non-surgical periodontal treatment reduces cardiovascular risk in refractory hypertensive patients:...

$: Non-surgical periodontal treatment reduces cardiovascular risk in refractory hypertensive patients: a pilot study$
Non-surgical periodontaltreatment reducescardiovascular risk in refractoryhypertensive patients: a pilotstudyVidal F, Cordovil I, Figueredo CMS, Fischer RG. Non-surgical periodontaltreatment reduces cardiovascular risk in refractory hypertensive patients: a pilotstudy. J Clin Periodontol 2013; 40: 681–687. doi: 10.1111/jcpe.12110.

AbstractAim: To evaluate the effects of non-surgical periodontal treatment on left ventric-ular mass (LVM), arterial stiffness, systolic and diastolic blood pressure andplasma levels of inflammatory markers (C-reactive protein (CRP), fibrinogen andinterleukin-6) in refractory hypertension patients.Material and Methods: This interventional prospective cohort pilot studyincluded 26 patients (53.6 � 8.0 years old) diagnosed with refractory hyperten-sion and generalized chronic periodontitis. Subjects received non-surgical peri-odontal treatment according to their needs. Plasma levels of systemicinflammation (CRP; fibrinogen and interleukin-6) and established cardiovascularrisk factors [systolic and diastolic blood pressure (SBP and DBP), left ventricularmass (LVM) and arterial stiffness] were assessed at three time points (baseline,3 months after baseline and 6 months after periodontal therapy).Results: Periodontal therapy significantly reduced all cardiovascular risk markersevaluated. Median values of SBP and DBP were reduced by 12.5 mmHg and10.0 mmHg, respectively, whereas left ventricular mass (LVM) reduced by 12.9 gand pulse wave velocity reduced by 0.9 m/s (p < 0.01). Levels of CRP, IL-6 andfibrinogen lowered by 0.5 mg/dl, 1.4 pg/dl and 37.5 mg/dl (p < 0.01), respectively,6 months after periodontal therapy.Conclusions: Periodontal therapy significantly reduced levels of CRP, IL-6, fibrin-ogen, blood pressure, LVM and arterial stiffness, lowering cardiovascular risk inrefractory hypertensive patients.

F�abio Vidal1,3, Ivan Cordovil2,Carlos Marcelo Silva Figueredo3

and Ricardo Guimar~aes Fischer3

1Est�acio de S�a University, Rio de Janeiro,

Brazil; 2National Institute of Cardiology, Rio

de Janeiro, Brazil; 3Rio de Janeiro State

University, Rio de Janeiro, Brazil

Key words: C-reactive protein; endothelial

dysfunction; fibrinogen; hypertension;

interleukin 6; left ventricular mass;

periodontal therapy

Accepted for publication 28 March 2013

Inflammation may play an importantrole on the development of hyperten-sion (Boos & Lip 2005). A chroniclow-grade inflammatory state hasbeen associated with endothelial dys-function (Fichtlscherer et al. 2000)and arterial stiffness (Vlachopouloset al. 2002), important conditionsthat lead to higher blood pressure

levels and increased mortality amonghypertensive patients (Laurent et al.2001). Some of the main inflamma-tory markers associated with increasedcardiovascular risk, such as C-reactiveprotein (CRP), fibrinogen and interleu-kin 6 (IL-6) may present higherlevels in periodontal patients (Looset al. 2000, Paraskevas et al. 2008,

Conflict of interest and source of

funding statement

The authors declare that they have noconflicts of interest. The study wasself-supported with resources fromRio de Janeiro State University

© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd 681

J Clin Periodontol 2013; 40: 681–687 doi: 10.1111/jcpe.12110

Vidal et al. 2009). In addition, peri-odontitis has also been associatedwith left ventricular hypertrophy(Angeli et al. 2003), hypertension(Holmlund et al. 2006, Franek et al.2009, Tsakos et al. 2010, Vidal et al.2011, Peres et al. 2012) and endothe-lial dysfunction (Seinost et al. 2005,Blum et al. 2007, Higashi et al. 2009).

Periodontitis is a low-grade chronicinflammatory disease of the tooth sup-porting tissues that may lead to toothloss (Moutsopoulos & Madianos 2006)and may increase blood levels ofinflammatory markers, including IL-6,CRP and fibrinogen (Loos et al. 2000,Paraskevas et al. 2008, Vidal et al.2009).

