Periodontal disease is characterized by progressive periodontal pathogens. It is known that coronary heart disease is

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1 ISSN: X CODEN: IJPTFI Available Online through Research Article PREVALENCE OF PERIODONTAL DISEASES IN PATIENTS WITH CORONARY HEART DISEASE Niha Naveed* BDS student, Saveetha Dental College and Hospitals, Chennai. Received on: Accepted on: Abstract: Periodontal disease is characterized by progressive periodontal pathogens. It is known that coronary heart disease is the leading cause for morbidity and mortality throughout the world. A case control study was performed to demonstrate the association between periodontal disease and coronary artery disease. The study was conducted on 200 subjects, 100 individuals with verified CHD from Department of Cardiology, Saveetha Medical College; Department of Cardiology, Government General Hospital, Chennai; and private practitioners clinics and 100 individuals with no past history of cardiac problems as the control group. Factors such as gender, probing depth, clinical attachment loss and number of periodontally affected teeth were taken into consideration for reaching the conclusion. The present study showed a positive association between periodontal disease and CHD in agreement with previous studies. Keywords: Periodontal problems, CHD, probing depth, clinical attachment loss. Introduction: An association between oral infection and systemic diseases has always been an area of interest for researchers for many centuries. The effect of oral health on the rest of body was proposed by Assyrians as early as the 7th century B.C (1). The focal infection theory, given by William Hunter in 1911, was discarded due to lack of scientific evidence (2).Coronary artery disease is a leading cause ofadult mortality and morbidity throughout theworld. The development of coronary artery diseasecan result from genetic and several environmental risk factors such as age, abnormal serum lipids, diabetes, smoking and hypertension (3). These well known risk factors independently or combined are involved in both atherosclerosis and myocardial infarction. Recent studies have shown that viral and bacterial infections may also contribute to acute thromboembolic events in susceptible people (4). Periodontal disease is an encompassing term relating to thedestructive inflammatory disorders of the hard IJPT June-2017 Vol. 9 Issue No Page 29841

2 and soft tissuessurrounding teeth. Periodontaldiseases are a group of inflammatorydiseases in which bacteria and their byproducts on endothelial cells are the principle etiologic agents. There is growing evidence that poor dental health, especially the presence of periodontal disease increases the risk of occurrence of coronary heart disease.long term plaque accumulation induces chronicinflammation of the periodontal tissues, which may lead to destructionof the attachment of the periodontal ligament and bone. This could occur via the host s immuno-inflammatory mediators that are elicited in response to bacteria, bacterial toxins or localized tissue response. These locally produced inflammatory mediators enterthe systemic circulation along with micro-organisms and this immuno-inflammatory response of periodontal tissues and systemic vascular response can offer an explanation for shift in causality anddirectionality of oral and systemic diseases (5)-(7). Materials and Methods: Inclusion Criteria: Patient Selection: 200 patients, 100 with CHD (61 male, 39 female) of age group 51±11 years and 100 without CHD (62 male, 38 female) of age group 47±8 years were included in the study. Case Selection: The cases selected in the CHD group were patients with verified CHD from the Department of Cardiology, Saveetha Medical College; Department of Cardiology, Government General Hospital, Chennai; and known sources. Selection: The cases in non-chd or control group were patients without any past history of cardiac problems. Exclusion Criteria: Edentulous patients, patients with chronic inflammatory disease, HIV, a history of organ transplant, or any cancer treatment 6 months before examination were excluded from the study. Medical History: Patients from both groups were interviewed about their medical status andcommon habits. Data on hypertension, diabetes andsmoking status were recorded. Measurement of Periodontal Status: Clinical examinations were performed using a Williams-type periodontal probe No. 23 to determine probing depth (Distance between the gingival margin and base of the pocket) in millimetre and level of clinical attachment loss (Distance between the cemento-enamel junction and base of the pocket) in millimeter. Probing depth was checked for 6 sites per tooth (mesiobuccal, direct buccal, distobuccal, mesiolingual/palatal, direct lingual/palatal, and distolingual/palatal).the number of missing teeth were also recorded. IJPT June-2017 Vol. 9 Issue No Page 29842

