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ORIGINAL RESEARCH  
Year : 2012  |  Volume : 23  |  Issue : 1  |  Page : 69-74
Impaired neutrophil and monocyte chemotaxis in chronic and aggressive periodontitis and effects of periodontal therapy


Department of Periodontics, College of Dental Sciences, Davangere, Karnataka, India

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Date of Submission16-Aug-2008
Date of Decision29-Jan-2009
Date of Acceptance09-Sep-2011
Date of Web Publication26-Jul-2012
 

   Abstract 

Background and Objectives: Depressed chemotactic activity of polymorphoneutrophil (PMN) and monocyte (MN) appears to be one of the significant risk factors in the development of periodontal disease. Although bacteria are the primary etiologic factor in periodontal disease, the patient's host response is a determinant of disease susceptibility. Depressed chemotaxis of PMN and MN could lead to periodontal destruction by altering the host response i.e. impairment of the normal host response in neutralizing infection and alterations that result in destruction of the surrounding periodontal tissues.
Materials and Methods: Thirty patients (10 healthy subjects, 10 chronic periodontitis, and 10 with aggressive periodontitis) participated in this study. Clinical parameters like plaque index, gingival index, probing pocket depth, and radiographic assessment were done. The peripheral blood PMNs and MNs were isolated from the patient and the chemotactic response was studied. Statistical analysis was performed using post-hoc Newman-Keul range test.
Results: PMN and MN chemotaxis was found to be statistically significant (P<0.05) at baseline and three months after periodontal therapy in chronic and aggressive periodontitis group compared to healthy subjects. However on comparison between chronic and aggressive periodontitis group statistical significance was not found (P>0.05).Comparision between chronic periodontitis, aggressive periodontitis with healthy subjects, PMN and MN chemotaxis showed statistical significance (P<0.05) at baseline and three months after periodontal therapy, Whereas statistically there was no difference when chronic periodontitis was compared with aggressive periodontitis
Interpretation and Conclusion: Depressed chemotaxis of PMN and MN results in increased periodontal destruction. In this study, depressed PMN and MN chemotaxis is seen in both aggressive periodontitis group and chronic periodontitis group and the response was altered although to a lesser degree after periodontal therapy in both groups indicating that effect of treatment does exist.

Keywords: Aggressive periodontitis, chemotaxis, chronic periodontitis, neutrophils, monocytes

How to cite this article:
Kumar R S, Prakash S. Impaired neutrophil and monocyte chemotaxis in chronic and aggressive periodontitis and effects of periodontal therapy. Indian J Dent Res 2012;23:69-74

How to cite this URL:
Kumar R S, Prakash S. Impaired neutrophil and monocyte chemotaxis in chronic and aggressive periodontitis and effects of periodontal therapy. Indian J Dent Res [serial online] 2012 [cited 2021 May 7];23:69-74. Available from: https://www.ijdr.in/text.asp?2012/23/1/69/99042
Studies over the decades have clearly implicated bacterial substances in dental plaque as a primary etiological factor responsible for the initiation of gingival and periodontal diseases. However, individual susceptibility as well as severity and extent of periodontal destruction appears to be influenced both by the response of the host to these microbial products as well as qualitative and quantitative differences in the composition of oral microflora. [1]

Substantial evidence indicates that the polymorphoneutrophils (PMNs) and monocytes (MNs) constitute a most important pathway for defense in gingival sulcus. Functional defects in the phagocytic cells appear to predispose individuals to the development of early onset severe periodontitis. [2] Patients with PMN disorders characteristically have increased the susceptibility to infection and are of particular interest as there is reported evidence of the presence of

severe periodontal disease associated with several of this disorders. [3]

Hence, the present investigation was undertaken to study PMN and MN chemotaxis in patients with chronic and aggressive periodontitis using modified Boyden's chamber [Figure 1] technique before and after one and three months of active periodontal therapy.
Figure 1: Modified Boyden's chamber with chemotaxis in progress

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   Materials and Methods Top


The patients for this case-control study were selected from the Out Patient Department of Periodontics of our institute. Ethical clearance was obtained from ethical committee of our institute and informed consent was obtained from all the patients who participated in the study.

