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Assessment of serum levels of triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol in periodontitis patients.
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PMID:  23633769     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND OBJECTIVES: Periodontal disease is a destructive inflammatory disease inducing profound changes in the plasma concentrations of cytokines leading to a catabolic state characterized by altered lipid metabolism and hypertriglyceridemia. The main objective of the present study was to evaluate the effect of periodontal infection on serum levels of triglycerides (TGL), total cholesterol (TC), high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol.
MATERIALS AND METHODS: A sample of 90 subjects; 30 periodontally healthy individuals, 30 chronic gingivitis cases (n=30), and 30 chronic periodontitis cases (n=30) with an age range of 25 to 65 years were included in the study. Periodontal parameters including Plaque Index, Gingival Index, Probing Depth, and Clinical Attachment Level were recorded. Venous blood samples were obtained after 12 hours fasting period from antecubital vein and serum levels of TGL, TC, HDL, and LDL cholesterol were measured.
RESULTS: The levels of TGL, TC, and LDL cholesterol were significantly higher for periodontitis group (P<0.05) as compared to gingivitis and periodontally healthy groups. HDL cholesterol levels were significantly lower in periodontitis group (P<0.05) as compared to periodontally healthy and gingivitis groups.
CONCLUSION: The results of the present study indicate that periodontal infection has a definite role in altering lipid metabolism leading to hyperlipidemia. However, further studies are required to clarify the relationship between periodontitis and serum lipid levels and to determine whether oral healthcare has the potential to reduce serum lipid levels in otherwise systemically healthy individuals.
Authors:
Swati Penumarthy; Gautami S Penmetsa; Satheesh Mannem
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of Indian Society of Periodontology     Volume:  17     ISSN:  0972-124X     ISO Abbreviation:  J Indian Soc Periodontol     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-05-01     Completed Date:  2013-05-02     Revised Date:  2013-05-03    
Medline Journal Info:
Nlm Unique ID:  101499342     Medline TA:  J Indian Soc Periodontol     Country:  India    
Other Details:
Languages:  eng     Pagination:  30-5     Citation Subset:  -    
Affiliation:
Department of Periodontics, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India.
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Journal Information
Journal ID (nlm-ta): J Indian Soc Periodontol
Journal ID (iso-abbrev): J Indian Soc Periodontol
Journal ID (publisher-id): JISP
ISSN: 0972-124X
ISSN: 0975-1580
Publisher: Medknow Publications & Media Pvt Ltd, India
Article Information
Copyright: © Journal of Indian Society of Periodontology
open-access:
Received Day: 03 Month: 7 Year: 2011
Accepted Day: 02 Month: 11 Year: 2012
Print publication date: Season: Jan-Feb Year: 2013
Volume: 17 Issue: 1
First Page: 30 Last Page: 35
PubMed Id: 23633769
ID: 3636940
Publisher Id: JISP-17-30
DOI: 10.4103/0972-124X.107471

Assessment of serum levels of triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol in periodontitis patients
Swati Penumarthyaff1
Gautami S. Penmetsaaff1
Satheesh Mannemaff1
Department of Periodontics, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India
Correspondence: Address for correspondence: Dr. Satheesh Mannem, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India. E-mail: satheeshmannem@gmail.com

INTRODUCTION

Chronic inflammatory periodontal disease represents a primarily anaerobic Gram-negative oral infection that leads to gingival inflammation, destruction of periodontal tissues, loss of alveolar bone, and eventual exfoliation of teeth in severe cases.[1, 2]

Several studies have indicated that subjects with periodontal disease may have a higher risk for cardiovascular disease.[36] Thus, one can speculate that periodontal disease as a chronic infection may be related to cardiovascular disease through infection-related mediators, hyperactivity of white blood cells, and altered lipid metabolism leading to hyperlipidemia. Chronic local and acute systemic infections have been demonstrated to induce profound changes in the plasma concentrations of cytokines leading to a catabolic state characterized by altered lipid metabolism. The main features of this altered metabolism are hypertriglyceridemia and lipid oxidation.[7]

