Dibetes Final

8/13/2019 Dibetes Final

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By- Krishan Gulia


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INTRODUCTIONHISTORYDIABETES MELLITUSORAL MANIFESTATIONS OF DIABETES

DIABETES AND PERIODONTAL DISEASEMICROBIOLOGYPATHOGENESISEFFECTS OF PERIODONTAL INFECTION ON

GLYCEMIC CONTROL OF DIABETESDIABETES AND DENTAL IMPLANT THERAPY


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PATIENT EVALUATION MANAGEMENT OF KNOWN DIABETIC

PATIENTS

MANAGEMENT OF UNCONTROLLED OR

POORLY CONTROLLED DIABETIC PATIENTS ORAL MEDICATIONS FOR DIABETIC

CONTROL

MANAGEMENT OF DIABETIC EMERGENCIES

SUMMARY REFERENCES


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Diabetes mellitus (DM) refers to a group of common metabolicdisorders that share the phenotype of hyperglycemia. Severaldistinct types of DM are caused by a complex interaction ofgenetics and environmental factors. Depending on the etiologyof the DM, factors contributing to hyperglycemia include

reduced insulin secretion, decreased glucose utilization, andincreased glucose production. The metabolic dysregulationassociated with DM causes secondary pathophysiologicchanges in multiple organ systems that impose a tremendousburden on the individual with diabetes and on the health caresystem. In the United States, DM is the leading cause of end-

stage renal disease (ESRD), nontraumatic lower extremityamputations, and adult blindness. It also predisposes tocardiovascular and periodontal diseases.


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Globally, as of 2010, an estimated 285 million people haddiabetes, with type 2 making up about 90% of thecases.Its incidence is increasing rapidly, and by 2030,this number is estimated to almost double. Diabetesmellitus occurs throughout the world, but is more

common (especially type 2) in the more developedcountries. The greatest increase in prevalence is,however, expected to occur in Asia and Africa, wheremost patients will probably be found by 2030.Theincrease in incidence in developing countries follows thetrend of urbanization and lifestyle changes, perhaps mostimportantly a "Western-style" diet. This has suggested anenvironmental (i.e., dietary) effect, but there is littleunderstanding of the mechanisms at present.


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India has more diabetics than any other country inthe world, according to the International DiabetesFoundation,although more recent data suggestthat China has even more.The disease affects

more than 50 million Indians - 7.1% of the nation'sadults - and kills about 1 million Indians a year.Theaverage age on onset is 42.5 years.The highincidence is attributed to a combination of geneticsusceptibility plus adoption of a high-calorie, low-

activity lifestyle by India's growing middle class.


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HISTORY

Gaw et al(1955) defined

diabetesmellitus as a

syndromecharacterized

byhyperglycemia

due to anabsolute or

relative lack ofinsulin orinsulin

resistance.

Malins (1968)-defined

diabetes as a

chronicdisorder of

carbohydratemetabolism

characterizedby

hyperglycemiaand glycosuria.

Nationaldiabetes datagroup (1979)

defined


genetically andclinically

heterogenousgroup of

disorders thatshared glucoseintolerance in

common.

Ervasti et al(1985)-defined


metabolicdisorder withdisturbances in

the intrinsicproduction, ofinsulin leadingto an abnormal

fat,carbohydrateand protein

metabolism .

Bennet(1994)defined this as

a syndromecharacterized

by

hyperglycemiaanddisturbances ofcarbohydrate,fat and protein

metabolismassociated with

absolute orrelative

deficiencies ininsulin actionand secretion.


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The term diabetes mellitus describes a metabolic

disorder of multiple etiology characterized by

chronic hyperglycaemia with disturbances of

carbohydrate, fat and protein metabolismresulting from defects in insulin secretion, insulin

action, or both.


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Type I diabetes: Insulin dependent

diabetes mellitus

Type II diabetes: non- insulin dependent

diabetes mellitus

Gestational diabetes


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Formerly called Insulin-Dependent Diabetes Mellitusand Juvenile-Onset Diabetes.

