Effectiveness of Full-Mouth andPartial-Mouth Scaling and Root Planingin Treating Chronic Periodontitis inSubjects With Type 2 DiabetesVanessa Renata Santos,* Jadson Almeida Lima,* Adriana Cutrim De Mendoncxa,*Maria Beatriz Braz Maximo,* Marcelo Faveri,* and Poliana Mendes Duarte*

Background: This study evaluated the clinical and meta-bolic effects of full-mouth scaling and root planing (FMSRP)compared to partial-mouth scaling and root planing (PMSRP)in patients with type 2 diabetes and chronic periodontitis, andit assessed the impact of the glycemic status on the clinicaland metabolic response to periodontal therapy.

Methods: In this clinical trial, 18 subjects with diabetesreceived FMSRP in a maximum of 24 hours, and 18 subjectsreceived PMSRP in a maximum of 21 days. Visible plaqueaccumulation, bleeding on probing, suppuration, probingdepth, clinical attachment level (CAL), and glycosylatedhemoglobin (HbA1c) levels were obtained at baseline and at3 and 6 months post-therapy. Baseline HbA1c values ‡9%and <9% defined subjects with poorly and better-controlleddiabetes, respectively.

Results: All clinical parameters improved after therapy(P <0.05). No significant differences were observed betweentreatment groups for clinical and metabolic parameters atany time (P >0.05). There were no changes in the HbA1c levelsafter therapy (P >0.05). No subject reported any adverse ef-fects during the study. Individuals with better-controlled dia-betes achieved a lower mean CAL at 6 months post-therapy,when FMSRP and PMSRP were evaluated together (P <0.05).

Conclusions: FMSRP and PMSRP were equally effective intreating chronic periodontitis in subjects with type 2 diabetes,without significant improvements in the glycemic control at 3and 6 months. Considering the periodontal therapy as a whole(FMSRP plus PMSRP), subjects with better-controlled diabetesexhibited a benefit in CAL at 6 months compared to subjectswith poorly controlled disease. J Periodontol 2009;80:1237-1245.

KEY WORDS

Chronic periodontitis; dental scaling; diabetes mellitus;root planing; therapy.

Specific bacterial biofilm is wellestablished as the etiologic agentof periodontal diseases;1 however,

evidence suggests that the severity andprogression of periodontal destructionmay be related to some environmentaland systemic modifiers, such as smok-ing and diabetes mellitus (DM).2,3 DM isa metabolic disease characterized byabnormal glucose tolerance and hyper-glycemia that can be involved in severaloral and systemic long-term complica-tions.4-5 Type 2 DM is the most preva-lent type of DM among middle-agedsubjects; it results from changes ininsulin molecules and/or their cell re-ceptors, impairing insulin function.5

A number of studies2,3,6-10 reportedhigh prevalence, severity, and progres-sion of periodontal diseases in subjectswith diabetes, providing substantial evi-dence to support DM as a risk factor forperiodontal diseases. It was also sug-gested that DM and periodontitis mayhave a mutual influence because at thesame time that DM predisposes to peri-odontal diseases, the established peri-odontitis may intensify the DM.11,12 Thechronic challenge of the periodontalpathogens may provide a constantsource of proinflammatory cytokinesthat may be associated with tissue insulinresistance and poor glycemic control insubjects with diabetes.13,14 Based on this

* Department of Periodontology, Dental Research Division, Guarulhos University,Guarulhos, SP, Brazil.

doi: 10.1902/jop.2009.090030

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theory, it was hypothesized that the successful controlof periodontal infection could improve the clinical signsofperiodontitis as well as the metaboliccontrol ofDM.13

Various investigations15-20 demonstrated that scal-ing and root planing (SRP), associated or not with an-tibiotics, yielded clinical benefits in subjects withdiabetes, including a reduction in probing depth(PD), bleeding on probing (BOP), and suppuration(SUP) and a gain in clinical attachment level (CAL).Simultaneously, these interventional studies15-23 as-sessed the potential effects of different types of peri-odontal therapy on glycemic control in subjects withdiabetes, as measured by glycosylated hemoglobin(HbA1c) levels. Some investigations13,15,21,22 sug-gested that improvements in periodontal conditionpositively affect metabolic control, whereas otherstudies16,20,23,24 did not find this beneficial effect.