Hyperlipidemia is a condition where there is an elevation of the serum levels of total cholesterol (TC) and triglycerides (TGL) due to the lipid metabolism alteration, with an increase in the liver lipogenesis and lipolysis in the adipocytes.[8] TGL are the glycerol esterified at each of its three hydroxyl groups by a fatty acid and are most abundant lipids comprising 85-90% of body lipids. Cholesterol is the most abundant steroid in animal tissues, especially food rich in animal fats; circulates in the plasma complexed to proteins of various densities and plays an important role in the pathogenesis of atheroma formation in the arteries; a precursor of steroid hormones. Low-density lipoprotein (LDL) is the compound containing both lipid and protein, which transport cholesterol to tissues other than the liver. High-density lipoprotein (HDL) is the compound containing both lipid and protein, which transport cholesterol to the liver for excretion in the bile.[9]

There have been several proinflammatory cytokines implicated in the immunopathology of periodontitis; however, some of the most convincing evidence for destruction of periodontium involves IL-1β and TNF-α. These cytokines are significantly elevated in diseased periodontal ligament sites demonstrating inflammation and during periods of active tissue destruction.[10]

Conversely, systemic exposure to infectious challenges such as bacterial lipopolysaccharide can alter fat metabolism and promote hyperlipidemia.[7, 10]

Various studies have shown that P. gingivalis can invade deep connective tissues/vascular endothelium associated with the periodontium, can be found within vascular pathological plaques, and can elicit circulating antibody response.[11] This suggests that even in a localized oral infection, such as periodontitis, the potential exists for chronic low-level systemic exposure to microorganisms/LPS leading to generalized alterations in lipid metabolism.

Thus, it has been stated that a relationship exists between chronic periodontitis and hyperlipidemia that involves the inflammatory response to LPS from periodontal pathogens such as Porphyromonas gingivalis.[7]

Hence, an attempt was made to evaluate the linkage between periodontal disease and changes in serum lipid parameters.


MATERIALS AND METHODS
Study design

A Sample of 90 subjects (30 periodontally healthy subjects [n=30], 30 chronic gingivitis cases [n=30], and 30 chronic periodontitis cases [n=30]) were selected from patients attending Department of Periodontics, Vishnu Dental College, Bhimavaram. Prior ethical committee approval was obtained before commencement of the study.

Inclusion criteria

Patients aging between 25 to 65 of years and having ≥10 teeth were included in the study.

Exclusion criteria

Patients with systemic diseases, history of drug treatment for hyperlipidemia, pregnant women, alcoholics, and smokers were excluded from the study.

Methodology

Patient's detailed case history was recorded which included general information of the patient, medical history, drug history, history of smoking and alcoholism. Anthropometric measurements such as height in meters and weight in kilograms were recorded. Body mass index was calculated using the formula BMI = Weight/(Height)2. Plaque Index (Silness and Loe 1964)[12] and Gingival Index (Loe and Silness 1963)[13] were recorded. Probing Depth (PD) and Clinical Attachment Level (CAL) were measured by using by using UNC–15 periodontal probe.

Even though patients aging between 25 to 65 of years and having ≥10 teeth were included in the study, These patients were divided into 3 groups, i.e., healthy group, gingivitis group, and periodontitis group. Individuals with a gingival index score of 0 were considered as periodontally healthy and individuals with gingival index score of more than 1 without periodontal pockets were considered as chronic gingivitis patients. All periodontitis patients had pocket depth of ≥ 6 mm involving more than 30% of sites or clinical attachment loss of 3 to 4 mm and radiographic evidence of bone loss.

PD and CAL measurements were recorded at six sites (mesiobuccal, mid buccal, distobuccal, mesiolingual/palatal, midlingual/palatal, distolingual/palatal) by using UNC-15 periodontal probe.