In Type I Diabetes a persons body does not produceinsulin or produces it in very small amounts.Thesymptoms usually appear suddenly during childhood,usually around the age of puberty.In type I diabetes,theimmune system attacks the insulin producing cells(called "islets") in the pancreas, making this anautoimmune disease.

Patients with type I diabetes present with thesymptoms traditionally associated with diabetes,including polyphagia, polydipsia, polyuria, andpredisposition to infection.


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Formerly called Non-Insulin Dependent Diabetes Mellitus andAdult-Onset Diabetes.In Type II Diabetes, both the bodysability to produce insulin and to use insulin may change.Thepancreas may start producing only very small amounts ofinsulin or the cells of the body may become resistant to the

action of the insulin.

The symptoms usually develop gradually over several yearsand the person may not realize they are ill for quite a while.Those symptoms include increased infections or skin sores,slow healing of infections, tiredness, and tingling or numbness

of hands or feet. There is a strong relationship between obesityand type II diabetes.

Type II diabetes usually develops after age 45, but instances inyounger people are increasing as obesity rates increase.


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Glucose intolerance developing during pregnancy isclassified as gestational diabetes.In this condition,somewomen experience in the second half of their pregnancywhen blood sugar levels become abnormally high.

The condition usually goes away after the pregnancy but insome people it does not. Insulin resistance is related to themetabolic changes of late pregnancy, and the increasedinsulin requirements may lead to diabetes.

GDM occurs in 7% (range 210%) of pregnancies in theUnited States; most women revert to normal glucosetolerance postpartum but have a substantial risk (3560%)of developing DM in the next 1020 years.


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Insulin is the principal hormone that regulates uptakeof glucosefrom the blood into most cells (primarilymuscle and fat cells, but not central nervous systemcells). Therefore, deficiency of insulin or theinsensitivity of its receptorsplays a central role in allforms of diabetes mellitus.

Insulin is released into the blood by beta cells (-cells),found in the islets of Langerhans in the pancreas, inresponse to rising levels of blood glucose, typically

after eating. Insulin is used by about two-thirds of thebody's cells to absorb glucose from the blood for useas fuel, for conversion to other needed molecules, orfor storage.
http://en.wikipedia.org/wiki/Glucosehttp://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Glucose


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Insulin is also the principal control signal for conversionof glucose to glycogenfor internal storage in liver andmuscle cells. Lowered glucose levels result both in thereduced release of insulin from the -cells and in thereverse conversion of glycogen to glucose whenglucose levels fall. This is mainly controlled by thehormone glucagon, which acts in the opposite mannerto insulin. Glucose thus forcibly produced from internalliver cell stores (as glycogen) re-enters thebloodstream; muscle cells lack the necessary export

mechanism. Normally, liver cells do this when the levelof insulin is low (which normally correlates with lowlevels of blood glucose).
http://en.wikipedia.org/wiki/Glycogenhttp://en.wikipedia.org/wiki/Glucagonhttp://en.wikipedia.org/wiki/Glucagonhttp://en.wikipedia.org/wiki/Glycogen


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1.Diabetic Ketoacidosis

2.Hyperglycemic Hyperosmolar State

3.Hypoglycemia

4.Diabetic Nephropathy

5.Diabetic Retinopathy

6.Diabetic Neuropathy

7.High Blood Pressure8.Slow Healing


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Xerostomia and parotid gland enlargement

(Sreebny LM et al.1992)

burning mouth syndrome

Altered taste sensation

Candidiasis (Fisher BM, 1987)

increased caries rate

Oral lichen planus (Bagan-Sebastian JV,1992)

Alterations in the flora of the oral cavity with greater predominance of Candidaalbicans, hemolytic Streptococci and Staphylococci.


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increased gingival inflammation in response tobacterial plaque. (Cianciola LJ et al.1982, De

Pommereau V et al.1992)

Pronounced gingival enlargement.

Goldman and Cohen in (1973) - Granular subgingivalproliferations

Periodontitis

Multiple lateral periodontal abscesses

Sessile or pedunculated gingival polyps


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undiagnosed or poorly

controlled diabetes mellitus

multiple or recurrentperiodontal abscesses

unexplained edematousgingival enlargement

rapid destruction ofalveolar bone

delayed healing


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The glucose content of gingival fluid and blood is higher inindividuals with diabetes than without, with similar Plaque andGingival Index scores.

