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ORIGINAL ARTICLE
Year : 2020  |  Volume : 11  |  Issue : 3  |  Page : 117-122

Correlation of C-reactive proteins with chronic periodontitis


Department of Oral and Maxillofacial Pathology, Yamuna Institute of Dental Sciences and Research, Yamuna Nagar, Haryana, India

Date of Submission29-Feb-2020
Date of Acceptance01-Sep-2020
Date of Web Publication15-Oct-2020

Correspondence Address:
Prof. Shailja Chatterjee
3/1323, Chatterjee Cottage, Janak Nagar, Bajoria Road, Saharanpur, Uttar Pradesh
India
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DOI: 10.4103/srmjrds.srmjrds_17_20

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  Abstract 

Background: Acute-phase reactant proteins are synthesized in human body in response to chronic periodontal states. C-reactive protein (CRP) is a similar protein produced in response to chronic inflammatory conditions. Aim: The aim of the study was to correlate CRP levels in chronic periodontitis when compared to normal controls. Materials and Methods: A total of 45 individuals suffering from chronic periodontitis and an equal numbers of controls were included in the study. Blood samples were drawn from all individuals after obtaining informed consent, and CRP levels were estimated using an ELISA kit. Unpaired t-test was performed for statistical analysis. Results: The mean CRP levels were found to be higher in periodontitis individuals as compared to normal controls. However, no statistical significance was observed on comparing both the groups. Conclusion: An elevated CRP level was obtained in the diseased group, confirming the inflammatory background response to periodontal diseases.

Keywords: C-reactive protein, periodontitis, serum


How to cite this article:
Chatterjee S. Correlation of C-reactive proteins with chronic periodontitis. SRM J Res Dent Sci 2020;11:117-22

How to cite this URL:
Chatterjee S. Correlation of C-reactive proteins with chronic periodontitis. SRM J Res Dent Sci [serial online] 2020 [cited 2020 Nov 28];11:117-22. Available from: https://www.srmjrds.in/text.asp?2020/11/3/117/298257


  Introduction Top


Periodontitis is an inflammatory disorder which affects the tooth-supporting structures. It is loss of clinical junctional epithelial attachment. “Clinical attachment loss” is the pathological loss of attachment of collagen to cemental surface along with apical junctional epithelial migration. Aggressive periodontitis is diagnosed based on clinical and radiographic features and is generally found in individuals younger than 35 years. Other associated features include an increased Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis; abnormal phagocytic activity; and increased interleukin (IL)-1β and prostaglandin E2 production. Aggressive periodontitis can be classified into – (a) localized (<30% affected teeth) and (b) generalized forms (>30% affected teeth). Severity of aggressive periodontitis can be categorized as – (a) slight (1–2 mm clinical attachment loss); (b) moderate (3–4 mm attachment loss); and (c) severe (>5 mm attachment loss).[1]

Etiological agents of periodontitis include mainly virulent bacterial pathogens derived from P. gingivalis, Treponema denticola, etc. These inflammatory reactions release a variety of inflammatory mediators such as chemokines.[2]

C-reactive protein (CRP) is produced in response to infection, trauma, and hypoxia and is reduced with conditions such as obesity, smoking, and diabetes alongside periodontal diseases. Patients suffering from aggressive periodontitis demonstrate statistically significant elevation in serum CRP levels.[1] Surgical intervention has been shown to undergo marked reduction in serum CRP levels.[2] High-sensitivity CRP (Hs-CRP) levels are considered to be more sensitive than regular CRP as these levels demonstrate significant decrease following periodontal treatment.[3]

Serum CRP levels can show an elevation of more than thousand times in inflammatory states with a half-life of 19 hours. It is considered a stable biomarker and a sensitive indicator of an ongoing inflammatory process. It is highly conserved protein found in all vertebrates and few invertebrates.[4] CRP levels can be found elevated in a variety of conditions such as infections of bacterial, viral, fungal, or mycobacterial origin; allergic response in rheumatic fever; inflammatory conditions such as Crohn's disease, Reiter's disease, systemic vasculitis, and ankylosing spondylitis; necrosis associated with myocardial infarction and acute pancreatitis; trauma secondary to burns, fractures etc.; and malignancies which include carcinomas, sarcomas, and lymphomas[Table 1].[5]
Table 1: Various conditions associated with increase in C-reactive protein concentration

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Muller et al. have demonstrated an elevated concentration of Hs-CRP linked with the risk of lung carcinoma in past as well as active smokers.[6]

CRPs are biological indicators of inflammation. These proteins may be demonstrating individual variations due to variations in immunological responses which can vary in various stages of treatment. This study was designed to work upon the novel idea of studying CRPs' levels based on inflammatory responses at periodic intervals of treatment.

