7.diabetes and periodontal disease

8/15/2019 7.Diabetes and Periodontal Disease

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VISHNU DENTAL COLLEGE

DEPARTMENT OF PERIODONTICS AND IMPLANTOLOGY

SEMINAR ON

DIABETES MELLITUS AND PERIODONTAL DISEASE

2013-2016

GUIDED BY: Dr. C.D.DWARAANATH

PRESENTED BY: Dr. .SAI SUDHA


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CONTENTS:

• Introduction

• History

• Classification• Diagnosis

• Management

• Complications

• Oral findings in diabetes mellitus

• Periodontal disease as a sit! complication

• Effect on periodontium

• DM and "ingi#al inflammation

• DM and periodontitis• $lterations in subgingi#al microbiota

• C!anges in !ost Immune%Inflammatory response

• Effect of periodontal infection on glycemic control

• &esponse to periodontal treatment

• T'o 'ay relation s!ip

• Periodontal Management of patients 'it! DM

I!"r#$%&"'#!• Diabetes mellitus is a clinically and genetically !eterogeneous group of metabolic

disorders manifested by abnormally !ig! le#els of glucose in t!e blood

Definition: (HO )***

• T!e term diabetes mellitus describes a metabolic disorder 'it! !eterogeneous

aetiologies '!ic! is c!aracteri+ed by c!ronic !yperglycemia and disturbances of


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carbo!ydrate, fat and protein metabolism resulting from defects in insulin secretion,

insulin action, or bot!-

Periodontal diseases are inflammatory, infectious diseases affecting t!e periodontium and

resulting in t!e loss of toot! support

History:

• ).// 0C 1 Egyptian p!ysician Hesy%&a 2Ebers Papyrus3 Earliest 4no'n record of

diabetes mentioned on 5rd Dynasty Egyptian papyrus by p!ysician Hesy%&a6

mentions polyuria 7fre8uent urination9 as a symptom-

• ./ 0C 1 "ree4 p!ysician $rateus defined diabetes as ;t!e softening do'n of limbs

and fles! into urine-<• He described t!e term 2 Diabetes3 from "ree4 'ord 2 Diabaino3 '!ic! means sip!on

or 'ater pipe

o =o!n &ollo: mellitus )>/*

o ?atin @ !oney

• Sus!rut and C!ara4 7.t! century 0C 9%Sugary urine-

• T!in and obese patients distinguis!ed-

• C!ara4a and sus!ruta %T!e greatest disco#ery concerning t!e treatment of diabetes

occurred in =uly of )*), '!en t'o Canadian in#estigators, Arederic4 0anting and

C!arles 0est, from t!e Bni#ersity of Toronto 'it! t!e !elp of Macleod and collip %

Noble pri+e in )*

• Macleod : term insulin

• Country 'ide associations

• Portuguese $ssociation for t!e Protection of Poor Diabetics, founded in )* by

Ernesto &oma

• 0ritis! Diabetic $ssociation, and no' Diabetes B 'as establis!ed in )*5F by &obin

?a'rence

•

$merican Diabetic $ssociation % )*F/• International associations

• International Diabetes Aoundation 'as establis!ed in )*./ and

• T!e European $ssociation for t!e Study of Diabetes 7E$SD9 in )*F

C()**'+&)"'#!:(!o )***

(HO re#isited t!e classification in )*** as did t!e $merican Diabetes $ssociation 7$D$9

&etained type ) and and remo#ed t!e terms IDDM and NIDDM


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Ne' classification attempted to encompass bot! etiology and clinical stages of t!e disease as

'ell as being useful clinically- T!is 'as based on t!e suggestion of u+uya and Matsuda

• Type ) 7beta%cell destruction, usually leading to absolute insulin deficiency9

• Autoimmune

• Idiopathic

• Type 7may range from predominantly insulin resistance 'it! relati#e insulin

deficiency to a predominantly secretory defect 'it! or 'it!out insulin resistance9

• "estational diabetes

• Ot!er specific types

&is4 class : I"T and IA" 'as introduced as anot!er ris4 state-

Ot!er types

"enetic defects of beta%cell function

• C!romosome /, HNAFG7MOD)9

• C!romosome , gluco4inase 7MOD9

• C!romosome ), HNA) G 7MOD59

• C!romosome )5, IPA%) 7MODF9

• Mitoc!ondrial DN$ 5F5 mutation

• Ot!ers

"enetic defects in insulin action

• Type $ insulin resistance

• ?eprec!aunism

• &abson%Menden!all syndrome

•

?ipoatrop!ic diabetes• Ot!ers

Ot!er types

Diseases of t!e eocrine pancreas

• Aibrocalculous pancreatopat!y

• Pancreatitis

• Trauma pancreatectomy

• Neoplasia


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0ased on etiology it can be grouped into

