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Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus …
Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20
Original ResearchReceived: 18th
 April 2015  Accepted: 10th
 July 2015  Conflicts of Interest: None
Source of Support: Nil
Relationship between Severity of Periodontal Disease and Control of Diabetes (Glycated
Hemoglobin) in Patients with Type 1 Diabetes Mellitus
Ankita Jindal1
, Anuj Singh Parihar2
, Meenakshi Sood3
, Pinojj Singh4
, Nandini Singh5
Contributors:
1
Senior Lecturer, Department of Periodontology, RKDF Dental
College and Research Centre, Bhopal, Madhya Pradesh, India;
2
Post-graduate Student, Department of Periodontology, People’s
College of Dental Sciences and Research Centre, Bhopal, Madhya
Pradesh, India; 3
Post-graduate Student, Department of Oral
Medicine and Radiology, People’s College of Dental Sciences
and Research Centre, Bhopal, Madhya Pradesh, India; 4
MDS,
Department of Periodontology, Dr. D.Y. Patil Dental College and
Hospital, Navi Mumbai, Maharashtra, India; 5
Private Practitioner,
Lucknow, Uttar Pradesh, India.
Correspondence:
Dr. Parihar AS. Department of Periodontology, People’s College
of Dental Sciences and Research Centre, Bhopal - 462 037,
Madhya Pradesh, India. Phone: +91-8827047003.
Email: Dr.anujparihar@gmail.com
How to cite the article:
Jindal A, Parihar AS, Sood M, Singh P, Singh N. Relationship
between severity of periodontal disease and control of diabetes
(glycated hemoglobin) in patients with Type 1 diabetes mellitus.
J Int Oral Health 2015;7(Suppl 2):17-20.
Abstract:
Background: Both diabetes mellitus (DM) and periodontitis
are chronic diseases affecting large number of the population
worldwide. Changes in human behavior and lifestyle over the
last century have resulted in a dramatic increase in the incidence
of diabetes in the world. This study was designed to evaluate the
relationship between severity of periodontal disease and control of
diabetes (glycated hemoglobin [HBA1c]) in patients with Type 1
DM in a hospital based study.
Materials and Methods: Fifty patients (n = 50) with Type 1
diabetes were enrolled in the study. They were divided into three
groups based on the degree of glycemic control by measuring
HbA1c levels as: “Good” (HBA1c ≤7) Group A, fair (HBA1c = 7-8)
Group B and poor (HBA1c >8) Group C. All enrolled patients
underwent detailed history and dental checkup. Evaluation for
periodontal disease was done by measuring dental plaque (plaque
index), inflammation of gums (gingival index), probing pocket
depth (PPD), and clinical attachment level.
Results: Type 1 diabetics with poor glycemic control had
increased gingival inflammation (P < 0.05), more dental plaque
(P < 0.05), increased PPDs (P < 0.05) and attachment loss
(P < 0.05) as compared to those with fair and good glycemic
control, respectively.
Conclusion: Severity of periodontal disease increases with poor
glycemic control in patients with Type 1 DM.
Key Words: Glycated hemoglobin levels, periodontal disease,
Type 1 diabetes mellitus
Introduction
Diabetes mellitus (DM) and periodontal diseases are
common chronic diseases observed worldwide. DM is
a heterogeneous chronic metabolic disorder principally
characterized by persistent hyperglycemia resulting
from defects in insulin action and/or insulin secretion.1
It affects more than 171 million individuals worldwide
and has reached epidemic status.2
DM results from a
malfunction of insulin-dependent glucose homeostasis.
Classically, they present a triad of symptoms including
polyuria, polyphagia, and polydipsia. These are the direct
result of hyperglycemia and osmotic imbalance.3
The
disease is characterized by an increased susceptibility to
infection, poor wound healing, and increased morbidity
and mortality associated with disease progression. Type 1,
insulin-dependent DM is characterized by abrupt onset
at any age, destruction of 80-90% of the pancreatic islet
cells that produce insulin, and dependence on exogenous
insulin to prevent ketosis and preserve life. The beta cell
destruction is an autoimmune process which occurs in
genetically susceptible individuals. The most frequent
onset of new cases occurs around the age of puberty. About
15% of diabetics are Type 1.4
Long-term poor glycemic
control in Type 1 DM patients leads to macrovascular
and microvascular complications. Periodontal disease has
been reported as the sixth complication of diabetes along
with neuropathy, nephropathy, retinopathy, and micro and
macrovascular diseases.5
Periodontal diseases are a group of inflammatory diseases
that affect the periodontal attachment apparatus (gingiva,
periodontal ligament, alveolar bone, and cementum).