The aim of the study was to correlate any association between periodontitis and CRP concentrations in serum.


  Materials and Methods Top


Study design

A total of 45 individuals (age range between 30 and 60 years) were recruited by periodontal selection. Periodontal status was evaluated in individuals with probing depths of ≥5 mm and with ≥2 of clinical attachment loss between the age range of 25 and 50 years with a mean age of 28.9 ± 1.3 years.

Ethical clearance was obtained from the hospital authorities, and the study purpose was well explained to the participants. Informed consent was obtained as per “Declaration of Helsinki's” guidelines.

Patient visit planning was planned at intervals of the first visit (for oral prophylactic procedures), second visit (at 6 months), and third visit (after 12 months of the first visit).

Deep scaling and root planing procedures were performed 3 months prior to the first collection of C-reactive samples. Periodontal assessment and CRP level measurement were done regularly at 6-month interval (second visit) and 12 months after initiating periodontal procedure (3rd visit). Inclusion criteria included – (a) good general physical health; (b) patients without any medication; and (c) informed patient consent. Exclusion criteria included – (a) any systemic disease; (b) pregnant or lactating females; (c) hypertensive individuals; (d) individuals with sleep-related disorders; (e) individuals with alcohol intake; (f) smokers; and (g) those with depression.

Plaque index (Silness and Loe), gingival index (Loe and Silness), pocket depth, and clinical attachment loss (Glavind and Loe) were assessed by a single investigator using a Williams's periodontal probe by avoiding bias.

Periodontal assessment

All cases with periodontal pockets were evaluated during oral examination with any of the following parameters – (a) clinical attachment loss of >2 mm; (b) bleeding on probing observed in nearly ≥35% of all the tooth-associated sites examined; and (c) there was a minimum of one involved site in four different teeth with pocket depth measuring more than 4 mm. Radiographic analysis was performed using either a panoramic (orthopantomograph) or intra-oral periapical radiograph.

Pocket depth was evaluated at each visit using a periodontal probe (William's probe) along with clinical loss of attachment by moving the probe at six sites around a tooth – mesiobuccal, middle, distobuccal and mesiolingual, lingual, and distolingual. The probing depth was measured from the gingival margin to the base of the pocket (millimeters), while clinical attachment levels were evaluated from recession and probing depth measurements and were represented as distance from the cemento-enamel junction to the base of the pocket (millimeters).

The participants were placed into three groups based on the following clinical assessment:

  1. Group 1 – Controls with a clinically healthy periodontium with probing depth measuring ≤2 mm with no attachment loss
  2. Group 2 – Individuals with probing depth measuring ≥5 mm and/or clinical attachment loss at more than 30% sites with varying severity of disease
  3. Group 3 – Individuals with probing depth measuring ≥5 mm and/or clinical loss of attachment on 8 or greater number of teeth including first permanent molars and incisors with varying severity.


The control group comprised of 45 individuals with no periodontal involvement under all the above-mentioned inclusion and exclusion criteria.

Blood collection was performed both in cases and controls before as well as at 6-month intervals to a maximum period of 12 months.

  1. Method of blood collection and storage.[7]


  2. A volume of 10 ml of blood sample was drawn from the branchial vein and transferred in a test tube which was then centrifuged at 3000 rpm for a duration of 10 min. The separated serum was stored at −80°C till further analysis was done.

  3. Quantification of CRP levels


Serum CRP levels were evaluated using commercially available ELISA kit from IMMUNOTECHA, Beckman Coulter Immunotech Company, Mersailles, France.

The mean ± standard deviation levels were calculated for periodontitis and control groups and comparisons were made using unpaired t-test for analyzing statistical significance. P < 0.05 was considered statistically significant.


