effect of non surgical periodontal therapy on serum lipid ... - Aosr.co.in

EFFECT OF NON SURGICAL PERIODONTAL THERAPY ON
SERUM LIPID LEVELS IN CHRONIC PERIODONTITIS.
Nishanth S.Rao * , Pavan Bajaj * , Savitha B. Naik † , A.R.Pradeep *
ABSTRACT
Background: The aim <strong>of</strong> the present study was to investigate the <strong>effect</strong> <strong>of</strong> <strong>non</strong> <strong>surgical</strong> <strong>periodontal</strong> <strong>therapy</strong> (NSPT) on the
lipid pr<strong>of</strong>iles in patients with chronic periodontitis.
Methods: The study population consisted <strong>of</strong> 50 <strong>non</strong> smokers with chronic periodontitis. The serum lipid levels, probing
pocket depth, <strong>periodontal</strong> attachment level & modified sulcus bleeding index was recorded at baseline and 3 months following
NSPT.
Results: At third month there was significant reduction in Total Cholesterol, Low Density Lipoprotein, Very Low Density
Lipoprotein, Triglyceride and increase in High Density Lipoprotein after NSPT. Also, the reduction in bleeding on probing,
pocket depth and attachment level were statistically significant in the treatment group.
Conclusion: The results <strong>of</strong> our study showed that <strong>periodontal</strong> destruction and serum lipid levels are positively correlated and
<strong>non</strong>-<strong>surgical</strong> <strong>periodontal</strong> treatment resulted in improved control on lipid pr<strong>of</strong>iles in chronic periodontitis patients.
AOSR 2011;1(2):60-64.
KEY WORDS: Chronic periodontitis; dental prophylaxis; lipoproteins.
Archives <strong>of</strong> Oral Sciences & Research
* Department <strong>of</strong> Periodontics, Govt. Dental College & Research Institute Fort, Bangalore- 560002, Karnataka, India.
† Department <strong>of</strong> Conservative Dentistry and Endodontics, Government Dental College and Research Institute, Fort,
Bangalore - 560002, Karnataka, India.
INTRODUCTION:
Periodontitis represents a chronic oral infection that leads
to gingival inflammation, destruction <strong>of</strong> tooth supporting
tissues, namely <strong>periodontal</strong> ligament and alveolar bone
and eventual exfoliation <strong>of</strong> teeth. The etiological agents
for periodontitis are the Gram negative, anaerobic microorganisms
present within the dental plaque. Recent studies
have proven that <strong>periodontal</strong> disease can produce disorders
in systemic health by changing the blood chemistry with
a rise in inflammatory mediators, proteins and lipids
in the serum. 1-3 Periodontitis is <strong>of</strong>ten associated with
endotoxemia and mild systemic inflammatory reactions,
and <strong>periodontal</strong> pathogens have been identified in early
atherosclerotic lesions. 4-6 Several studies have indicated
that subjects with <strong>periodontal</strong> disease may have a higher
risk for cardiovascular diseases when compared to subjects
with a healthy periodontium. 7-11
Factors that place individuals at risk for periodontitis may
also place them at risk for cardiovascular disease; that
means that periodontitis and cardiovascular disease may
share common risk factors, such as smoking, diabetes,
behavioural factors, ageing and male gender. 12 Periodontitis
has been shown to be associated with increased levels
<strong>of</strong> proatherogenic plasma lipoproteins. 5,6,13,14 Evidence
suggests that low level, chronic exposure to gram negative
microrganisms and/or their lipopolysaccharide (LPS) can
manifest a state <strong>of</strong> altered lipid metabolism; the main features
<strong>of</strong> which are hypertriglyceridemia and lipid oxidation.
The underlying mechanism for these alterations is the
release <strong>of</strong> TNF-α and IL-1β in response to Gram negative
LPS exposure. This increase in plasma concentrations
<strong>of</strong> cytokines leads to a state <strong>of</strong> altered lipid metabolism.