Gingivitis is defined as inflammation of the gingiva. It is
characterizedbyrednessandedemaofgingivaltissue,bleeding
on provocation, changes in contour and presence of calculus
or plaque with no radiographic evidence of crystal bone
loss.6
Periodontitis is defined as an inflammatory disease
of the supporting tissues of the teeth caused by specific
microorganisms, resulting in progressive destruction of the
periodontalligamentandalveolarbonewithpocketformation,
recession or both. The clinical feature that distinguishes
periodontitis from gingivitis is the presence of clinically
detectable attachment loss. This is often accompanied by
periodontal pocket formation and changes in the density and
height of subjacent alveolar bone.7
18
Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus …
Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20
In Type 1 DM chronic hyperglycemia leads to formation of
biologically active glycated proteins and lipids that promote
inflammatory responses.8,9
Long-term poor control of DM
in Type 1 patients leads to microvascular damage of the
periodontium,alterationincompositionofgingivalcrevicular
fluid, host bacterial flora of the gingiva and impaired healing
response of periodontium. Increased levels of inflammatory
markers such as C-reactive protein, tumor necrosis factor-α,
interleukin-6 (IL-6), IL-1, prostaglandin E2, and IL-10
observedinpatientswithdiabetesmayplayaroleinperiodontal
damage.10
Thepresentstudywasdesignedtoinvestigatetherelationship
between severity of periodontal disease and glycemic control
in patients with Type 1 DM.
Materials and Methods
FiftypatientswererecruitedfromtheDepartmentofMedicine,
People’s College of Medical Sciences and Research Centre.
Inclusion criteria were: Age between 12 and 25 years and with
a diagnosis of Type 1 DM for more than 3 months duration.
Patientswereexcludedfromthestudyiftheywerenon-Type 1
diabetics, undergoing active orthodontic treatment, patients
with any chronic inflammatory diseases and on long-term
medications that could influence the studied parameters such
asantibioticsandantiepilepticimmunosuppressivedrugs.The
individuals were classified according to their glycemic control
as“good”(glycatedhemoglobin[HBA1c]≤7)11
Group A,fair
(HBA1c=7-8)11
Group B,andpoor(HBA1c8)11
Group Cin
this study. The periodontal status was examined by recording
the following parameters: Plaque index (PI); Silness and
Loe (1964)12
, gingival index (GI); Loe and Silness (1963)12
,
probing pocket depth (PPD)13
and clinical attachment level
(CAL)13
after adjusting for age, gender, frequency of prior
dental visits and dental examiner.
Dental plaque is a soft, non-mineralized deposit that forms on
the tooth surface. PI assessed the thickness of plaque at the
gingival area of the tooth surface. A dental explorer was used
to evaluate the cervical third of tooth. GI assessed the severity
of gingivitis, by examining qualitative changes of gingival soft
tissue. A blunt instrument such as periodontal probe was
used to assess the bleeding potential of tissues. PPD and CAL
measured the distance from the gingival margin to the base of
gingival sulcus and distance from cementoenamel junction to
base of sulcus respectively.12,13
PPD and CAL were obtained from six exploratory points
for each tooth with a calibrated North Carolina probe, by a
single examiner. The pockets were classified into two groups
according to the depth: Medium pockets with depth 4-5 mm
and deep pockets with depth 6 mm. The CAL was classified
into three groups: CAL 2 mm (mild periodontitis), CAL
3-4 mm (moderate periodontitis), CAL ≥5 mm (severe
periodontitis).13
Results
Thestudygroupconsistedof50subjectsdiagnosedwithType 1
DM. The subjects were divided into three groups depending
on the HbA1c levels: “Good” (HBA1c ≤7)11
Group A, “fair”
(HBA1c=7-8)11
Group Band“poor”(HBA1c8)11
Group C
in this study. The number and percentage of subjects in each
group were Group A - 15 (30%), Group B - 16 (32%), and
Group C - 19 (38%) (Table 1). The number and percentage
ofmalesandfemalesinthestudygroupweremales - 32 (64%),
females - 18 (36%). The mean and standard deviation of
periodontal parameters PI, GI, PPD, and CAL in Group A
(HBA1c ≤7) were 2.93 ± 0.59, 3.33 ± 0.48, 1.25 ± 0.20, and
1.25 ± 0.34, respectively. The mean and standard deviation
of periodontal parameters PI, GI, PPD, and CAL in Group B
(HBA1c = 7-8) were 3.81 ± 0.75, 4.43 ± 0.62, 1.82 ± 0.45,
and 1.43 ± 0.33, respectively. The mean and standard
deviation of periodontal parameters in Group C (HBA1c 8)
were 5.31 ± 0.20, 6.15 ± 1.38, 2.39 ± 0.18, and 2.01 ± 0.29,
respectively(Table 2).Comparisonofperiodontalparameters
among the three groups was done by applying the ANOVA
test. P  0.05 was considered to be statistically significant for
all analysis.