It was hypothesized that partial-mouth SRP(PMSRP) would lead to reinfection of the already in-strumented sites from sites not yet treated and/orother intraoral niches, whereas the short-term full-mouth elimination of pathogens would help to preventsuch reinfection.25,26 Particularly in a group suscepti-ble to infection, e.g., subjects with diabetes, full-mouth SRP (FMSRP) could present some advantagesover PMSRP, such as a decrease in the number ofvisits to the dentist and an abrupt reduction in bacte-rial infection. Despite evidence of the effect of FMSRPin subjects with diabetes,16,19,27 to the best of ourknowledge, no study has evaluated the long-termclinical and glycemic impact of FMSRP comparedto PMSRP in subjects with type 2 diabetes.

Cross-sectional studies28-31 observed that subjectswith poor glycemic control had more severe peri-odontitis than individuals with well-controlled disease.Although many studies15-23 evaluated the effect ofvarious periodontal treatments for subjects with diabe-tes, they focused on the clinical and metabolic re-sponses to these therapies, considering the diabeticgroup as a whole. Few interventional studies32,33 dif-ferentiated the glycemic status of the subjects with di-abetes to assess the effect of periodontal therapy inindividuals with better- and poorly controlled disease.

Therefore, the aims of the present study were toevaluate the clinical and metabolic effects of FMSRPin subjects with type 2 diabetes and chronic peri-odontitis compared to PMSRP at 3 and 6 months fol-low-up and to assess the impact of the glycemic statuson the clinical and metabolic response to non-surgicalperiodontal therapy.

MATERIALS AND METHODS

Sample Size CalculationThe ideal sample size to ensure adequate power forthis clinical trial was calculated considering differ-ences ‡1 mm for CAL and a standard deviation of

0.94 mm between groups in initially deep periodontalpockets (>6 mm). Based on these calculations, it wasdecided that 14 subjects per group were necessary toprovide 80% power with a = 0.05.

Subject PopulationThirty-six subjects (age range: 36 to 70 years) diag-nosed with type 2 DM and chronic periodontitis wereselected from the population referred to the Periodon-tal Clinic of Guarulhos University, from July 2007 untilJanuary 2008. Detailed medical and dental recordswere obtained. Subjects who fulfilled the inclusion/ex-clusion criteria were invited to participate in the study.All eligible subjects were thoroughly informed of thenature, potential risks, and benefits of the study andprovided written informed consent. The study proto-col was approved by Guarulhos University’s EthicsCommittee in Clinical Research.

Inclusion and Exclusion CriteriaData on the duration of DM and medications were re-trieved from the medical records of the subjects at thebeginning of the study. All subjects had received a di-agnosis of type 2 DM within the past 5 years and wereunder insulin supplementation, a diet regimen, and/ororal hypoglycemic agents. Subjects were diagnosedwith generalized chronic periodontitis, based on theclinical and radiographic criteria proposed by the1999 World Workshop for Classification of Periodon-tal Diseases and Conditions.34 All subjects were >30years old; had ‡15 teeth, excluding third molars andteeth with severe periodontitis and/or caries, indi-cated to surgical extraction; and >30% of sites withPD and CAL ‡5 mm at baseline.

Exclusion criteria were pregnancy, lactation, cur-rent smoking or smoking within the past 5 years, peri-odontal and/or antibiotic therapies in the previous 6months, use of mouthrinses containing antimicrobialsin the preceding 2 months, any systemic condition(except DM) that could affect the progression of peri-odontal disease (e.g., immunologic disorders), andthe long-term administration of anti-inflammatoryand immunosuppressive medications. Subjects withperiapical pathology, orthodontic appliances, andmultiple systemic complications of DM were also ex-cluded from the study.