Metabolic parameters

Enzymatic analysis of cholesterol levels and TGL was done using enzymes manufactured by Ensure Biotechprivate limited™ and ELICO UV-Vis™ spectrophotometer SL 159 version 6.1.

Venous blood samples were obtained after 12 hours fasting period from antecubital vein. TC and HDL cholesterol levels were determined by Trinder CHOD/POD End Point method under the principle of enzymatic determination of TC using the following reactions: Cholesterol ester is converted into cholesterol and fatty acids in the presence of cholesterol esterase. Cholesterol is oxidized in the presence of cholesterol oxidase to produce hydrogen peroxide. Hydrogen peroxide reacts with Phenol and 4-Aminoantipyrin in the presence of peroxidases to give Quinone and water molecule to produce red color. The optical density is read at 500 nm against blank.

TGL were determined by GPO/POD method. TGL are hydrolyzed by lipase to glycerol and free fatty acids. Glycerol is phosphorylated by ATP in the presence of glycerol kinase to Glycerol-3-phosphate which is oxidized by the enzyme Glycerol-3-phosphate oxidase producing hydrogen peroxide. Hydrogen peroxide so formed reacts with 4-Aminoantipyrine and 4-Chlorophenol in the presence of enzyme peroxidases to produce red Quinoneimine. The intensity of color developed is proportional to the TGL concentration.

LDL cholesterol was assessed according to the formula by Friedewald et al. in 1972, in which LDL = TC – (HDL + TG/5).

Cutoff points were taken as follows: For TGL, ≥150 mg/dl; TC, ≥200 mg/dl; HDL-cholesterol, ≤60 mg/dl; and LDL–cholesterol, ≥130 mg/dl.[14, 15]


RESULTS

This study included 90 subjects (47 male and 43 female subjects) with age group ranging from 25 to 65 years who satisfied the selection criteria. The selected subjects were explained about the study and an informed consent was obtained. The demographic data, periodontal parameters, and serum lipid profile were obtained. The obtained data were statistically analyzed using Microsoft Excel and Statistical software (SPSS version 16). For all these tests, a P value of 0.05 or less was set for statistical significance (S). Kruskal-Wallis ANOVA test was done for multiple group comparisons. The Mann Whitney U test was done to compare between two groups. Unpaired T test was done to compare lipid parameters between male and female subjects. Pearson correlation coefficient (r) was used to describe correlations between age, BMI, lipid parameters, and periodontal parameters.

Significant differences were found when comparison of Age (P=0.0), BMI (P=0.01), TGL (P=0.001), TC (P=0.005), LDL (P=0.001), and HDL (P=0.0) were done between 3 groups as shown in Table 1 and Figures 16.

Significant difference were found when comparison of Age (P=0.001), BMI (P=0.016), TGL (P=0.02), and HDL (P=0.004) were done between group I and II. When compared between Group I and III, significant differences were found with Age (P=0.0), BMI (P=0.005), TGL (P=0.001), TC (P=0.003), LDL (P=0.001), and HDL (P=0.00). When compared between Group II and III, significant differences were found with Age (P=0.0), TC (P=0.019), LDL (P=0.003), and HDL (P=0.00) as shown in Table 2.

When comparison of lipid parameters between males and females within group I, group II, and group III was done, none of the parameters are significant, as shown in Table 3.

When comparison of lipid parameters between age, gender, and BMI within group I, group II, and group III was done, none of the parameters are significant, as shown in Table 4.

When comparison of lipid parameters between GI and PI within group I, group II, and group III was done, none of the parameters are significant. Probing Pocket Depth (P=0.01) and CAL (P=0.004) were significant within group 3 only, as shown in Table 5.


DISCUSSION

Over many years, the prevailing view was that periodontal infections were localized only to the periodontium and rarely had systemic implications in healthy individuals. More recent evidence, however, has shown that periodontitis induces increased systemic inflammation, as indicated by raised serum levels of various inflammatory markers leading to development of variable systemic complications such as cardiovascular disease, cerebrovascular disease, respiratory diseases, pregnancy complications, altered glycemic control, and renal disease.[16]

A significant association between periodontitis and cholesterol has been reported.[7, 10] Hence, this study was designed for better understanding the association between periodontal disease and serum lipid levels.