  Results Top


Blood sample collection for analyzing CRP levels and clinical oral examinations were performed at study steps stratified at three visits – first visit (baseline); 3-month visit (second), and visit at 12 months of commencing the analysis.

CRP levels were found to be reduced during treatment period with mean values of 2.6 ± 2.4 mg/dL (males) and 2.3 ± 2.2 mg/dL (females); 1.9 ± 1.7 mg/dL (males) and 1.8 ± 1.5 mg/dL (females); 0.8 ± 0.6 mg/dL (males) and 0.6 ± 2.1 mg/dL (females) during the first, second, and third visits, respectively in diseased state, whereas in the control group, the mean values were 0.9 ± 2.3 mg/dL (males) and 0.5 ± 0.3 mg/dL (females) [Table 2], [Graph 1] and [Graph 2]. A statistically significant difference (P = 0.04) was noted between the study and control groups. However, comparing serum CRP levels with gender distribution (n = 30 and 20 males in case and control groups, respectively, and n = 25 and 25 females in case and control groups, respectively) showed no statistical significant difference (P = 0.3).
Table 2: Comparison of serum C-reactive protein levels in both study groups in subsequent groups (age range of 25–50 years; mean age=28.9±1.3 years)

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There was a significant reduction in mean pocket depth among males as- 3.5± 0.7 mm ; 2.4± 0.5mm and 1.7±0.6 mm in follow-up visits. Similar, reduction was noted among females, 2.5 ± 0.9 mm, 2.2 ± 0.7 mm, and 1.6 ± 0.5 mm at subsequent visits. The mean pocket depths of the controls were noted (males – 0.9 ± 0.5 and females – 0.7 ± 0.4 mm). A P value of 0.5 and 0.4 were obtained on making gender comparisons.

At subsequent visits, clinical loss of attachment was noted among both the genders, males – 4.12 ± 0.98 mm, 3.98 ± 0.4 mm, and 1.09 ± 0.7 mm and females – 3.09 ± 0.8 mm, 2.09 ± 0.45 mm, and 1.75 ± 0.5 mm, respectively. On comparing both the genders, P value of 0.4 and 0.35 were noted [Table 3].
Table 3: Pocket depth recorded at subsequent visits (gender-wise distribution)

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On comparing all the parameters using ANOVA, a P value of 0.45 was obtained [Table 4].
Table 4: Intragroup comparisons between pocket depth, clinical loss of attachment, and serum C-reactive protein levels using ANOVA

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No statistically significant value (P = 0.06) was observed when the mean plaque and gingival indices were compared at subsequent visits [Table 5].
Table 5: Mean plaque and gingival indices

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  Discussion Top


An acute-phase protein increases or decreases by 25% in an inflammatory disease, which may be either acute or chronic in nature. These proteins include complement system proteins, proteinaceous components of coagulation and fibrinolytic systems, and mediators of inflammatory processes.[8],[9] Leite et al. in their study showed a significant association between periodontitis and reduction in high-density lipoprotein-cholesterol. This correlation has been linked with localized inflammatory cytokine production and initiation of lipid metabolic pathway.[10]

The CRP is an acute-phase protein first discovered by Tillet and Francis (1930). It was discovered as a protein which precipitated pneumococcal cell wall polysaccharide.[8] CRP is produced by liver as a response to inflammatory cytokines such as IL-1 and -6 and tumor necrosis factor-alpha Circulating CRP levels are markers of systemic inflammation and are closely linked with periodontal disease. It is considered a gold standard for inflammatory load assessment.[10] The synthesis of CRPs takes place in hepatocytes at the expense of albumin and other important constitutive proteins (reprioritization of hepatic protein synthesis). Various risk factors determining CRP levels include old age, smoking, and bacterial infections.[11]