Hyperlipidaemia is a state <strong>of</strong> abnormal lipid pr<strong>of</strong>ile,
which is characterized by elevated blood concentrations
<strong>of</strong> triglycerides (TG), elevated levels <strong>of</strong> total cholesterol
(TC) and low-density lipoprotein-cholesterol (LDL), and
decreased levels <strong>of</strong> high-density lipoprotein-cholesterol
(HDL). HDL have several antiatherogenic properties,
such as an ability to promote the efflux <strong>of</strong> cholesterol from
cells, to function as an important antioxidant by inhibiting
LDL oxidation, to prevent or interrupt foam cell formation
and to retard inflammatory activity, for instance. 15 These
properties may prevent the harmful <strong>effect</strong>s <strong>of</strong> infections,
and conversely, infections may have a more detrimental
<strong>effect</strong> in the absence <strong>of</strong> functioning HDL.
However, to date, there have been no studies reporting
the <strong>effect</strong> <strong>of</strong> <strong>periodontal</strong> treatment on lipid levels in <strong>non</strong>
smokers with chronic periodontitis in an Indian population.
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Non-<strong>surgical</strong> <strong>periodontal</strong> <strong>therapy</strong> & lipid levels
Hence, the aim <strong>of</strong> the present study was to investigate the
<strong>effect</strong> <strong>of</strong> <strong>non</strong> <strong>surgical</strong> <strong>periodontal</strong> <strong>therapy</strong> (NSPT) on the
lipid levels in <strong>non</strong> smokers with chronic periodontits.
MATERIAL AND METHODS
Subjects:
The subjects for the study were selected from patients
who attended the Outpatient Section, Department <strong>of</strong>
Periodontics, Government Dental College and Research
Institute, Bangalore, from February 2010 to June 2010.
The Ethics Committee and Review Board <strong>of</strong> Government
Dental College & Research Institute, Bangalore approved
the study protocol. The protocol was clearly explained to
all the patients and informed consent was obtained from all
recruits. Smoking history was collected by means <strong>of</strong> selfreporting
following a standardized questionnaire. Subjects
were classified as smokers and <strong>non</strong> smokers based on
criteria established by the Centre for Disease Control and
prevention (CDC), “current smokers” were defined as those
who had smoked 100 or more cigarettes over their lifetime
and smoked at the time <strong>of</strong> interview; “former smokers” had
smoked 100 or more cigarettes over their lifetime but were
not currently smoking; and “<strong>non</strong> smokers” had not smoked
100 or more cigarettes over their lifetime. Former smokers
and current smokers were excluded from the study. All
subjects with more than 3 pockets with a probing pocket
depth (PPD) ≥ 4 mm or with a <strong>periodontal</strong> attachment
level (PAL) ≥ 3mm were included in the study. The study
population consisted <strong>of</strong> 50 <strong>non</strong>-smokers (24 females and
26 males) with chronic periodontitis (mean age: 34.79
+ 6.17). Body weight was assessed by using body mass
index (BMI) and only <strong>non</strong> obese individuals (BMI: 18-
22.9 Kg/m2) were enrolled in the study. The exclusion
criteria for the study were dental treatment during the past
6 months, smoking, alcoholics, pregnant, lactating and
post menopausal women, aggressive periodontitis, cardiac
diseases, rheumatoid arthritis, obesity, patients taking any
drug against hypercholesterolaemia and any other systemic
disease which can alter the course <strong>of</strong> <strong>periodontal</strong> disease or
serum lipid levels.
Measurement <strong>of</strong> serum lipids:
Serum lipids were determined in the Infosys laboratory,
Victoria Hospital using routine enzymatic methods. To
identify subjects with pathologic values, the following
cut<strong>of</strong>f points were used according to the laboratory’s
recommendation: TC > 200 mg/dL, LDL > 130 mg/dL,
HDL < 35 mg/dL, VLDL > 40 mg/dL and TG > 200 mg/
dL. The serum lipid levels was recorded at baseline (day 0)
and 3 months following the scaling and root planing.
*
Hu-Friedy, Chicago, IL, USA.
†
SPSS statistical package version 17, SPSS Inc., Chicago, IL, USA.