$utoimmune Diabetes Mellitus

Idiopat!ic

$utoimmune Diabetes Mellitus

Synonyms: Insulin1dependent diabetes 7IDDM9, Type ) diabetes, or u#enile1 onset diabetes,

It results from autoimmune mediated destruction of t!e beta cells of t!e pancreas-

ariations

T!e rate of destruction is 8uite #ariable, being rapid in some indi#iduals and slo' in ot!ers-

• T!e rapidly progressi#e form: commonly obser#ed in c!ildren, but also may occur in

adults-

• T!e slo'ly progressi#e form: generally occurs in adults and is sometimes referred to

as latent autoimmune diabetes in adults 7?$D$9-

?$D$

• latent autoimmune diabetes of adult!ood3 7?$D$9, )-. diabetes3, or 2slo'ly

progressi#e IDDM3

• $pproimately .L1)/L of adult Caucasian patients '!o present 'it! a type diabetes

p!enotype also !a#e islet cell autoantibodies , particularly "$D.$, '!ic! predict

insulin dependency-

Humoral: Islet cell autoantibodies 7IC$9

Cellular : auto reacti#e CD> T lymp!ocytes2

Idiopat!ic DM

• No 4no'n aetiology-

• Hig!ly in!eritable but !as neit!er H?$ associations nor detectable islet cell

autoantibodies

• Some of t!ese patients !a#e permanent insulinopenia and are prone to 4etoacidosis, but

!a#e no e#idence of autoimmunity- T!is form of diabetes is more common among

indi#iduals of $frican and $sian origin-

• In anot!er form found in $fricans an absolute re8uirement for insulin replacement

t!erapy in affected patients may come and go, and patients periodically de#elop


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4etoacidosis-

Type II

•

Synonyms: Non1 insulin1dependent diabetes 7NIDDM9, or adult1onset diabetes-

Aeatures:

• T!is form of diabetes is fre8uently undiagnosed for many years because t!e

!yperglycaemia is often not se#ere enoug! to pro#o4e noticeable symptoms of diabetes-

• Increased ris4 of de#eloping macro#ascular and micro #ascular complications

• T!e primary abnormality is insulin resistance and t!e b%cell dysfunction arises from

t!e prolonged, increased secretory demand placed on t!em by t!e insulin resistance .

Insulin secretion is defecti#e in t!ese patients and insufficient to compensate for insulin

resistance-

Most patients 'it! t!is form of diabetes are obese or may !a#e an increased percentage of

body fat distributed predominantly in t!e abdominal region- $dipose tissue plays an

important role in t!e de#elopment of insulin resistance- Aree fatty acids contribute to insulin

resistance by in!ibiting glucose upta4e, glycogen synt!esis, and glycolysis, and by increasing

!epatic glucose production

G,*")"'#!)( D'),",* ,(('"%*

Definition: "estational diabetes is carbo!ydrate intolerance resulting in !yperglycaemia of

#ariable se#erity 'it! onset or first recognition during pregnancy-

"estational diabetes mellitus represents nearly */L of all pregnancies complicated by

diabetes6 it usually !as its onset in t!e t!ird trimester of pregnancy and ade8uate treatment

'ill reduce perinatal morbidity

Pat!op!ysiology

Human placental lactogen t!at interferes 'it! susceptible insulin receptors leading to insulin

resistance

Type $): abnormal oral glucose tolerance test 7O"TT9, but normal blood glucose le#els

during fasting and t'o !ours after meals6 diet modification is sufficient to control glucose

le#els

Type $: abnormal O"TT compounded by abnormal glucose le#els during fasting andor

after meals6 additional t!erapy 'it! insulin or ot!er medications is re8uired-

D')/!#*'*

$merican Diabetes $ssociation criteria for t!e diagnosis of diabetes mellitus, impairedglucose tolerance 7I"T9, and impaired fasting glucose 7IA"9


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Normal Diabetes IGT IFG

Aasting glucose 7mgdl9 )// Q ) )//1).

