Journal of Baghdad College of Dentistry, Vol. 34, No. 4 (2022), ISSN (P): 1817-1869, ISSN (E): 2311-5270 9 Research Article Assessment of serum levels of monocyte chemoattractant protein 1 (MCP 1) in patients with periodontitis and atherosclerotic cardiovascular disease Safa Ali Hamad 1*, Maha Shukri Mahmood2 1 Master student, ministry of health, Baghdad. 2 Professor, Department of periodontics, College of Dentistry, University of Baghdad. Bab Almoadham, P.O. Box 1417, Baghdad, Iraq * Correspondence: safa.almahamdah@yahoo.com Abstract: Background: Monocyte chemotactic protein-1 (MCP-1) is a chemokine expressed by inflammatory and endothelial cells. It has a crucial role in initiating, regulating, and mobilizing monocytes to active sites of periodontal inflammation. Its expression is also elevated in response to pro-inflammatory stimuli and tissue injury, both of which are linked to atherosclerotic lesions. Aim of the study: To determine the serum level of MCP-1 in patients with periodontitis and atherosclerotic cardiovascular disease in comparison to healthy control and evaluate the biomarker's correlations with periodontal parameters. methods: This study enrolled 88 subjects, both males and females, ranging in age from 36-66 years old, and divided into four groups: 1ST group with atherosclerotic cardiovascular disease (ASCVD) without periodontal disease (25 patients), 2nd group with periodontitis and systemically healthy, (25 patients),3rdgroup having both ASCVD and periodontitis (25 patients), and the 4th is the control group without any systemic disease and with good oral hygiene (13 subjects). The clinical periodontal parameters plaque index (PL I), Bleeding on probing (BOP), Probing Pocket depth (PPD) and clinical attachment level (CAL) were used to evaluate periodontal health status. Atherosclerotic cardiovascular disease patients were chosen after clinical examination by specialists and diagnoses confirmed with catheterization. Following clinical assessment, 5ml of venous blood was drawn from each participant MCP-1 levels in the blood were then measured using enzyme-linked-immunosorbent assay (ELISA). Results: According to the findings of this study, the mean values of PLI and BOP were higher in periodontitis group and athero+periodontitis group than in athero group and control group, PPD and CAL mean values were greater in athero+periodontitis group than in periodontitis group. The serum level of MCP-1 was higher in athero+periodontitis group than in athero, periodontitis and control groups. Regarding the correlations between MCP-1 and clinical periodontal parameters. In periodontitis group there was a positive correlation with PPD and CAL and there was a positive correlation with CAL in athero+periodontitis. Conclusion: This study revealed that periodontitis with higher MCP-1 level may be linked to an increased risk of atherosclerosis. Keywords: Periodontitis, Cardiovascular, Plasminogen activators, Monocyte chemoattractant. Introduction Periodontal diseases (PDs) are inflammatory diseases that affect the tissues that support the teeth. Periodontitis is defined as a loss of supportive periodontal tissue, manifested clinically as clinical loss of attachment with gingival bleeding, and pocketing, while loss of alveolar bone is determined by radiography (1). Atherosclerosis is a chronic inflammatory disease of the arteries caused by cholesterol accumulation and other physiological factors, and it is the leading cause of heart disease. Cardiovascular disease (CVD) is the leading cause of death worldwide. CVD is anticipated to kill 17.3 million people per year, accounting for 30% of all fatalities, and this figure is expected to rise to 23.3 million Received date: 10-01-2022 Accepted date: 26-02-2022 Published date: 15-12-2022 Copyright: © 2022 by the authors. The article is published under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org /licenses/by/4.0/). https://doi.org/10.2647 7/jbcd.v34i4.3272 mailto:safa.almahamdah@yahoo.com https://creativecommons.org/licenses/by/4.0/ https://creativecommons.org/licenses/by/4.0/ https://doi.org/10.26477/jbcd.v34i3.3214 https://doi.org/10.26477/jbcd.v34i3.3214 J. Bagh. Coll. Dent. Vol. 34, No. 4. 