Anda di halaman 1dari 5

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || Click here to download free Android application for this journal

Original Article

The effect of ketoprofen in chronic periodontitis: A clinical double-blind study

M. Srinivas, Sangeetha Medaiah, S. Girish, M. Anil, Jagadish Pai, Amit Walvekar

Department of Periodontics, Coorg Institute of Dental Sciences, Coorg, Karnataka, India

Access this article online

Website:

www.jisponline.com

DOI:

10.4103/0972-124X.85670

Quick Response Code:

Access this article online Website: www.jisponline.com DOI: 10.4103/0972-124X.85670 Quick Response Code:

Address for

correspondence:

Dr. Sangeetha Medaiah, Coorg Institute of Dental Sciences, KK Campus, Maggula Village, Virajpet - 571 218, Coorg, Karnataka, India. E-mail:

sangeethamedaiah@

yahoo.com

Submission: 18-01-2011 Accepted: 21-08-2011

Abstract:

Background: The objective of this double-blind clinical trial was to evaluate the effects of the nonsteroidal anti- inflammatory drug (NSAID), ketoprofen, on patients with chronic periodontitis. Materials and Methods:Two similar local drug delivery preparations of a poloxamen gel containing 1.5% ketoprofen and a placebo were indigenously prepared for this purpose. Ten subjects aged 33-55 years with moderate to severe chronic periodontitis were recruited and were monitored for a period of 90 days. Three sites in each patient (total 30 sites) with a probing pocket depth of 5-8 mm were selected and divided randomly into three groups: 1) group A: scaling and rootplaning (SRP) + drug A; 2) group B: SRP + drug B; and 3) group C: SRP. Clinical parameters and blood smear (from intracrevicular blood) were assessed to determine the differential count and Arneth index. All parameters were assessed at baseline, 30 days and 90 days, respectively. Results: Highly significant values were achieved for plaque index (P=0.00), and significant values were obtained for gingival index (P=0.044). Reduction in bleeding on probing was found to be highly significant. Probing depth and clinical attachment level showed no inter group variation. Conclusion: The results of this double-blind trial indicate that the combined effect of locally delivered ketoprofen with SRP was more effective in controlling periodontal disease than SRP alone.

Key words:

Arneth index, bleeding on probing, ketoprofen gel, placebo

 
 

INTRODUCTION

that endotoxin-stimulated monocytes secreted

modifying the response of the host to the process

P eriodontitis is an inflammatory disease caused by microorganisms. The progression of the disease, however, is

P eriodontitis is an inflammatory disease caused by microorganisms. The progression

of the disease, however, is determined by host

two to three times more PGE than subjects without disease. [3] Ketoprofen has the added advantage of directly inhibiting monocytes

and macrophages, which are predominant

factors. One of the mediators that influence this progression is the prostaglandins (PGs)

cells involved in the synthesis of PGs, thereby

which are formed from arachidionic acid under

of inflammation.

the influence of cyclooxygenase enzymes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown therapeutic benefits

For a locally delivered drug to be effective, an adequate concentration of the drug

in slowing down the rate of progression of periodontal disease by the effective inhibition of PG synthesis. [1]

requires to be present at the desired site. The vehicle therefore plays an important role in determining the mode of application as well as

Local drug delivery is aimed at site-specific therapy; it helps to avoid systemic complications and at the same time achieve high concentrations

to other agents in blocking human periodontal

anti-bradykinin activity and stabilization of

obtaining sufficient concentrations. Presently, thermo-reversible hydrogels are the most commonly used vehicle in most pharmaceutical applications. [4]

of the drug at the diseased site. Most research initially conducted utilized antimicrobial agents. This principle is now applied to NSAIDs. One such NSAID that can be used for this purpose is ketoprofen. This propionic acid derivative exhibits a marked potency relative

PGE2 synthesis in vitro . [2] Other in vitro anti- inflammatory effects of ketoprofen include an

Arneth index is usually considered to estimate the age of the neutrophil. A number of conditions are present wherein older, multilobed neutrophils have been found. recovering from a longstanding infection has been demonstrated as a possibility. [5]

This study was directed at modulating the host response by utilizing an indigenously prepared

lysosomal membranes. A number of studies have

anti-inflammatory drug containing ketoprofen.

shown that differences in disease susceptibility

The study was double blinded in order to

between patients are primarily due to the fact

eliminate the possibility of a bias.

Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011

255

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || C

Srinivas, et al.: Ketoprofen as local drug delivery in chronic periodontitis

MATERIALS AND METHODS

RESULTS

This double-blind clinical trial was conducted to evaluate the effects of the NSAID, ketoprofen, on patients with chronic periodontitis. Two similar local drug delivery preparations of a poloxamen gel containing 1.5% ketoprofen and a placebo were indigenously prepared for this purpose. The drug release pattern of the gel was obtained through static diffusion analysis. This demonstrated an initial burst with

approximately 20% of the drug being released in the first hour

and the remaining released in a linear manner over a period of 3 days [Figure 1].

The overall oral hygiene status showed a considerable

improvement. Highly significant values were achieved for plaque index (P=0.00), and significant values were obtained for gingival index (P=0.044).

BOP which was measured by contingency coefficient showed

a mean reduction of 86.7% in relation to group B (SRP +

ketoprofen) (P=0.000), which was found to be highly significant, versus 33.3% (P=0.024) for group A and 20.0% (P=0.15) in group C.

The sample constituted 10 subjects aged 33-55 years with moderate to severe chronic periodontitis reporting to the outpatient department, C. I. D. S. Three sites in each patient (total of 30 sites) with a probing depth of 5-8 mm were selected. The patients were recruited and monitored for a period of 90 days. Informed consent was obtained from each patient prior to the initiation of the study.

The overall reduction in probing depth was statistically significant (P=0.001) and although group B (SRP + ketoprofen) demonstrated the greatest reduction in probing depth inter-

group variations were not found to be statistically significant

[Table 1].

The same pattern was observed when changes in CAL from

Patients with a history of allergy to propionic acid derivatives, subjects under chronic treatment with NSAIDs within 1 month, subjects under medication likely to induce gingival hyperplasia, pregnant women and subjects with systemic diseases or habits that might modify the periodontal status were excluded from the study.

baseline were compared. Clinical attachment gain was greatest in relation to the ketoprofen group, but failed to show

statistically significant inter-group variations [group A (SRP +

placebo) 2.5 mm; group B (SRP + ketoprofen) 3.2 mm; group C (SRP) 2.8 mm] [Table 2].

60 50
60
50

Differential count in all the three sites did not show any variation and was consistent with the systemic count.

All subjects received oral hygiene instructions. Scaling and rootplaning (SRP) was performed and the patients were recalled after a week. Persistent sites were taken into consideration and were randomly divided into three groups in each patient:

Group A: SRP + drug A (ketoprofen, [Figure 2]) Group B: SRP + drug B (placebo) Group C: SRP

In vitro diffusion study of ketoprofen gel 40 30 20 10 0 0123 4 5 6
In vitro diffusion study of ketoprofen gel
40
30
20
10
0
0123
4
5
6
7
8
9
Time (in hours)
% Release

Figure 1: Drug release pattern of ketoprofen

The clinical parameters taken into consideration were the plaque index (Silness and Loe), gingival index (Loe and Silness), both of which are considered to determine the oral hygiene status of the patient.

Clinical attachment level (CAL) and Probing pocket depth (PPD) (standardized using an acrylic stent) were measured using a Williams Periodontal Probe [Figures 3 and 4].

Bleeding on Probing (BOP) was recorded as present or absent at the time of conventional probing at each site.

In addition, a blood smear to determine the differential count and Arneth index (from intracrevicular blood) were assessed from the selected three sites. Intracrevicular blood was obtained with the help of capillary tubes [Figure 5]. A systemic

count was obtained by a finger prick (peripheral smear) and

the values were compared. All parameters were assessed at baseline, 30 days and 90 days.