Casual glucose 7mgdl9 Q //

%! P" 7mgdl9 )F/ Q // Q )F/ but //

M)!)/,,!"

C#('&)"'#!*Diabetes !as been classically associated 'it! a group of micro#ascular and macro#ascular

complications- T!e micro#ascular complications of retinopat!y, nep!ropat!y and neuropat!y

are specifically associated 'it! diabetes, and t!e ris4 of macro#ascular disease is greatly

increased in diabetic patients- Diabetic patients !a#e a dramatically increased ris4 for #isual

impairment or blindness, 4idney failure, limb amputation, stro4e, and myocardial infarction-

Sustained !yperglycemia plays a primary role in bot! t!e onset and progression of t!ese

complications- Periodontitis 'as added as sit! complication by ?oe in )**5-

Macro#ascular complications are strongly associated 'it! t!e increased at!erosclerosis

common in diabetes- Hyperglycemia results in alterations in lipid metabolism as 'ell as

nonen+ymatic glycation of proteins suc! as collagen- T!ese c!anges result in altered function

of cell membranes and c!anges in cell1cell and cell1matri interactions- T!is may t!en lead

to increased #essel 'all t!ic4ness and formation of at!eromas and microt!rombi in large

#essels, and alterations in endot!elial cell function and #ascular permeability in t!e

micro#asculature-


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T!e glycation of proteins, lipids and nucleic acids in diabetic patients results in accumulation

of t!ese glycated proteins in t!e small blood #essels of endorgans suc! as t!e retina,

glomerulus and endoneurial region, and in t!e 'alls of large blood #essels- T!ese glycated

proteins, 4no'n as ad#anced glycation end%products 7$"Es9, form in diabetic and non%

diabetic indi#iduals6 !o'e#er, t!eir accumulation is greatly increased in diabetic patients 'it!sustained !yperglycemia- T!e result of t!eir accumulation is increased basement membrane

t!ic4ness in t!e retina and around t!e ner#es, t!ic4ening of t!e mesangial matri in t!e

glomerulus, and accumulation of collagen in larger #essels- T!e cumulati#e effect is a

progressi#e narro'ing of t!e #essel lumen and decreased perfusion of affected organs-

$"Es form on collagen, causing increased collagen cross%lin4ing, and resulting in formation

of !ig!ly stable collagen macromolecules t!at are resistant to normal en+ymatic degradation

and tissue turno#er- In t!e blood #essel 'all, $"E%modified collagen accumulates, t!ic4ening

t!e #essel 'all and narro'ing t!e lumen- $"E formation occurs in bot! central and

perip!eral arteries, and is t!oug!t to contribute significantly to t!e macro#ascular complications of diabetes- $"E%modified collagen in #essel 'alls co#alently cross%lin4s 'it!

circulating lo' density lipoprotein, contributing to at!erosclerosis- $"E modification of

collagen also occurs in t!e basement membrane of small blood #essels- $gain, $"E%modified

collagen accumulates and increases basement membrane t!ic4ness, altering normal

!omeostatic transport across t!e membrane-

$"Es !a#e maor effects at t!e cellular le#el- $ receptor for $"Es 4no'n as &$"E 7receptor

for $"E9 !as been identified on t!e surface of endot!elial cells, neurons, smoot! muscle

cells, and monocytes macrop!ages- Hyperglycemia results in increased epression of t!e

receptor and increased $"E1&$"E interaction- T!e effect on endot!elial cells is an increase

in #ascular permeability and t!rombus formation- $"Es are c!emotactic for monocytes-

Interaction bet'een $"Es and t!e receptor, &$"E, on monocytemacrop!age membranes

induces increased cellular oidant stress and acti#ates t!e transcription factor NA%40- T!is

signals a c!ange in t!e monocytemacrop!age p!enotype and results in increased production

of proinflammatory cyto4ines suc! as interleu4in%) 7I?%)9 and tumor necrosis factor, and

gro't! factors suc! as platelet%deri#ed gro't! factor and insulin%li4e gro't! factor- T!ese

cyto4ines and gro't! factors contribute to t!e c!ronic inflammatory process in at!eroma

formation-

Oral Manifestations of Diabetes

Numerous oral c!anges !a#e been described in diabetics, including c!eilosis, mucosal drying

and crac4ing, burnRing mout! and tongue, diminis!ed sali#ary flo', and alRterations in t!e

flora of t!e oral ca#ity, 'it! greater preRdominance of Candida albicans, !emolytic

streptococci, and stap!ylococci- $n increased rate of dental caries !as also been obser#ed in

poorly controlled diaRbetes- It s!ould be noted t!at t!ese c!anges are not al'ays present, are

not specific, and are not pat!ognomonic for diabetes- Aurt!ermore, t!ese c!anges are less

li4ely to be obser#ed in 'ell%controlled diabetics- InRdi#iduals 'it! controlled diabetes !a#e

a normal tissue response, a normally de#eloped dentition, a normal deRfense againstinfections and no increase in t!e incidence of caries-