2022 Hamad and Mahmood 10 by 2030 owing to enhanced aging and obesity prevalence (2). For over a century, there has been speculation that there is a link between dental health and CVD and according to epidemiological data, persons with periodontitis are more prone to develop the atherosclerotic disease than people without (3). The investigation into potential links between periodontitis and atherosclerosis has intensified, and various correlations and causalities are being studied (4,5) Two publications looked at the scientific evidence for these associations: one looked at the function of invading microbes and infections (6), whereas the other is based on inflammatory processes (7). This academic evidence now suggests that periodontitis leads to the entry of bacteria or their products into the circulatory system, which increases the host's inflammatory response through numerous pathways, favoring the formation and worsening of atheromatous lesions (8). Monocyte chemoattractant protein-1 (MCP-1) is a strong factor for macrophage and monocyte chemotaxis, reflecting the very first identified. human CC chemokine with monocyte chemotactic functions (9). A number of various cells, such as epithelial, endothelial, smooth muscle, astrocytic, mesangial, microglial, monocytic, and fibroblastic cells producing MCP-1 Following oxidative stress, particular cytokine or growth factor action which is either biologically derived or stimulated (9). The key role of MCP-1 is the regulation of monocytes, macrophages, natural killer (NK) cells, and memory T lymphocyte recruitment and aggregation (10). In atherosclerotic CVD, research findings have shown that MCP-1 promotes endothelial cell activity with chemokine receptors and enhances the vulnerability of plaques (11). Furthermore; MCP-1 was shown to be selectively present at affected periodontal sites and displayed a distinct distribution pattern in the periodontium, as it is expressed in the inflammatory infiltrate along the basal layer of the oral epithelium and by endothelial cells, fibroblasts, and mononuclear phagocytes (12). Material and methods Study design Eighty-eight subjects were selected according to inclusion and exclusion criteria in a period from March to July 2021. The study protocol was approved by the ethical committee of the College of the Dentistry/University of Baghdad follow the guidelines of Helsinki and Tokyo for humans (the reference no.249 in 18/2/2021). All the individuals were informed about the purpose of this investigation. Informed consent was obtained from each participant, and a questionnaire was used to record the background information. Subjects were divided into four main groups: •Athero group, 25 Patients with Atherosclerotic Cardiovascular Disease (ASCVD) who have had catheterization for less than one year and are taking anticoagulant medicines (Plavix) and have stenosis of about fifty percent or more of at least one coronary artery and with healthy periodontium. • Periodontitis group, 25 patients diagnosed to have periodontitis and didn’t have any systemic disease. A patient is a periodontitis case in the context of clinical care with Interdental CAL is detectable at ≥2 non-adjacent teeth, or buccal or oral CAL ≥3 mm with pocketing >3 mm is detectable at ≥2 teeth (13). •Athero+periodontitis group, 25 patients with both periodontitis and atherosclerosis, •control group, 13 subjects with clinically healthy periodontium and no systemic disease, in which bleeding on probing less than 10% and Probing pocket depth of ≤ 3 mm (14). This group represents baseline data for the serum level of MCP-1. The exclusion criteria were: Patients with a history of another chronic, systemic disease with a known link with periodontitis, such as diabetes mellitus, rheumatoid arthritis, and so on, medication (anti- inflammatory or antibacterial medication) during the past three months and smokers, pregnancy, and contraceptive pills. J. Bagh. Coll. Dent. Vol. 34, No. 4. 2022 Hamad and Mahmood 11 Examiner alignment For inter-examiner calibration, the periodontal parameters (BOP, PPD, and CAL) for 5 subjects were measured by the researcher and the supervisor at the same time. The measurements were assessed using interclass correlation coefficient (ICC), and there was a good level of agreement for all parameters 0.785,0.760, and 0.753 respectively. For intra examiner calibration, the periodontal parameters (BOP, PPD, and CAL) for 5 subjects were measured twice by the researcher with a two-hour interval between the two measurements. There was a good level of agreement for BOP and PPD, and excellent for CAL (16). Clinical assessment Assessment of the periodontal status was carried out for all participants in which full mouth plaque score by O’Leary (1972 ) is used to detect presence or absence of plaque at four