Statistical analysis

Descriptive statistics was used for all data. Repeated measure analysis of variance (ANOVA) was used to analyze mean

changes from baseline. Contingency coefficient was used for data with continuous efficacy variables.

Table 1: Symmetric measure showing levels of

significance

GPS

Value

Approx.

 

Significance

A Nominal by nominal contingency

0.447

0.024

coefficient N of valid cases B

30

Nominal by nominal contingency

0.707

0.000

coefficient N of valid cases

30

C

Nominal by nominal contingency

0.333

0.153

coefficient N of valid cases

30

256

Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || Click here to download free Android application for this journal

Srinivas, et al.: Ketoprofen as local drug delivery in chronic periodontitis

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || <a href=Click here to download free Android application for this journal Srinivas, et al .: Ketoprofen as local drug delivery in chronic periodontitis Figure 2: Placement of ketoprofen gel Figure 3: Probing depth in group B (SRP + ketoprofen) at 30 days Figure 4: Probing depth in group B at 90 days Figure 5: Obtaining intracrevicular blood Estimated marginal means of Measure_1 0 20 10 Estimated marginal means 1 2 3 Groups C B A Change Figure 6: Graphic representation of Arneth index Table 2 : Comparison of clinical attachment levels in three site Groups Mean Std. Deviation N CALBASE A 5.7000 0.6749 10 B 5.7000 0.8233 10 C 5.5000 0.5270 10 Total 5.6333 0.6687 30 CAL 30 A 3.9000 0.3162 10 B 3.3000 0.6749 10 C 3.7000 0.6749 10 Total 3.6333 0.6149 30 CAL 90 A 3.5000 0.7071 10 B 2.5000 0.7071 10 C 3.3000 1.0593 10 Total 3.1000 0.9229 30 The Arneth index demonstrated a statistically significant change in group B (SRP + ketoprofen) at 30 days, wherein the number of hyper-segmented neutrophils had increased ( P< 0.01) and these values returned to normal at 90 days [Figure 6]. DISCUSSION The current concept of periodontal disease pathogenesis states that microorganisms and their products are capable of inducing inflammatory mediators and the resulting Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011 257 " id="pdf-obj-2-10" src="pdf-obj-2-10.jpg">

Figure 2: Placement of ketoprofen gel

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || <a href=Click here to download free Android application for this journal Srinivas, et al .: Ketoprofen as local drug delivery in chronic periodontitis Figure 2: Placement of ketoprofen gel Figure 3: Probing depth in group B (SRP + ketoprofen) at 30 days Figure 4: Probing depth in group B at 90 days Figure 5: Obtaining intracrevicular blood Estimated marginal means of Measure_1 0 20 10 Estimated marginal means 1 2 3 Groups C B A Change Figure 6: Graphic representation of Arneth index Table 2 : Comparison of clinical attachment levels in three site Groups Mean Std. Deviation N CALBASE A 5.7000 0.6749 10 B 5.7000 0.8233 10 C 5.5000 0.5270 10 Total 5.6333 0.6687 30 CAL 30 A 3.9000 0.3162 10 B 3.3000 0.6749 10 C 3.7000 0.6749 10 Total 3.6333 0.6149 30 CAL 90 A 3.5000 0.7071 10 B 2.5000 0.7071 10 C 3.3000 1.0593 10 Total 3.1000 0.9229 30 The Arneth index demonstrated a statistically significant change in group B (SRP + ketoprofen) at 30 days, wherein the number of hyper-segmented neutrophils had increased ( P< 0.01) and these values returned to normal at 90 days [Figure 6]. DISCUSSION The current concept of periodontal disease pathogenesis states that microorganisms and their products are capable of inducing inflammatory mediators and the resulting Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011 257 " id="pdf-obj-2-15" src="pdf-obj-2-15.jpg">