OncomparisonoftheperiodontalparametersPI,GI,PPD,and
CAL between group A, B, and C the values were found to be
significantlyhigher(P0.05)inGroup CfollowedbyGroup B
Table 1: Number and percentage of individuals in each group.
Groups Number of individuals (%)
A 15 (30)
B 16 (32)
C 19 (38)
Table 2: Mean and standard deviation of periodontal parameters
in Group A, B, C.
Glycemic control PPD CAL PI GI
Group A (HBA1c≤7) 2.93±0.59 3.33±0.48 1.25±0.20 1.25±0.34
Group B (HBA1c=7‑8) 3.81±0.75 4.43±0.62 1.82±0.45 1.43±0.33
Group C (HBA1c8) 5.31±0.20 6.15±1.38 2.39±0.18 2.01±0.29
PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
Table 3: Comparison between Groups A and B.
Periodontal parameter Group A Group B P value
PPD 2.93±0.59 3.81±0.75 0.05
CAL 3.33±0.48 4.43±0.62 0.05
PI 1.25±0.20 1.82±0.45 0.05
GI 1.25±0.34 1.43±0.33 0.05
PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
Table 4: Comparison between Groups B and C.
Periodontal parameter Group B Group C P value
PPD 3.81±0.75 5.31±0.2 0.05
CAL 4.43±0.62 6.15±1.38 0.05
PI 1.82±0.45 2.93±0.18 0.05
GI 1.43±0.33 2.01±0.29 0.05
PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
19
Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus …
Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20
and lowest in Group A (Tables 3-5). The results of this study
showed that there is increased severity of periodontal disease
with poor glycemic control in Type 1 diabetics.
Discussion
Inthisstudy,thepatientswithpoorglycemiccontrol(Group C)
had deeper pockets and more attachment loss which was in
accordance with the findings of studies conducted by Llambés
etal.2005,Silvestreetal.2009,14,15
Tsaietal.2002,16
andSeppälä
etal.1993,1997.17,18
TervonenandOliver19
demonstratedthisin
a cross-sectional study into the association between long-term
diabeticcontrolandperiodontalstatus.Diabeticswereassessed
using HbA1c and for plaque, calculus, probing depth, and
attachmentloss.Basedontheircontrolofbloodglucoselevels,
they were grouped into “good control,” “moderate control,”
and“poorcontrol”ofbloodglucoselevels.Itwasfoundthatthe
prevalenceofsevereattachmentlossincreasedwithdecreasing
controlofdiabetes.Thisstudyfoundthat10%ofwellcontrolled
and 27% of poorly controlled diabetics had loss of attachment
5 mm.19
Thesefindingshavebeenconfirmedbyotherstudies
- bothcross-sectional20
andlongitudinal.17,21
Thepresentstudy
showedthatsubjectswithpoorglycemiccontrolharboredmore
plaque and had more severe gingival inflammation as evident
bythehigherscoresofGIandPI.Similarresultswereobtained
in a study conducted by Lalla et al. 200722
who found higher PI
scores and greater gingival inflammation in a large cohort of
Type 1 diabetics as compared to non-diabetic controls. High
blood glucose sustained over time appears to give rise to a
situationofchronicinflammatorymediatorsecretion,andthus
to an exaggerated periodontal response. However, from the
oppositeperspective,itcouldbepostulatedthattheseverityof
PDcouldaffectDMcontroldespiteadequateintegraltreatment
and patient cooperation.15
Conclusion
Periodontaldiseasescanbepreventedinsusceptibleindividuals
at an early stage23,24
if regular oral screenings and periodontal
treatment programs are considered as a standard of care for
young patients with Type 1 diabetes.
References
1.	 AmericanDiabetesAssociation.Diagnosisandclassification
of diabetes. Diabetes Care 2009;32:S62-7.
