Periodontitis as a Risk Factor in non-diabetic Patients with coronary artery disease
Introduction
Coronary artery disease (CAD) remains the principal cause of death in most countries, despite significant preventive and therapeutic advances. It has many known risk factors like, Hypertension, Hyperlipidemia, Diabetes mellitus, Positive Family history, Smoking and so on. But many
conditions increase risk of CAD yet, through atherosclerosis (1,3).
Recent studies illustrate the existence of a relation between periodontal disorders and coronary artery disease, which power the probable effect of periodontal disease as a risk factor for(CAD(4 and 5).Otherwise another were experienced insignificant relation between (CAD) and periodentitis(8-10). Periodontitis is associated with endotoxemia, leakage of lipopolysaccharides ( LPS )deriving from periodontal pathogens into circulation(4,20). LPS is one of the potent stimulators of systemic inflammation and intima wall macrophage-derived foam cell formation, and therefore it is considered a proatherogenic compound,
through the response to increasing levels of acute phase proteins (CRP) (7, 8 and 9) .
Also recent epidemiologic studies show that high CRP as a risk factor is considered for cardiovascular events (10). Also, an intervention study statement on whether the treatment of gingival inflammation (periodentitis) leads to reduced CHD mortality is not done (6).
Patients and Methods
A cohort study was done on 152 patients referring to Mazandaran Heart Center in North of Iran between 2008-2009. Inclusion criteria: Age over the 40 years who's Coronary artery disease as defined by previous or current detection of 50% stenosis of a main coronary artery by coronary angiography .Or no significant stenosis of coronary artery.
Exclusion criteria: Diabetic, Periodontal treatment and/or antibiotic therapy during the last 6 months, Pregnancy, Current alcohol or drug abuse, or psychological reasons that make study participation impractical
Drugs which are potential causal for gingival hyperplasia such as (Hydantoin, Nifedipine, Cyclosporin A, and other)
The people studied divided in two groups by coronary angiography results.. Demographic information were derived from questions asked during the interviewed to age, sex, literacy level, weight, LDL and HDL, exercise, , smoking, blood pressure for all the two groups. Then a periodontal examination was done (by general dentist and periodontitis) for all participants of the study, who was unaware from the result of patient's angiography.
Coronary artery disease defined by stenosis more than 50% lumen in at least one coronary artery in angiography .Periodontal disease is an inflammatory disease of tissues or teeth holder tissue that gradually causes the destruction of tissues and loss of teeth.
Clinical periodontal examination included measuring plaque (plaque terms), bleeding on examination with the probe (Barnett bleeding indexes), Probing packet depth at the mesial , distal, Bucal, Palatal or Lingual surface of all teeth except the third molar has been done
and CAL (Clinical Attachment Level) was calculated.
Plaques were recorded according to Silness & loe index. Plaque depth measuring, the entrance depth of probe in longitudinal axis of tooth and also CAL as mm is registered and the number of teeth remaining were recorded.
Plaque index (Silness & loe): accumulation of debries in gingival margins of tooth that is determined with the scale of 0 to 3.
0 = No plaque
1 =A film of plaque adhering to the free gingival margin and adjacent area of the tooth. The plaque may be observed in situ only after application of a disclosing solution or by using a probe on the tooth surface.
2 = moderate accumulation of soft deposits within gingival pocket, or on the tooth and gingival margin, that can be seen with the naked eye.
3 = an abundance of soft matter within the gingival pocket, on the tooth and gingival margin, in all these areas.
Modified papillary Bleeding Index (Barnett) bleeding after the probing of gums sulcus bleeding gums, diffuse marginal inflammation, and swollen red papillae is determined with the Scale of zero to 3  :
Zero: the lack of bleeding after 30 seconds
One: bleeding after 30 seconds
Two: bleeding 2 to 30 seconds
Three: bleeding less than 2 seconds
Gingival groove depth: Shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other, V shaped. Sulcus depth can be measured by a periodontal probe.Histologic depth is about 1.8mm,probing depth is2-3 mm.
