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DENTAL SCIENCE - REVIEW ARTICLE
Year : 2015  |  Volume : 7  |  Issue : 5  |  Page : 184-189  

Serum ferritin level and red blood cell parameters in healthy controls and chronic periodontitis patients


1 Department of Periodontics, K. G. F. Dental College and Hospital, Karnataka, India
2 Department of Oral Pathology and Microbiology, K. G. F. Dental College and Hospital, Karnataka, India
3 Department of Periodontics, Rajah Muthiah Derntal College and Hospital, Chidambaram, Tamil Nadu, India
4 Department of Oral Pathology and Microbiology, Sree Balaji Dental College and Hospital, Bharath University, Chennai, Tamil Nadu, India

Date of Submission31-Oct-2014
Date of Decision31-Oct-2014
Date of Acceptance09-Nov-2014
Date of Web Publication30-Apr-2015

Correspondence Address:
Dr. L Malathi
Department of Oral Pathology and Microbiology, Sree Balaji Dental College and Hospital, Bharath University, Chennai, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-7406.155896

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   Abstract 

Periodontitis, which is a chronic inflammatory disease causes reduction in the number of erythrocytes and hemoglobin. It is found to be caused by specific pathogenic subgingival plaque bacteria. Periodontitis is host mediated through release of pro inflammatory cytokines by local tissues and immune cells in response to bacterial flora and its products, especially lipopolysacharides. Periodontitis is found to have systemic effect and the cytokines produced inhibit proliferation and differentiation of erythrocytes leading to anaemia. This study evaluate level of hemoglobin erythrocytes, hematocrit and serum ferritin levels in healthy subjects and periodontitis patient.

Keywords: Anemia, periodontitis, serum ferritin


How to cite this article:
Latha S, Thirugnanamsambandan S, Arun R T, Masthan K, Malathi L, Rajesh E. Serum ferritin level and red blood cell parameters in healthy controls and chronic periodontitis patients. J Pharm Bioall Sci 2015;7, Suppl S1:184-9

How to cite this URL:
Latha S, Thirugnanamsambandan S, Arun R T, Masthan K, Malathi L, Rajesh E. Serum ferritin level and red blood cell parameters in healthy controls and chronic periodontitis patients. J Pharm Bioall Sci [serial online] 2015 [cited 2020 Nov 26];7, Suppl S1:184-9. Available from: https://www.jpbsonline.org/text.asp?2015/7/5/184/155896

Periodontitis is a chronic inflammatory disease which causes a reduction in a number of erythrocytes and consequently lowers hemoglobin level in periodontitis patients. It has been recognized as a chronic inflammatory oral disease caused by specific pathogenic subgingival plaque bacteria. Periodontal destruction is host-mediated through release of pro-inflammatory cytokines by local tissues and immune cells in response to bacterial flora and its products, especially lipopolysaccharides. In periodontitis, the levels of interleukin-β (IL-1β) and tumor necrosis factor-α (TNF-α) [1] are significantly elevated in gingival crevicular fluid and enters systemically, falling within the detectable range of biological serum assays. [2]

Periodontitis-induced pro-inflammatory cytokines play a major role in development of variety of systemic disease [3] epidemiological studies [4] suggest that periodontitis is associated with an increased risk for systemic diseases such as cardiovascular diseases, cerebrovascular ischemia, and atherosclerosis. These associations indicate that periodontitis has systemic effects, and most likely systemic inflammation must also be present. It has been observed that infection is associated with profound disturbances in iron metabolism and decreased incorporation of iron into hemoglobin give rise to anemia. A pro-inflammatory cytokines from the chronic disease processes are involved in the pathogenesis of anemia. These cytokines inhibit proliferation and differentiation of erythrocyte progenitors, [5] modulate iron metabolism, [6] and suppress erythropoietin production [7] with resultant anemia. Hence, the present study is undertaken to substantiate that periodontitis may cause anemic state.


   Materials and Methods Top


The subjects for this study were selected from the outpatients attending the Department of Periodontics, Tamil Nadu government dental college and hospital Chennai, after informed consent.