Selection criteria

Patients with chronic periodontitis (CP), aggressive periodontitis (AP), and healthy periodontium (controls) as evidenced clinically and radiographically were selected. Chronic periodontitis patients were in the age range between 30-45 years (mean±SD = 37.9 ± 2.7), >30% of sites involved, pocket depth ≥6 mm, radiologically bone loss (≥50% of the root length); and aggressive periodontitis patients were under 30 years of age (mean±SD = 25.1 ± 7.7), involvement of at least three teeth other than 1 st molars and incisors, pocket depth ≥6 mm, history of familial aggregation, radiolologically bone loss (≥50% of the root length especially in first molars and incisors). Patients with 25-45 years (mean±SD = 29.1 ± 3.6) were considered as healthy with sulcus depth ≤3 mm and radiologically without bone loss. [4]

From previous experience (by the investigator and similar studies), about 20 PMN and MN chemotaxis difference was expected between control and experimental groups. Level of significance was 5% and estimated power of the study was 80%. With this information, sample size was determined by computer using statistical package for social sciences (SPSS) program which gave about nine in each group. Finally, power of the study was yielded to be 90%.

Thorough medical and dental histories were taken from all patients and control subjects. The patients for this double blind study were recruited consecutively as and when they reported. Controls were selected concurrently and included volunteered dental students and dental hygienists.

Age matching between AP (25 years), CP (38 years), and controls (29 years) was done. Sex matching was not done.

Criteria for exclusion included systemic illness likely to affect periodontal status, such as diabetes mellitus, chronic ingestion of drugs, including anti-inflammatory agents, antibiotics in the past month, smoking, previous periodontal therapy other than routine tooth cleaning, and a lack of a desire to participate.

Clinical parameters like plaque index (Silness and Loe), gingival index (Loe and Silness), and probing pocket depth were recorded. These data were used only to establish a diagnosis and they are not presented in the present paper. Control subjects had no clinical manifestations of periodontitis, no history of periodontal therapy other than routine tooth cleaning, and probing depth ≤3 mm. Patients were assigned a diagnosis of CP or AP on the basis of selection criteria. [4]

Periodontal therapy: (active therapy) [5] includes

  • Initial therapy (documentation, data collection, and treatment planning for the patient and oral hygiene Instructions, scaling and root planning, occulsal adjustment, tetracycline therapy for 14 days).
  • Surgical therapy which includes modified Widman flap in areas not resolved by initial therapy.
  • Maintenance therapy includes the recall visit at 1 st and 3 rd months after active therapy.


Active therapy was considered finished when comparatively minimal bleeding on probing.

Sample collection

Ten ml of venous blood was collected from antecubital vein; 30 days and three months following the completion of active periodontal therapy. Venous blood was mixed with ethylene diamine tetraacetic acid.

The collected sample was centrifuged and washed thrice with phosphate buffer solution to get leukocyte suspension. Chemotaxis was studied using a modified Boyden's chamber [6] [Figure 1]. Since the assessments were done by a blinded microbiologist with standardized instrument, method error was negligible. However, the mean of two measurements on each of three replicate filters was designated as the chemotactic migration score and taken for results and analysis.

Statistical analysis

Paired 't' test was used for intragroup comparisons. Intergroup comparisons were made by one way analysis of variance (ANOVA) followed by post hoc Neuman-Keul's range test for group wise comparisons. For all tests, P value of 0.05 or less was considered to be statistically significant.


   Results Top


PMN chemotaxis [Table 1], [Table 2], [Table 3] and [Table 4] and [Figure 2]

The mean increase in PMN chemotaxis from baseline to 90 th day post-treatment was statistically highly significant (P<0.001) in CP patients and statistically significant in AP patients. When healthy subjects, chronic periodontitis, and aggressive periodontitis were compared at baseline, PMN chemotaxis was statistically significant (P<0.05), but at 90 th day, post treatment was statistically not significant; and when compared between CP patients and AP patients at baseline and at 90 th day, post treatment was statistically not significant.
Figure 2: Photomicrograph showing PMN chemotaxis in Harris Hematoxylin staining under ×40 power magnification

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Table 1: PMN and monocyte chemotaxis in AP

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Table 2: PMN and monocyte chemotaxis in CP

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Table 3: PMN and monocyte chemotaxis in healthy subjects



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Table 4: PMN chemotaxis

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Monocyte chemotaxis: [Table 1], [Table 2], [Table 3], [Table 5] and [Figure 3]

In chronic and aggressive periodontitis groups, the mean increase of the MN chemotaxis was found to be statistically significant. However, on intergroup comparison, mean increase of MN chemotaxis was found to be statistically significant between control and aggressive periodontitis groups and statistically not significant between control and chronic periodontitis. The mean difference in MN chemotaxis when compared between CP and AP at baseline and 90 th day, post treatment was statistically not significant.
Figure 3: Photomicrograph showing monocyte chemotaxis in Harris Hematoxylin staining under ×40 power magnification

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Table 5: Monocyte chemotaxis

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   Discussion Top


Periodontal disease like the acquisition of infection, in general, is dependent upon host related issues of which PMN dysfunction is one of the many contributing factors. A causal relationship between impaired chemotaxis and increased susceptibility of periodontal disease is not established. [1] PMN and MN dysfunction which in turn alters the host defense mechanism can act as predisposing factor for causation of periodontal disease in an individual.