Non-surgical periodontal therapymay reduce systemic inflammation innormotensive (D’Aiuto et al. 2004,2007, Marcaccini et al. 2009) andhypertensive patients (Vidal et al.2009), and improve endothelial func-tion (Mercanoglu et al. 2004, Seinostet al. 2005, Blum et al. 2007, Tonettiet al. 2007, Higashi et al. 2009). Onthe other hand, there are only fewstudies regarding the possible effectsof periodontal therapy and the reduc-tion in the inflammatory burden onblood pressure levels and left ventric-ular hypertrophy, which are some ofthe main targets of anti-hypertensivetreatment. Thus, the primary aim ofthis study was to evaluate the effectsof non-surgical periodontal therapyon clinical parameters such as bloodpressure levels, arterial stiffness andLVM on a population of refractoryhypertensive patients. The secondaryoutcome was to observe the effects onplasma levels of inflammatory markersassociated with chronic periodontalinflammation and increased cardio-vascular risk, such as CRP, IL-6 andfibrinogen.

Material and Methods

Experimental design and patient selection

The present pilot study was an inter-ventional prospective cohort revisedand approved by the Hospital’s Ethi-cal Board. All patients gave theirwritten consent to be part of thestudy. One hundred and sixty-twopatients diagnosed with severe essen-tial refractory hypertension and fol-lowed by the clinical board of theHypertension Department of theNational Institute of Cardiology

(Rio de Janeiro, Brazil) for at least2 years were initially enrolled at thestudy. Refractory hypertension isdiagnosed when blood pressure levelsremain above 140 9 90 mmHg, evenwhen the patient is engaged in atreatment programme and uses threeor more classes of anti-hypertensivedrugs including a diuretic (Choba-nian et al. 2003). The patients wereunder supervision of a cardiologist,and were medicated with beta-block-ers, angiotensin-converting enzyme(ACE) inhibitors and a diuretic. Thepatients were under treatment in theCardiology department for 5–8 years.The study was conducted betweenSeptember 2010 and February 2012.

All 162 patients were examined bythe same experienced periodontist(FV). After the initial screening, 26 ofthese patients who met the inclusioncriteria were included in the study.The inclusion criteria were that sub-jects: (i) have at least 12 teeth; (ii)have a diagnosis of generalizedadvanced chronic periodontitis(Armitage 1999); (iii) have a minimumof 2 years of anti-hypertensive treat-ment with good adherence; (iv) be� 40 years old; (v) have no previousperiodontal therapy and (vi) have nottaken antibiotics for the preceding6 months. The exclusion criteriaincluded pregnancy, previous peri-odontal therapy, history of infectiveendocarditis, use of medications suchas antibiotics or anti-inflammatorydrugs, and systemic conditions thatcontra-indicated periodontal therapyor that might affect the progressionor treatment of periodontitis.

The study design consisted ofthree stages (Fig. 1). On stage 1(baseline), periodontal examination,cardiological exams and laboratorialanalyses were performed. A completeperiodontal examination was per-formed, including patient medical his-tory (assessed by a questionnaire),visible plaque index (VPI), probingpocket depth (PPD), clinical attach-ment level (CAL) and bleeding onprobing (BOP). All patients wereexamined by the same calibratedexaminer (FV), using a manual UNC15-mm periodontal probe at six sitesper tooth (excluding residual roots),except for the VPI (Ainamo & Bay1975), which was assessed at four sitesper tooth. An intra-examiner calibra-tion was performed. Ten non-studysubjects were used for the calibration

of the examiner. The patients wereexamined twice within an interval of72 hours (kappa = 0.91). In stage 2(90 days after baseline), all clinicalperiodontal parameters were reas-sessed and cardiological exams andlaboratorial analysis were repeated.Periodontal treatment was conductedby a single experienced periodontist(FV). Subjects received oral hygieneinstructions, including a demonstra-tion of utilization of dental floss andbrushing technique (Bass technique),supragingival scaling using man-ual instruments (Gracey curettes,Hu-friedy, Chicago, IL, USA) and asonic device (Sonic Borden 2000N,Kavo, Joinville, SC, Brazil). Subgin-gival scaling and root planing wereperformed at each site withPPD � 4 mm. There was no limitof appointments but, in general,patients were seen four to six timesfor 60 minutes sessions of subgingi-val scaling within a 2-week period.The oral hygiene instructions werereinforced at each appointment dur-ing this stage. Local anaesthesia wasused whenever necessary and bloodpressure was constantly monitoredduring the sessions. After the treat-ment phase, patients were instructedto follow oral hygiene instructions,were given a manual toothbrush,toothpaste containing sodium fluo-ride and dental floss and wererecalled 6 months later. In stage3 (180 days after stage 2), all peri-odontal parameters were reassessed,and new cardiological exams andlaboratorial analysis were performed.