Inclusion criteria (for both groups):

  • Age groups 40-50 years
  • Either sex
  • Systemically healthy subjects.


Exclusion criteria (for both groups):

  • History of peptic ulcer, tuberculosis, bronchiectasis, pneumonia, lung abscess, bacterial endocarditis, chronic renal failure, hepatic disease, rheumatoid arthritis, systemic lupus erythematosus, malaria, viral infection, diabetes, menorrhagia, hodgkins disease, carcinoma, traumatic injuries, gastric surgeries, allergy, pregnancy, smokers and alcoholic.


Control group

Control group included any periodontal sight which had probing depth (PD) of ≤ 3 mm and with no clinical attachment loss (CAL).

Study group

Study group included any periodontal site which had PD of ≥4 mm and with CAL.

Study design

Examination was preceded by a thorough medical history of both he groups. A complete periodontal examination was undertaken using a mouth mirror, and Williams graduated periodontal probe. Periodontal status was assessed using the clinical parameters such as PD and level of the CAL. Full mouth intraoral periapical radiographs were taken for both the groups and 5 mm of venous blood samples were collected from antecubetal fossa.

Hematological investigations are done with blood samples, consisting erythrocyte count, white blood cell count, estimation of hemoglobin, erythrocyte sedimentation rate (ESR), and peripheral smear examination and for biochemical investigation such as blood glucose, blood urea, serum creatinine, and serum ferritin.

Probing depth

Probing depth is measured from the gingival margin to the base of the pocket using a calibrated periodontal probe. The probe is passed under the gingiva along the circumference of the tooth. Three measurements are made in the buccal aspect and three on the lingual aspect of each tooth total of six sites per tooth (mesio buccal, midbuccal, distobuccal, mesiolingual, midlingual, distolingual).



Clinical attachment level

Clinical attachment level is measured from the cemento-enamel junction to the base of the pocket using a calibrated periodontal probe.

When the gingival margin is located on the anatomical crown, the level of attachment is determined by subtracting from the pocket the distance from the gingival margin to cemento-enamel junction. If both are the same, the loss of attachment is zero.


   Collection of Blood Sample Top


Five ml of venous blood samples was obtained by venipuncture of cubital vein in the anticubibetal fossa using 5 ml disposable syringe 23 gauge needles. The blood was then transferred to sterile vacuum tube containing ethylene diamine tetra acetic acid and transported to the clinical laboratory for processing within 4 h of venepuncture.


   Results Top


Twenty-eight subjects were selected from the outpatients attending the Department of Periodontics, Tamil Nadu government dental college and hospital, Chennai. Fourteen subjects with PD ≤ 3 mm and no CAL were taken as a control group and the remaining 14 patients with PD ≥ 4 mm and with CAL ≥ 1 mm were taken as study group.

Clinical periodontal parameters used in this study consisted of measuring the PD and clinical attachment level in mm. Hematological and biochemical investigations performed for both the groups included erythrocyte count, estimation of hemoglobin, hematocrit, ESR, and estimation of serum ferritin. Statistical analyses were done using Student's t-test and Pearson correlation analysis.

[Table 1] and [Table 2] show the values of clinical parameters, hematological and biochemical investigations in control and study group.
Table 1: Values of clinical periodontal parameters, hematological investigations, and biochemical investigations in control group

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Table 2: Values of clinical periodontal parameters, hematological investigations, and biochemical investigations in study group

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[Table 3] and [Table 4] show the peripheral blood smear examination in control and study group. Four subjects in the control group and 2 patients in study group had microcytes, the remaining patients had macrocytes.
Table 3: Peripheral blood smear examination in the control group

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Table 4: Peripheral blood smear examination in study group

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[Table 5] shows number of the control group and study group with values red blood cell parameters and serum ferritin levels above or below the reference range. In hemoglobin levels, 100% of the control and study group were anemic. 42.9% controls and 50% of the study group were anemic concerning hematocrit levels. Further, 14.2% of the controls and 28.4% of the study group were anemic concerning number of erythrocytes. Finally, slightly a higher proportion of study group (42.9%) had an elevated ESR compared to the control (21.4%).
Table 5: Number an percentage control and study groups with values with RBC parameters and serum ferritin below or above reference range

