive periodontitis.

Inhibition of Alveolar Bone Loss in Beagles with the NSAID Naproxen

Article

Dec 1991

The non-steroidal anti-inflammatory drug(NSAID) naproxen was studied in 11 beagle dogs over a 13-month period to determine its effect on the progression of periodontitis. Following a 6-month pretreatment period, 5 dogs received naproxen daily at a dosage of 2.0 mg/kg for 1 month, then 0.2 mg/kg for 6 months. Six control dogs received a gelatin capsule daily as placebo. Standardized radiographs were used to measure the rate of bone loss during the pretreatment and treatment periods. In the control dogs, the rate of bone loss was seen to increase during the treatment period although the increase was not statistically significant. In dogs treated daily with naproxen, the rate of bone loss in the treatment period was significantly less at 4 months of treatment; however, at 7 months the difference, though lower than pretreatment rate, was not significant. When the percent change in rate of bone loss during the overall 7-month treatment period was compared with pretreatment rate, the control dogs demonstrated a 38% increase in rate of bone loss during the treatment period contrasting with a 61% decrease in bone loss rate in naproxen-treated dogs. The data indicate that the non-steroidal anti-inflammatory drug naproxen can significantly inhibit alveolar bone loss in beagles. At 4 months of treatment the rate of bone loss in the naproxen-treated dogs was significantly less than pretreatment, but at 7 months of treatment the rate was no longer statistically significantly less than baseline. This probably reflects a dose response to naproxen treatment for, after 30 days of the treatment period, the naproxen dosage was reduced 10-fold due to tolerance by the beagle.

Periodontal Disease in Pregnancy. I. Prevalence and Severity

Article

Dec 1963

Gingival inflammation assessed by histology, 3H-estrone metabolism and prostaglandin E2 levels

Article

Dec 1977
J PERIODONTAL RES

Gingival samples were histologically evaluated and placed in two groups, 7 samples each. Group 1 was normal gingiva with no or very few inflammatory cells and group 2 was inflamed gingiva with moderately dense accumulation of inflammatory cells in isolated areas, and sparse distribution in other areas. One hundred to three hundred mg gingival tissue samples were separately homogenized in 7 ml of 0.1 M potassium phosphate buffer (pH 7.4) and incubated with 1.51 X 10−4μM of 3H-estrone in the presence of NADPH at 37° for three hours. Organic solvent extracts of the homogenates were separated by silica gel thin layer chromatograpy and the radioactivity incorporated in estrone (E1) and estradiol-17 β (E2) zones was extracted with methanol and measured by liquid scintillation spectrometry. The rate of conversion of (E1) to (E2) in normal and inflamed gingiva was 4.4 and 8.3 X 10−7μM/g/min respectively. Prostaglandin E2 levels in 3 normal and 2 inflamed gingival samples were 37.8 and 448.7 pmole/g respectively. The significant increase in the biosynthesis of (E2) and PGE2 in inflamed as compared with normal gingiva could be a systemic factor in aggravating gingival inflammation due to the hyperemic effects of these hormones.

The Inflammatory Response

Article

Mar 1972

D.A. Willoughby

Plaque induced periodontal disease in beagle dogs. A 4 year clinical, roentgenographical and histometrical study