Fasting Plasma Glucose (FPG) and GlycosylatedHemoglobin LevelsAll blood analyses were performed by a single labora-tory (Guarulhos University Clinical Analysis Labora-tory). Blood samples were taken from each subjectat baseline and at 3 and 6 months post-therapy.FPG, measured using the glucose oxidase method,was expressed in milligrams per deciliter (normalhealthy range, 60 to 110 mg/dl). HbA1c, measuredbyhigh-pressure liquidchromatography,wasexpressed

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as a percentage (normal healthy range, 4.5% to 8%).Baseline HbA1c values ‡9% were considered poorlycontrolled DM, and baseline HbA1c levels <9% wereconsidered better-controlled DM.35

Clinical MonitoringAll clinical examinations were performed by one ex-aminer (VRS), calibrated according to the methoddescribed by Araujo et al.36 The intraexaminer vari-ability was 0.21 mm for PD and 0.25 mm for CAL.The examiner was able to provide repeatable PD andCAL measurements of under 0.5 mm of differences.The clinical parameters registered dichotomously,i.e., BOP and SUP, were evaluated by the Kappa-Lighttest, and the intraexaminer agreement was >0.85.The examiner was unaware of the treatment assign-ment and the metabolic status of the subjects.

The following parameters were assessed at six sitesof all teeth, excluding third molars (mesio-buccal,medio-buccal, disto-buccal, mesio-lingual, medio-lingual, and disto-lingual) using a manual periodontalprobe (15 mm):† visible plaque accumulation (plaqueindex; PI): presence or absence of plaque alongthe cervical margin;37 BOP: presence or absence ofbleeding up to 15 seconds after gentle probing;SUP: presence or absence of spontaneous SUP orSUP on probing; PD: distance between the gingivalmargin and the bottom of the sulcus/pocket; andCAL: distance between the cemento-enamel junctionand the bottom of the sulcus/pocket. Clinical exami-nations were performed at baseline and at 3 and 6months post-therapy.

Experimental Design and Treatment ProtocolsAll subjects were submitted to the hygiene phase ofperiodontal therapy, including supragingival plaqueand calculus removal, exodontia, provisional restora-tion, and removal of overhangs of fillings. They wereinstructed to perform a brushing technique using asoft toothbrush, dental floss, and interdental tooth-brushes, as necessary. Moreover, all volunteers re-ceived the same brand of toothpaste to use duringthe course of the study.‡

In this prospective, parallel, masked, randomized,and controlled clinical trial, 36 subjects with type 2diabetes and chronic periodontitis were randomlyassigned, by the toss of a coin by the same assessor(PMD), to the control or test group.

FMSRP (test group; n = 18): SRP was completed intwo appointments, lasting ;120 minutes each, per-formed under local anesthesia (3% prilocaine withfelypressin) using periodontal curets§ and an ultra-sonic device.i SRP of all teeth was concluded in a max-imum of 24 hours on two consecutive days, startingwith the right maxillary and mandibular quadrants.

PMSRP (control; n = 18): SRP was completed in fourappointments, lasting ;60 minutes each, performed

under local anesthesia (3% prilocaine with fely-pressin) using periodontal curets¶ and an ultrasonicdevice.# Treatment of all teeth was concluded in amaximum of 21 days, starting in the right maxillaryquadrant, followed by the right mandibular, left max-illary, and left mandibular quadrants.

SRP in both groups was performed by the sameoperator without the use of any antibiotics or localantimicrobials. The supportive therapy, includingprofessional plaque control with an abrasive sodiumcarbonate air-powder system** and reinstruction oforal hygiene, was performed at 3 and 6 monthspost-therapy. The subjects were asked to report anychanges in their DM treatment regimen at the fol-low-up appointments. To assess the effects of theperiodontal treatments on metabolic control, nochanges in the medication or diet were made duringthe study period (6 months).