Table 1 - distribution of people with coronary heart disease and without coronary heart disease according to gender
CHD
Gender
Patients With CHD (percent)
Patients Without CHD(percent)
Total
Male
37
(44.6)
46
(55.4)
83
Women
39
(56.5)
30
(43.5)
69
Illiterate or elementary
51
(67.1)
25
(32.9)
76
Guidance school
10
(43.5)
13
(56.5)
23
High School
11
(44)
14
(56)
25
Higher diploma
4
(14.3)
24
(85.7)
28
Clinical Attachment Level: The amount of space between attached periodontal tissues and a fixed point, usually the cement enamel junction.
A measurement used to assess the stability of attachment as part of a periodontal maintenance program.
Statistical significance was set at 0.05, and the unit of analysiswas the person.. Bivariate relationships were assessed by t tests or Kolmogorov-Smirnovtests for continuous variables and Cochran Mantel-Haenszel 2 statistics and odds ratios and 95% CIs for categoricalvariables.. Potential confounders were basedon the literature and our previous findings on the relationshipbetween clinical periodontal disease and CAD. (13-20).
Result
152 patients were included in this study.
There were 54.6% (83)men and the 45.4% (69) were female. The mean age for case group was 51.1+/-7.3(mean+/-SD) and 51.3+/-10.3 years for
control group. In male participants, 37 patients (44.6%) had coronary artery disease and among women 39 cases (56.5%) had CAD, which sex difference was not significant (p= 0.96) (Table 1).
The level of education and physical activity , has contrary effect on CAD and this difference was statistically significant (p <0.05). (Table 2,)
Table 6 - distribution of people with coronary heart disease and coronary heart disease based on GI.
CHD
GI
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Score 0
0
(0)
13
(100)
13
Score 1
5
(19.2)
21
(80.8)
26
Score 2
31
(55.4)
25
(44.6)
56
Score 3
40
(70.2)
17
(29.8)
57
Other risk factors comparable hypertension, hyperlipidemia, and smoking were higher significantly in CAD group than the other group one (p <0.05) (table 3,4,5).The level of physical activity in patients with CAD is significant less than other group.(table 2)
Mean BMI in patients without coronary artery disease is 25.72±2.95 and the mean BMI in people with CAD are30.29±5.34 that this relationship is statistically significant (P <0.05) .
Table 2 - Distribution of people with coronary heart disease and without coronary heart disease according to sport
CHD
Exercise
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Loss of
Physical
Activity
66
(73.3)
24
(26.7)
90
Regular exercise
1
(3)
32
(97)
33
Irregular exercise
9
(31)
20
(69)
29
Table 3 - distribution of people with coronary heart disease without coronary heart disease by smoking
CHD
Cigarettes
Patients With CHD (percent)
Patients Without CHD
(percent)
Total
Smoking
32
(80)
8
(20)
40
Non-smoking
44
(39.3)
68
(60.7)
112
Table 4 - distribution of people with coronary heart disease without coronary heart disease based on HPL
CHD
Hyperlipidemi(TC,LDL)
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
TC>250
LDL>180
34
(77.3)
10
(22.7)
44
TC<250
LDL<180
42
(38.9)
66
(61.1)
108
Table 5 - distribution of people with coronary heart disease without coronary heart disease based on history of hypertension
Heart   disease
Hypertension
Number of people
With heart disease (percent)
Number of people
Without heart disease
(percent)
Total
History of hypertension
51
(85)
9
(15)
60
Without History of hypertension
25
(27.2)
67
(72.8)
92
The gingival index( GI) average was higher in patients with CAD (70.2%) than control group(29.8%) ,as like Bleeding index(BI) and this difference is statistically significant. (P <0.05) (Table 6,7)
The relationship between Entrance depth of
probe and CAD was not statistically significant. P = 0.5 (Table 9)
Table 7 - Distribution individuals with coronary heart disease and coronary heart disease according to Index of bleeding
Heart     disease
Bleeding index
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Score 0
7
(28)
18
(72)
25
Score 1
17
(47.2)
19
(52.8)
36
Score 2
31
(59.6)
21
(40.46)
52
Score 3
21
(53.8)
18
(46.2)
39
Measurement of clinical attachment level more likely reflects periodontal disease. The statistically significant difference was found in the clinical attachment level
(p<0.005), where a higher mean value was in patients with coronary artery disease
(53.8%) compared with patients
without CAD (46.2%).(Table 10)
Table 8- Distribution of individuals with coronary heart disease without coronary heart disease based on depth of Probe entrance
Heart        disease
Entrance depth of probe
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
2 mm
8
(40)
12
(60)
20
3 mm
20
(45.5)
24
(54.5)
44
4 mm
14
(41.2)
20
(58.8)
34
5 mm
6
(54.5)
5
(45.5)
11
6 mm
9
(81.8)
2
(18.2)
11
7 mm
13
(65)
7
(35)
20
8 mm
6
(50)
6
(50)
12
Table 9 - Distribution of individuals with coronary heart disease and without coronary heart disease based on the amount of clinical adhesion.