Although numerous host defense mechanisms are called into action on bacterial onslaught at the gingival sulcus, substantial evidence indicate that the phagocytic cells specifically the PMNs and MNs constitute the most important pathway of defense for this area. Functional defects in phagocytic cells appear to predispose individuals having them to the development of early and severe periodontitis. With several recent reports [7],[8] demonstrating that the patients with these forms of periodontitis manifests high frequency of defects in PMNs chemotaxis. However, studies of MN chemotaxis are scarce. [2]

Hence, this study was taken up to evaluate the chemotactic responses of PMNs and MNs in chronic and aggressive periodontitis patients before and after periodontal therapy.

PMN chemotaxis

The proportion of depressed PMN chemotaxis response was greater (50%) in AP patients compared to normal healthy subjects which were statistically significant. The results confirm with earlier studies by Clark et al., [9] Ciancialo et al. [10] Altman et al.[11] which indicates that abnormalities of PMN chemotaxis is associated with various forms of early onset periodontitis.

The depressed migration of PMN may be due to the presence of an inhibitor in serum. [10] It was reported that serum abnormalities were frequently evident in patients with the most profound decrease in cell responsiveness. [11]

It was observed in the study that out of five (2, 5, 6, 7, 9) patients with depressed chemotaxis at baseline, one patient's (7) PMN chemotactic response was restored immediately after three months of periodontal therapy; and in other two patients (6, 9), it was restored after three months; and in two (2, 5) patients, it was not restored.

In CP, PMN chemotaxis was suppressed to a lesser degree (30%) compared to normal subjects, which was found to be statistically significant. In three patients (11, 13, 14), PMNs have shown depressed cell response at baseline. But studies on PMN chemotaxis in chronic periodontitis showed no chemotactic abnormality. [10],[12] However, studies with adult patients with severe periodontitis, [6] adult patients with active periodontitis, have shown depressed PMN chemotaxis. Gothier DE [13] in his study showed patients with advanced CP have shown presence of serum inhibitors of PMN chemotaxis which modify the PMN chemotactic response. It was observed in this study that out of three (11, 13, 14) patients with depressed chemotaxis at baseline, one patient's (14) chemotactic response was restored immediately and three months after periodontal therapy. In other two (11, 13), it was not restored even after three months post-operative therapy.

In CP and AP groups, the PMN chemotaxis defect was reconstituted following periodontal therapy which was statistically significant. The finding correlates with the earlier studies done by Suzuki JB et al.[5] wherein they have shown a reconstitution of a neutrophil chemotaxis defect in two of 58 localized juvenile periodontitis patients immediately following active periodontal treatment with one additional patient reversing the cell defect one year later. Van dyke et al.[3] studied 23 adult patients with severe periodontitis and 43% exhibited elevated chemotaxis. Four of the patients exhibited elevated chemotaxis when tested repeatedly over an eight month period during which time they underwent conventional periodontal therapy. However, Clark R.A. et al.[9] showed contradictory results; where no improvement in PMN chemotaxis was observed after periodontal therapy.

Monocyte chemotaxis

Monocyte chemotaxis has not been well established and few studies have been performed on monocyte chemotaxis from patients with various types of early onset periodontitis other than juvenile periodontitis. The documentation regarding the monocyte chemotaxis put forth by Cianciola et al., [10] reported monocytes from juvenile periodontitis patients to be chemotactically normal, but other investigators have reported otherwise like Altman et al., [11] Bowen et al., [2] and Page RC et al., [2] who assessed monocyte chemotaxis in children with prepubertal periodontitis, in all cases chemotaxis of monocyte was significantly depressed. In this study, monocyte chemotaxis was suppressed to a greater extent (40%) in aggressive periodontitis patients compared to healthy subjects. These results correlate with the studies of Altman et al., [11] and Bowen et al.[2] It was observed in this study that out of four (2, 5, 6, 7) patients with depressed MN chemotaxis at baseline, one patient (7) showed normal chemotactic response immediately after three months of periodontal therapy; and one patient (6) showed normal result after three months whereas in other two patients (2, 5), no improvement was seen.