Blood pressure

Systolic and diastolic blood pressurelevels were assessed using an ambu-latory blood pressure monitoringdevice (TM 2430�, A&D, SantaClara, CA, USA). This techniquepresents the means of both, SBP andDBP, after a 24-hour period, accord-ing to the current ambulatory bloodpressure monitoring guidelines(O’Brien et al. 2005).

Left ventricular mass

Left ventricular mass was estimatedafter transthoracic Doppler echocar-diographic evaluation (CV70TM, Sie-mensTM, Munich, Germany). Afterobtaining the measures of the leftventricle, it is possible to estimate

© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

682 Vidal et al.

LVM by applying a mathematic for-mula (Alfakin et al. 2006).

Arterial stiffness

Arterial stiffness was measuredthrough the detection of pulse wavevelocity (PWV). PWV was deter-mined using the Complior� system(Complior�, Colson, Garges lesGenosse, France). In this method,two sensors are positioned in theskin above the arterial segment to beanalysed. The distance between thesensors is measured as the pulsewave shock and is registered in bothsensors. This information is sent to acontrol CPU containing the softwarethat estimates the time lapse betweenthe pulses, thus allowing ascertainingthe pulse wave velocity. PWV is avalid and reliable method of measur-ing arterial stiffness, as a conse-quence of endothelial dysfunction

(Muiesan et al. 2010, Rusak et al.2010).

Plasma inflammatory markers

Nine ml of blood samples weretaken at each stage, to evaluateplasma levels of inflammatory mark-ers potentially associated with highercardiovascular risk. High-sensitivityCRP (Dade Behring�, Amsterdam,Netherlands), IL-6 (Immulite�, Sie-mens Medical Solutions Diagnostics,Los Angeles, CA, USA) and fibrino-gen (Sigma�, St. Louis, MO, USA)were assessed with ELISA kits,according to the protocols recom-mended by the manufacturers.

Data management and statistical analysis

Based on a previous study (Vidalet al. 2009) the sample size calcula-tion indicated that with a sample size

of 22 patients, there was a 80%power to detect, at a 0.05 level, a50% reduction in the mean% ofsites with PPD and PAL � 6 mm. Apost hoc calculation showed thatwith a sample size of 24 patients,there was an 80% power to detect,at a 0.05 level, a mean reduction of1.2 m/s of the PWV values. Twenty-six patients were included expectingfor dropouts. As all the patientscompleted the study, all 26 patientswere included in the analysis.Kolmogorov–Smirnov and Shapiro–Wilk tests were used to assess if vari-ables were normally distributed.Normally distributed variables werereported as mean (� SD), whereasnon-normally distributed data weredescribed as median (inter-quartilerange). To verify differences betweenclinical and laboratory values atbaseline, 3 months after baseline and6 months after periodontal therapy,

Fig. 1. Flow chart of the study.


Periodontal treatment in hypertension 683

paired t-test and Wilcoxon ranktest were used to compare normallydistributed and non-normally distrib-uted data respectively. All statisticalanalyses were carried out with a sta-tistical programme (IBM SPSS 19.0,SPSS Inc., Chicago, IL, USA) witha significance level of 5% (p < 0.05).

Results

The studied group consisted of 26patients (9 men, 17 women, meanage = 53.6 � 8.0). There were 16 non-white patients and 3 smokers (>10cigarettes per day). The mean (�SD)number of teeth was 18 (�6). Furtherbaseline characteristics of the subjectsstudied are summarized in Table 1.

No significant difference wasdetected between the clinical peri-odontal data between baseline andthe 3 months re-evaluation previousto periodontal therapy, except forBOP and percentage of sites withPPD � 6 mm. Mean percentage ofsites with VPI, BOP, PPD � 4 mm,PPD 4–5 mm, PPD � 6 mm, CAL4–5 mm and CAL � 6 mm was sig-nificantly reduced 6 months afterperiodontal treatment (Table 2).

Six months after periodontal treat-ment, a significant reduction in themedian values of SBP and DBP andof the mean values of LVM and PWVwas observed. The median values ofthe inflammatory markers, CRP, IL-6and fibrinogen were significantlyreduced 6 months after periodontaltreatment (Table 3).