CAL
clinical attachment
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
1 mm
0
(0)
1
(100)
1
2 mm
10
(43.5)
13
(56.5)
23
3 mm
20
(37)
34
(63)
54
4 mm
16
(61.5)
10
(38.5)
26
5 mm
15
(65.2)
8
(34.8)
23
6 mm
10
(58.8)
7
(41.2)
17
Coefficient of plaque index with entrance depth of Probe is 0.659 that is statistically significant (P <0.05)
Coefficient of plaque index with clinical adhesion rate is 0.664 that is statistically significant (p<0.05)
Coefficient of bleeding index with entrance depth of probe is 0.685 that is statistically significant (p<0.05)
Coefficient of bleeding index with clinical adhesion rate is 0.686 that is statistically significant (p<0.05)
coefficient of entrance depth of probe with clinical adhesion rate is 0.894 that is statistically significant (p<0.05) .
Conclusion
This study suggests a possible association between Periodontitis and CAD.
Since 3 main indices out of 4 indices for periodontal diseases such as swollen red papillae, bleeding gums, or diffuse marginalinflammation, correlated with increased risk of coronary artery disease in our research and most other studies, periodontal disease may be regarded as an independent risk factor for coronary artery disease.
Discussion
The present study demonstrated higher abnormal Periodontal Indices in patients with coronary artery disease than normal groups as independent risk factor.
Several theories exist to explain the link between periodontal disease and heart disease. One theory is that oral bacteria can affect the heart when they enter the blood stream, attaching to fatty plaques in the coronary arteries (heart blood vessels) and contributing to clot formation. Coronary artery disease is characterized by a thickening of the walls of the coronary arteries due to the buildup of fatty proteins. Blood clots can obstruct normal blood flow, restricting the amount of nutrients and oxygen required for the heart to function properly. This may lead to heart attacks.
Another possibility is that the inflammation caused by periodontal disease increases plaque build up, which may contribute to swelling of the arteries.
Researchers have found that people with periodontal disease are almost twice as likely to suffer from coronary artery disease as those without periodontal disease. (American Academy of periodontology,5)
The association between periodontitis and  CAD may be because of common risk factors such as smoking,diabet,male gender and socioeconomic factors ,but there is also good evidence of periodontitis being an independent risk factor for CAD.(2,15)  Furthermore, periodontal pathogens have been identified in early as well as advanced atherosclerotic lesions. (16) There is also some evidence that periodontitis is associated with increased plasma concentrations of pro-atherogenic Lipoproteins (17, 18). A study done by Buhlin K. And colleagues on the Range 143 women aged 43 to 79 years of age with CAD as a case group and 50 women 45 to 77 years old without CAD. OPG (Orthopanogram) were obtained for all patients and they were matched as viewpoints of other risk factors. The result of this study was, the women with CAD had lower oral and dental health conditions than women without CAD and there has been a significant relationship between periodontal disease and CAD. (19,20)
However multivariableanalyses indicate that periodontal status is not significantlyassociated with CHD in either ever smokers or never smokers.
Clinical signs of periodontal disease werenot associated with CAD, whereas systemic antibody responsewas associated with CAD in ever smokers and never smokers. Thesefindings indicate that the quality and quantity of the hostresponse to oral bacteria may be an exposure more relevant tosystemic atherothrombotic coronary events than clinical measures.(21)
References
[1] Wood,D MS,FRCP,FRCPE,FPHM,FESC,et al,.Established and emerging Cardiovascular risk factors. A H J ,2001 Vol; 141,Num,2, S49-S57.