Article

Dec 1975

The present investigation was carried out in order to study some aspects of the clinical, roentgenographical and histopathological alterations of periodontal tissues in dogs which during a 4-year period were allowed freely to accumulate plaque.Twenty inbred Beagle dogs, at the start of the study 10 months of age, were used. During a preparatory period of eight weeks the animals were once weekly subjected to a careful prophylaxis and had their teeth brushed twice daily. At the end of this period the dogs were divided into two groups of ten (test and control). From day zero of experimentation and onwards the teeth of the control dogs were twice daily subjected to meticulous toothbrushing, whereas the teeth of the test dogs were not cleaned. Examinations of the periodontal tissues were performed at days 0, 7, 14, 21, 28 and after 2, 4, 6, 8, 12, 18, 24, 36 and 48 months. Biopsies of different tooth regions were made on day zero and after 6, 12, 18, 24, 36 and 48 months of experiment. In the sections were measured (i) the distance from the cemento-enamel junction (CEJ) to the most apical cells of the dento-gingival epithelium, and (ii) the distance from CEJ to the level of the marginal alveolar bone.The study demonstrated that it is possible in dogs to establish and maintain a normal gingiva simply by eliminating calculus and then subjecting the animals to daily repeated and carefully performed tooth cleanings. Dogs allowed freely to accumulate plaque rapidly developed signs of gingivitis and eventually also clinical, radiographical and histopathological signs of periodontal tissue breakdown. The observations show that at least one type of periodontal disease is induced by factors within the dental plaque.

Reductions in proportions of dental plaque streptococci following a 5 day Kanamycin treatment

Article

Feb 1977

A 5 day topical kanamycin treatment of the dental gingival surfaces in institutionalized mentally retarded subjects significantly reduced the plaque mass on the tooth surfaces compared to a placebo treatment. This reduction occurred in the absence of any mechanical hygiene procedures and lasted for 4 or more weeks, which was longer than the kanamycin could have been expected to be present in the mouth. This suggested that the kanamycin had caused an alteration of the plaque flora which should be discernible by quantitative culturing procedures. Plaque was removed and cultured, using an anaerobic serial dilution procedure, before and after kanamycin or placebo treatments. The reduction in plaque weight was associated with reduced levels of streptococci in the plaque. This could be demonstrated by intergroup comparison of the placebo - and kanamycin treated subjects, and by intragroup comparisons of the kanamycin treated subjects prior to treatment and at 4 and 8 weeks after treatment. The streptococci species accounted for 30% of the plaque colony forming units (CFU) prior to kanamycin treatment. At 4 weeks after treatment, the streptococci had decreased to 3% of the CFU and at 8 weeks after treatment, the streptococci had increased slightly to account for 14% of the CFU. The streptococci appeared to be Streptococcus sanguis and Streptococcus mitis. The observations indicate that the topical kanamycin was effective in reducing supragingival plaque because of its ability to decrease the proportions of streptococci in the plaque.

Periodontal status of patients with abnormalities of the immune system

Article

Feb 1978

Effect of controlled oral procedures on caries and periodontal disease in adults

Article

Jun 1978

Identification of inflamed gingival surfaces

Article

May 1979

. The present study was undertaken to clarify whether visual inflammation or gingival bleeding on probing is the earlier indicator of gingivitis. A dental prophylaxis was given to 90 male students and 1 month later the gingiva adjacent to the mesio-buccal, mid-buccal and mid-lingual surfaces of all teeth was evaluated. Two subsequent examinations were done at 1-month intervals. Each gingival margin was examined visually and classified as either non-inflamed or inflamed and these same surfaces were then probed for bleeding. The number of gingival surfaces at each examination was 6990 and, at the first examination, 16798 of these combined absence of visual inflammation and bleeding (healthy). One month later only 766 of these surfaces were still healthy. Inspection of the data from the surfaces which had changed since the first examination showed that there were a significantly greater number of surfaces which bled after probing compared to either a color change only or combined both a color change plus bleeding. The same trend was seen between the second and third examinations. It was concluded that substantial changes in healthy gingival surfaces occur in as brief a period as 1 month. When healthy gingival surfaces (no visual inflammation and no bleeding) developed clinically detectable signs under investigation, a significantly greater number manifested bleeding alone compared to either visual inflammation alone or a combination of visual inflammation plus bleeding. These findings support an emphasis on gingival bleeding indices for detection of early deviations from health.