Statistical AnalysisThe statistical analysis was performed using a com-mercially available software program.†† The biostat-istician was unaware of the treatment assignment orthe metabolic status of the subjects. Data were exam-ined first for normality using the Kolmogorov-Smirnovtest; because they did not achieve normality, analysiswas performed using non-parametric methods. Theprimary variables were the changes in PD andCAL levels from baseline to 3 and 6 months. The sec-ondary variables were the changes in the other clinicalparameters and in the levels of HbA1c and FPG. Thepercentage of sites with visible plaque, BOP, and SUPand mean PD, CAL, HbA1c, and FPG levels werecomputed for each subject. Clinical parameters wereaveraged across subjects and in the therapeutic(PMSRP and FMSRP) and glycemic (better or poorlycontrolled DM) groups. HbA1c and FPG data werealso averaged in the therapeutic and glycemic groups.The changes in PD and CAL over time were examinedin subsets of sites for both therapeutic groups, accord-ing to the initial PD: £3 mm (shallow), 4 to 6 mm (in-termediate), and ‡7 mm (deep). Values for eachclinical parameter were averaged separately withinthe three PD categories in each subject and then aver-aged across subjects in the treatment groups. The sig-nificance of the clinical and metabolic differencesbetween FMSRP and PMSRP, as well as betweensubjects with better- and poorly controlled disease,was compared using the Mann-Whitney U test. The

† UNC15, Hu-Friedy, Chicago, IL.‡ Colgate Total, Anakol Industria e Comercio, – Kolynos do Brasil – Colgate

Palmolive, Sao Bernardo do Campo, SP, Brazil.§ Hu-Friedy.i Jet Sonic, Gnatus, Ribeirao Preto, SP, Brazil.¶ Hu-Friedy.# Jet Sonic, Gnatus.** Jet Sonic, Gnatus.†† SPSS for Windows version 12.0, SPSS, Chicago, IL.

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significance of differences in age and duration of DMbetween FMSRP and PMSRP groups was also com-pared using the Mann-Whitney U test. The Friedmantest was used to detect statistically significant differ-ences within each therapeutic or glycemic groupamong the three time points. When there were signif-icant differences by the Friedman test, a pairwisecomparison was performed using the Wilcoxon test.The x2 test was used to detect differences in the fre-quencies of gender between FMSRP and PMSRPgroups. The level of significance was set at 5%.

RESULTS

Subject RetentionNo subject dropped out of the study. Thus, 36 subjectscompleted the study: 18 in the control group (PMSRP)and 18 in the test group (FMSRP). No subject reportedany adverse effects, such as fever or indisposition,during the study.

Clinical ResultsThe demographic characteristics of the subjects atbaseline for both therapeutic groups are presentedin Table 1. No statically significant differences wereobserved between PMSRP and FMSRP groups with re-gard to age, duration of DM, gender, glycemic control,and distribution of DM treatment regimens.

Table 2 presents the mean full-mouth values for theclinical parameters at baseline and at 3 and 6 months

after therapy. No statistically significant differenceswere observed between therapeutic groups for anyclinical parameters at any time point (P >0.05). Boththerapies led to a statistically significant decrease inthe mean percentage of sites with visible plaque andBOP and the mean PD and CAL at 3 months (P<0.05). In addition, these improvements were sus-tained at 6 months post-therapy (P <0.05). SUP pro-gressively decreased in the FMSRP group over time (P<0.05). However, the percentage of sites exhibitingSUP significantly decreased in the PMSRP group onlyat 6 months (P <0.05).

The mean changes in PD and CAL for both treat-ment groups between baseline and 3 months andbetween baseline and 6 months post-therapy arepresented in Figure 1. The results are organized ac-cording to full-mouth values as well as different base-line PD categories: shallow (£3 mm), intermediate (4to 6 mm), and deep (‡7 mm) sites. FMSRP and PMSRPgroups showed similar reductions in PD and CAL,considering full-mouth values and all PD categoriesat 3 and 6 months post-therapy. For both groups,the initially deep sites had the greatest reduction inmean PD and CAL, followed by the intermediateand shallow sites.