2.	 Wild S, Roglic G, Green A, Sicree R, King H. Global
prevalence of diabetes: Estimates for the year 2000 and
projectionsfor2030.DiabetesCare2004;27(5):1047-53.
3.	 Soskolne WA, Klinger A. The relationship between
periodontal diseases and diabetes: An overview. Ann
Periodontol 2001;6(1):91-8.
4.	 PapapanouPN.Epidemiologyofperiodontaldiseases:An
update. J Int Acad Periodontol 1999;1(4):110-6.
5.	 Lowe GD. The relationship between infection,
inflammation, and cardiovascular disease: An overview.
Ann Periodontol 2001;6:1-8.
6.	 Parameter on plaque-induced gingivitis. American
academyofperiodontology.J Periodontol2000;71:851-2.
7.	 Novak MJ. Classification of diseases and conditions
affecting the periodontium. In: Newman MG, (Editor).
Carranza’sTextBookofClinicalPeriodontology,10th ed.
Missouri: Elsevier Publication; 2006. p. 100-9.
8.	 Verma S. C-reactive protein incites atherosclerosis. Can J
Cardiol 2004;20 Suppl B:29B-31.
9.	 IacopinoAM.Periodontitisanddiabetesinterrelationships:
Roleofinflammation.AnnPeriodontol2001;6(1):125-37.
10.	 MealeyBL,OcampoGL.Diabetesmellitusandperiodontal
disease. Periodontol 2000 2007;44:127-53.
11.	 Rose LF, Genco RJ, Cohen DW, Mealey BL. Periodontal
Medicine, Hamilton, BC Decker Inc.; 2000. p. 130-42.
12.	Carranza FA, Newman MG. Clinical Periodontology,
8th
 ed. Oxford: W B Saunders Co.; 1996. p. 64-8.
13.	Newman MG, Takei HH, Klokkevold PR. Carranza’s
Clinical Periodontology, 10th
 ed. Noida, India: Elsevier;
2006. p. 551-3.
14.	Llambés F, Silvestre FJ, Hernández-Mijares A, Guiha R,
Caffesse R. Effect of non-surgical periodontal treatment
withorwithoutdoxycyclineontheperiodontiumoftype 1
diabetic patients. J Clin Periodontol 2005;32(8):915-20.
15.	Silvestre FJ, Miralles L, Llambes F, Bautista D, Solá-
Izquierdo E, Hernández-Mijares A. Type 1 diabetes
mellitus and periodontal disease: Relationship to
different clinical variables. Med Oral Patol Oral Cir Bucal
2009;14(4):E175-9.
16.	Tsai C, Hayes C, Taylor GW. Glycemic control of
type 2 diabetes and severe periodontal disease in the
US adult population. Community Dent Oral Epidemiol
2002;30(3):182-92.
17.	Seppälä B, Seppälä M, Ainamo J. A longitudinal study
on insulin-dependent diabetes mellitus and periodontal
disease. J Clin Periodontol 1993;20(3):161-5.
18.	Seppälä B, Sorsa T, Ainamo J. Morphometric analysis of
cellular and vascular changes in gingival connective tissue
in long-term insulin-dependent diabetes. J Periodontol
1997;68(12):1237-45.
19.	Tervonen T, Oliver RC. Long-term control of
diabetes mellitus and periodontitis. J Clin Periodontol
1993;20(6):431-5.
20.	Tervonen T, Karjalainen K, Knuuttila M,
HuumonenS.Alveolarbonelossintype 1diabeticsubjects.
J Clin Periodontol 2000;27(8):567-71.
21.	Seppälä B, Ainamo J. A site-by-site follow-up study
on the effect of controlled versus poorly controlled
insulin-dependent diabetes mellitus. J Clin Periodontol
1994;21(3):161-5.
Table 5: Comparison between Groups A and C.
Periodontal parameter Group A Group C P value
PPD 2.93±0.59 5.31±0.2 0.05
CAL 3.33±0.48 6.15±1.38 0.05
PI 1.25±0.2 2.93±0.18 0.05
GI 1.25±0.34 2.01±0.29 0.05
PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
20
Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus …
Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20
22.	 LallaE,ChengB,LalS,KaplanS,Softness B,GreenbergE,
etal.Diabetes-relatedparametersandperiodontalconditions
in children. J Periodontal Res 2007;42(4):345-9.
23.	 MehtaA.Riskfactorsassociatedwithperiodontaldiseases
andtheirclinicalconsiderations.IntJContempDentMed
Rev 2015;2015:Article ID: 040115. doi: 10.15713/ins.
ijcdmr.31.