CRP acts by binding to plasma lipoproteins, phospholipids, phosphocholine, and on cell membranes of apoptotic or dead cells. This CRP bound to a ligand triggers inflammatory process, opsonization, and complex solubilizing complement system. This is an acute-phase reaction representing a nonspecific, early, and complex reaction of an organism to injuries of bacterial, viral, and parasitic infestations. The levels of CRPs are indicators of severity of an inflammatory disease condition.[12] It is a pentameric pattern recognition molecule which binds to specified molecular configuration on pathogen surface. This protein belongs to Pentraxin family exhibiting calcium-dependent reactivity. It has five noncovalent identical 23 kDa protomers with a symmetrical arrangement around a central axis. Each protomer is made of lectin fold, which is comprised of a β-sheet structure, while the opposite face contains single α-helix. CRP binding to chromatin takes place through histone interactions as its binding cannot take place with naked DNA. CRP acts by binding to C3 complement. The bound CRP produces secondary binding sites for factor “H,” regulating the alternate pathway and C5 convertase. As CPR is an acute-phase protein, its elevated levels fall sharply with removal of cause.[13]

The current study showed higher CRP levels in periodontitis individuals as compared to normal controls in the control group. These findings have been corroborated by numerous studies published earlier. Koppolu et al. (2013) in their investigation found that the baseline CRP concentrations reduced at 8-week interval.[2]

Salzberg et al. in their study also supported the view that serum CRP levels correspond to periodontitis severity. These levels were found to be significantly higher in localized as well as generalized aggressive periodontitis (1.0138 and 2.0538 mg/dL, respectively) when compared to controls (0.659 mg/dL).[14]

CRP levels have been found to fluctuate in conditions of hypertension, smoking, chronic fatigue, sleep disabilities, alcoholism, and in pregnant and lactating females. Podzimek et al. observed lowest levels of CRP in gingival recession cases when compared to chronic and aggressive periodontitis. Individuals with lowest CRP levels were seen in gingival recession cases followed by gingivitis and progressively in chronic and aggressive periodontitis. The bleeding on probing index showed better correlation with CRP levels in aggressive periodontitis when compared with chronic periodontitis cases.[15]

Shojaee et al. assessed CRP levels in saliva samples. They observed mean CRP levels of 5332 ± 5051.63 pg/mL in periodontitis and 35.45 ± 3061 pg/mL in gingivitis, while mean value of 3108 ± 3574 pg/mL was seen in healthy controls. A statistically significant difference (P = 0.045) was observed between the disease and control groups.[16]

Thakare et al. (2010) in their analysis surmised an increased risk of atherosclerosis due to elevated serum CRP levels. CRP acts by binding to ligands exposed in damaged tissues followed by the activation of complement pathway. Periodontal pathogens such as P. gingivalis, Tannerella forsythensis, and Actinobacillus actinomycetemcomitans have been isolated from atherosclerotic plaques, thus proving their close association between both conditions.[17]

Gupta et al. demonstrated increased mean CRP levels (5.8595 mg/L) in periodontitis patients with comparison to healthy controls with a high statistical significance (P = 0.000). However, smoking habit did not show any statistically significant association with periodontitis (P = 0.541) and CRP levels (P = 0.344).[18]

Al-Zahrani and Alghamdi observed a reduction in serum CRP concentrations pretreatment as compared to posttreatment samples (0.78 ± 0.51 and 0.55 ± 0.41 mg/dL, respectively, with a high statistical significance (P = 0.001) although treatment response was not found to have any significant association with obesity.[19]

Incidence of periodontitis during pregnancy has been linked with elevated CRP levels. This may result in preterm deliveries and low-birth weight infants in pregnant as compared to nonpregnant females.[20]

Alade et al. found a statistically significant association (P = 0.006) of an increased serum CRP with an increased severity of chronic periodontitis in hypertensive patients.[21]

Bolla et al. corroborated a higher mean CRP level in chronic periodontitis when compared with generalized aggressive periodontitis, but no statistical significance was found.[22]

Savitha and Shasmita showed elevated salivary CRP concentrations in periodontitis (60% of patients had 0.2 mg/mL) when compared to normal controls (≤1 mg/mL).[23]

Serum levels of CRP increase with in 4–8 hours following the onset of an acute event which can double at 8- hour interval while peaking at 50 hours. The protein levels can fall drastically after the removal of causative agent.[24]

Tian et al. investigated the association between IL-6, IL-12, CRP, vascular endothelial growth factor, and β-defensin-1 polymorphism and susceptibility of periodontitis development in 122 disease patients and 532 healthy individuals. Serum CRP levels and their genotypes were found to be associated with chronic periodontitis although their allele frequency demonstrated no significant difference between chronic periodontitis patients and normal controls.[25]

