Relationship between periodontal disease and

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Saudi Journal of Oral Sciences ORIGINAL ARTICLE

Relationship between periodontal disease and carotid atheromatous plaque: A clinico-ultrasound study Surekha Ramrao Rathod, Farooque Khan, Trup Sa sh Sarda, Anubha Raj1 Departments of Periodontology and 1Periodon cs, VSPM Dental College and Research Ins tute, Nagpur, Maharashtra, India

Abstract

Aim: The aim of this study was to determine the rela onship between Caro d atheromatous plaque in caro d artery with periodontal health and disease clinically and ultrasonographically and secondarily whether these rela ons are dependent on the level of serum high-density lipoprotein (HDL) cholesterol. Materials and Methods: The cross-sec onal study was carried out on 60 subjects. Of which 30 subjects with chronic periodon s and 30 subjects with healthy periodon um were recruited and they underwent ultrasound scanning of common caro d arteries to determine caro d plaque thickness. Clinical parameters measured were probing pocket depth, clinical a achment loss, plaque index, gingival index and biochemical parameters included total cholesterol, triglycerides, and HDL levels. Results: Periodontal disease is posi vely associated with caro d atherosclerosis. Plaque thickness and prevalence of caro d atheromatous plaque were significantly higher in the test group as compared to the control group. In the test group the mean caro d atheromatous plaque thickness was found to be 2.18 mm whereas in the control group it was found to be 0.14 mm. In test group, there was a posi ve and highly significant correla on of probing depth (PD) with triglycerides and total cholesterol levels and caro d atheromatous plaque thickness but a nega ve correla on between PD and HDL, triglycerides and total serum cholesterol levels in healthy subjects. HDL was significantly less in test group when compared with a control group with a P = 0.004. Conclusion: An inter-rela onship between periodontal disease and the presence of atheromatous plaque exists. The prevalence of both periodon s and atherosclerosis is very high. Periodon s should be diagnosed and treated at its earliest and hence that clinician and public health prac oner can control the epidemic of cardiovascular diseases and reduce mortality. Key words: Caro d Doppler, caro d atheromatous plaque, cardiovascular diseases, periodon

s

Introduc on

connec ve ssue as well as in the loss of suppor ve alveolar bone.[1]

Periodontal disease is a mul factorial infec ous disease influenced by several risk factors such as genetic, environmental and host immune system. Although microorganisms are implicated as the e ologic agent responsible for the inflammatory lesion, the products of inflamma on play an important role in the loss of

Chronic infec ons have been reported as one of the risk factors for coronary heart disease such as ischemic stroke and the major contribu ng factor in the majority of cases of cardiovascular disease, and cerebrovascular disease is atherosclerosis.[2] One of the outcomes of this disease process is the narrowing of the arteries resulting from the subendothelial deposi on of cholesterol, cholesterol esters and calcium within the vessel walls. Rupture of the

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Address for correspondence: Dr. Surekha Ramrao Rathod, A-20, Mahalgi Nagar, Ring Road, Nagpur, Maharashtra, India. E-mail: [email protected]

DOI: 10.4103/1658-6816.160760

S J Oral Sci Vol 2 No 2

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Jul-Dec 2015


Rathod, et al.: Periodontitis and carotid atheromatous plaque

atherosclero c plaque yield thrombi that travel distally to occlude arteries, resul ng in myocardial infarc on and stroke.[3]

medical condi on apart from periodon s, any type of cardiovascular disease, smokers and pregnant women. The study was conducted in a joint collabora on with the Department of Periodon cs, Department of General Radiology, and Department of Biochemistry.

High Density Lipoprotein (HDL) have several antiatherogenic properties, such as an ability to promote the efflux of cholesterol from cells to func on as an important an oxidant by inhibi ng Low-Density lipoprotein (LDL) oxida on to prevent or interrupt foam cell forma on and to retard inflammatory ac vity, for instance these proper es may prevent harmful effects of infec ons and conversely infec ons may have a more detrimental effect in the absence of func oning HDL. Therefore considering the possible biologic mechanism by which chronic bacterial infections increase the risk of atherosclerosis, the role of -HDL appears to be par cularly interes ng.[4]

Determining the presence and thickness of carotid plaque in common caro d artery: The ultrasonographic assessment of carotid arteries was done according to the method described in Atherosclerosis Risk In Communities study.[1,5] A duplex ultrasound system with 7.5 MHz linear array transducer was used to scan the arteries. The machine used to scan the arteries was Mylab 50 Esoate. The caro d arteries were visualized with transverse and longitudinal scans to check the presence of significant focal atheroma which is defined as a localized protrusion within the vascular lumen. The presence or absence of atherosclero c plaque and the caro d atheromatous plaque thickness was evaluated in the caro d arteries using Caro d Doppler Ultrasound in both the groups [Figure 1]. The inves ga ons were done by a single, trained and experienced inves gator who was blinded about the periodontal status.

The aim of the present study was to determine the relationship between atheromatous plaque in the carotid artery with periodontal health and disease clinically and ultrasonographically and secondarily whether these rela ons are dependent on the level of HDL cholesterol. The objec ves of the study were to evaluate the presence of caro d atheromatous plaque in healthy and periodontally diseased subjects and to correlate and compare caro d atheromatous plaque and HDL, total serum cholesterol and triglycerides levels in periodontal health and disease.

Analysis of Systemic condi ons: Overall adiposity was es mated by a body mass index which was calculated by the formula weight in kilograms divided by height in meters squared. Par cipants were asked to fast before coming to the clinical visit and fas ng venous blood samples were taken by venipunture in the antecubital fossa in a tube. From these tubes, serum was prepared and was stored at −20°C until all samples from all par cipants were collected.