Ficara AI, Levin MP in 1975found that the increased glucosein the gingival fluid and blood of individuals with diabetes could

change the environment of the microflora, inducing qualitativechanges in bacteria that could account for the severity ofperiodontal disease observed in poorly controlled individuals withdiabetes.

Patients with type 1 diabetes with periodontitis have been

reported to have a subgingival flora composed mainly ofCapnocytophaga, anaerobic vibrios, andActinomycesspecies.Porphyromonas gingivalis, Prevotella intennedia,andActinobacillus actinomycetemcomitans, which arecommon inperiodontal lesions of individuals without diabetes, are present inlow numbers in those with the disease .


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Gusberti F, Grossman N, Loesche in 1982 andShklar G et al in 1962 however, found scarceCapnocytophagaand abundant A.actinomycetemcomitans and black-pigmentedBacteroides, as well as P. intermedia,P.melaninogenica, and Campylobacter rectus.

Mascola B in 1970 and Sastrowijoto SH et al in1989 found blackpigmented species, especially P.gingivalis, P. intermedia,and C. rectus, are prominent

in severe periodontal lesions of Pima Indians with type2 diabetes .These results point to an altered flora in theperiodontal pockets of patients with diabetes.


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Increased collagenase activity and decreased collagensynthesis is found in individuals with diabetes withchronic hyperglycemia. Decreased collagen synthesis,osteoporosis, and reduction in the height of alveolarbone occur in diabetic animals, with comparable

osteoporosis in other bones. The periodontal ligamentand cementum are not affected, but glycogen isdepleted in the gingiva.

Bissada NF in 1966found ,generalized osteoporosis,

resorption of the alveolar crest, and gingivalinflammation and periodontal pocket formationassociated with calculus have been described inChinese hamsters with hereditary diabetes underinsulin replacement therapy.


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Chronic hyperglycemia adversely affects the synthesis,maturation, and maintenance of collagen andextracellular matrix. In the hyperglycemic state,numerous proteins and matrix molecules undergo anonenzymatic glycosylation, resulting in advancedglycation end products (AGES).

The formation of AGES can occur at normal glucoselevels, but in hyperglycemic environments, AGEformation is excessive. AGE formation cross-links

collagen, making it less soluble and less likely to benormally repaired or replaced. As a result, collagen inthe tissues of poorly controlled diabetics is aged andmore susceptible to breakdown.


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Periodontitis has been referred to as the sixthcomplication of diabetes(Loe. H, 1993)

. A number of studies found a higher prevalence of

periodontal disease among diabetic patients thanamong healthy controls.

Available data reveals strong evidence that

diabetes is a risk factor for gingivitis andperiodontitis, and the level of glycemic controlappears to be an important determinant in thisrelationship.( Papapanou PN in 1996)


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It was suggested that periodontal destruction can startvery early in life in diabetes, becomes more prominent aschildren become adolescents (Lalla et al. 2006),and isrelated to the level of metabolic control (Lalla et al.2007).

In adults with type 1 diabetes, the overall degree ofgingival inflammation was similar between diabeticsubjects as a whole and non-diabetic control subjects withsimilar plaque accumulation(Sastrowijoto S in 1990 and

Karjalainen K in 1996).


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Ervasti T et al in 1985, foundgreater gingivalinflammation was also seen in adults with type 2diabetes than in non-diabetic controls, with the highestlevel of inflammation in subjects with poor glycemiccontrol.

Cutler CW et al in1999 ,showed more rapid andpronounced development of gingival inflammation inrelatively well-controlled adult type 1 diabetic subjectsthan in non-diabetic controls, despite similar levels of

plaque accumulation and similar bacterial compositionof plaque, suggesting a hyperinflammatory gingivalresponse in diabetes.


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In a large cross-sectional study, by Grossi et al in1994showed that diabetic patients were twice aslikely as nondiabetic subjects to have attachment loss.