surfaces of each tooth (buccal, palatal/lingual, mesial & distal) by using a disclosing agent (15), full mouth bleeding on probing score recorded as present (1) or absent (0), probing pocket depth and clinical attachment level were recorded using a periodontal probe of William’s (marking at 1,2,3,5,7,8,9 and 10 mm). PPD was measured from the gingival margin to the base of the pocket while CAL is the distance measured from cemento-enamel junction to the base of the pocket/sulcus at six sites per tooth. MCP-1 measurement 5ml of venous blood was collected from each participant from the cubital fossa using 5ml plastic disposable syringe, then transferred into jell separating tubes, centrifuged for 5 minutes at (3000 RPM) and then sera were separated, then the tubes were labeled and stored at (-20°C) for later analysis by Enzyme-Linked Immuno-Sorbent Assay (ELISA) for the quantitative determination of serum MCP-1. Statistical analysis Data description, analysis, and presentation were performed using Statistical Package for Social Science (SPSS version 21) (Chicago, USA, Illinois). Mean, and standard deviation (SD) for nominal variables, also Inferential Statistics as Levene test, Pearson correlation (r), interclass correlation coefficient (ICC), two independent sample T-test, Shapiro Wilk and D'agostino Pearson test for the normality distribution of the quantitative variables, and One Way Analysis Of Variance (ANOVA) with Games-Howell posthoc test and Tukey Kramer HSD (according to levene's p-value) were used to analyze data. Results All studied variables were found to be normally distributed (parametric data) using Shapiro-Wilk and D’Agostino Pearson at (p˃0.05). For PLI analysis, the mean value of PLI was found to be higher in athero+periodontitis group followed by periodontitis group then athero group, and lowest in the control group with a significant difference at P.value ˂0.05. While in BOP it was found to be higher in periodontitis group, followed by athero+periodontitis group, then athero group, and also lowest in control group with a significant difference at P.value ˂0.05 table.1 Levene statistics=1.904, p value=0.135 NS, * = Significant at p<0.05. for PLI Levene statistics=15.375, p value=0.000 sig., *= Significant at p<0.05.for BOP Following multiple pairwise comparisons (MPC), the only non-significant finding was found when comparing control group with athero group and periodontitis group with athero+periodontitis group while other results were significant, BOP showed the same results table 2. For PPD and CAL, athero+periodontitis group showed J. Bagh. Coll. Dent. Vol. 34, No. 4. 2022 Hamad and Mahmood 12 a higher mean value and SD than periodontitis group with a significant difference between them at P.value ˂0.05 as shown in table 3. Table 1: Statistical test of PLI and BOP among groups using One Way ANOVA. Groups PLI (Mean±SD) of Score 1 P-value BOP (Mean±SD) of Score 1 P-value Athero 25.080±8.411 0.000 Sig 5.080±1.656 0.000 Sig periodontitis 70.400±13.342 39.360±18.154 Athero+periodontitis 70.640±11.139 35.440±15.594 control 24.538±13.956 5.154±2.853 Table 2: Inter groups multiple pairwise comparisons of the mean values of PLI and BOP. (A) Groups (B) Groups Mean Difference (A-B) of PLI P-value Mean Difference (A-B) of BOP P-value Athero Periodontitis -45.3200 0.000 * -34.2800 0.0000 * Athero+periodontitis -45.5600 0.000 * -30.3600 0.0000 * Control 0.5415 0.9991 ^ -0.0738 0.9998 ^ periodontitis Athero+periodontitis -0.2400 0.9999 ^ 3.9200 0.8452 ^ Control 45.8615 0.000 * 34.2062 0.0000* Athero+periodontitis Control 46.1015 0.000 * 30.2862 0.0000* *=significant at p<0.05, ^=not significant at p>0.05 Table 3: A statistical test of PPD and CAL among groups using Independent Sample T- test. Variables Periodontitis Athero+periodontitis T-test P-value PPD (mean±SD) 4.759±0.727 5.169±0.583 2.202 0.032* Sig CAL (mean±SD) 3.459±1.033 4.649±0.999 4.143 0.000* Sig *=significant at p˂0.05 Primary outcomes The current study showed that MCP-1 was higher in athero+periodontitis group followed by athero group, and then periodontitis group, while lower in control group with a significant difference at P.value ˂0.05 table 4. After doing MPC the only non-significant result was found when comparing athero group with periodontitis group while other findings were significant as shown in table 5. Concerning the correlation of MCP-1 and clinical periodontal parameters in the current study, there was a significant strong positive correlation with PPD (r=0.503; p=0.0104), and CAL (r=0.501; p=0.0107) in periodontitis group and there was a significant strong positive correlation with CAL (r=0.510; p=0.009) in athero+periodontitis group table 6. J. Bagh. Coll. Dent. Vol. 34, No. 4. 