Materials and Methods A randomized cross-sectional observational study was carried out consis ng of 60 subjects, ≥38 years of age, repor ng to the Department of Periodon cs and Implantology (from October 2013 to September 2014). The inclusion criterion was chosen to ensure the adult onset of periodon s in the pa ent group and along with it the disease may have had me to affect the process of atherosclerosis. The test group included 30 subjects who were referred to the department of Periodontology and were diagnosed with moderate to severe periodon s. In the control group the 30 subjects were recruited from the pa ents coming to the hospital for regular dental check-ups or for the restorative dental procedure. Thus, pa ents in the control group had healthy periodon um. The purpose of this study was explained verbally as well as wri en informa on was provided to all the study participants. Written ethical clearance was obtained from ins tu onal ethics commi ee. On the basis of extensive medical history by interview, the following subjects were considered for exclusion: Individuals with any given disease or chronic


Measurement of biochemical parameters: Levels of total serum cholesterol, HDL and triglycerides were determined in the aliquots of plasma that were stored

Figure 1: Caro d atheromatous plaque thickness calculated using caro d doppler ultrasound scan

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Rathod, et al.: Periodontitis and carotid atheromatous plaque

nega ve correla on between PD and HDL, triglycerides and total serum cholesterol levels in healthy subjects. The mean levels of HDL, triglycerides and total cholesterol levels in the test group were 30.69, 206.9 and 191.6 respec vely whereas in the control group the mean values were 31.47, 139.5 and 171.2 respec vely. Body mass index was also calculated in both the groups and the mean values for the test group, and the control group were 25.46 Kg/m2 and 20.44 Kg/m2 respec vely. HDL, which is protec ve cholesterol, was significantly less in periodon s group when compared with healthy subjects (control group) with a P = 0.004 [Table 1].

at −20°C. Plasma levels of HDL and total cholesterol were measured with standard enzyma c assays. All the above measurements were made blinded with respect to periodontal status. Measurement of clinical parameters: The clinical parameters that were recorded in subjects of both the groups at the me of study included Plaque index (PI) (Tureskey and Gilmore), (1970)[6] Gingival index (GI) (Loe and Silness, 1963),[7] Probing depth (PD) and Clinical a achment level (CAL). Parameters were recorded using Williams Graduated probe. Sta s cal analysis

Discussion

It was performed using EPI info so ware version 7. Pearson’s correla on coefficient test was performed to find out correla on between parameters and student t-test was used to check the level of significance (α = 0.05)

Connective tissue breakdown or degradation is the hallmark of both cardiovascular and periodontal diseases. The primary enzymes leading to collagen breakdown are matrix metalloproteinases. These enzymes degrade the fibrous cap in atherosclerosis, leading to myocardial infarction. [8] Similarly, in periodon s, these enzymes degrade the connec ve ssue which results in tooth loss.[9] Thus there exists parallelism between periodontal ssue destruc on and cardiovascular disease, both mediated and/or regulated by a similar pathway, in this case one associated with MMPs. Matsumura, et al., 2005 had concluded from his study that there is increasing evidence that inhibi on of MMPs, already shown to be effec ve for inhibi on of periodontal a achment loss, can also inhibit the development of cardiac failure.[10] Literature has shown that systemic and/or local infec ons may lead to the

Results The study was carried out on a total of 60 subjects (37 males and 23 females). The test group consisted of 30 systemically healthy individuals showing a mean age of 43.4 years affected by severe periodon s. The control group consisted of 30 systemically healthy subjects showing a mean age of 44 years. There was no significant difference in mean age of both the groups. Pa ents in the test group showed a mean probing pocket depth (PPD) of 4.769 mm and those in the control group showed a mean PPD of 1.305 mm. There was a sta s cally significant difference with respect to PPD when compared between the two groups. The mean CAL for the test group was 5.86 mm and for the control group mean CAL was 0 mm. The mean GI and PI in the test group were 1.86 and 2.77 respec vely whereas in the control group, it was 0 and 2.42 respec vely.

Table 1: Descrip ve sta s cs and details of clinical and biochemical parameters for the control group (group I) and the test group (group II) Parameter PPD*

In the present study, we found that, periodontal disease is posi vely associated with caro d atherosclerosis. Plaque thickness and prevalence of plaque were significantly higher in the test group as compared to the control group. In the test group, the mean plaque thickness was found to be 2.18 mm, whereas in the control group it was found to be 0.14 mm. Thus in chronic periodon s subjects, we found a posi ve correla on between periodontal disease status and caro d artery plaque thickness sugges ng that periodontal disease has an associa on with atheroma forma on. In chronic periodon s subjects (test group) we found a posi ve and highly significant correla on of PD with triglycerides and total cholesterol levels and plaque thickness but a


CAL† GI‡ PI§ PT$ HDL# Cholesterol Triglyceride

Group

n

Mean

SD

t

P

1 2 1 2 1 2 1 2 1 2 1 2 1 2 1 2

30 30 30 30 30 30 30 30 30 30 30 30 30 30 30 30

1.3050 6.62±0.28 0.00 5.86 0.00 1.86 2.422 2.770 0.14 2.18 31.47 30.69 171.217 191.600 139.517 206.987

0.30911 1.01332 0.00 0.9 0.000 0.384 0.3821 1.0131 0.785 3.462 0.960 1.080 7.0745 18.7019 17.9604 27.7053

−17.91