Shah et al. showed a progressive increase in CRP levels in periodontitis with disease severity.[26]

Musalaiah et al. in their study demonstrated that chronic periodontitis can lead to the development of anemia, hence reducing high-sensitive CRP levels in individuals with chronic periodontitis.[27] Jayaprakash et al. demonstrated an increase in CRP levels in gingival crevicular fluid in periodontitis patients.[28]


  Conclusion Top


CRPs are acute-phase reactant proteins synthesized in response to chronic inflammatory states. Their levels have been studied in chronic periodontal disease over the years and have uniformly reported an elevation as compared to normal controls. The current study also reported similar observation in chronic periodontitis-affected individuals. However, because the study aims to analyze a biological protein in a clinical disease, it must be studied over varied population subsets belonging to different demographic locations and also, a larger sized population subset would be substantiating or providing more essential data on this analysis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Mysak J, Podzimek S, Vasakova J, Mazanek J, Vinsu A, Duskova J. C-reactive protein in patients with aggressive periodontitis. J Dent Sci 2017;12:368-74.  Back to cited text no. 1
    
2.
Moeintaghavi A, Arab HR, Moghaddam MA, Shahmohammadi R, Bardan BY, Soroush Z. Evaluation of effect of surgical and nonsurgical periodontal therapy on serum C-reactive protein, triglyceride, cholesterol, serum lipoproteins and fasting blood sugars in patients with severe chronic periodontitis. Open Dent J 2019;13:15-21.  Back to cited text no. 2
    
3.
Ertugrul AS, Bozoglan A, Taspınar M. The effect of nonsurgical periodontal treatment on serum and gingival crevicular fluid markers in patients with atherosclerosis. Niger J Clin Pract 2017;20:361-8.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Paffen E, DeMaat MP. C-reactive protein in atherosclerosis: A causal factor? Cardiovasc Res 2006;71:30-9.  Back to cited text no. 4
    
5.
Pepys MB, Hirschfield GM. C-reactive protein: A critical update. J Clin Invest 2003;111:1805-12.  Back to cited text no. 5
    
6.
Muller DC, Lacose TL, Hodge A, Guide F, Langhammer A, Grankvist K, Meyer K et al. Circulating high sensitivity C reactive protein concentrations and risk of lung cancer: nested case-control study within lung cancer cohort consortium. BMJ 2018;364:k4981-7.  Back to cited text no. 6
    
7.
Koppolu P, Durvasula S, Palaparthy R, Rao M, Sagar V, Reddy SK, et al. Estimate of CRP and TNF-alpha level before and after periodontal therapy in cardiovascular disease patients. Pan Afr Med J 2013;15:92.  Back to cited text no. 7
    
8.
Mir RA, Saima S, Shah GA, Bashir B. Effect of ultrasonic scaling on C-reactive protein levels in chronic periodontitis patients: A research article. Int J Appl Dent Sci 2019;5:163-4.  Back to cited text no. 8
    
9.
Kalra N, Pradeep AR, Priyanka N, Kumari M. Association of stem cell factor and high-sensitivity C reactive protein concentrations in crevicular fluid and serum in patients with chronic periodontitis with and without type 2 diabetes. J Oral Sci 2013;55:57-62.  Back to cited text no. 9
    
10.
Leite AC, Carneiro VM, Guimarães Mdo C. Effects of periodontal therapy on C-reactive protein and HDL in serum of subjects with periodontitis. Rev Bras Cir Cardiovasc 2014;29:69-77.  Back to cited text no. 10
    
11.
Moeintoghavi A. Association of periodontal diseases with c reactive proteins. J Med Sci 2008;8:191-5.  Back to cited text no. 11
    
12.
Deepa D, Gupta C, Gupta A. Assessment of high-sensitivity C-reactive protein values in chronic periodontitis patients with or without cardiovascular disease: A cross-sectional study. J Clin Prev Cardiol 2016;5:108-12.  Back to cited text no. 12
  [Full text]  
13.
Gupta S, Gupta I, Gupta R, Gupta P. Role of C-reactive protein in periodontal disease – A review. Int J Contemp Med Res 2017;4:980-5.  Back to cited text no. 13
    