2022 Hamad and Mahmood 13 Table 4: A statistical test of MCP-1 among groups using One Way ANOVA. Groups Mean ±SD P-value athero 83.857 33.742 0.000* Sig Periodontitis 82.433 26.499 Athero+peridontitis 148.177 51.693 control 48.594 14.586 Table 5: Inter groups multiple pairwise comparisons of the mean values of MCP-1 Multiple Comparisons ( Games-Howell) Dependent Variable: MCP-1 (ng/L) (A) Groups (B) Groups Mean Difference (A-B) Sig. Athero Periodontitis 1.4244 0.9983 ^ Athero+periodontitis -64.3200 0.0000* control 35.2632 0.0004* Periodontitis Athero+periodontitis -65.7444 0.0000* control 33.8388 0.0001* Athero+periodontitis control 99.5832 0.0000* Levene statistics=3.730, p value=0.014 Sig. *= significant at p<0.05 *=significant at p<0.05, ^=not significant at p>0.05 Table 6: Correlation between MCP-1 and periodontal parameters by each group.. MCP-1 (ng/ L) r p-value Athero. PLI 0.477 0.016 * BOP 0.215 0.302 Periodontitis PLI 0.071 0.736 BOP 0.079 0.709 PPD (mm) 0.503 0.0104* CAL (mm) 0.501 0.0107* Athero+periodontitis PLI 0.291 0.158 BOP 0.318 0.121 PPD (mm) 0.011 0.958 CAL (mm) 0.510 0.009* Control PLI 0.175 0.569 BOP -0.028 0.927 Discussion The current study showed that the mean values of PPD and CAL in athero+periodontitis group were greater than in periodontitis group with significant difference between them. These results agreed with other previous studies (17-20). This could be due to an increase in plaque and bacterial invasion with its toxin, which induces further damage of the alveolar bone tissue, sulcular and junctional epithelium, and other supporting tissue, ultimately increasing the supply of nutrients required for the multiplication of bacteria (21). In terms of increased periodontal damage when atherosclerosis is present, there are two possible explanations: either a direct effect of atherosclerosis on the immune system, resulting in the release of enzymes and pro-inflammatory cytokines such as IL-1α, IL-6, MMPs, and TNF-α, or the effect of plaque accumulation. Endothelial dysfunction has also been linked to more periodontal destruction (22). Also, the increased loss of periodontal attachment may be due to the host immune responses to the presence of pathogens leading to collagen and bone destruction by the production of cytokines from cells such as PMNs and monocytes that played an active role in inflammatory processes and were involved in numerous activities that would enhance the amount of damage. Furthermore, the existence of atherosclerosis would result in a rise in cytokine release, greater damage, and hence an increase in CAL levels (23). Results as well showed that the mean value of serum MCP-1 was higher in athero+periodontitis group than in athero group, periodontitis group and the control group with highly significant difference between them this agreed with previous findings (21). Regarding the increased level of MCP-1 with J. Bagh. Coll. Dent. Vol. 34, No. 4. 2022 Hamad and Mahmood 14 periodontitis, the possible explanation is that Pathogens such as (P. gingivalis, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans) may cause local production of MCP-1 by various cells at diseased periodontal sites, attracting circulating monocytes to the periodontal tissues, where they mature into macrophages upon exposure to various stimuli, including cytokines. Macrophages are found in large numbers in inflamed gingival tissues in periodontal disease and are considered to have a key role in pathogen killing and the production of pro-inflammatory mediators and cytokines. In addition to that, IL-1 and TNF-α, which are produced by macrophages, are known to cause bone resorption in addition to their pro-inflammatory characteristics (24). Regarding the increased level of MCP-1 with atherosclerosis, the observed increase of MCP-1 protein levels in the circulation of individuals with atherosclerosis can be attributed to at least two processes.1st , it might be a direct result of the progression of atherosclerosis. Endothelia and macrophage-like cells are the major sources of MCP-1, which are known to play a key role in the development of atherosclerosis and plaque formation. Endothelial cells can generate MCP-1 in response to low-density lipoprotein (LDL), a key atherosclerotic trigger factor, according to in vitro studies (25, 26). 