[3] Wilson PW, DAgostino RB, levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories Circulation 1998 May 12; 97(18): 1837-47.
[4] Beck J, Garicia R, Heiss G,Vokonas PS,Offenbacher S. Periodontal disease and cardiovascular disease.J Periodontal .1996 Oct; 67:1123-37.
[5]Loesche WJ, Schork A, Terpenning MS,Chen YM, ,Kerr C,Dominguez BL. The relation ship between dental disease and cerebral vascular accident in elderly United States veterans. Ann Periodontal 1998Jul; 3(1):161-74.
[6] Hujoel, PP..Does chronic periodontitis cause coronary heart disease? A review of the literature. J Am Dental Assoc. 2002 Vol 133,No suppl._1, 31S- 36S.
[7] Offenbacher S.Beck JD.A Perspective on the potential cardio protective benefits of periodontal therapy. Am Heart J. 2005 Jun; 149(6): 950-4.
[8] Renvert S, Pettersson T, Ohlsson O, Persson GR. Bacterial profile and burden of periodontal infection in subjects with a diagnosis of acute coronary syndrome. J Periodontal. 2006 Jul; 77(7):1110-9
[9] Spahr A.,Klein E,Khuseyinova N,Boeckh C,Muche R,Kunze M,Rothenbacher D,Pezeshki G,Hoffmeister A,Koenig W. Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal disease (CORODONT) study. Arch Intern Med. 2006 Mar 13; 166(5): 554-9.
[10] Ridker PM, Hennekens CH, Buring JE, Rifai N. C- reactive protein and other markers of inflammation in the prediction of cardiovascular disease. N Engl J Med. 2000 Mar 23; 342(12):836-43.
[11] DeStefano F., Anda R.F., Kahn, H.S., Â Â Willamson, D.F. Russell CM .Dental disease and risk of coronary heart disease and mortality. BMJ. 1993 Mar 13; 306(6879): 688-91.
[12] Hujoel PP, Drangsholt M., Spiekerman C. DeRouen, T.A.Periodontal disease and coronary heart disease risk. JAMA. 2000 Sep 20; 284(11), 1406-10.
[13] Hujoel PP, Drangsholt M.., Spiekerman C. DeRouen, TA. Pre-existing cardiovascular disease and periodontitis: a follow-up study. Juornal of dental Research 2002 Mar; 81(3): 186-91.
[14] Wu T., Trevisan M., Genco R., Dorn J et al,.Periodontal disease and risk of cerebrovascular disease: the first national health and nutrition examination survey and its fallow up study. Arch Intern Med. 2000 Oct 9;Vol: 160 (18), 2749-55.
[15] Janket SJ., Baird AE., Chuang SK., Jones JA. Meta- analysis of periodontal disease and risk of coronary heart disease and storke. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003 May; 95(5):559-69.
[16] Madianos PN., Bobetsis GA., Kinane DF. Is Periodontitis with an increased risk of coronary heart disease and preterm and/ or low birth weight births? J Clin Periodontal 2002; 29 Suppl 3:22-36.
[17] Silness J., Loe H.. Periodental Disease in Pregnancy: II.Correlation Between Oral Hygiene and Periodontal Condition. Acta Odontol Scand 1964 Feb; 22:121-35.
[18] Brigg JE.,.Mckeown.PP, Crawtord.VL,.Woodside.JV,.Stout.RW, Evans.A, and,.Linden GJ. Angiographically confirmed coronary heart disease and periodontal disease in middle-Aged Males. J Periodontal, 2006 Jan; 77(1):95-102.
[19] Buhlin K., Gustafsson A., Ahnve S., Janszky I., Tabrizi F., Klinge B., Oral Health in Woman With Coronary Heart disease. J Periodontology 2005 Apr;Vol. 76 ,N(4),Page: 544-50.