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T!e influence of diabetes on t!e periodontium !as been t!oroug!ly in#estigated- $lt!oug! it

is difficult to ma4e definiti#e conclusions about t!e specific effects of diabetes on

periodontium, a #ariety of c!anges !a#e been described, including a tendency to'ard

enlarged gingi#a, sessile or pedunculated gingi#al polyps, polyRpoid gingi#al proliferations,

abscess formation, periodontitis, and loosened teet!- Per!aps t!e most stri4ing c!anges inuncontrolled diabetes are t!e reduction in defense mec!anisms and t!e increased

susceptibility to infections leading to destructi#e periodontal disease-

Perioo!tal isease as a si"t# $ompli$atio!%%%

Herald loe and "enco &=: Type II DM : )>/ Pima Indians7)*>5%)*>>9

?oe H )*>:)/ Danis! men

H$&$?D ?OE )**5


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Aindings from studies of type ) and type persons !a#e demonstrated t!at bot! types of

diabetes are predictors of periodontal disease, and t!at periodontal disease s!ould be

considered as a sit! complication of diabetes mellitus-

I!&l'e!$e o& DM o! perioo!ti'm

&ay and Orban )*./

• Degeneration of tissues

• Presence of calcified bodies in and around small blood #essels of t!e gingi#a-

Sil#a =$ et al. //>

• $trop!y and pleomorp!ism of t!e gingi#al epit!elium, 'it! decreased cellular

organelles and increased intercellular spaces,

• a t!ic4ened 4eratin layer 'it! t!e reduction of !eig!t of dermal papilla-

$driana Monea /): in#estigated !istological c!anges t!at occur in t!e periodontium of

subects 'it! type DM 'it!out signs of PD

$t epit!elial le#el,

• $ccelerated Mitosis In 0asal Epit!elial ?ayer,

• $cant!osis In Spinocelular ?ayer,

• Para4eratosis $nd Hyper4eratosis In Superficial ?ayer-

$t connecti#e tissue le#el,

• Dilated capillaries 'it! #ascular stasis and t!rombosis

• "ingi#al epit!elium penetrates underlying c!orion and epit!elial cells islands occur

into t!e connecti#e tissue-

&ic! lymp!oplasmocytary infiltrate, '!ic! disorgani+es t!e structure of conuncti#e fibers

$ll t!ese c!anges depend on t!e duration of diabetic status and on t!e le#el of metabolic

control of t!e disease, 'orsening as t!e diabetes is more poorly controlled and t!ey are

independent of t!e presence or absence of periodontal disease-

DM )!$ /'!/')( '!))"'#!


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Summary : T!ese studies s!o' t!at t!e presence of diabetes mellitus is often, but not al'ays,

associated 'it! increased gingi#al inflammation6 furt!ermore, t!e le#el of glycemic control

may play a role in t!e gingi#al response to bacterial pla8ue in many indi#iduals


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DM a! Perioo!titis

Summary: Some diabetic patients 'it! poor glycemic control de#elop etensi#e periodontal


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destruction, '!ile ot!ers do not-

Con#ersely, many 'ell controlled diabetic patients !a#e ecellent periodontal !ealt!, but

ot!ers de#elop periodontitis-It is important to note t!at periodontal disease pre#alence and

se#erity #aries greatly 'it!in t!e non%diabetic population, ust as it does in t!e population