3 Statistical Analysis: The data was tabulated and subjected to statistical analysis by SPSS version 22.0using the independent sample t-test to compare the variables between the two groups and within each group among genders separately. The proportion of risk factors present in individuals of both groups were calculated in percentage. Results: The CHD group showed significantly higher probing depth, clinical loss of attachment and percentage of periodontally affected teeth (TABLE 1). The males were found to have higher probing depth and clinical attachment loss than females in CHD group (TABLES 2&3). But the females had higher percentage of periodontally affected teeth than males in the CHD group (TABLES 2&3). In the control group, the males have higher probing depth, clinical loss of attachment and percentage of periodontally affected teeth than females. From this,we know that males are more at risk than females. It was also found that CHD group had poorer oral hygiene. Oral Candidiasis was severe in the CHD group individuals compared to thecontrol group (TABLE 4). TABLE 5 shows the proportion of major risk factors in both the groups. Table 1: Independent sample t-test to compare the mean values between s. Variable N Mean Std. Dev t-value P-Value Age (years) CHD Mean PD CHD Mean CAL CHD <1 Percentage of PDL affected teeth CHD Table 2: Independent sample t-test to compare the mean values between genders in CHD and s separately. Variable Gender N Mean Std. Dev t-value P-Value CHD Age (years) Female IJPT June-2017 Vol. 9 Issue No Page 29843

4 Mean PD Female Mean CAL Female Percentage of PDL affected teeth Female Age (years) Female Mean PD Female Mean CAL Female Percentage of PDL affected teeth Female Table 3: Independent sample t-test to compare the mean values between s among s and Females separately. Gender Variable group N Mean Std. Dev t-value P-Value Age (years) CHD Mean PD CHD Mean CAL CHD Percentage of PDL affected teeth CHD Female Age (years) CHD IJPT June-2017 Vol. 9 Issue No Page 29844

5 Mean PD CHD Mean CAL CHD Percentage of PDL affected teeth CHD Table 4: Patients with Oral candidiasis in both groups. N No. of patients with severe Oral Candidiasis CHD Table 5: Percentage of patients with other risk factors. Risk factors CHD % of hypertensives % of smokers % of diabetics Chart 1: Mean Age of Both s Mean Age (years) IJPT June-2017 Vol. 9 Issue No Page 29845

6 Chart 2: Mean PD Mean PD Chart 3: Mean Cal Mean CAL Chart 4: Mean % of PDL affected teeth. Mean Percentage of PDL affected teeth IJPT June-2017 Vol. 9 Issue No Page 29846

7 Chart 5: Mean age (years) Fe Chart 6: Mean PD Fe Chart 7: Mean CAL Fe IJPT June-2017 Vol. 9 Issue No Page 29847

8 Chart 8: 10 8 Mean Percentage of PDL affected teeth Fe Chart 9: Mean Age (years) Female Co Gender Chart 10: 5.00 Mean PD Female Co Gender IJPT June-2017 Vol. 9 Issue No Page 29848

9 CHART 11: Mean CAL Female Co Gender Chart 12: Mean Percentage of PDL affected teeth Female Gender Discussion: Periodontitis, although not a cause of mortality, is also a major public health concern because of its high prevalence in the population and its negative impact on oral health, ability to chew, appearance, quality of life, dental care costs and tooth loss. In addition, as a progressive, chronic inflammatory disease, untreated periodontitis has the potential to undermine overall health and even exacerbate other inflammatory conditions, such as CHD (8). Periodontitis has been shown to increase the risk of a CHD independent of other known cardiovascular risk factors. The size of the increase in risk varies according to the age and gender (9). In my study, I found that males are more at risk than females. This may be due to the influence of hormone oestrogen in females. Although some risk factors, such as smoking and diabetes, are known to play a role in the development of both periodontitis and CHD, their presence IJPT June-2017 Vol. 9 Issue No Page 29849