Figure 3: Probing depth in group B (SRP + ketoprofen) at 30 days

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || <a href=Click here to download free Android application for this journal Srinivas, et al .: Ketoprofen as local drug delivery in chronic periodontitis Figure 2: Placement of ketoprofen gel Figure 3: Probing depth in group B (SRP + ketoprofen) at 30 days Figure 4: Probing depth in group B at 90 days Figure 5: Obtaining intracrevicular blood Estimated marginal means of Measure_1 0 20 10 Estimated marginal means 1 2 3 Groups C B A Change Figure 6: Graphic representation of Arneth index Table 2 : Comparison of clinical attachment levels in three site Groups Mean Std. Deviation N CALBASE A 5.7000 0.6749 10 B 5.7000 0.8233 10 C 5.5000 0.5270 10 Total 5.6333 0.6687 30 CAL 30 A 3.9000 0.3162 10 B 3.3000 0.6749 10 C 3.7000 0.6749 10 Total 3.6333 0.6149 30 CAL 90 A 3.5000 0.7071 10 B 2.5000 0.7071 10 C 3.3000 1.0593 10 Total 3.1000 0.9229 30 The Arneth index demonstrated a statistically significant change in group B (SRP + ketoprofen) at 30 days, wherein the number of hyper-segmented neutrophils had increased ( P< 0.01) and these values returned to normal at 90 days [Figure 6]. DISCUSSION The current concept of periodontal disease pathogenesis states that microorganisms and their products are capable of inducing inflammatory mediators and the resulting Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011 257 " id="pdf-obj-2-20" src="pdf-obj-2-20.jpg">

Figure 4: Probing depth in group B at 90 days

Figure 5: Obtaining intracrevicular blood
Figure 5: Obtaining intracrevicular blood

Estimated marginal means of Measure_1

0 20 10 Estimated marginal means
0
20
10
Estimated marginal means
  • 1 2

3

Groups

C B A
C
B
A

Change

Figure 6: Graphic representation of Arneth index

Table 2 : Comparison of clinical attachment levels in

three site

Groups

Mean

Std. Deviation

N

CALBASE

A

5.7000

0.6749

10

B

5.7000

0.8233

10

C

5.5000

0.5270

10

Total

5.6333

0.6687

30

CAL 30

A

3.9000

0.3162

10

B

3.3000

0.6749

10

C

3.7000

0.6749

10

Total

3.6333

0.6149

30

CAL 90

A

3.5000

0.7071

10

B

2.5000

0.7071

10

C

3.3000

1.0593

10

Total

3.1000

0.9229

30

The Arneth index demonstrated a statistically significant change in group B (SRP + ketoprofen) at 30 days, wherein the number of hyper-segmented neutrophils had increased ( P< 0.01) and these values returned to normal at 90 days [Figure 6].

DISCUSSION

The current concept of periodontal disease pathogenesis states that microorganisms and their products are capable of inducing inflammatory mediators and the resulting

Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011

257

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || Click here to download free Android application for this journal

Srinivas, et al.: Ketoprofen as local drug delivery in chronic periodontitis

inflammation presents as the hallmark of the disease. PGs

formed by the arachidionic acid-cyclooxygenase pathway are one of the key mediators of the disease. Two isoforms of the enzyme cyclooxygenase exist: cox-1 is constitutively expressed and the resulting PGs are responsible for physiological functions (e.g. gastric mucosal secretions, renal homeostasis) and cox-2 is inducible and is said to be produced during inflammation. [2] NSAIDs, with the exception of selective cox-2 inhibitors, inhibit both the isoforms of cyclooxygenase, resulting in adverse effects (gastritis, peptic ulcers, impaired renal function).

In previous reports, use of NSAIDs to control inflammation and as an adjunct to conventional periodontal therapy [1,2] has proven beneficial in comparison with controls. The drawbacks

of systemic NSAIDs can be avoided by using a local drug delivery that allows the concentration of a particular drug at the desired site. Ketoprofen, a propionic acid derivative, has

test and control groups with regard to PPD, CAL and loss of alveolar bone. [1]

In this study, although there was a highly significant overall

gain in CAL and reduction of PPD, inter-group variations

were not found to be statistically significant. This variability in

responsiveness may be attributed to differences in study design in terms of duration and due to the lack of a standardized drug regimen.