[20] Lopez R., Oyarzun M., Naranjo C., Cumsille F., Ortiz M., Baelum V. Coronary hearth disease and periodontitis- a case control study in Chilean adults, JClin Periodontal 2002 May; 29(5): 468-73
[20] Ozlem Fentoglu ,F.Yesim ,Bozkurt,
The Bi_Directional Relationship between
Periodontal Disease and Hyperlipidemia,
Eur.J.Dent.2008 Apr;2:142-146
Coronary artery disease (CAD) remains the principal cause of death in most countries, despite significant preventive and therapeutic advances. It has many known risk factors like, Hypertension, Hyperlipidemia, Diabetes mellitus, Positive Family history, Smoking and so on. But many
conditions increase risk of CAD yet, through atherosclerosis (1,3).
Recent studies illustrate the existence of a relation between periodontal disorders and coronary artery disease, which power the probable effect of periodontal disease as a risk factor for(CAD(4 and 5).Otherwise another were experienced insignificant relation between (CAD) and periodentitis(8-10). Periodontitis is associated with endotoxemia, leakage of lipopolysaccharides ( LPS )deriving from periodontal pathogens into circulation(4,20). LPS is one of the potent stimulators of systemic inflammation and intima wall macrophage-derived foam cell formation, and therefore it is considered a proatherogenic compound,
through the response to increasing levels of acute phase proteins (CRP) (7, 8 and 9) .
Also recent epidemiologic studies show that high CRP as a risk factor is considered for cardiovascular events (10). Also, an intervention study statement on whether the treatment of gingival inflammation (periodentitis) leads to reduced CHD mortality is not done (6).
Patients and Methods
A cohort study was done on 152 patients referring to Mazandaran Heart Center in North of Iran between 2008-2009. Inclusion criteria: Age over the 40 years who's Coronary artery disease as defined by previous or current detection of 50% stenosis of a main coronary artery by coronary angiography .Or no significant stenosis of coronary artery.
Exclusion criteria: Diabetic, Periodontal treatment and/or antibiotic therapy during the last 6 months, Pregnancy, Current alcohol or drug abuse, or psychological reasons that make study participation impractical
Drugs which are potential causal for gingival hyperplasia such as (Hydantoin, Nifedipine, Cyclosporin A, and other)
The people studied divided in two groups by coronary angiography results.. Demographic information were derived from questions asked during the interviewed to age, sex, literacy level, weight, LDL and HDL, exercise, , smoking, blood pressure for all the two groups. Then a periodontal examination was done (by general dentist and periodontitis) for all participants of the study, who was unaware from the result of patient's angiography.
Coronary artery disease defined by stenosis more than 50% lumen in at least one coronary artery in angiography .Periodontal disease is an inflammatory disease of tissues or teeth holder tissue that gradually causes the destruction of tissues and loss of teeth.
Clinical periodontal examination included measuring plaque (plaque terms), bleeding on examination with the probe (Barnett bleeding indexes), Probing packet depth at the mesial , distal, Bucal, Palatal or Lingual surface of all teeth except the third molar has been done
and CAL (Clinical Attachment Level) was calculated.
Plaques were recorded according to Silness & loe index. Plaque depth measuring, the entrance depth of probe in longitudinal axis of tooth and also CAL as mm is registered and the number of teeth remaining were recorded.
Plaque index (Silness & loe): accumulation of debries in gingival margins of tooth that is determined with the scale of 0 to 3.
0 = No plaque
1 =A film of plaque adhering to the free gingival margin and adjacent area of the tooth. The plaque may be observed in situ only after application of a disclosing solution or by using a probe on the tooth surface.
2 = moderate accumulation of soft deposits within gingival pocket, or on the tooth and gingival margin, that can be seen with the naked eye.
3 = an abundance of soft matter within the gingival pocket, on the tooth and gingival margin, in all these areas.
Modified papillary Bleeding Index (Barnett) bleeding after the probing of gums sulcus bleeding gums, diffuse marginal inflammation, and swollen red papillae is determined with the Scale of zero to 3  :
Zero: the lack of bleeding after 30 seconds
One: bleeding after 30 seconds
Two: bleeding 2 to 30 seconds
Three: bleeding less than 2 seconds
Gingival groove depth: Shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other, V shaped. Sulcus depth can be measured by a periodontal probe.Histologic depth is about 1.8mm,probing depth is2-3 mm.