HbA1c ranged from 4.8% to 8.7% and from 9% to12% for the subjects with better- and poorly controlleddisease, respectively. The comparisons between bet-

ter and poor control were made considering thenon-surgical periodontal therapy as a whole(FMSRP plus PMSRP). Statistical comparisonsamong four groups (poorly controlled diseasetreated by FMSRP, better-controlled diseasetreated by FMSRP, poorly controlled diseasetreated by PMSRP, and better-controlled dis-ease treated by PMSRP) were not possible be-cause of the small sample size per group, asobserved in Table 1. The clinical parametersof subjects with better- (HbA1c level <9%)and poorly controlled (HbA1c level ‡9%) dis-ease at baseline and at 3 and 6 months post-therapy are presented in Table 3. A statisticallysignificant decrease in the mean percentage ofsites with visible plaque, BOP, and SUP and inmean PD and CAL was observed for subjectswith poor and good metabolic control at 3and 6 months post-therapy (P <0.05). Al-though not statistically significant, subjectswith diabetes with poor metabolic control hada tendency for higher visible plaque accumula-tion (82.9% – 22.6%) than those with goodmetabolic control (56.9% – 34.5%) at baseline(P >0.05). The mean percentage of sites withBOP and SUP and the mean PD and CAL weresimilar for subjects with better- and poorly con-trolled disease at baseline (P >0.05). There

Table 1.

Demographic Characteristics at Baseline forFMSRP and PMSRP Groups

Characteristic

FMSRP

(n = 18)

PMSRP

(n = 18)

Age (years)Mean – SD 52.3 – 9.4 53.0 – 9.2Range 37 to 70 36 to 67

Gender (n)Male 8 8Female 10 10

Glycemic control (n)Poor 11 10Better 7 8

DM treatment regimen (n)Diet 2 4Diet + insulin 3 2Diet + oral hypoglycemic agents 11 10Diet + oral hypoglycemic

agents + insulin2 2

Duration of DM (years; mean – SD) 6.8 – 1.1 6.3 – 0.8

There are no differences between groups at baseline regarding age and duration of DM(Mann-Whitney test) and regarding gender, glycemic control, and DM treatmentregimen (x

2 test; P >0.05).

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were no differences with regard to any clinical param-eter between these two groups at 3 months after peri-odontal treatment (P >0.05). However, subjects withbetter-controlled disease had a lower mean CAL(3.1 – 0.7 mm versus 3.5 – 0.8 mm) at 6 months afterSRP (P <0.05).

Metabolic ResultsThere were no statistically significant differences be-tween FMSRP and PMSRP groups in the mean HbA1cand FPG levels at baseline and at 3 and 6 monthspost-therapy (P >0.05). In addition, there were nochanges in the HbA1c values from baseline to 3months and to 6 months for any therapeutic group(P >0.05). A statistically significant increase in meanFPG level was observed for the FMSRP group at 3 and6 months and for the PMSRP group at 6 months aftertherapy (Table 2). The distribution of subjects strati-fied by changes in HbA1c from baseline to 3 and 6months are presented in Table 4. A ‡0.5% increase

or decrease from baseline to the follow-up examina-tion was considered a change; otherwise, the levelof glycemic control was considered stable. As ex-pected, the mean level of HbA1c was higher for sub-jects with poorly controlled disease at baseline. Thisdifference was also observed at 6 months after ther-apy but not at 3 months after therapy. There wereno changes in HbA1c over time for subjects withpoorly controlled disease. Unexpectedly, the meanlevels of HbA1c increased from baseline to 3 monthspost-therapy for the individuals with better-controlleddisease (7.3% – 1.2% to 9.1% – 1.8%). FPG levels werehigher for subjects with poor glycemic control than forthose with good control at all experimental times.There was an increase in the FPG levels in the groupwith poorly controlled disease at 3 and 6 months aftertreatment, whereas these values remained unchangedfor the group with better-controlled disease (Table 3).