The differential count was estimated in order to assess the effect of ketoprofen on monocytes (in vitro studies have demonstrated that ketoprofen can suppress monocytes and macrophage). [9] This study did not demonstrate any inter-group variation in the proportion of WBCs which remained constant throughout the study. This difference may be attributed to the fact that this was an in vivo study.

been found to be effective against a number of inflammatory

conditions and is currently under investigation as a potential adjunct to conventional periodontal therapy. [2] Besides its ability to block the cyclooxygenase pathway, in vitro reports have also demonstrated an anti-lipoxygenase activity, [2] and hence the added ability of the drug to inhibit leukotriene formation.

Arneth’s index is the result of computations based on nuclear structures. It is a method of estimating the relative age of a neutrophil. Neutrophils with less lobes are younger forms, while those with greater number of lobes represent older cells. An increase in the number of lobes (shift to right) was demonstrated at 30 days following application of drug B. The values returned to normal when examined at 90 days. During recovery from an infection, there is a shift to the right. This is because the number of young cells entering the site is decreased and the cells already present are somewhat effected by the toxemia of the infectious process. [5] Another explanation could be the fact that ketoprofen is capable of inhibiting interleukin (IL)-8-induced chemotaxis. [8]

In this study, a local drug delivery system containing 1.5% ketoprofen gel was used in conjunction with SRP in order to assess periodontal outcomes in subjects with chronic periodontitis.