14.
Salzberg TN, Overstreet BT, Rogers JD, Califano JV, Best AM, Schenkein HA. C-reactive protein levels in patients with aggressive periodontitis. J Periodontol 2006;77:933-9.  Back to cited text no. 14
    
15.
Podzimek S, Mysak J, Janatova T, Duskova J. C-reactive protein in peripheral blood of patients with chronic and aggressive periodontitis, gingivitis, and gingival recessions. Mediators Inflamm 2015;2015:564858.  Back to cited text no. 15
    
16.
Shojaee M, Fereydooni Golpasha M, Maliji G, Bijani A, Aghajanpour Mir SM, Mousavi Kani SN. C-reactive protein levels in patients with periodontal disease and normal subjects. Int J Mol Cell Med 2013;2:151-5.  Back to cited text no. 16
    
17.
Thakare SS, Deo V, Bhongade ML. Evaluation of the C-reactive protein serumlevels in periodontitis patients with or without atherosclerosis. Ind J Dent Res 2010;21:326-30.  Back to cited text no. 17
    
18.
Gupta S, Pradhan S, Sushil KC, Shakya S, Giri M. C-reactive protein in periodontitis and its comparison with body mass index and smoking behavior. J Nepal Med Assoc 2017;56:226-33.  Back to cited text no. 18
    
19.
Al-Zahrani MS, Alghamdi HS. Effect of periodontal treatment on serum C-reactive protein level in obese and normal-weight women affected with chronic periodontitis. Saudi Med J 2012;33:309-14.  Back to cited text no. 19
    
20.
Navkiran, Kaur A, Singh S, Verma A. Relationship of chronic periodontitis and plasma C-reactive protein during pregnancy. Int J Med Dent Sci 2016;5:1208-13.  Back to cited text no. 20
    
21.
Alade GO, Ayanbadejo PO, Umeizudike KA, Ajuluchukwu JN. Association of elevated C-reactive protein with severe periodontitis in hypertensive patients in Lagos, Nigeria: A pilot study. Contemp Clin Dent 2018;9:S95-9.  Back to cited text no. 21
    
22.
Bolla V, Kumari PS, Munnangi SR, Kumar DS, Durgabai Y, Koppolu P. Evaluation of serum C-reactive protein levels in subjects with aggressive and chronic periodontitis in comparison with healthy controls: A clinic-biochemical study. Int J App Basic Med Res 2017;7:121-4.  Back to cited text no. 22
[PUBMED]  [Full text]  
23.
Savitha P, Shasmita R. Comparison of salivary CRP level in chronic periodontitis and healthy individuals. J Pharm Sci Res 2015;7:729-30.  Back to cited text no. 23
    
24.
Shafiq F, Hingorjo MR, Qureshi MA. Level of C-reactive protein in periodontal patients before and after treatment in a teaching hospital selected population. JPDA 2011;20:145-8.  Back to cited text no. 24
    
25.
Tian Y, Li JL, Hao L, Yue Y, Wang M, Loo WT, et al. Association of cytokines, high sensitive C-reactive protein, VEGF and beta-defensin-1 gene polymorphisms and their protein expressions with chronic periodontitis in the Chinese population. Int J Biol Markers 2013;28:100-7.  Back to cited text no. 25
    
26.
Shah MA, Shah BK, Modi BB, Shah EB, Dave DH. Hs-CRP levels in patients with periodontitis – A cross sectional study. J Integ Health Sci 2015;3:15-20.  Back to cited text no. 26
    
27.
Musalaiah SV, Anupama M, Nagasree M, Krishna CM, Kumar A, Kumar PM. Evaluation of nonsurgical periodontal therapy in chronic periodontitis patients with anemia by estimating hematological parameters and high-sensitivity C-reactive protein levels. J Pharm Bioallied Sci 2014;6:S64-9.  Back to cited text no. 27
    
28.
Jayaprakash D, Aghanashini S, Vijayendra RR, Chatterjee A, Rosh RM, Bharwani A. Effect of periodontal therapy on C-reactive protein levels in gingival crevicular fluid of patients with gingivitis and chronic periodontitis: A clinical and biochemical study. J Indian Soc Periodontol 2014;18:456-60.  Back to cited text no. 28
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    Tables

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



 

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