24.	Nategh B, Moghaddam MA, Nodehi D, Sharbaf DA.
Periodontitisandoralhealth.IntJContempDentMedRev
2015;2015:ArticleID:020515.doi:10.15713/ins.ijcdmr.76.

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Relationship between Severity of Periodontal Disease and Control of Diabetes (Glycated Hemoglobin) in Patients with Type 1 Diabetes Mellitus

  • 1. 17 Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus … Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20 Original ResearchReceived: 18th  April 2015  Accepted: 10th  July 2015  Conflicts of Interest: None Source of Support: Nil Relationship between Severity of Periodontal Disease and Control of Diabetes (Glycated Hemoglobin) in Patients with Type 1 Diabetes Mellitus Ankita Jindal1 , Anuj Singh Parihar2 , Meenakshi Sood3 , Pinojj Singh4 , Nandini Singh5 Contributors: 1 Senior Lecturer, Department of Periodontology, RKDF Dental College and Research Centre, Bhopal, Madhya Pradesh, India; 2 Post-graduate Student, Department of Periodontology, People’s College of Dental Sciences and Research Centre, Bhopal, Madhya Pradesh, India; 3 Post-graduate Student, Department of Oral Medicine and Radiology, People’s College of Dental Sciences and Research Centre, Bhopal, Madhya Pradesh, India; 4 MDS, Department of Periodontology, Dr. D.Y. Patil Dental College and Hospital, Navi Mumbai, Maharashtra, India; 5 Private Practitioner, Lucknow, Uttar Pradesh, India. Correspondence: Dr. Parihar AS. Department of Periodontology, People’s College of Dental Sciences and Research Centre, Bhopal - 462 037, Madhya Pradesh, India. Phone: +91-8827047003. Email: Dr.anujparihar@gmail.com How to cite the article: Jindal A, Parihar AS, Sood M, Singh P, Singh N. Relationship between severity of periodontal disease and control of diabetes (glycated hemoglobin) in patients with Type 1 diabetes mellitus. J Int Oral Health 2015;7(Suppl 2):17-20. Abstract: Background: Both diabetes mellitus (DM) and periodontitis are chronic diseases affecting large number of the population worldwide. Changes in human behavior and lifestyle over the last century have resulted in a dramatic increase in the incidence of diabetes in the world. This study was designed to evaluate the relationship between severity of periodontal disease and control of diabetes (glycated hemoglobin [HBA1c]) in patients with Type 1 DM in a hospital based study. Materials and Methods: Fifty patients (n = 50) with Type 1 diabetes were enrolled in the study. They were divided into three groups based on the degree of glycemic control by measuring HbA1c levels as: “Good” (HBA1c ≤7) Group A, fair (HBA1c = 7-8) Group B and poor (HBA1c >8) Group C. All enrolled patients underwent detailed history and dental checkup. Evaluation for periodontal disease was done by measuring dental plaque (plaque index), inflammation of gums (gingival index), probing pocket depth (PPD), and clinical attachment level. Results: Type 1 diabetics with poor glycemic control had increased gingival inflammation (P < 0.05), more dental plaque (P < 0.05), increased PPDs (P < 0.05) and attachment loss (P < 0.05) as compared to those with fair and good glycemic control, respectively. Conclusion: Severity of periodontal disease increases with poor glycemic control in patients with Type 1 DM. Key Words: Glycated hemoglobin levels, periodontal disease, Type 1 diabetes mellitus Introduction Diabetes mellitus (DM) and periodontal diseases are common chronic diseases observed worldwide. DM is a heterogeneous chronic metabolic disorder principally characterized by persistent hyperglycemia resulting from defects in insulin action and/or insulin secretion.1 It affects more than 171 million individuals worldwide and has reached epidemic status.2 DM results from a malfunction of insulin-dependent glucose homeostasis. Classically, they present a triad of symptoms including polyuria, polyphagia, and polydipsia. These are the direct result of hyperglycemia and osmotic imbalance.3 The disease is characterized by an increased susceptibility to infection, poor wound healing, and increased morbidity and mortality associated with disease progression. Type 1, insulin-dependent DM is characterized by abrupt onset