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[Table 6] shows the mean, standard deviation and test of significance of mean values between control and study group. Statistical analysis by Student's independent t-test showed than the mean PD in the study group (4.7 ± 0.5) is significantly higher than the control group (1.6 ± 0.2) (P < 0.001). Similarly, the mean CAL in the study group (5.5 ± 0.8) is significantly higher than control group (0.0 ± 0.0) (P < 0.0001). However, no other variables are statistically significant between the control and study group (P > 0.005).
Table 6: Mean, SD, and test off significance of mean values between control and study group

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[Table 7] shows the mean, standard deviation, and test of significance of mean values between the control and study group males. Statistical analysis showed that the mean PD and CAL are significantly higher in the study group males (PD = 4.8 ± 0.6, CAL = 6.0 ± 0.7) than the control group.
Table 7: Mean, SD, and test off significance of mean values in control and study males

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Males (PD = 1.6 ± 0.2; CAL = 0.0 ± 0.0) (P < 0.0001).

[Table 8] shows the mean, standard deviation, and test of significance of mean values between the control and study group females. Statistical analysis showed that the mean PD and CAL are significantly higher in the study group females (PD = 4.7 ± 0.5, CAL = 4.9 ± 0.6) than control group females (PD = 1.6 ± 0.2, CAL = 0.0 ± 0.0) (P < 0.0001).
Table 8: Mean, SD and test off significance of mean values in control and study females

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[Table 9] shows the correlation analysis of clinical periodontal parameters with hematological and biochemical investigations in control and study group. Pearson correlation analysis showed that there is a significant positive linear relationship between hemoglobin and CAL in study group (r = 0.45, P = 0.05).
Table 9: Correlation analysis of clinical periodontal parameters with RBC parameters in control and study group


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[Table 10] shows the correlation analysis of clinical periodontal parameters with hematological and biochemical investigations in control and study group males.
Table 10: Correlation analysis of clinical periodontal parameters with RBC parameters in control and study group males

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[Table 11] shows the correlation analysis of clinical periodontal parameters with hematological and biochemical investigations in control and study group females. There is a significant positive linear relationship between packed cell volume and PD for females in the study group (r = 0.70, P = 0.04)
Table 11: Correlation analysis of clinical periodontal parameters with RBC parameters in control and study group females

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   Discussion Top


Periodontitis is initiated by a specific bacteria, predominantly Gram-negative anaerobes [8] that activate tissue mechanism that produces a series of inflammatory and immunologic changes leading to destruction [9],[10] of periodontium. Periodontal tissue destruction is host-mediated through release of proinflammtory cytokines by local tissue and immune cells in response to bacterial flora and its product. There have been several proinflammatory cytokines implicated in the immunopathology of periodontitis, however recent studies [11] have shown that IL-1® and TNF-α are most commonly involved in the destruction of the periodontium.

Earlier paradigms have maintained that periodontitis is an oral disease and that the tissue destruction respond remains localized between the periodontium, limiting it effects to oral tissues supporting the teeth. Recent studies have indicated that periodontitis also produces alterations in the systemic health. It has significant association with acute cerebral infarction, failure of organ replacement and kidney dialysis, [12] coronary heart disease, [13] preterm low birth weight, [14] aspiration pneumonia, [15] and diabetes. [16] It has been shown that patients with moderate to severe periodontitis had a lower number of erythrocytes, lower levels of hemoglobin and hematocrits indicating possible anemia.