Table 1 - distribution of people with coronary heart disease and without coronary heart disease according to gender
CHD
Gender
Patients With CHD (percent)
Patients Without CHD(percent)
Total
Male
37
(44.6)
46
(55.4)
83
Women
39
(56.5)
30
(43.5)
69
Illiterate or elementary
51
(67.1)
25
(32.9)
76
Guidance school
10
(43.5)
13
(56.5)
23
High School
11
(44)
14
(56)
25
Higher diploma
4
(14.3)
24
(85.7)
28
Clinical Attachment Level: The amount of space between attached periodontal tissues and a fixed point, usually the cement enamel junction.
A measurement used to assess the stability of attachment as part of a periodontal maintenance program.
Statistical significance was set at 0.05, and the unit of analysiswas the person.. Bivariate relationships were assessed by t tests or Kolmogorov-Smirnovtests for continuous variables and Cochran Mantel-Haenszel 2 statistics and odds ratios and 95% CIs for categoricalvariables.. Potential confounders were basedon the literature and our previous findings on the relationshipbetween clinical periodontal disease and CAD. (13-20).
Result
152 patients were included in this study.
There were 54.6% (83)men and the 45.4% (69) were female. The mean age for case group was 51.1+/-7.3(mean+/-SD) and 51.3+/-10.3 years for
control group. In male participants, 37 patients (44.6%) had coronary artery disease and among women 39 cases (56.5%) had CAD, which sex difference was not significant (p= 0.96) (Table 1).
The level of education and physical activity , has contrary effect on CAD and this difference was statistically significant (p <0.05). (Table 2,)
Table 6 - distribution of people with coronary heart disease and coronary heart disease based on GI.
CHD
GI
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Score 0
0
(0)
13
(100)
13
Score 1
5
(19.2)
21
(80.8)
26
Score 2
31
(55.4)
25
(44.6)
56
Score 3
40
(70.2)
17
(29.8)
57
Other risk factors comparable hypertension, hyperlipidemia, and smoking were higher significantly in CAD group than the other group one (p <0.05) (table 3,4,5).The level of physical activity in patients with CAD is significant less than other group.(table 2)
Mean BMI in patients without coronary artery disease is 25.72±2.95 and the mean BMI in people with CAD are30.29±5.34 that this relationship is statistically significant (P <0.05) .
Table 2 - Distribution of people with coronary heart disease and without coronary heart disease according to sport
CHD
Exercise
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Loss of
Physical
Activity
66
(73.3)
24
(26.7)
90
Regular exercise
1
(3)
32
(97)
33
Irregular exercise
9
(31)
20
(69)
29
Table 3 - distribution of people with coronary heart disease without coronary heart disease by smoking
CHD
Cigarettes
Patients With CHD (percent)
Patients Without CHD
(percent)
Total
Smoking
32
(80)
8
(20)
40
Non-smoking
44
(39.3)
68
(60.7)
112
Table 4 - distribution of people with coronary heart disease without coronary heart disease based on HPL
CHD
Hyperlipidemi(TC,LDL)
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
TC>250
LDL>180
34
(77.3)
10
(22.7)
44
TC<250
LDL<180
42
(38.9)
66
(61.1)
108
Table 5 - distribution of people with coronary heart disease without coronary heart disease based on history of hypertension
Heart   disease
Hypertension
Number of people
With heart disease (percent)
Number of people
Without heart disease
(percent)
Total
History of hypertension
51
(85)
9
(15)
60
Without History of hypertension
25
(27.2)
67
(72.8)
92
The gingival index( GI) average was higher in patients with CAD (70.2%) than control group(29.8%) ,as like Bleeding index(BI) and this difference is statistically significant. (P <0.05) (Table 6,7)
The relationship between Entrance depth of
probe and CAD was not statistically significant. P = 0.5 (Table 9)
Table 7 - Distribution individuals with coronary heart disease and coronary heart disease according to Index of bleeding
Heart     disease
Bleeding index
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
Score 0
7
(28)
18
(72)
25
Score 1
17
(47.2)
19
(52.8)
36
Score 2
31
(59.6)
21
(40.46)
52
Score 3
21
(53.8)
18
(46.2)
39
Measurement of clinical attachment level more likely reflects periodontal disease. The statistically significant difference was found in the clinical attachment level
(p<0.005), where a higher mean value was in patients with coronary artery disease
(53.8%) compared with patients
without CAD (46.2%).(Table 10)
Table 8- Distribution of individuals with coronary heart disease without coronary heart disease based on depth of Probe entrance
Heart        disease
Entrance depth of probe
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
2 mm
8
(40)
12
(60)
20
3 mm
20
(45.5)
24
(54.5)
44
4 mm
14
(41.2)
20
(58.8)
34
5 mm
6
(54.5)
5
(45.5)
11
6 mm
9
(81.8)
2
(18.2)
11
7 mm
13
(65)
7
(35)
20
8 mm
6
(50)
6
(50)
12
Table 9 - Distribution of individuals with coronary heart disease and without coronary heart disease based on the amount of clinical adhesion.