'it! diabetes mellitus- Presence of periodontal disease in some diabetic indi#iduals may be

related more to ot!er ris4 factors for periodontitis suc! as poor oral !ygiene and smo4ing

t!an to t!e mere presence of diabetes-

Alteratio!s i! s'b(i!(i)al mi$robiota

• T!e glucose content of gingi#al fluid and blood is !ig!er in indi#iduals 'it! diabetes

t!an 'it!out, 'it! similar Pla8ue and "ingi#al Inde scores-

• T!e increased glucose in t!e gingi#al fluid and blood of indi#iduals 'it! diabetes could

c!ange t!e en#ironment of t!e micro%flora, inducing 8ualitati#e c!anges in bacteria t!at

could account for t!e se#erity of periodontal disease obser#ed in poorly controlled

indi#iduals 'it! diabetes-

Type ) diabetes 7gusberti )*>,slots )*>5,sastrao'ioto )**/,Ebersole //>9

• Capnocytophaga

• $naerobic #ibrios

•

Actinomyces species• Porphyromonos gingivalis

• Prevotella intermedia

• Actinobacillus actinomycetemcomitans

• Campylobacter rectus

• E- nodatum 7lalla //9

Type diabetes 7genco:)*>,+ambon:)*>>9

• Porphyromonos gingivalis

• Prevotella intermedia

• C. rectus

arco et al- /)

• ?imitation of t!ese studies is t!e restricted analysis of biofilm species6 global 7and

unbiased9 analysis of t!e pla8ue microbiota using t!e tec!ni8ues of microbiomics and

metagenomics could re#eal more detailed information about t!e influence of diabetes

on t!e oral microbiome-


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=o!n =- Taylor, P!ilip M- Pres!a' /)5

• It is not al'ays clear if identified differences in t!e periodontal microbiota bet'een

diabetic and non%diabetic patients result truly from an impact of t!e diabetic state on t!e

periodontal bacteria, or simply result from more se#ere periodontitis

• T!e presence of diabetes 7T)DM or TDM9 !as no significant effect on t!e composition

of t!e periodontal microbiota- Aurt!ermore, t!e le#el of glycaemic control in people

'it! diabetes also does not significantly influence t!e composition of t!e subgingi#al

biofilm-

*#a!(es i! #ost imm'!o i!&lammatory respo!se

PMN abnormalities

• $bnormalities of t!e cytos4eleton, of t!e endocytosis and of t!e transduction

mec!anism, due to !yperglycemia

• c!emotais, ad!erence and p!agocytosis

• Usuperoide production

Monocyte macrop!ages

• Hyperresponsi#e: $"E :&$"E interactions

Pro inflammatory cyto4ines: TNAG,P"E, interleu4in%)b

$lteration in collagen metabolism

Offenbac!er )**:

• Not all people 'it! diabetes mellitus !a#e a !yper%responsi#e monocytemacrop!age

p!enotype, and it is li4ely t!at t!ere is a genetic component to t!is p!enomenon

Sc!midt et al )**F

$ccumulation of $"Es in t!e periodontium stimulates migration of monocytes,PMN


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Outcome

T!ese alterations in t!e !ost immunoinflammatory response

• pre#ent effecti#e elimination of bacteria and bacterial products-

• persistence in bacterial c!allenge may t!en be met 'it! an ele#ated

monocytemacrop!age response, '!ic! results in increased tissue destruction-

Differences b' type ) and type

$spriello SD 7/))9

• "ingi#al cre#icular fluid le#els of I?%)b and TNA%a in P%T)DM subects 'ere

significantly !ig!er t!an in P%TDM subects-

• $ significant and negati#e correlation in P%T)DM subects bot! bet'een t!e duration of

T)DM and gingi#al cre#icular fluid I?%)b and bet'een t!e duration of T)DM and

gingi#al cre#icular fluid TNA%a-

Altere *olla(e! Metabolism

• Decreased collagen synt!esis

• $ffects t!e synt!esis, maturation, and maintenance of collagen and etracellular matri-

• Ne'ly formed collagen is susceptible to degradation by collagenase '!ic! is ele#ated

in diabetic tissues, including t!e periodontium-

• Source: Neutrop!ils

• Aibroblast apoptosis

• Increased oidant stress diabetic tissues % 'idespread #ascular inury

• $"E formation also stimulates proliferation of arterial smoot! muscle cells, increasing

t!ic4ness of #essel 'alls and decreasing t!e #essel lumen-

• $"E % increased cross%lin4ing of collagen, reducing collagen solubility and decreasing

turno#er rate-

• &ate of collagen production can be restored by administration of insulin to normali+e

blood glucose le#els-

E&&e$ts o! #eali!( a! treatme!t respo!se

(ound !ealing is impaired due to t!e cumulati#e effects on cellular functions

)- Decreased synt!esis of collagen by fibroblasts


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- Increased degradation by collagenase