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || <a href=Click here to download free Android application for this journal Srinivas, et al .: Ketoprofen as local drug delivery in chronic periodontitis inflammation presents as the hallmark of the disease. PGs formed by the arachidionic acid-cyclooxygenase pathway are one of the key mediators of the disease. Two isoforms of the enzyme cyclooxygenase exist: cox-1 is constitutively expressed and the resulting PGs are responsible for physiological functions (e.g. gastric mucosal secretions, renal homeostasis) and cox-2 is inducible and is said to be produced during inflammation. NSAIDs, with the exception of selective cox-2 inhibitors, inhibit both the isoforms of cyclooxygenase, resulting in adverse effects (gastritis, peptic ulcers, impaired renal function). In previous reports, use of NSAIDs to control inflammation and as an adjunct to conventional periodontal therapy has proven beneficial in comparison with controls. The drawbacks of systemic NSAIDs can be avoided by using a local drug delivery that allows the concentration of a particular drug at the desired site. Ketoprofen, a propionic acid derivative, has test and control groups with regard to PPD, CAL and loss of alveolar bone. In this study, although there was a highly significant overall gain in CAL and reduction of PPD, inter-group variations were not found to be statistically significant. This variability in responsiveness may be attributed to differences in study design in terms of duration and due to the lack of a standardized drug regimen. The differential count was estimated in order to assess the effect of ketoprofen on monocytes ( in vitro studies have demonstrated that ketoprofen can suppress monocytes and macrophage). This study did not demonstrate any inter-group variation in the proportion of WBCs which remained constant throughout the study. This difference may be attributed to the fact that this was an in vivo study. been found to be effective against a number of inflammatory conditions and is currently under investigation as a potential adjunct to conventional periodontal therapy. Besides its ability to block the cyclooxygenase pathway, in vitro reports have also demonstrated an anti-lipoxygenase activity, and hence the added ability of the drug to inhibit leukotriene formation. Arneth’s index is the result of computations based on nuclear structures. It is a method of estimating the relative age of a neutrophil. Neutrophils with less lobes are younger forms, while those with greater number of lobes represent older cells. An increase in the number of lobes (shift to right) was demonstrated at 30 days following application of drug B. The values returned to normal when examined at 90 days. During recovery from an infection, there is a shift to the right. This is because the number of young cells entering the site is decreased and the cells already present are somewhat effected by the toxemia of the infectious process. Another explanation could be the fact that ketoprofen is capable of inhibiting interleukin (IL)-8-induced chemotaxis. In this study, a local drug delivery system containing 1.5% ketoprofen gel was used in conjunction with SRP in order to assess periodontal outcomes in subjects with chronic periodontitis. The results of this double-blind clinical trial of 10 patients with moderate to severe chronic periodontitis at 30 and 90 days following SRP and oral hygiene index (OHI) indicate that the overall oral hygiene status showed considerable improvement ( P= 0.00 for plaque index; P= 0.044 for gingival index). As far as the limitations of this study are concerned, a larger sample size with a longer duration of follow-up would have proven to be beneficial. Since NSAIDs are currently in an experimental stage, a standardized drug regimen would have established desired concentrations of the drug within the gingival crevice for the required period of time. BOP is considered the first clinical sign that denotes inflammation, and is therefore a valuable indicator in assessing the status of the inflammatory component. All sites treated with SRP showed improvement at 30 and 90 days, respectively. At 90 days, reduction of BOP with ketoprofen was found to be highly significant ( P= 0.00) in comparison with the other two groups. Results in relation to group A (SRP + placebo) were found to be significant ( P= 0.24), while BOP did not achieve statistically significant values in relation to group C, indicating that group B (SRP + ketoprofen) demonstrated a significant reduction in the clinical signs of gingival inflammation. This is in conjunction with previous reports of reduced inflammatory components following the application of a similar gel. CONCLUSION Ketoprofen has important anti-inflammatory properties, and is therefore beginning to be utilized in periodontics. In this study, locally delivered ketoprofen in conjunction with mechanical periodontal therapy has proven to be beneficial in controlling the clinical signs of inflammation. However, further long-term studies are required to substantiate this effect of ketoprofen as an adjunct to conventional periodontal therapy. REFERENCES The presence of increased levels of PGs has been implicated in the loss of attachment and alveolar bone loss. Controlling PG synthesis can therefore reduce bone loss and maintain attachment levels. Recently published data utilizing different concentrations of a topically applied ketoprofen gel demonstrated decreased PG levels in gingival crevicular fluid (GCF). A number of investigations using anti-inflammatory medications as an adjunct to SRP have reported significant differences between 1. Jeffcoat MK, Reddy MS, Haigh S, BuchananW, Doyle MJ, Meredith MP, et al . A comparison of topical ketrolac, systemic flurbiprofen, and placebo for the inhibition of bone loss in adult periodontitis. J Periodontol 1995;66:329-38. 2. Paquette DW, Lawrence HP, Maynor GB, Wilder R, Binder TA, Troullos E, et al . Pharmacodynamic effects of ketoprofen on crevicular fluid prostanoids in adult periodontitis. J Clin Periodontol 2000;27:558-66. 3. Garrisons W, Nichols FC. LPS elicited secretory responses in monocytes: Altered release of PGE2 but not IL-1 beta in patients with adult periodontitis. J Periodontal Res 1989;24:88-95. 258 Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011 " id="pdf-obj-3-61" src="pdf-obj-3-61.jpg">

The results of this double-blind clinical trial of 10 patients with moderate to severe chronic periodontitis at 30 and 90 days following SRP and oral hygiene index (OHI) indicate that the overall oral hygiene status showed considerable improvement (P=0.00 for plaque index; P=0.044 for gingival index).

As far as the limitations of this study are concerned, a larger sample size with a longer duration of follow-up would have

proven to be beneficial. Since NSAIDs are currently in an

experimental stage, a standardized drug regimen would have established desired concentrations of the drug within the gingival crevice for the required period of time.