Periodontal parameters:
All subjects were examined by the same examiner. All
<strong>periodontal</strong> parameters were assessed at 6 different sites
around each tooth (Mesio-buccal, Buccal, Disto-buccal,
Mesio-lingual, Lingual and Disto-lingual). The examining
investigator was unaware <strong>of</strong> the group assignments. The
parameters assessed were: PPD, PAL & modified sulcus
bleeding index (mSBI). PPD & PAL assessments were
carried out with the UNC 15 probe * with 1mm graduations.
The <strong>periodontal</strong> parameters were recorded at baseline (day
0) and 3 months following the scaling and root planing.
The patients received oral hygiene instructions and fullmouth
scaling and root planing (NSPT) performed under
local anaesthesia after recording the baseline parameters.
STATISTICAL METHODS:
Data are presented as mean and standard deviation.
Differences between means were proved for significance
using the Student’s t-test. The data were analyzed using
statistical s<strong>of</strong>tware. †
RESULTS:
Table 1 demonstrates the demographic data and patient
characteristics <strong>of</strong> the study population. The lipid levels
were determined for <strong>non</strong> smokers at baseline and at
end <strong>of</strong> 3 months. As shown in Table 2, there was
significant reduction in the TC, LDL, VLDL and TG
at the end <strong>of</strong> 3 months after NSPT. Also there was a
statistically significant increase in HDL after NSPT. The
clinical <strong>periodontal</strong> parameters also showed significant
improvement after treatment. Thus suggesting that
<strong>periodontal</strong> destruction and higher TC, LDL, VLDL and
TG are positively correlated, while HDL is positively
correlated with <strong>periodontal</strong> health.
Table 1. Characteristics <strong>of</strong> the study subjects
Characteristic N= 50
Age (mean+ S.D.) 34.79 + 6.17
Male (%) 52
Female (%) 48
Body Mass Index
(mean + S.D.)
20.41 + 1.53
Daily brushing
habit (times/day) (%)
0 times/day 2
1 time/day 76
2 times/day 22
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Nishanth S.Rao et al.
DISCUSSION:
Coronary heart disease has become a public health
problem and major cause <strong>of</strong> death, both in developed and
developing countries. 16,17 There is increasing concern about
the blood lipid levels, as a risk factor for the development <strong>of</strong>
coronary heart disease. Studies have also shown a positive
correlation between periodontitis and increased serum
lipid pr<strong>of</strong>ile. 5,12,13,18,19 Changes in concentrations <strong>of</strong> these
markers have also been associated with acute and chronic
infections, and in this respect, bacterial infections have
been implicated as a possible risk factor in the etiology <strong>of</strong>
coronary heart disease. 5,20
* P value < 0.05 significant
Table 2: Comparison <strong>of</strong> variables at baseline and 3 months
Non-smokers (n=50)
Baseline 3 months P value
Total cholesterol 167.48 + 10.42 142.07 + 7.16 0.001*
HDL 38.83 + 2.39 40.48 + 2.57 0.001*
LDL 117.97 + 10.43 99.38 + 3.18 0.001*
VLDL 26.76 + 3.64 25.10 + 3.38 0.001*
Triglyceride 142.97 + 9.65 140.62 + 10.13 0.002*
Probing pocket depth 4.95 + 0.36 3.76 + 0.46 0.001*
Periodontal attachment
level
4.48 + 0.35 3.75 + 0.38 0.001*
Modified sulcus
bleeding index
2.96 + 0.35 1.85 + 0.25 0.001*
Data <strong>of</strong> our study suggests that periodontitis may trigger
alterations in lipid levels by possibly eliciting an increased
systemic inflammatory response. The data <strong>of</strong> the present
study indicate that periodontitis causes changes in serum
TC, HDL, LDL, VLDL and TG levels. Periodontitis is a
chronic, inflammatory, destructive disease that affects the
supporting tissues <strong>of</strong> the teeth, and is <strong>of</strong>ten associated with
enhanced concentrations <strong>of</strong> proatherogenic plasma lipids,
i.e., TC and LDL as well as TG. 12,13,19 The outcomes <strong>of</strong>
our study support this overall conclusion. But most <strong>of</strong> the
above mentioned studies were unable to infer a positive
correlation with all the parameters <strong>of</strong> lipid pr<strong>of</strong>ile (i.e.