Till date, there are no studies on monocyte chemotaxis in chronic periodontitis. The proportion of depressed monocyte chemotaxis was about 20% compared to normal healthy subjects and it was not statistically significant. It was observed that out of two patients (13, 14) with depressed MN chemotaxis at baseline, one patient (14) showed normal chemotaxis response after three months of periodontal therapy and in other patient (13) there was no improvement. The proportion of patients after successful treatment that restored to normal chemotactic response has shown statistically significant results, both in chronic and aggressive periodontitis which indicate that treatment effect does exist.


   Conclusion Top


In this study, PMN and MN cell responsiveness was found to be depressed both in CP and AP compared to normal subjects. However, in AP, the proportion of patients with depressed PMN and MN chemotaxis was greater. After periodontal therapy (immediately, after one month and three months), the chemotactic response altered in both cell types, suggesting periodontal treatment may have an effect on the chemotactic response though it was found to a lesser degree.

Hence, it can be concluded that this defect may be an important causative factor in the pathogenesis of the disease. A causal relationship between impaired chemotaxis and increased susceptibility of periodontal disease is not established. PMN and MN dysfunction which in turn alters the host defense mechanism can act as predisposing factor for causation of periodontal disease in an individual.

Hence, the evaluation of PMN and MN chemotaxis is a valuable adjunct to the clinical and radiographic diagnosis of periodontal disease, particularly in younger age group with rapid and severe periodontitis. Future studies have to be conducted with large sample sizes and advanced equipments to evaluate the functions of PMNs and monocytes.

 
   References Top

1.Lavine WS, Maderazo EG, Stolman J, Ward PA, Cogen RB, Greenblat I, et al. Impaired neutrophil chemotaxis in patients with juvenile and rapidly progressing periodontitis. J Periodontal Res 1979;14:10-9.  Back to cited text no. 1
    
2.Page RC, Sims TJ, Geissler F, Altman LC, Baab DA. Defective neutrophil and monocyte motality in patients with early onset periodontitis. Infect Immun 1985;47:169-75.  Back to cited text no. 2
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3.Van Dyke TE, Horoszewicz, Cianciola LJ, Genco RJ. Neutrophil chemotaxis dysfunction in human periodontitis. Infect Immun 1980;27:124-32.  Back to cited text no. 3
    
4.Tonetti MS, Mombelli A. Consensus Report: Chronic periodontitis and Aggressive periodontitis. Ann Periodontol 1999;4:38-52.  Back to cited text no. 4
[PUBMED]    
5.Suzuki JB, Rison L, Falkler WA Jr, Collison C, Bowers G. Effect of periodontal therapy on spontaneous lymphocyte response and neutrophil chemotaxis in localized and generalized juvenile periodontitis patients. J Clin Periodontol 1985;12:124-34.  Back to cited text no. 5
    
6.Thompson RA. Neutrophil leukocyte function tests in techniques in clinical immunology; 2 nd ed; Philadelphia: Blackwell Scientific Publication; 1978. p. 273-93.  Back to cited text no. 6
    
7.Leino L, Hurttia H. A potential role of an intracellular signaling defect in neutrophil functional abnormalities and promotion of tissue damage in patients with localized juvenile periodontitis. Clin Chem Lab Med 1999;37:215-22.  Back to cited text no. 7
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8.Hart TC, Shapira L, Van Dyke TE. Neutrophil defects as risk factors for periodontal diseases. J Periodontol 1994;65:521-9.  Back to cited text no. 8
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9.Clark RA, Page RC, Wilde G. Defective neutrophil chemotaxis in Juvenile periodontitis. Infect Immun 1977;18:694-700.  Back to cited text no. 9
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10.Cianciola LJ, Genco RJ, Patters MR, Meckenna J, Oss CJ. Defective polymorphonuclear leukocyte function in a human periodontal disease. Nature 1977;265:445-7.  Back to cited text no. 10
    
11.Altman LC, Page RC, Vandesteen GE, Dixon LI, Bradford C. Abnormalities of leukocyte chemotaxis in patients with various forms of periodontitis. J Periodontal Res 1985;20:553-63.  Back to cited text no. 11
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12.Ellegaard B, Borregaard N, Ellegaard J. Neutrophil chemotaxis and phagocytosis in juvenile periodontitis. J Periodont Res 1984;9:261-8.  Back to cited text no. 12
    
13.Gothier DE, Gaumer HR, Philstrom BL, Folke LE. Elevation of a serum component in periodontal disease capable of modulating chemotactic infiltration. J Periodontal Res 1975;10:65-72.  Back to cited text no. 13
    

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Correspondence Address:
Shobha Prakash
Department of Periodontics, College of Dental Sciences, Davangere, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.99042

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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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