DISCUSSION

There is increasing interest in the developmentof efficient periodontal therapies for subjects withdiabetes, a group considered at risk for periodontaldiseases. In addition, various studies15-21,23 aimedto elucidate the effects of periodontal therapy on theglycemic control of subjects with diabetes. The pres-ent study evaluated the clinical and metabolic effectsof FMSRP compared to PMSRP in subjects with type 2diabetes and chronic periodontitis. In addition, the im-pact of non-surgical SRP on clinical and metabolic

Table 2.

Clinical and Metabolic Parameters(mean – SD) for FMSRP and PMSRPGroups at Baseline and at 3 and6 Months Post-Therapy

Parameter Time Point FMSRP (n = 18) PMSRP (n = 18)

PI (%) Baseline 70.0 – 31.0a 74.1 – 31.0a

3 months 33.9 – 28.1b 26.2 – 14.3b

6 months 34.2 – 23.5b 26.2 – 16.5b

BOP (%) Baseline 53.8 – 26.1a 53.0 – 36.0a

3 months 8.9 – 8.2b 11.9 – 10.2b

6 months 8.0 – 10.9b 11.4 – 12.1b

SUP (%) Baseline 2.9 – 5.8a 2.5 – 4.6a

3 months 1.4 – 3.1b 2.5 – 6.9a

6 months 0.5 – 1.1c 1.0 – 1.9b

PD (mm) Baseline 3.2 – 0.5a 3.5 – 0.6a

3 months 2.4 – 0.6b 2.5 – 0.7b

6 months 2.6 – 0.3b 2.8 – 0.5b

CAL (mm) Baseline 3.8 – 0.7a 4.2 – 0.9a

3 months 3.2 – 0.7b 3.5 – 0.7b

6 months 3.2 – 0.6b 3.5 – 0.9b

HbA1c (%) Baseline 9.1 – 2.1a 9.2 – 1.9a

3 months 9.8 – 2.3a 9.6 – 2.0a

6 months 9.5 – 1.9a 10.3 – 2.6a

FPG (mg/dl) Baseline 160.8 – 64.7a 177.6 – 54.3a

3 months 193.9 – 76.8b 175.0 – 53.9a

6 months 190.6 – 86.0b 200.8 – 64.1b

Different letters indicate statistically significant differences over time by theFriedman and Wilcoxon tests (P <0.05). There were no differences betweenthe treatment groups at any time point; Mann-Whitney test (P >0.05).

Figure 1.Mean – SD changes in PD and CAL for the full mouth and at sites withinitial PD £3, 4 to 6, and ‡7 mm between baseline and 3 and 6 monthsfor FMSRP and PMSRP groups. There were no differences between thetreatment groups at any time point. Mann-Whitney test; P >0.05.

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parameters was observed in subjects with better- andpoorly controlled disease.

In this study, SRP in 24 hours was not superior toquadrant-wise SRP performed over a 3-week intervalin subjects with diabetes. Thus, both FMSRP andPMSRP may be considered effective in the treatmentof subjects with diabetes and chronic periodontitis,producing reductions in PD and BOP and gain inCAL. Our results from subjects with diabetes are inagreement with previous studies26,38 and systematicreviews,39,40 which demonstrated that an improve-ment in clinical parameters in subjects with chronicperiodontitis and without diabetes could be achievedequally by FMSRP and PMSRP after 6 months.

SRP alone or in association with antimicrobialsyielded improvements in the periodontal conditionof subjects with diabetes and periodontitis.15-20,22

The favorable clinical response observed for thePMSRP group in our study corroborates the findingsof previous investigations17,18,20,22 evaluating thisconventional therapy. Also, our results for the FMSRPgroup are consistent with studies15,19 that focused onthe reduction of periodontal infection in a short-terminterval and found improvements in the periodontalstatus of subjects with diabetes.