10 does not fully explain the observed link between periodontitis and the increased cardiovascular risk. Moreover, additional risk due to periodontitis was shown in people who had never smoked and was also apparent in studies that controlled for diabetes status (10). It is possible, however, that there are as yet unknown genetic factors that may influence both of these inflammatory diseases and may therefore explain the association found in clinical studies (11). At the moment, there is not enough evidence to show whether periodontitis could increase the probability of a second CHD event in patients with established CHD who have previously suffered an event. The most likely explanation for how periodontitis affects CHD is that periodontal bacteria and their products (e.g. endotoxin) from periodontal pockets enter the circulation and provoke an acute-phase and subsequent inflammatory response. Mediators produced as part of this host response then promote the development, maturation and instability of fatty lesions (atheroma) in the arteries, increasing the risk of an CHD adverse event. Research shows that the likelihood of periodontal bacteria entering the bloodstream (bacteraemia) after chewing, brushing, flossing or scaling depends upon the patient s periodontal health(12)-(14). Bacteraemia is more common, and involves a wider range of bacteria (including periodontal pathogens), in patients with periodontitis, compared with patients who have gingivitis or healthy mouths. Another possible mechanism by which periodontitis might contribute to CHD risk is that antibodies produced in response to plaque bacteria may promote the development of atheroma by cross- reacting with the cells lining the arteries (endothelial cells) and with blood lipids(11)(13)(14). Studies have demonstrated that periodontal treatment reduces the overall level of inflammation within the circulation. Specifically, periodontal therapy had favourable effects on two key factors known to be important in CHD risk: levels of a pro-inflammatory acute-phase protein agent called C-reactive protein (CRP); and measures of endothelial cell function(13)-(16). Conclusion: In the present study we observed a positive association between periodontal disease & CHD. References: 1. Case Study To Assess Association Between Periodontal Infection And Coronary Heart Disease Jyoti Mohitey1*, Rahul Redasani1 JKIMSU, Vol. 1, No. 2, July-Dec ISSN Periodontal Disease and Coronary Heart Disease,Balwant Rai et al., JK science, Vol. 11 No. 4, Oct-December Coronary Artery Disease and Periodontitis: A Prospective Study. Sumit Malhotra et al. JIMSA April - June 2013 Vol. 26 No Asikainen SE. Periodontal bacteria and cardiovascular problems. Future Microbiol 2009 ;4: IJPT June-2017 Vol. 9 Issue No Page 29850

11 5. Renvert S, Lindahl C, Roos-Jansåker AM, Lessem J. Shortterm effects of an anti inflammatory treatment on clinical parameters and serum levels of C-reactive protein and proinflammatory cytokines in subjects with periodontitis. J Periodontol 2009;80(6): Mattilka K. Does periodontitis cause heart disease? Eur Heart J 2003; 24: Beck JD, Offenbacher S, Williams R, Gibbs P, Garcia R. Periodontitis : a risk factor for coronary heart disease? Ann Periodontol 1998; 3: Slavkin HC. Does the mouth put the heart at risk? J Am Dent Assoc 1999; 130(1): Grossi SG. Dental plaque attack: The connection between periodontal disease, heart disease and diabetes mellitus. Compend Contin Educ Dent 2001; 22(1): Ross R. Atherosclerosis: An inflammatory disease. N Engl JMed. 1999; 340(2): Rohde LEP, Hennekens CH, Ridker PM. Survey of C-reactive protein and cardiovascular risk factors in apparently healthy men. Am J Cardiol. 1999; 84: Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes. [Part I] New Engl J Med1992; 326: Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronaryartery disease and the acute coronary syndromes.[part II] New Engl J Med1992; 326: Hegele RA. The pathogenesis of atherosclerosis. Clin Chim Acta 1996; 246: Kinane DF, Lindhe J. Pathogenesis of periodontitis. In: Lindhe J, Karring T, Lang NP, Eds. Clinical Periodontology and Implant Dentistry, 3rd ed. Copenhagen: Munksgaard, 1997, Cochran D. Periodontology in the age of inflammation: a changing landscape. J Am Coll Dent 2009 ;76(1): IJPT June-2017 Vol. 9 Issue No Page 29851