Effect of tetracycline and/or scaling on human periodontal disease. Clinical, microbiological and histological observations

Article

Dec 1978

Suppression of Inflammation and Bone Resorption by Indomethacin During Experimental Periodontitis in Dogs

Article

Oct 1979

1. The placement of cotton floss ligatures in a position apical to the gingival margin of premolars and molars in young dogs induced an acute inflammatory reaction in the periodontal tissues resulting in loss of connective tissue attachment and alveolar bone. 2. Bone resorption could be observed histologically within 7 days, and radiographically within 2 to 3 weeks after ligature placement. 3. Daily administration of indomethacin interfered with the periodontal tissue response to ligature placement. Indomethacin was shown to (i) delay the onset and to suppress the magnitude of the acute inflammatory reaction, and (ii) decrease the degree of alveolar bone resorption.

Testing therapeutic measures for controlling chronic gingivitis in man: The results of two studies

Article

Dec 1976

A previous paper described a suggested protocol which could be used for testing therapeutic measures. In this paper the protocol has been used as a basis for testing experimental toothpastes over short and medium periods of time. The effects on plaque and gingivitis of a chlorhexidine paste used for 4 weeks, and of two other experimental products used over 8 weeks, have been investigated. Statistically significant improvements in gingivitis were observed during the use of chlorhexidine and one of the experimental pastes compared with their respective placebo pastes. The benefit observed for the experimental paste became evident when the data were analyzed considering only participants with 'frank' gingivitis. The findings have also been presented in various ways in attempts to express the benefits of the therapeutic measures in clinical terms by using arbitrarily determined success criteria.

Human breast tumor-induced osteolysis and prostaglandins

Article

Apr 1976
Prostag Other Lipid Mediat

Hypercalcemia is a common complication of advanced human mammary cancer and is generally associated with skeletal metastases. Whilst it is assumed that the hypercalcemia is due, in most cases, to calcium release, consequent upon progressive destruction of bone by the tumor metastases, the precise mechanism is unknown. Previous investigations on this problem using organ cultures of human breast tumors and an in vitro bone resorption bioassay showed that the majority of mammary carcinomas could stimulate in vitro the release of calcium from bone into the surrounding tissue culture medium and that this stimulation could be reduced significantly by the addition of aspirin to the medium. Some prostaglandins stimulate in vitro bone resorption. These results indicate that whilst osteolytically active PGE and PGF are released by the carcinomas in most cases, some other osteolytic principle is released as well.

Experimental gingivitis in man. 3. Influence of antibiotics on gingival plaque development

Article

Feb 1967

Prostaglandins Stimulation of Bone Resorption in Tissue Culture

Article

Jul 1970

Some Perspectives on the Pathogenesis of Periodontal Disease

Article

Jun 1974

N S Taichman

Periodontal disease in pregnancy acta

Article

Jan 1964

Periodontal Disease in Pregnancy II. Correlation Between Oral Hygiene and Periodontal Condition

Article

Mar 1964

Experimental gingivitis in Man III

Article

May 1965

During a 5 day period without oral hygiene, 4 groups each consisting of 3 subjects with healthy gingivae, rinsed their mouths with solutions of tetracycline, vancomycin, polymyxin B or distilled water. Gingival plaque accumulated rapidly in the group rinsing with water, while tetracycline, and to a lesser degree vancomycin and polymyxin B inhibited plaque formation. Clinical gingivitis was not observed in any of the participants, but gingival exudate and leukocyte emigration were noted and seen to increase during the experimental period, especially in the water group. Rinsing with antibiotics inhibited these signs of subclinical inflammation to varying degrees. The bacterial composition of the gingival plaque changed in the water group during the experimental period towards a higher percentage of gram-negative bacteria, following the pattern observed in previous investigations. Tetracycline markedly reduced the numbers of gingival plaque organisms, while polymyxin B favored a proliferation of gram-positive cocci and short rods and depressed gram-negative bacteria. Rinsing with vancomycin resulted in a pronounced shift towards an almost pure gram-negative plaque flora. It is concluded that local administration of antibiotics with a limited spectrum may be useful for the study of the pathogenicity of the different components of the gingival microbial flora.

The Periodontal Status of Subjects Receiving Non-Steroidal Anti-Inflammatory Drugs

Abstract

No full-text available

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