CAL
clinical attachment
Number of people
With CHD (percent)
Number of people
Without CHD
(percent)
Total
1 mm
0
(0)
1
(100)
1
2 mm
10
(43.5)
13
(56.5)
23
3 mm
20
(37)
34
(63)
54
4 mm
16
(61.5)
10
(38.5)
26
5 mm
15
(65.2)
8
(34.8)
23
6 mm
10
(58.8)
7
(41.2)
17
Coefficient of plaque index with entrance depth of Probe is 0.659 that is statistically significant (P <0.05)
Coefficient of plaque index with clinical adhesion rate is 0.664 that is statistically significant (p<0.05)
Coefficient of bleeding index with entrance depth of probe is 0.685 that is statistically significant (p<0.05)
Coefficient of bleeding index with clinical adhesion rate is 0.686 that is statistically significant (p<0.05)
coefficient of entrance depth of probe with clinical adhesion rate is 0.894 that is statistically significant (p<0.05) .
Conclusion
This study suggests a possible association between Periodontitis and CAD.
Since 3 main indices out of 4 indices for periodontal diseases such as swollen red papillae, bleeding gums, or diffuse marginalinflammation, correlated with increased risk of coronary artery disease in our research and most other studies, periodontal disease may be regarded as an independent risk factor for coronary artery disease.
Discussion
The present study demonstrated higher abnormal Periodontal Indices in patients with coronary artery disease than normal groups as independent risk factor.
Several theories exist to explain the link between periodontal disease and heart disease. One theory is that oral bacteria can affect the heart when they enter the blood stream, attaching to fatty plaques in the coronary arteries (heart blood vessels) and contributing to clot formation. Coronary artery disease is characterized by a thickening of the walls of the coronary arteries due to the buildup of fatty proteins. Blood clots can obstruct normal blood flow, restricting the amount of nutrients and oxygen required for the heart to function properly. This may lead to heart attacks.
Another possibility is that the inflammation caused by periodontal disease increases plaque build up, which may contribute to swelling of the arteries.
Researchers have found that people with periodontal disease are almost twice as likely to suffer from coronary artery disease as those without periodontal disease. (American Academy of periodontology,5)
The association between periodontitis and  CAD may be because of common risk factors such as smoking,diabet,male gender and socioeconomic factors ,but there is also good evidence of periodontitis being an independent risk factor for CAD.(2,15)  Furthermore, periodontal pathogens have been identified in early as well as advanced atherosclerotic lesions. (16) There is also some evidence that periodontitis is associated with increased plasma concentrations of pro-atherogenic Lipoproteins (17, 18). A study done by Buhlin K. And colleagues on the Range 143 women aged 43 to 79 years of age with CAD as a case group and 50 women 45 to 77 years old without CAD. OPG (Orthopanogram) were obtained for all patients and they were matched as viewpoints of other risk factors. The result of this study was, the women with CAD had lower oral and dental health conditions than women without CAD and there has been a significant relationship between periodontal disease and CAD. (19,20)
However multivariableanalyses indicate that periodontal status is not significantlyassociated with CHD in either ever smokers or never smokers.
Clinical signs of periodontal disease werenot associated with CAD, whereas systemic antibody responsewas associated with CAD in ever smokers and never smokers. Thesefindings indicate that the quality and quantity of the hostresponse to oral bacteria may be an exposure more relevant tosystemic atherothrombotic coronary events than clinical measures.(21)
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