2nd, elevated MCP-1 levels may reflect the progression of the inflammatory response in the heart and brain. MCP-1 and Macrophage inflammatory protein-1beta (MlP-lbeta) are two major chemokines that coordinate the infiltration of blood-derived monocytes and lymphocytes into the ischemic region, according to several research on animal models of stroke. In addition, a significant positive correlation was found with PPD and CAL. Our results were in agreement with (27-29), The possible explanation for these findings is that in periodontal disease, MCP- 1/CCL2 is thought to be the main chemoattractant for macrophages. Macrophages are abundant in inflamed gingival tissues and are hypothesized to play a key role in pathogen killing as well as the release of pro-inflammatory mediators such TNF-, IL-1, and nitric oxide (24, 30, 31). These mediators also promote the cellular immune response, which could help with periodontopathogen control. In contrast, macrophages produce inflammatory products that have been shown to promote osteoclast formation and maturation, which leads to bone resorption (31). As a result, the attraction of macrophages by MCP-1 may result in increased periodontal disease severity, a theory confirmed by data revealing that more macrophages were detected in active periodontitis sites. MCP1/CCL2 is also linked to osteoclast chemotaxis and differentiation, most likely due to its interaction with the CCR2 receptor (32, 33) Conclusion According to the findings of this study the significant positive correlations between serum level of MCP-1 and clinical periodontal parameters (PPD and CAL) in both periodontitis and athero+periodontitis group and assuming that serum MCP-1 level rise proportionally to the severity of periodontal disease, and suggesting that MCP-1 could be used as an inflammatory biomarker in periodontal disease. Conflict of interest: None. References 1. Peres MA, Macpherson LM, Weyant RJ, Daly B, Venturelli R, Mathur MR, et al. Oral diseases: Glob. Public Health. The Lancet. 2019;394(10194):249-60. J. Bagh. Coll. Dent. 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Biochem. 2006;97(3):512-8. في مرضى التهاب دواعم االسنان و مرض التصلب العصيدي 1العنوان: تقييم مستويات مصل الدم للبروتين الجاذب ألحادي الخلية مها شكري محمود , صفا علي حمد الباحثون: : المستخلص وتنظيم بدء في مهما دوًرا يلعبو والبطانية، االلتهابية لخاليا ا بواسطة عنها التعبير يتم كيميائية مادة هو 1– الخلية ألحادي الجاذب البروتين الخلفية: مرتبط وكالهما األنسجة، وإصابة لاللتهابات المؤيدة للمنبهات استجابةً أيًضا تعبيره يرتفع اللثة. اللتهاب النشطة المواقع في االحادية الخاليا وتعبئة الجيوب عمق مؤشر وقيم التسبير عند النزف ومؤشر الجرثومية الصفيحة مؤشر مثل اللثوية السريرية المعلمات قياس األهداف:.الشرايين تصلب بآفات المرتبط، لألنزيم المناعية االمتصاصية المقايسة فحص باستخدام 1– الخلية ألحادي الجاذب للبروتين المصل مستويات قياس الرابطة، االنسجة وفقدان والضبط الدراسة مجموعات في 1– الخلية ألحادي الجاذب للبروتين المصل مستويات ومقارنة الضبط، ومجموعة الدراسة مجموعات من كل في 66 إلى 36 من أعماره تراوحت وإناثًا، ذكوًرا شخصا، 88 الدراسة هذه ضمت العمل: وطرق المواد األشخاص، اللثوية. السريرية بالمعلمات وربطها 25 تضم الثانية المجموعة سليمة، لثة مع العصيدي التصلب مرض لديهم شخصا 25 تضم األولى المجموعة مجموعات: أربع إلى تقسيمهم تم عاًما، تضم الرابعة والمجموعة المرضين كال لديهم شخصا 25 تضم الثالثة المجموعة جهازية، امراض أي وبدون االسنان دواعم التهاب مرض لديهم شخصا تم السريري، التقييم وبعد .للثة الصحية الحالة لتقييم اللثوية السريرية المعلمات استخدام تم مزمن. جهازي مرض أي وبدون سليمة لثة لديهم شخصا 13 المقايسة فحص باستخدام MCP-1 الخلية ألحادي الجاذب البروتين مستوى لقياس الدم مصل وفصل مشارك كل من الوريدي لدم ا من مل 5 سحب كان التسبير عند النزف ومؤشر الجرثومية الصفيحة مؤشر قيم فإن الدراسة، هذه لنتائج وفقًا النتائج:. ELISAالمرتبط لألنزيم المناعية االمتصاصية في منها 3 المجموعة في أكبر الرابطة االنسجة وفقدان الجيوب عمق مؤشر قيم كانت المقابل. في .4و 1 المجموعة في منه 2و 3 مجموعة في أعلى يتعلق وفيما ، 4 و2 و 1 المجموعة في منه 3 المجموعة في أعلى الدم مصل في الخلية ألحادي الجاذب البروتين مستوى ان وجد كما ،2 المجموعة االنسجة وفقدان الجيوب عمق مؤشر قيم مع معنوي إيجابي ارتباط هناك كان 2 المجموعة في اللثوية. السريرية والمعلمات MCP -1 بين باالرتباطات الجاذب البروتين مستوى أن الدراسة هذه كشفت االستنتاج: الرابطة. االنسجة فقدان مؤشر مع معنوي إيجابي ارتباط هناك كان 3 المجموعة وفي الرابطة مستوى ارتفاع يرتبط قد لذلك، نتيجة والثانية. األولى المجموعة في منه ملحوظ بشكل أعلى كان الثالثة المجموعة في الدم مصل في الخلية ألحادي الشرايين. بتصلب اإلصابة خطر بزيادة االسنان دواعم بالتهاب المرتبط الخلية ألحادي الجاذب البروتين