Discussion

Our results showed a reduction inboth SBP and DBP. Among the 26patients, 18 showed a reduction in

systolic blood pressure levels and 20patients showed a reduction in DBPlevels. In general, the reduction inclinical parameters of periodontaldisease led to the improvement ofblood pressure levels for most of thepatients. According to the literature,even small differences of 5 mmHgcan reduce cardiovascular mortalityin the long term (Dyer et al. 1994).There is a lack of studies aimed pri-marily at blood pressure reductionafter periodontal therapy. D’Aiutoet al. (2006) found a discrete reduc-tion (7 � 3 mmHg) in systolic bloodpressure levels after periodontal treat-ment associated with minocyclinespheres. Graziani et al. (2010) founda significant reduction in both SBP(8.3 mmHg) and DBP (4.9 mmHg),in an exploratory trial on the effectsof periodontal therapy on renalfunction, which further corroboratesour hypothesis. However, the authorsanalysed non-hypertensive patients,and this hinders the comparison withour data. The majority of thestudies available used casual blood

pressure measures on non-hyperten-sive patients, and aimed primarily atother end points such as endothelialdysfunction. The significant reductionin blood pressure levels in some of thepatients from our group may be par-tially explained by the fact that theywere already under pharmacologicalanti-hypertensive treatment for atleast 2 years and the periodontaltreatment provided the removal ofthe potential modifying risk factorsassociated with chronic infection ofperiodontal tissues, consequentlyreducing the inflammatory burdenthat can impair endothelial functionand lead to poorer response to theanti-hypertensive therapy.

According to recently publisheddata, endothelial dysfunction medi-ated by reduced levels of nitrousoxide seems to be the link betweeninflammation and higher blood pres-sure levels (Tsioufis et al. 2011). Theresults obtained in our study showedan improved endothelial function6 months after periodontal treat-ment. Many studies showed signifi-

Table 1. Means (� SD) of body massindex (BMI) and years of anti-hypertensivetreatment and frequencies of patients withhistory of acute myocardial infarction(AMI)/stroke, diabetes mellitus and smok-ing (N = 26)

Variables Mean (�SD)

BMI 30.6 (�8.0)Anti-hypertensivetreatment(years)

4.8 (�1.7)

History ofAMI/Stroke (%)

23.1

Diabetics (%) 15.4Smokers (%) 11.5

Table 2. Mean (�SD) number of teeth, percentages (�SD) of sites with visible plaqueindex (VPI), bleeding on probing (BOP), probing pocket depth (PPD) and clinical attach-ment level (CAL) at baseline (0), 3 months after baseline (1) and 6 months (2) after peri-odontal treatment

0 1 2

Number of teeth 18 (�6) 18 (�6) 18 (�6)VPI (%) 65.6 (�23.1) 73.8 (�20.0)* 45.1 (�20.6)¶

BOP (%) 46.1 (�22.3) 47.3 (�22.7) 17.4 (�12.8)¶

%PPD � 4 mm 31.1 (�15.1) 31.7 (�14.1) 12.7 (�7.8)¶

%PPD 4–5 mm 22 (�12.4) 22.1 (�11.2) 9.0 (�5.2)¶

%PPD � 6 mm 9.1 (�6.1) 9.5 (�6.2)* 3.7 (�4.0)¶

%CAL 4–5 mm 27.6 (�13.7) 27.4 (�13.5) 20.6 (�10.9)¶

%CAL � 6 mm 18.4 (�16.5) 18.4 (�16.7) 13 (�13.9)¶

*significantly higher as compared with the values from baseline (0).¶significantly lower as compared with the values from baseline (0) and 6 months after peri-odontal treatment (1).

Table 3. Medians (inter-quartile range) of C-reactive protein (CRP), interleukin 6 (IL-6),fibrinogen (FIB), systolic (SBP) and diastolic (DBP) blood pressure and mean (�SD) of leftventricular mass (LVM) and pulse wave velocity (PWV) at baseline (0), 3 months after base-line (1) and 6 months (2) after periodontal treatment

0 1 2

CRP (mg/dL) 0.6 (1.1) 0.8 (0.8) 0.3 (0.5)*IL-6 (pg/ml) 2.1 (4.3) 2.3 (3.9) 0.9 (0)*FIB (mg/dL) 376 (193) 381.5 (203.8) 344 (139.5)*SBP (mmHg) 175 (38.8) 170 (28.8) 157.5 (40)*DBP (mmHg) 105 (21.3) 105 (21.3) 95 (11.3)*LVM (g) 234.4 (�79.6) 232.3 (�74.5) 219.4 (�69.2)*PWV (m/s) 13.7 (�2.4) 13.4 (�2.4) 12.5 (�1.9)*

*significantly lower as compared with the values from baseline (0) and 6 months after peri-odontal treatment (1).