5- "lycosylation of eisting collagen at 'ound margins

F- Defecti#e remodelling and rapid degradation of ne'ly synt!esi+ed, poorly cross%lin4ed

collagen-

R,*#!*, "# ,r'#$#!")( "r,)",!":

E&&e$t o& perioo!tal i!&e$tio! o! (ly$emi$ $o!trol


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S'mmary

0orgna44e (S,/)5

Current e#idence for effects of periodontal disease on glycaemic control is scarce- Ho'e#er,

it suggests t!at compared to periodontally !ealt!y indi#iduals, people 'it! poor periodontal

!ealt! and:

• Type diabetes or no diabetes: !a#e greater ris4 of de#eloping poorer glycaemic

control

•Type ) or type diabetes: !a#e greater ris4 for diabetes related complications

• No diabetes: !a#e greater ris4 of de#eloping manifest diabetes-

Conse8uently, large%scale, definiti#e studies of long duration and in multiple different

population groups in many different countries are needed

T# )4 r,()"'#!*5'


19/21

Management of patient 'it! DM

Coordination of Care bet'een Dentist and P!ysician

Dental Treatment Modifications

T!e 'ell%controlled diabetic can usually be managed con#entionally to include most surgical

procedures-

Precautions

Modify insulin protocols to insure a stable postoperati#e outcome- Patients may re8uire

reduction of insulin dose immediately prior to oral surgical procedures t!at 'ill result in

reduced calorie oral inta4e so as to pre#ent unintended !ypoglycemia

Marginally or poorly controlled diabetics: caution

• Electi#e dental treatment s!ould be a#oided until t!e patient is stabili+ed-

• $ntibiotic co#erage s!ould be considered for emergency surgical procedures re8uired to

treat acute oral infection-

• Aor surgical t!erapy, as4 t!e patients to bring t!eir glucometer to t!e appointment if

t!ey !a#e one and !a#e t!em ta4e and record t!eir preoperati#e plasma glucose le#el

prior to t!e procedure

Plan dental treatment to occur eit!er before or after periods of pea4 insulin acti#ity- T!is

reduces t!e ris4 of perioperati#e !ypoglycemic reactions, '!ic! occur most often during pea4

insulin acti#ity-

• lispro insulin :5/ to */ minutes

• &egular insulin: to 5 !ours

• ?ente insulin: F to )/ !ours

• Sulfonylureas, pea4 insulin acti#ity depends on t!e indi#idual drug ta4en-


20/21

• Metformin and t!e t!ia+olidinediones rarely cause !ypoglycemia-

Intra Operati#e care

• Surgical patients are best sc!eduled in t!e morning after a normal meal and after using

normal insulin or oral anti%diabetic medications-

• Insulin%using patients s!ould be 8ueried about last food inta4e to assure blood sugar

le#els 'ill be ade8uately maintained until net meal time-

• Office stress reduction protocols

• Profound local anest!esia,

• Tissues s!ould be !andled as atraumatically and as minimally 7!rs9 as possible

• pro#ide analgesics as necessary for postoperati#e discomfort

Post operati#e management

• ?arge doses of non%steroidal anti%inflammatory drugs 7NS$IDs9 or aspirin may increase

t!e !ypoglycemic effect of insulin or oral !ypoglycemic drugs-

• Diet recommendations to maintain a proper glucose balance

• Are8uent recall and fastidious !ome oral care

Emergencies

• 0e prepared to manage diabetic emergencies

Hyperglycemia:

• $dminister oygen, monitor #ital signs, and perform CP& if needed

Hypoglycemia

"i#e approimately ). g of carbo!ydrate 7F1 o+ of fruit uice,51F tsp sugar, glucose tablet-

I access is present, gi#e ) mg glucagon intramuscularly or subcutaneously-

Patient s!ould respond fully 'it!in ). minutesMonitored for at least ) !our-

C#!&(%*'#!

• The extensive literature on this subject and the overall impression of

clinicians point to the fact that periodontal disease in diabetics follows no

consistent or distinct pattern.

• Warrants further well controlled randomized control trials

• Awareness among physicians and patients

• Dental professionals with a thorough understanding of current medical

treatment regimens and the implications of diabetes on dental care are


21/21

able to help their diabetic patients achieve and maintain the best possible

oral health.

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7.diabetes and periodontal disease

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