Ninety subjects with age range between 25 to 65 years having ≥10 natural teeth were included. Age matching could not be done as most of the periodontitis patients were of higher age group.

The mean BMI for all the three study groups was <25. This suggests that the subjects were in normal weight range.[17] Thus, the potential effect of obesity on lipid profile levels was eliminated.

Highest mean values of TGL, TC, and LDL were observed for periodontitis group and least mean values were observed for periodontally healthy group. On the other hand, HDL value was highest in the periodontally healthy group and least for periodontitis group after eliminating potential confounders. This elevated lipid parameters in periodontitis group is mainly due to the elevated proinflammatory cytokines produced by chronic periodontitis.

Periodontal infection induces the APR leading to multiple alterations in lipid and lipoprotein metabolism. Plasma TGL levels increase from increased VLDL secretion as a result of adipose tissue lipolysis, increased de novo hepatic fatty acid synthesis, and suppression of fatty acid oxidation. Hypercholesterolemia occurs attributable to increased hepatic cholesterol synthesis and decreased LDL clearance, conversion of cholesterol to bile acids, and secretion of cholesterol into the bile.[18]

IL-1β and TNF-α exert an effect on lipid metabolism by influencing production of other cytokines, altering hemodynamics/amino acid utilization of various tissues involved in lipid metabolism, or modifying the hypothalamic-pituitary-adrenal axis increasing plasma concentrations of adrenocorticotropic hormone, cortisol, adrenaline, noradrenaline, and glucagon.[10]

Further studies have explained this concept by highlighting the fact that periodontal disease results in elevated serum levels of aspartate aminotransferase, alanine aminotransferase, cholinesterase, and an aspartate aminotransferase-to-alanine aminotransferase ratio less than one, suggesting that they have a tendency toward steatohepatitis leading to hepatic dyslipidemia.[18]

In contrast to the results of the present study, no raise in levels of TGL and cholesterol were observed in periodontitis group when compared to control group.[19] This could be due to the collection of non-fasting venous blood in that study that might have altered the plasma lipid values. In our present study, blood was drawn after 12 hours of fasting as food intake may alter the serum TGL levels.

The present study showed a significant increase in the TGL value and a significant decrease in the HDL value in the gingivitis group compared to the periodontally healthy group. This increase in TGL value may be because of the difference in the physical activity, food habits, and socioeconomic conditions of the subjects in the two groups. But, the difference in mean TC and LDL values between the two groups was not significant. This might be due to the less severity of proinflammatory cytokine production in gingivitis compared to periodontitis condition leading to minimal systemic manifestations. To the best of our knowledge, no study has been reported in the literature comparing the lipid profile in periodontally healthy group and gingivitis group.

A significant increase in TC, LDL values and a significant decrease in HDL values were seen in periodontitis group when compared to gingivitis group. This signifies that inflammation of the superficial structures of the periodontium may not alter the lipid metabolism. However, absence of significant difference in TGL values may be due to a variation in dietary and exercise pattern which could not be excluded as dietary records were not kept, that might have affected along with socioeconomic conditions.

When comparing the lipid profile between male and female subjects in periodontally healthy group and gingivitis group, TGL and HDL values were more for females when compared to male subjects. However, TC and LDL values were more for male subjects than females. Moreover, in periodontitis group, TGL, TC, and HDL values were more for male subjects and LDL value was more for female subjects. But, the values were not statistically significant. This shows the absence of consistent pattern of variation among male and female subjects. This can be due to the unequal distribution of male and female subjects in each group.