684 Vidal et al.

cant improvement of endothelialfunction, and consequently, thereduction in arterial stiffness, afterperiodontal therapy conducted onhealthy patients (Seinost et al. 2005,Blum et al. 2007, Tonetti et al. 2007),hypertensive patients (Higashi et al.2008) and atherosclerotic diseasepatients (Mercanoglu et al. 2004,Higashi et al. 2009). Although endo-thelial dysfunction was measured by adifferent methodology (flow-mediateddilation) in the studies cited above,their results can be interpreted thesame way as ours. Therefore, peri-odontal therapy, leading to the reduc-tion in clinical and systemic infectionand inflammation, seems to improveendothelial function.

To our knowledge, our study wasthe first one to evaluate the possiblebeneficial effects of periodontal ther-apy on left ventricular hypertrophy.It has been shown that severe formsof periodontitis were associated withLVM in hypertensive patients, andalso that the re-establishment of thenitrous oxide pathway is an impor-tant therapeutic target for left ven-tricular hypertrophy (Angeli et al.2003, Franek et al. 2009). The reduc-tion in LVM observed in some ofthe patients in our study may becompared with the reductiondescribed after some types of multi-drug protocols (Okin et al. 2004,Miller et al. 2010). Hence, it couldbe inferred that non-surgical peri-odontal therapy may, indirectly, helpreduce left ventricular mass, proba-bly due to improved endothelialfunction and lower blood pressurelevels. As LVM reduction is associ-ated with lower cardiovascular mor-bidity and mortality (Verdecchiaet al. 2003, Devereux et al. 2004,Okin et al. 2008), it is possible toconsider that periodontal healthre-establishment may be beneficialand reduce cardiovascular risk insome patients.

The effects of periodontal therapyon blood levels of inflammatorymarkers associated with cardiovascu-lar diseases have been described inthe literature. Most studies showedreduction in plasma and/or serumlevels of IL-6, fibrinogen, CRP andother acute-phase proteins and inter-leukins after non-surgical periodon-tal therapy (Iwamoto et al. 2003,D’Aiuto et al. 2004, Montebugnoliet al. 2005, Higashi et al. 2008,

Marcaccini et al. 2009, Offenbacheret al. 2009, Vidal et al. 2009, Shimadaet al. 2010, Bokhari et al. 2012). Themethods and recall intervals variedbetween studies ranging from 1 to6 months. Some studies, however,did not observe reduction in theblood levels of inflammatory mark-ers, as a consequence of periodontaltherapy (Ide et al. 2003, Yamazakiet al. 2005). The population studiedin both cases differs from our groupbecause they presented either mild tomoderate periodontitis or extremelylow levels of the inflammatory mark-ers on baseline evaluation. Offenb-acher et al. (2009), in a controlledrandomized multi-centred clinicaltrial (PAVE - Periodontitis and Vas-cular Events), observed that despitebeing effective on reducing CRP lev-els in patients with initially highervalues (>3 mg/l) and preventing theelevation in patients with CRP levelsinitially between 1 and 3 mg/l, peri-odontal therapy had little effect onobese patients and patients with low(<1 mg/l) CRP levels on baseline.The individual inflammatory profileof each subject, and the variety ofpossible modifiers (such as smoking,overweight, non-periodontal infec-tions, inflammatory diseases otherthan periodontitis) may interfere onthe response to periodontal therapy,explaining why some patients do notshow reduction in the inflammatorymarkers analysed, despite having animprovement of clinical periodontalparameters. In this regard, D’Aiutoet al. (2004) described a more evi-dent reduction in inflammatorymarkers in patients who had betterresponse to periodontal therapy.

The reduction in CRP levelsobserved on our group (0.5 mg/dL),after periodontal therapy, can beconsidered relevant and even com-pared with the reduction observedafter pharmacological therapy withstatins (Ridker et al. 1998) withoutthe potential collateral effects of suchdrugs. The periodontal therapy doesnot increase the risk of cardiovascu-lar events in hypertensive patients(Beck et al. 2008) and causes little orno discomfort (Fardal et al. 2002).