TC, HDL, LDL, VLDL and TG) to arrive at a definitive
conclusion on the association between periodontitis and
increased lipid pr<strong>of</strong>ile.
Lösche W. et al. 5 found only LDL to be significantly
associated with the clinical parameters <strong>of</strong> inflammation
and <strong>periodontal</strong> tissue destruction in periodontitis subjects.
Iacapino and Cutler 21 reported that existence <strong>of</strong> an
association between periodontitis and serum lipid levels
does not establish whether <strong>periodontal</strong> disease causes
elevations in lipid levels or whether elevations in serum
lipids predispose to periodontitis. Hence these studies in
actual fact do not depict a strong correlation between serum
lipid levels and <strong>periodontal</strong> disease. One possible reason to
explain the differences between the results <strong>of</strong> this study
and previous studies is the difference in how periodontitis
is defined. We defined chronic periodontitis as subjects
with more than 3 pockets with a probing depth ≥ 4 mm
and PAL≥ 3mm whereas Katz et al 13 for example, used
CPITN scores for determining periodontitis. A possible
explanation for the association between hyperlipidaemia
and <strong>periodontal</strong> infection was postulated by Noack et al 22
by assessing neutrophil respiratory burst by whole blood
chemiluminescence and they found significant increases
in both chemiluminescence and pocket depth on a group
<strong>of</strong> patients with hyperlipidaemia. They suggested that the
association <strong>of</strong> hyperlipidaemia with periodontitis could be
due to the dysfunction <strong>of</strong> polymorfonuclear leucocytes.
The results <strong>of</strong> the present study show that local <strong>periodontal</strong>
treatment resulted in a significant decrease in TC, LDL,
VLDL and TG levels. The reduction <strong>of</strong> TC, LDL, VLDL,
TG and rise in HDL after treatment suggests a potential
<strong>effect</strong> <strong>of</strong> periodontitis-driven systemic inflammation on
lipid metabolism. These findings are in concordance with
a report by Pussinen et al 14 who reported that periodontitis
is associated with a reduction <strong>of</strong> the HDL levels and
that <strong>periodontal</strong> <strong>therapy</strong> results in an increase in this
antiatherogenic lipid fraction. However, in another study
conducted by D’Aiuto et al 23 lipid marker changes were
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Non-<strong>surgical</strong> <strong>periodontal</strong> <strong>therapy</strong> & lipid levels
insignificant between standard <strong>periodontal</strong> treatment and
control groups, and some reductions <strong>of</strong> TC and LDL were
present only in the intensive <strong>periodontal</strong> treatment group.
There have been studies which reported that <strong>periodontal</strong>
treatment is associated with the reduction <strong>of</strong> proatherogenic
plasma lipid levels, i.e., TC and LDL as well as TG in
patients with severe periodontitis. 5,23 However this study
was the first to study the <strong>effect</strong> <strong>of</strong> <strong>periodontal</strong> <strong>therapy</strong> on
lipid pr<strong>of</strong>iles in an Indian population. Further investigations
are needed for further exploration <strong>of</strong> the relationship among
periodontitis, <strong>periodontal</strong> <strong>therapy</strong> and lipid metabolism.
Larger studies and clinical intervention trials are necessary
to better define the periodontitis subjects in whom local
infection causes significant systemic inflammation, and
whether these findings are true or confounded by other
important factors like nutrition, socioeconomic status, or
age.
CONCLUSION:
The present study indicates that <strong>non</strong> <strong>surgical</strong> <strong>periodontal</strong>
treatment in chronic periodontitis patients could cause
significant changes in lipid levels and help in preventing
any systemic complications due to the elevated lipid levels.
These results suggest a potential <strong>effect</strong> <strong>of</strong> periodontitisdriven
systemic inflammation on lipid metabolism.
ACKNOWLEDGEMENTS:
The authors express their thanks to Dr. Gangaboraiah,
a Statistician, Bangalore for carrying out all required
statistics.
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Correspondence:
Dr. Nishanth S Rao
Post Graduate Student
Department <strong>of</strong> Periodontics,
Government Dental College and Research Institute
Fort, Bangalore-560002, Karnataka, India.
E-mail: dr.nishurao@gmail.com
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