at any age, destruction of 80-90% of the pancreatic islet cells that produce insulin, and dependence on exogenous insulin to prevent ketosis and preserve life. The beta cell destruction is an autoimmune process which occurs in genetically susceptible individuals. The most frequent onset of new cases occurs around the age of puberty. About 15% of diabetics are Type 1.4 Long-term poor glycemic control in Type 1 DM patients leads to macrovascular and microvascular complications. Periodontal disease has been reported as the sixth complication of diabetes along with neuropathy, nephropathy, retinopathy, and micro and macrovascular diseases.5 Periodontal diseases are a group of inflammatory diseases that affect the periodontal attachment apparatus (gingiva, periodontal ligament, alveolar bone, and cementum). Gingivitis is defined as inflammation of the gingiva. It is characterizedbyrednessandedemaofgingivaltissue,bleeding on provocation, changes in contour and presence of calculus or plaque with no radiographic evidence of crystal bone loss.6 Periodontitis is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontalligamentandalveolarbonewithpocketformation, recession or both. The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically detectable attachment loss. This is often accompanied by periodontal pocket formation and changes in the density and height of subjacent alveolar bone.7
  • 2. 18 Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus … Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20 In Type 1 DM chronic hyperglycemia leads to formation of biologically active glycated proteins and lipids that promote inflammatory responses.8,9 Long-term poor control of DM in Type 1 patients leads to microvascular damage of the periodontium,alterationincompositionofgingivalcrevicular fluid, host bacterial flora of the gingiva and impaired healing response of periodontium. Increased levels of inflammatory markers such as C-reactive protein, tumor necrosis factor-α, interleukin-6 (IL-6), IL-1, prostaglandin E2, and IL-10 observedinpatientswithdiabetesmayplayaroleinperiodontal damage.10 Thepresentstudywasdesignedtoinvestigatetherelationship between severity of periodontal disease and glycemic control in patients with Type 1 DM. Materials and Methods FiftypatientswererecruitedfromtheDepartmentofMedicine, People’s College of Medical Sciences and Research Centre. Inclusion criteria were: Age between 12 and 25 years and with a diagnosis of Type 1 DM for more than 3 months duration. Patientswereexcludedfromthestudyiftheywerenon-Type 1 diabetics, undergoing active orthodontic treatment, patients with any chronic inflammatory diseases and on long-term medications that could influence the studied parameters such asantibioticsandantiepilepticimmunosuppressivedrugs.The individuals were classified according to their glycemic control as“good”(glycatedhemoglobin[HBA1c]≤7)11 Group A,fair (HBA1c=7-8)11 Group B,andpoor(HBA1c8)11 Group Cin this study. The periodontal status was examined by recording the following parameters: Plaque index (PI); Silness and Loe (1964)12 , gingival index (GI); Loe and Silness (1963)12 , probing pocket depth (PPD)13 and clinical attachment level (CAL)13 after adjusting for age, gender, frequency of prior dental visits and dental examiner. Dental plaque is a soft, non-mineralized deposit that forms on the tooth surface. PI assessed the thickness of plaque at the gingival area of the tooth surface. A dental explorer was used to evaluate the cervical third of tooth. GI assessed the severity of gingivitis, by examining qualitative changes of gingival soft tissue. A blunt instrument such as periodontal probe was used to assess the bleeding potential of tissues. PPD and CAL measured the distance from the gingival margin to the base of gingival sulcus and distance from cementoenamel junction to base of sulcus respectively.12,13 PPD and CAL were obtained from six exploratory points for each tooth with a calibrated North Carolina probe, by a single examiner. The pockets were classified into two groups according to the depth: Medium pockets with depth 4-5 mm and deep pockets with depth 6 mm. The CAL was classified into three groups: CAL 2 mm (mild periodontitis), CAL 3-4 mm (moderate periodontitis), CAL ≥5 mm (severe periodontitis).13 Results Thestudygroupconsistedof50subjectsdiagnosedwithType 1 DM. The subjects were divided into three groups depending on the HbA1c levels: “Good” (HBA1c ≤7)11 Group A, “fair” (HBA1c=7-8)11 Group Band“poor”(HBA1c8)11 Group C in this study. The number and percentage of subjects in each group were Group A - 15 (30%), Group B - 16 (32%), and Group C - 19 (38%) (Table 1). The number and percentage ofmalesandfemalesinthestudygroupweremales - 32 (64%), females - 18 (36%). The mean and standard deviation of periodontal parameters PI, GI, PPD, and CAL in Group A (HBA1c ≤7) were 2.93 ± 0.59, 3.33 ± 0.48, 1.25 ± 0.20, and 1.25 ± 0.34, respectively. The mean and standard deviation of periodontal parameters PI, GI, PPD, and CAL in Group B (HBA1c = 7-8) were 3.81 ± 0.75, 4.43 ± 0.62, 1.82 ± 0.45, and 1.43 ± 0.33, respectively. The mean and standard deviation of periodontal parameters in Group C (HBA1c 8) were 5.31 ± 0.20, 6.15 ± 1.38, 2.39 ± 0.18, and 2.01 ± 0.29, respectively(Table 2).Comparisonofperiodontalparameters among the three groups was done by applying the ANOVA test. P  0.05 was considered to be statistically significant for all analysis. OncomparisonoftheperiodontalparametersPI,GI,PPD,and CAL between group A, B, and C the values were found to be significantlyhigher(P0.05)inGroup CfollowedbyGroup B Table 1: Number and percentage of individuals in each group. Groups Number of individuals (%) A 15 (30) B 16 (32) C 19 (38) Table 2: Mean and standard deviation of periodontal parameters in Group A, B, C. Glycemic control PPD CAL PI GI Group A (HBA1c≤7) 2.93±0.59 3.33±0.48 1.25±0.20 1.25±0.34 Group B (HBA1c=7‑8) 3.81±0.75 4.43±0.62 1.82±0.45 1.43±0.33 Group C (HBA1c8) 5.31±0.20 6.15±1.38 2.39±0.18 2.01±0.29 PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index Table 3: Comparison between Groups A and B. Periodontal parameter Group A Group B P value PPD 2.93±0.59 3.81±0.75 0.05 CAL 3.33±0.48 4.43±0.62 0.05 PI 1.25±0.20 1.82±0.45 0.05 GI 1.25±0.34 1.43±0.33 0.05 PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index Table 4: Comparison between Groups B and C. Periodontal parameter Group B Group C P value PPD 3.81±0.75 5.31±0.2 0.05 CAL 4.43±0.62 6.15±1.38 0.05 PI 1.82±0.45 2.93±0.18 0.05 GI 1.43±0.33 2.01±0.29 0.05 PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
  • 3. 19 Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus … Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20 and lowest in Group A (Tables 3-5). The results of this study showed that there is increased severity of periodontal disease with poor glycemic control in Type 1 diabetics. Discussion Inthisstudy,thepatientswithpoorglycemiccontrol(Group C) had deeper pockets and more attachment loss which was in accordance with the findings of studies conducted by Llambés etal.2005,Silvestreetal.2009,14,15 Tsaietal.2002,16 andSeppälä etal.1993,1997.17,18 TervonenandOliver19 demonstratedthisin a cross-sectional study into the association between long-term diabeticcontrolandperiodontalstatus.Diabeticswereassessed using HbA1c and for plaque, calculus, probing depth, and attachmentloss.Basedontheircontrolofbloodglucoselevels, they were grouped into “good control,” “moderate control,” and“poorcontrol”ofbloodglucoselevels.Itwasfoundthatthe prevalenceofsevereattachmentlossincreasedwithdecreasing controlofdiabetes.Thisstudyfoundthat10%ofwellcontrolled and 27% of poorly controlled diabetics had loss of attachment 5 mm.19 Thesefindingshavebeenconfirmedbyotherstudies - bothcross-sectional20 andlongitudinal.17,21 Thepresentstudy showedthatsubjectswithpoorglycemiccontrolharboredmore plaque and had more severe gingival inflammation as evident bythehigherscoresofGIandPI.Similarresultswereobtained in a study conducted by Lalla et al. 200722 who found higher PI scores and greater gingival inflammation in a large cohort of Type 1 diabetics as compared to non-diabetic controls. High blood glucose sustained over time appears to give rise to a situationofchronicinflammatorymediatorsecretion,andthus to an exaggerated periodontal response. However, from the oppositeperspective,itcouldbepostulatedthattheseverityof PDcouldaffectDMcontroldespiteadequateintegraltreatment and patient cooperation.15 Conclusion Periodontaldiseasescanbepreventedinsusceptibleindividuals at an early stage23,24 if regular oral screenings and periodontal treatment programs are considered as a standard of care for young patients with Type 1 diabetes. References 1. AmericanDiabetesAssociation.Diagnosisandclassification of diabetes. Diabetes Care 2009;32:S62-7. 2. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: Estimates for the year 2000 and projectionsfor2030.DiabetesCare2004;27(5):1047-53. 3. Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: An overview. Ann Periodontol 2001;6(1):91-8. 4. PapapanouPN.Epidemiologyofperiodontaldiseases:An update. J Int Acad Periodontol 1999;1(4):110-6. 5. Lowe GD. The relationship between infection, inflammation, and cardiovascular disease: An overview. Ann Periodontol 2001;6:1-8. 6. Parameter on plaque-induced gingivitis. American academyofperiodontology.J Periodontol2000;71:851-2. 7. Novak MJ. Classification of diseases and conditions affecting the periodontium. In: Newman MG, (Editor). Carranza’sTextBookofClinicalPeriodontology,10th ed. Missouri: Elsevier Publication; 2006. p. 100-9. 8. Verma S. C-reactive protein incites atherosclerosis. Can J Cardiol 2004;20 Suppl B:29B-31. 9. IacopinoAM.Periodontitisanddiabetesinterrelationships: Roleofinflammation.AnnPeriodontol2001;6(1):125-37. 10. MealeyBL,OcampoGL.Diabetesmellitusandperiodontal disease. Periodontol 2000 2007;44:127-53. 11. Rose LF, Genco RJ, Cohen DW, Mealey BL. Periodontal Medicine, Hamilton, BC Decker Inc.; 2000. p. 130-42. 12. Carranza FA, Newman MG. Clinical Periodontology, 8th  ed. Oxford: W B Saunders Co.; 1996. p. 64-8. 13. Newman MG, Takei HH, Klokkevold PR. Carranza’s Clinical Periodontology, 10th  ed. Noida, India: Elsevier; 2006. p. 551-3. 14. Llambés F, Silvestre FJ, Hernández-Mijares A, Guiha R, Caffesse R. Effect of non-surgical periodontal treatment withorwithoutdoxycyclineontheperiodontiumoftype 1 diabetic patients. J Clin Periodontol 2005;32(8):915-20. 15. Silvestre FJ, Miralles L, Llambes F, Bautista D, Solá- Izquierdo E, Hernández-Mijares A. Type 1 diabetes mellitus and periodontal disease: Relationship to different clinical variables. Med Oral Patol Oral Cir Bucal 2009;14(4):E175-9. 16. Tsai C, Hayes C, Taylor GW. Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Community Dent Oral Epidemiol 2002;30(3):182-92. 17. Seppälä B, Seppälä M, Ainamo J. A longitudinal study on insulin-dependent diabetes mellitus and periodontal disease. J Clin Periodontol 1993;20(3):161-5. 18. Seppälä B, Sorsa T, Ainamo J. Morphometric analysis of cellular and vascular changes in gingival connective tissue in long-term insulin-dependent diabetes. J Periodontol 1997;68(12):1237-45. 19. Tervonen T, Oliver RC. Long-term control of diabetes mellitus and periodontitis. J Clin Periodontol 1993;20(6):431-5. 20. Tervonen T, Karjalainen K, Knuuttila M, HuumonenS.Alveolarbonelossintype 1diabeticsubjects. J Clin Periodontol 2000;27(8):567-71. 21. Seppälä B, Ainamo J. A site-by-site follow-up study on the effect of controlled versus poorly controlled insulin-dependent diabetes mellitus. J Clin Periodontol 1994;21(3):161-5. Table 5: Comparison between Groups A and C. Periodontal parameter Group A Group C P value PPD 2.93±0.59 5.31±0.2 0.05 CAL 3.33±0.48 6.15±1.38 0.05 PI 1.25±0.2 2.93±0.18 0.05 GI 1.25±0.34 2.01±0.29 0.05 PPD: Probing pocket depth, CAL: Clinical attachment level, PI: Plaque index, GI: Gingival index
  • 4. 20 Periodontal disease and control of diabetes (HBA1c) in Type 1 diabetes mellitus … Jindal A et al Journal of International Oral Health 2015; 7(Suppl 2):17-20 22. LallaE,ChengB,LalS,KaplanS,Softness B,GreenbergE, etal.Diabetes-relatedparametersandperiodontalconditions in children. J Periodontal Res 2007;42(4):345-9. 23. MehtaA.Riskfactorsassociatedwithperiodontaldiseases andtheirclinicalconsiderations.IntJContempDentMed Rev 2015;2015:Article ID: 040115. doi: 10.15713/ins. ijcdmr.31. 24. Nategh B, Moghaddam MA, Nodehi D, Sharbaf DA. Periodontitisandoralhealth.IntJContempDentMedRev 2015;2015:ArticleID:020515.doi:10.15713/ins.ijcdmr.76.