BOP is considered the first clinical sign that denotes inflammation, and is therefore a valuable indicator in

assessing the status of the inflammatory component. [10] All sites treated with SRP showed improvement at 30 and 90 days, respectively. At 90 days, reduction of BOP with ketoprofen was found to be highly significant (P=0.00) in comparison with the other two groups. Results in relation to group A (SRP + placebo) were found to be significant (P=0.24), while BOP did not achieve statistically significant values in relation

to group C, indicating that group B (SRP + ketoprofen)

demonstrated a significant reduction in the clinical signs of gingival inflammation. This is in conjunction with previous reports of reduced inflammatory components following the application of a similar gel. [2]

CONCLUSION

Ketoprofen has important anti-inflammatory properties,

and is therefore beginning to be utilized in periodontics. In this study, locally delivered ketoprofen in conjunction with

mechanical periodontal therapy has proven to be beneficial in controlling the clinical signs of inflammation. However,

further long-term studies are required to substantiate this effect of ketoprofen as an adjunct to conventional periodontal therapy.

REFERENCES

The presence of increased levels of PGs has been implicated in the loss of attachment and alveolar bone loss. [6] Controlling PG synthesis can therefore reduce bone loss and maintain attachment levels. [7]

Recently published data utilizing different concentrations of a topically applied ketoprofen gel demonstrated decreased

PG levels in gingival crevicular fluid (GCF). [2] A number of investigations using anti-inflammatory medications as an adjunct to SRP have reported significant differences between

  • 1. Jeffcoat MK, Reddy MS, Haigh S, BuchananW, Doyle MJ, Meredith MP, et al. A comparison of topical ketrolac, systemic flurbiprofen, and placebo for the inhibition of bone loss in adult periodontitis. J Periodontol 1995;66:329-38.

  • 2. Paquette DW, Lawrence HP, Maynor GB, Wilder R, Binder TA, Troullos E, et al. Pharmacodynamic effects of ketoprofen on crevicular fluid prostanoids in adult periodontitis. J Clin Periodontol 2000;27:558-66.

  • 3. Garrisons W, Nichols FC. LPS elicited secretory responses in monocytes: Altered release of PGE2 but not IL-1 beta in patients with adult periodontitis. J Periodontal Res 1989;24:88-95.

258

Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || Click here to download free Android application for this journal

Srinivas, et al.: Ketoprofen as local drug delivery in chronic periodontitis

  • 4. Escobar-Chávez JJ, López-Cervantes M, Naïk A, Kalia YN, Quintanar-Guerrero D, Ganem-Quintanar A. Applications of thermo-reversible Pluronic F -127 pharmaceutical formulations. J Pharm Pharm Sci 2006;9:339-58.

  • 5. Burns L. Studies in osteopathic sciences, cells of the blood. Vol.4 chapter 4, version 5.0. Available from: http://www. mcmillinmedia.com/eamt/files/burns4/bur4ch04.html [Last cited on 2011 Jan 03].

  • 6. Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E 2 levels as predictor of periodontal attachment loss. J Periodontal Res 1986;21:101-12.

  • 7. Feldman RS, Szeto B, Chauncey H, Goldhaber P. Nonsteroidal anti-inflammatory drugs in the reduction of human alveolar bone loss. J Clin Periodontol 1983;10:131-6.

  • 8. Bizzari C, Paglei S, Brandolini L. Selective inhibition of il-8

induced neutrophil chemotaxis by ketoprofen isomers. Biochem Pharmacol 2001;61:1429-37.

  • 9. Jackman BR, Moore JN, Barton MH, Morris DD. Comparison of the effects of ketoprofen and fluxin meglumine on the in vitro response of equine peripheral blood monocytes to bacterial endotoxin. Can J Vet Res 1994;58:138-43.

    • 10. Newman, Takei, Klokkevold, Carranza. Text book on Clinical Periodontology 10th ed, St Louis, Missouri: Saunders; 2006.

How to cite this article: Srinivas M, Medaiah S, Girish S, Anil M, Pai J, Walvekar A. The effect of ketoprofen in chronic periodontitis: A clinical double-blind study. J Indian Soc Periodontol 2011;15:255-9.

Source of Support: Nil, Conflict of Interest: None declared.