The population studied in thisstudy included refractory hyperten-sive patients, under treatment for atleast 2 years that, despite the goodadherence to the anti-hypertensivetherapy, remained with blood pres-

sure levels above 140 9 90 mmHg.This may suggest that other clinicalconditions besides the well-establishedcardiovascular risk factors may playan important role in the pathogenesisof hypertension, as well as, in theresponse to treatment. All the sub-jects included in the study presentedsevere generalized periodontitis, andreported that they had never receivedperiodontal therapy.

Non-surgical periodontal treat-ment was effective on reducing VPI,BOP, PPD and CAL 6 months afterperiodontal therapy completion. Theresults are in accordance with the lit-erature that shows that non-surgicalperiodontal treatment is an effectiveway of treating chronic periodontitis(Badersten et al. 1984). As expected,as no periodontal treatment was per-formed, nor significant changes inmedical condition were noticed, nosignificant differences were foundbetween baseline and the 3-monthevaluation. VPI showed higher valuesat the 3-month re-evaluation, butchanges in this parameter may beexplained by the fact that patientswere scheduled exclusively for the den-tist at the baseline appointment, butnot for the 3-month re-evaluation,that was conducted during routinecardiologic follow-up. This may haveled to a more careful oral health careprior to the dental appointment.Although VPI mean values were sig-nificantly reduced 6 months after peri-odontal treatment, levels were stillsomewhat high. The patients werefrom a low socioeconomic status andhad never received periodontal ther-apy, or dental care on a regular basis.Moreover, the patients were initiallyscheduled for cardiologic examina-tion, not specifically for dental care,were only seen 6 months after theperiodontal treatment and oralhygiene was only demonstrated instage 2, not reinforced during thestudy. On the other hand, there was asignificant reduction in BOP,indicating an improvement in the gin-gival conditions after periodontaltreatment.

In this study, no adverse reactionsor noteworthy complications occurredin the patients throughout the studyperiod. In fact, standard periodontaltherapy, divided into short sessions,presented itself as a relatively cheapand safe treatment, even for hyperten-sive patients. The protocols suggested



for the management of hypertensivepatients were followed (AmericanAcademy of Periodontology 2002).

Even though there is still no con-clusive evidence that the preventionand treatment of periodontitis mayreduce cardiovascular risk, the resultsof this study suggest that periodontaltherapy and the maintenance of ahealthy periodontium may interferein established and potential cardio-vascular risk factors. The authors areaware of the intrinsic limitations ofthe study presented. Firstly, althoughsample size estimation was calculated,the patient sample was relativelysmall. Secondly, no control groupwas enrolled to compare the long-term changes in cardiovascular riskfactors and inflammatory biomar-kers. Other studies, with higher num-ber of patients and other populationsshould be conducted to allow theextrapolation of these assertions.Although some questions are still tobe answered, we may recommend thathypertensive patients receive dentaland periodontal care since there-establishment of oral health itselfprovides evident benefits to thepatients (Needleman et al. 2004).

In conclusion, non-surgical peri-odontal therapy reduced plasma lev-els of CRP, IL-6 and fibrinogen in asample of refractory hypertensivepatients. Blood pressure, LVM andarterial stiffness, an indicator ofendothelial function, also improved6 months after the end of periodontaltreatment.

Acknowledgements

The authors thank Dr MarceloBarros and Ana Beatriz Lima for theirassistance with the study (NationalInstitute of Cardiology, Rio deJaneiro, Brazil).

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Address:Ricardo Guimar~aes FischerFaculdade de OdontologiaUniversidade do Estado do Rio de JaneiroBoulevard 28 de Setembro, 157Vila Isabel- Rio de Janeiro – RJ – BrazilCEP: 20551-030E-mail: [email protected]

Clinical Relevance

Scientific rationale for the study:Although there are studies suggest-ing that periodontal diseases mayinfluence the course of cardiovascu-lar diseases, there is still somecontroversy regarding the effectsof periodontal therapy, and the

consequent reduction in inflamma-tory burden, on plasma levels ofinflammatory markers and othercardiovascular risk factors.Principal findings: The present pilotstudy showed that non-surgical peri-odontal therapy led to the reductionof established cardiovascular risk

factors in refractory hypertensivepatients even after adjustment forpossible confounders.Practical implications: These find-ings may contribute to presentknowledge that periodontal therapymay be beneficial for individualswith refractory hypertension.



non-surgical periodontal treatment reduces cardiovascular risk in refractory hypertensive patients:...

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