The results of the present study demonstrated a positive correlation between probing depth and clinical attachment level with TGL, TC, LDL and a negative correlation with HDL values. This shows that with increasing probing depth and CAL, the values of TGL, TC, and LDL increased but the value of HDL decreased. This is in accordance with the study conducted by Katz et al. who hypothesized that there is a strong positive statistical association between the existence of periodontal pockets and plasma lipid levels, thereby confirming a positive relationship between periodontitis and hyperlipidemia.[20]

Machado et al. demonstrated a positive correlation between tooth loss and the levels of TGL, TC, and LDL and a negative correlation between tooth loss and the levels of HDL.[21] Similar results were obtained by Morita T et al. who showed that positive conversions of blood pressure and the blood lipid index were significantly associated with the presence of periodontal pockets.[22]

In contrast to the results of present study, the results of the study conducted by Chen L et al. showed no positive correlation of TC, HDL cholesterol, LDL cholesterol, and TGL with the mean probing depth. This might be due to the inclusion of diabetic patients in the study population, as diabetes acts as a potential risk factor for the development of hyperlipidemia. The advantage of present study is the elimination of all confounding factors.[23]


CONCLUSION

The present study indicates that periodontal infection has a definite role in altering lipid metabolism which supports the hypothesis that a relationship exists between chronic periodontitis and hyperlipidemia.

Based on our results, following conclusions can be drawn:

  • Periodontitis patients have a significant increase in TGL, TC, and LDL levels and decrease in HDL levels compared to periodontally healthy group and gingivitis group
  • A positive correlation exists between probing depth and CAL with TGL, TC, and LDL
  • A negative correlation exists between probing depth and CAL with HDL value
  • Gingival inflammation alone in the absence of probing depth and attachment loss has no effect on the serum lipid profile.

However, further studies are required to clarify the relationship between periodontitis and serum lipid levels and to determine whether oral healthcare has the potential to reduce serum lipid levels in otherwise systemically healthy individuals.


Notes

Source of Support: Nil

Conflict of Interest: None declared.