[Downloaded free from http://www.jisponline.com on Friday, May 04, 2012, IP: 82.137.10.209] || <a href=Click here to download free Android application for this journal Srinivas, et al .: Ketoprofen as local drug delivery in chronic periodontitis 4. Escobar-Chávez JJ, López-Cervantes M, Naïk A, Kalia YN, Quintanar-Guerrero D, Ganem-Quintanar A. Applications of thermo-reversible Pluronic F -127 pharmaceutical formulations. J Pharm Pharm Sci 2006;9:339-58. 5. Burns L. Studies in osteopathic sciences, cells of the blood. Vol.4 chapter 4, version 5.0. Available from: http://www. mcmillinmedia.com/eamt/files/burns4/bur4ch04.html [Last cited on 2011 Jan 03]. 6. Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E levels as predictor of periodontal attachment loss. J Periodontal Res 1986;21:101-12. 7. Feldman RS, Szeto B, Chauncey H, Goldhaber P. Nonsteroidal anti-inflammatory drugs in the reduction of human alveolar bone loss. J Clin Periodontol 1983;10:131-6. 8. Bizzari C, Paglei S, Brandolini L. Selective inhibition of il-8 induced neutrophil chemotaxis by ketoprofen isomers. Biochem Pharmacol 2001;61:1429-37. 9. Jackman BR, Moore JN, Barton MH, Morris DD. Comparison of the effects of ketoprofen and fluxin meglumine on the in vitro response of equine peripheral blood monocytes to bacterial endotoxin. Can J Vet Res 1994;58:138-43. 10. Newman, Takei, Klokkevold, Carranza. Text book on Clinical Periodontology 10th ed, St Louis, Missouri: Saunders; 2006. How to cite this article: Srinivas M, Medaiah S, Girish S, Anil M, Pai J, Walvekar A. The effect of ketoprofen in chronic periodontitis: A clinical double-blind study. J Indian Soc Periodontol 2011;15:255-9. Source of Support: Nil, Conflict of Interest: None declared. New features on the journal’s website Optimized content for mobile and hand-held devices HTML pages have been optimized of mobile and other hand-held devices (such as iPad, Kindle, iPod) for faster browsing speed. Click on [Mobile Full text] from Table of Contents page. This is simple HTML version for faster download on mobiles (if viewed on desktop, it will be automatically redirected to full HTML version) E-Pub for hand-held devices EPUB is an open e-book standard recommended by The International Digital Publishing Forum which is designed for reflowable content i.e. the text display can be optimized for a particular display device. Click on [EPub] from Table of Contents page. There are various e-Pub readers such as for Windows: Digital Editions, OS X: Calibre/Bookworm, iPhone/iPod Touch/iPad: Stanza, and Linux: Calibre/Bookworm. E-Book for desktop One can also see the entire issue as printed here in a ‘flip book’ version on desktops. Links are available from Current Issue as well as Archives pages. Click on View as eBook Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011 259 " id="pdf-obj-4-45" src="pdf-obj-4-45.jpg">

New features on the journal’s website

Optimized content for mobile and hand-held devices

HTML pages have been optimized of mobile and other hand-held devices (such as iPad, Kindle, iPod) for faster browsing speed. Click on [Mobile Full text] from Table of Contents page. This is simple HTML version for faster download on mobiles (if viewed on desktop, it will be automatically redirected to full HTML version)

 

E-Pub for hand-held devices

EPUB is an open e-book standard recommended by The International Digital Publishing Forum which is designed for reflowable content i.e. the text display can be optimized for a particular display device. Click on [EPub] from Table of Contents page. There are various e-Pub readers such as for Windows: Digital Editions, OS X: Calibre/Bookworm, iPhone/iPod Touch/iPad: Stanza, and Linux:

Calibre/Bookworm.

 

E-Book for desktop

One can also see the entire issue as printed here in a ‘flip book’ version on desktops. Links are available from Current Issue as well as Archives pages.

Click on

Click on View as eBook

View as eBook

Journal of Indian Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011

259