Cross-sectional studies28-31,41 demonstrated thatsubjects with poorly controlled disease have more se-vere periodontitis than subjects with well-controlleddiabetes. Tsai et al.30 noted that subjects with poorlycontrolled (HbA1c levels >9%) type 2 diabetes had ahigher prevalence of severe periodontal disease thanindividuals without diabetes. Lim et al.31 demonstratedthat subjects with type 1 or 2 diabetes with HbA1clevels <8% exhibitedabetterperiodontal condition thanindividuals with HbA1c levels ‡8%. However, the exist-ing interventional investigations evaluated the effectsof different therapies for diabetic groups as a whole,without considering their glycemic status. Therefore,to provide information about the impact of glycemiccontrol on the clinical and metabolic response toSRP, we divided the subjects with type 2 diabetes intothose with better-controlled disease (HbA1c <9%) orpoorly controlled disease (HbA1c ‡9%).

Although not statistically significant, there was atrend toward more plaque accumulation in the sub-jects with poorly controlled disease at baseline (Table3). The compliance of subjects with diabetes with oralhygiene was already associated with HbA1c levels,with improved compliance among those with betterglycemic control.24,42 When FMSRP and PMSRP wereevaluated together, the response to periodontal treat-ment was similar for subjects with better- and poorlycontrolled disease for almost all clinical parameters(Table 3); only the mean CAL was lower for the sub-jects with better-controlled disease at 6 months.

Table 3.

Clinical and Metabolic Parameters(mean – SD) of Subjects With Poorly andBetter-Controlled Diabetes at 3 and 6Months After Non-Surgical PeriodontalTherapy, Independent of Treatment Type

Parameter Time Point

Poor Control

(HbA1c ‡9%;

n = 21)

Better Control

(HbA1c <9%;

n = 15)

PI (%) Baseline 82.9 – 22.6a 56.9 – 34.5a

3 months 31.6 – 21.1b 30.2 – 26.4b

6 months 31.1 – 11.6b 28.8 – 29.1b

BOP (%) Baseline 55.2 – 32.0a 58.0 – 30.5a

3 months 10.7 – 8.0b 12.5 – 11.4b

6 months 7.7 – 7.8b 12.5 – 15.0b

SUP (%) Baseline 2.7 – 4.5a 2.6 – 6.1a

3 months 0.9 – 2.3b 0.6 – 1.3b

6 months 0.7 – 1.8b 0.7 – 1.3b

PD (mm) Baseline 3.4 – 0.6a 3.3 – 0.6a

3 months 2.7 – 0.4b 2.6 – 0.3b

6 months 2.7 – 0.5b 2.6 – 0.4b

CAL (mm) Baseline 4.2 – 0.7a 3.8 – 0.8a

3 months 3.6 – 0.8b 3.1 – 0.6b

6 months* 3.5 – 0.8b 3.1 – 0.7b

HbA1c (%) Baseline* 10.5 – 1.2a 7.3 – 1.2a

3 months 10.1 – 2.3a 9.1 – 1.8b

6 months* 10.7 – 2.0a 8.6 – 2.2a

FPG (mg/dl) Baseline* 193.0 – 57.7b 135.8 – 45.3a

3 months* 208.7 – 72.5b 150.5 – 36.0a

6 months* 223.8 – 76.8b 156.4 – 52.5a

Different letters indicate statistically significant differences over time byFriedman and Wilcoxon tests (P <0.05).* Difference between better- and poorly controlled disease; Mann-Whitney

test (P <0.05).

Table 4.

Distribution of Subjects (n) Stratified byChanges in HbA1c From Baseline to3 and 6 Months

FMSRP (n = 18) PMSRP (n = 18)

Change in HbA1c3

Months

6

Months

3

Months

6

Months

Decrease in HbA1c 5 8 8 6

Increase in HbA1c 9 7 7 10

No change in HbA1c 4 3 3 2

A ‡0.5% increase or decrease from baseline to the follow-up examinationwas considered a change; otherwise, the level of glycemic control wasconsidered stable.