In our study, the hematological investigations performed include erythrocyte count, estimation of hemoglobin, hematocrit, and ESR. And the present study also includes the estimation value of the white blood cells and peripheral smear examination. Total leukocytes count was taken into consideration to rule out parasitic infections and allergic reactions. Peripheral smear examination was performed to differentiate iron deficiency, macrocytic and normocytic anemia. Biochemical investigations such as blood glucose, blood urea, and serum creatinine were done to exclude the diabetic and renal failure patients. Estimation of serum ferritin was performed to show that in spite of low serum iron level in anemia due to chronic diseases also accompanied by a normal serum ferritin level. [17]

Pearson correlation analysis is used in this study to see the correlation between the clinical periodontal parameters and red blood parameters among the control and study groups. It showed a significant positive linear relationship between hemoglobin and CAL in study group (r = 0.45, P = 0.05), the significant relationship may indicate the beginning of subclinical or clinically evident anemic status.


   Conclusion Top


Both the groups showed iron deficiency and macrocytic anemia, no statistically significant correlation was found to exist between periodontitis and erythrocyte count, levels of hemoglobin, hematocrit, and serum ferritin since there is no normocytic anemia.

 
   References Top

1.
Heasman PA, Collins JG, Offenbacher S. Changes in crevicular fluid levels of interleukin-1 beta, leukotriene B4, prostaglandin E2, thromboxane B2 and tumour necrosis factor alpha in experimental gingivitis in humans. J Periodontal Res 1993;28:241-7.  Back to cited text no. 1
    
2.
Prabhu A, Michalowicz BS, Mathur A. Detection of local and systemic cytokines in adult periodontitis. J Periodontol 1996;67:515-22.  Back to cited text no. 2
    
3.
Ranney RR. Immunologic mechanisms of pathogenesis in periodontal diseases: An assessment. J Periodontal Res 1991;26:243-54.  Back to cited text no. 3
    
4.
DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. BMJ 1993;306:688-91.  Back to cited text no. 4
    
5.
Means RT Jr, Krantz SB. Progress in understanding the pathogenesis of the anemia of chronic disease. Blood 1992;80:1639-47.  Back to cited text no. 5
    
6.
Vreugdenhil G, Löwenberg B, Van Eijk HG, Swaak AJ. Tumor necrosis factor alpha is associated with disease activity and the degree of anemia in patients with rheumatoid arthritis. Eur J Clin Invest 1992;22:488-93.  Back to cited text no. 6
    
7.
Baer AN, Dessypris EN, Krantz SB. The pathogenesis of anemia in rheumatoid arthritis: A clinical and laboratory analysis. Semin Arthritis Rheum 1990;19:209-23.  Back to cited text no. 7
    
8.
Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol 2000 1994;5:78-111.  Back to cited text no. 8
    
9.
Narasinga Rao BS, Vijayasarathy C, Prabhavathi T. Iron absorption from habitual diets of Indians studied by the extrinsic tag technique. Indian J Med Res 1983;77:648-57.  Back to cited text no. 9
    
10.
Genco RJ. Assesment of risk of periodontal disease. Compendium 1994;18:S678-83.  Back to cited text no. 10
    
11.
Gemmell E, Marshall RI, Seymour GJ. Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease. Periodontol 2000 1997;14:112-43.  Back to cited text no. 11
    
12.
Lowe GD. Etiopathogenesis of cardiovascular disease: Hemostasis, thrombosis, and vascular medicine. Ann Periodontol 1998;3:121-6.  Back to cited text no. 12
    
13.
Dinant HJ, de Maat CE. Erythropoiesis and mean red-cell lifespan in normal subjects and in patients with the anaemia of active rheumatoid arthritis. Br J Haematol 1978;39:437-44.  Back to cited text no. 13
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14.
Dasanayake AP. Poor periodontal health of the pregnant woman as a risk factor for low birth weight. Ann Periodontol 1998;3:206-12.  Back to cited text no. 14
    
15.
Loesche WJ, Lopatin DE. Interactions between periodontal disease, medical diseases and immunity in the older individual. Periodontol 2000 1998;16:80-105.  Back to cited text no. 15
    
16.
Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: A two-way relationship. Ann Periodontol 1998;3:51-61.  Back to cited text no. 16
    
17.
Lukens JN. Control of erythropoiesis in rats with adjuvant-induced chronic inflammation. Blood 1973;41:37-44.  Back to cited text no. 17
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11]



 

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