REFERENCES
1. Socransky S,Haffajee AD. The bacterial etiology of destructive periodontal disease: Current conceptsJ PeriodontolYear: 199263322311573546
2. Offenbacher S. Periodontal diseases: PathogenesisAnn PeriodontolYear: 19961821789118282
3. Beck JD,Offenbacher S,Williams R,Gibbs P,Garcia R. Periodontitis: A risk factor for coronary heart diseaseAnn PeriodontolYear: 19983127419722697
4. Khader YS,Albashaireh ZS,Alomari MA. Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: A meta analysisJ PeriodontolYear: 20047510465315455730
5. Gotsman I,Lotan C,Soskolne WA,Rassovsky S,Pugatsch T,Lapidus L,et al. Periodontal destruction is associated with coronary artery disease and periodontal infection with acute coronary syndromeJ PeriodontolYear: 2007788495817470018
6. Vidal F,Figueredo CM,Cordovil I,Fischer RG. Periodontal therapy reduces plasma levels of interleukin-6, C- reactive protein, and fibrinogen in patients with severe periodontitis and refractory arterial hypertensionJ PeriodontolYear: 2009807869119405832
7. Cutler CW,Shinedling EA,Nunn M,Jotwani R,Kim BO,Nares S,et al. Association between periodontitis and hyperlipidemia: Cause or effect?J PeriodontolYear: 19997014293410632517
8. Wilkins WL. Definition of triglycerides and cholesterolStedman's medical dictionaryYear: 200528th edWolters Kluwer367
9. Fentoglu O,Oz G,Tasdelen P,Uskun E,Aykac Y,Bozkurt Y. Periodontal status in subjects with hyperlipidemiaJ PeriodontolYear: 2009802677319186967
10. Iacopino AM,Cutler CW. Pathophysiological relationships between periodontitis and systemic disease: Recent concepts involving serum lipidsJ PeriodontolYear: 20007113758410972656
11. Meyer DD,Mintz KP,Fives-Taylor PM. Models of invasion of enteric and periodontal pathogens into epithelial cells: A comparative analysisCrit Rev Oral Biol MedYear: 199783894099391752
12. Silness J,Loe H. Periodontal disease in pregnancy II. Correlation between oral hygiene and periodontal conditionActaOdontolScandYear: 19642212135
13. Loe H,Silness J. The gingival index, the plaque index and the retention index systemsJ PeriodontolYear: 19673861065237684
14. Ashavald TF,Todur SP,Dheral AJ. Establishment of reference intervals in indian populationIndian J Clin BiochemYear: 200520110823105542
15. Miller M,Stone NJ,Ballantyne C,Bittner V,Criqui MH,Ginsberg HN,et al. Triglycerides and cardiovascular disease: A special statement from the american heart associationCirculationYear: 2011123229233321502576
16. Garcia RI,Henshaw MM,Krall EA. Relationship between periodontal disease and systemic healthPeriodontol 2000Year: 200125213611155180
17. Barba C,Cavalli-Sforza T,Cutter J,Darnton-Hill I,Deurenberg P,Gill T. Appropriate body-mass index for asian populations and its implications for policy and intervention strategiesLancetYear: 20043631576314726171
18. Saito T,Murakami M,Shimazaki Y,Oobayashi K,Matsumoto S,Koga T. Association between alveolar bone loss and elevated serum c-reactive protein in japanese menJ PeriodontolYear: 2003741741614974814
19. Loos BG,Craandijk J,Hoek FT,Wertheim-van Dillen PM,Van der Velden U. Evaluation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patientsJ PeriodontolYear: 20007115283411063384
20. Katz J,Flugelman MY,Goldberg A,Heft M. Association between periodontal pockets and elevated cholesterol and low density lipoprotein cholesterol levelsJ PeriodontolYear: 20027349450012027250
21. Machado AC,Quirino MR,Nascimento LF. Relation between Chronic Periodontal Disease and Plasmatic Levels of Triglycerides, Total Cholesterol and FractionsBraz Oral ResYear: 200519284916491257
22. Morita T,Yamazaki Y,Mita A,Takada K,Seto M,Nishinoue N. A Cohort Study on the Association between Periodontal Disease and the Development of Metabolic SyndromeJ PeriodontolYear: 2010815121920367094
23. Chen L,Wei B,Liu F,Xuan D,Xie B,Zhang J. Association of Periodontal Parameters with Metabolic Level and Systemic Inflammatory Markers in Patients with Type-2 DiabetesJ PeriodontolYear: 2010813647120192862

Figures

[Figure ID: F1]
Figure 1 

Comparison of mean age between periodontally healthy, gingivitis and periodontitis groups. Age in years



[Figure ID: F2]
Figure 2 

Comparison of mean body mass index between periodontally healthy, gingivitis, and periodontitis groups. BMI (kg/m2)



[Figure ID: F3]
Figure 3 

Comparison of mean TGL values between periodontally healthy, gingivitis, and periodontitis groups TGL (mg/dL)



[Figure ID: F4]
Figure 4 

Comparison of mean total cholesterol. TC(mg/dL) values between periodontally healthy, gingivitis, and periodontitis groups. TC(mg/dL)



[Figure ID: F5]
Figure 5 

Comparison of mean low-density lipoprotein values between periodontally healthy, gingivitis, and periodontitis groups. LDL(mg/dL)



[Figure ID: F6]
Figure 6 

Comparison of mean high-density lipoprotein values between periodontally healthy, gingivitis, and periodontitis groups. HDL(mg/dL)



Tables
[TableWrap ID: T1] Table 1 

Comparison of demographic data and lipid parameters between periodontally healthy, gingivitis, and periodontitis groups



[TableWrap ID: T2] Table 2 

Comparison of age, BMI and lipid parameters between groups



[TableWrap ID: T3] Table 3 

Comparison of lipid parameters between male and female subjects



[TableWrap ID: T4] Table 4 

Correlations between age, gender, BMI, and lipid parameters



[TableWrap ID: T5] Table 5 

Correlations between periodontal and lipid parameters




Article Categories:
  • Original Article

Keywords: Cardiovascular disease, cytokines, hyperlipidemia, inflammation, periodontitis.

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