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Christgau et al.32 did not find a significant influence ofmetabolic control on the periodontal response in sub-jects with diabetes stratified according to differentlevels of HbA1c. However, the investigators includedtype 1 and 2 DM, and their sample of subjects withpoor glycemic control was too small (only three indi-viduals). Tervonen and Karjalainen33 observed aworse clinical response to periodontal therapy in sub-jects with type 1 diabetes with poor metabolic control,identified by medical history, compared to subjectswith well-controlled disease. However, the methodo-logic differences of these studies hampered a morestraight comparison to our results.

Based on the theory that infections are implicatedin tissue insulin resistance,43,44 it was hypothesizedthat DM and periodontitis could have reciprocal influ-ence.12,13 Consequently, the effective reduction ofpathogens after periodontal therapy could promotea better metabolic control. HbA1c, which estimatesthe stable glucose/hemoglobin binding over the prior3 months, is considered an accurate means of follow-ing glycemic control in a subject already diagnosedwith DM. In our study, the levels of HbA1c did notchange significantly at 3 and 6 months followingFMSRP or PMSRP (Table 2). These findings are inagreement with studies16,20,23-25 in which PMSRPand FMSRP resulted in improvements in the clinicalparameters without significant changes in the glyce-mic control in individuals with diabetes. Conversely,our results are in contrast with those from investiga-tions15,17,19,21,22 that showed improvements in glyce-mic control in individuals with type 2 DM after PMSRPor FMSRP. The contribution of periodontal therapy toimproving glycemic control in subjects with type 2 di-abetes remains controversial; caution should be usedin the interpretation of these findings because of dif-ferences in study designs, types of DM, initial levelsof HbA1c, therapeutic protocols, severity of peri-odontitis, and sample sizes. It was established that alarge sample size (‡246 subjects) is needed for anysignificant reduction in HbA1c to be observed.23

Surprisingly, many subjects had an increase inHbA1c levels after therapy (Table 4), and the increasewas statistically significant for subjects with better-controlled disease at 3 months after SRP (Table 3).Therefore, we noted that many subjects with diabetesare able to maintain intermittent control of glycemia.Tervonen et al.45 also observed that some subjectswith better- or poorly controlled type 1 diabetes hadimprovements in DM control after periodontal ther-apy, whereas the glycemic control remained stableor increased in other subjects. These findings maybe attributed to the role of other variables, such asdiet, physical activity, compliance with medications,other infectious diseases, and medical monitoring,on the glycemic status. This hypothesis can be rein-

forced by the observation of changes in the levels ofFPG, which reflect the glycemic control at a given timepoint and may vary rapidly according to diet, physicalactivity, and medications. In this way, the influence ofdiabetic status on the periodontal healing responseprobably becomes more significant when the meta-bolic control of DM is constantly poor or good. There-fore, the maintenance of lower CAL observed forsubjects with better-controlled disease at 6 monthsand the appearance of further clinical differences be-tween subjects with poorly and better-controlled dis-ease might be dependent on the long-term metaboliccontrol in these subjects.

CONCLUSIONS

PMSRP and FMSRP resulted in comparable improve-ments in periodontal parameters in subjects with type2 diabetes and chronic periodontitis at 3 and 6months. In addition, neither therapy resulted in im-provements in the HbA1c level at 3 and 6 months.Finally, subjects with better- and poorly controlleddiabetes showed similar clinical responses to SRP,with only a significantly lower CAL for subjects withbetter-controlled disease at 6 months. Longitudinalfollow-up is needed to evaluate the long-term out-comes in relation to periodontal health and the sys-temic implications for these subjects.

ACKNOWLEDGMENT

The authors report no conflicts of interest related tothis study.

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44. Ozdem S, Akcam M, Yilmaz A, Artan R. Insulin resis-tance in children with Helicobacter pylori infection.J Endocrinol Invest 2007;30:236-240.

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Correspondence: Dr. Poliana Mendes Duarte, GuarulhosUniversity – Dental Research Division, Dr. Nilo Pecxanha,81 – Centro, 07011-040, Guarulhos, SP, Brazil. Fax: 55-11-2464-1758; e-mail: pduarte@ung.br.

Submitted January 14, 2009; accepted for publicationMarch 26, 2009.

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