Firatli E et al in 1997followed type 1 diabetic patientsand healthy controls for 5 years and found that thepeople with diabetes had significantly more clinicalattachment loss than controls.


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Bridges RB et al in 1996in his cross sectional

study concludedthat diabetes affected all periodontal parameters,

including bleeding scores, probing depths, loss ofattachment and missing teeth.

A study by Moore PA et al in 1999 has shownthat diabetic patients are 5 times more likely to be

partially edentulous than nondiabetic subjects.


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A study by Weyant RJ et al in 1998showed thatpeople with type I and type 2 diabetes appear equallysusceptible to periodontal disease and tooth loss.

Chen I and Skrepcinski FB et al in 2000 found ,arelationship between diabetes and periodontaldisease,which appears to be very strong within certainpopulations, such as Aboriginalpeoples ,which indicates a genetic component.

Myers DE et al in 1999in his study found that,smoking increases the risk of periodontal disease bynearly 10 times in diabetic patients.


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In subjects with diabetes, chronically elevated blood glucoselevels lead to the accelerated formation of advanced glycationend products (AGEs). Endothelial cells and monocytespossess specific receptors for AGEs (i.e., RAGEs) located ontheir cell surfaces.

There is strong indication that the interaction of AGEs withtheir receptors plays an important role in the development ofdiabetic complications. The interaction of macrophages withAGEs has been shown to stimulate increased secretions ofpro-inflammatory mediators such as tumour necrosis factor a

(TNF-a) and interleukin-1 (IL-1). In subjects with type 2diabetes, deterioration of periodontal status was associatedwith elevated serum levels of AGEs (Salvi et al. 2008).


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The possible role of adipokines in periodontal diseaseand type 2 DM because these mediators may reflectcommon pathogenic processes relating toimunoregulatory changes (Preshaw et al. 2007 andLalla et al. 2001).

Other mechanisms by which diabetes may influencethe periodontium includes: vascular abnormalities,nonenzymatic glycosylation, imbalances in lipidmetabolism, altered collagen metabolism, neutrofil

dysfunction and altered monocytic response (Mealeyand Oates 2006 and Ryan et al. 2003)


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Diabetic people are 2-4 times more

susceptible to periodontal disease

Periodontal infection then complicates

glycemic control and enhances insulin

resistance and hyperglycemia

Poor glycemic control causes increased

susceptibility to re-infection and

more severe periodontal disease

Diabetes PeriodontalDisease


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Well controlled Diabetes mellitus subjects with moderate toadvanced periodontal disease, scaling and root planingresulted in similar clinical changes when compared to non-diabetes mellitus subjects with similar levels of periodontaldisease.(Christgau et al.in 1998)

Conversely, poorly controlled diabetes mellitus patients oftenhave a less favorable response to treatment than those withwell controlled diabetes.

Tervonen et al in 1997,found that the initial response to

scaling and root planing was good in diabetes mellitussubjects, but the incidence of disease recurrence over thesubsequent 12 months was greater in poorly controlleddiabetes mellitus individuals compared to well or moderatelycontrolled subjects.


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Westfelt et al in 1996, performed a longitudinal assessmentof periodontal therapy, including scaling and root planing,modified Widman flap surgery, and regular maintenance, indiabetes mellitus subjects and non-diabetes mellitus controlswith moderate to advanced periodontitis. At the 5-year re-

evaluation, diabetes mellitus patients had a similar percentageof sites gaining or losing attachment, and a similar percentageof sites with stable attachment levels, compared to non-diabetes mellitus subjects.

This data suggest that individuals with well controlled diabetes

mellitus respond to periodontal therapy in a fashion similar tonon-diabetes mellitus patients, but that poorly controlledpatients may have a less favorable response.


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There is little scientific evidence regarding thesuccess or failure of dental implant therapy indiabetic individuals. Diabetes is often considered arelative contraindication to implant placement, but

in well-controlled diabetes there is no reason toavoid implant therapy. Patients with poorlycontrolled diabetes may not respond well to anysurgical treatment, including implant placement,

due to impaired wound healing. The effect ofdiabetes on long- term clinical implant stability isalso unknown at this time.

Surgical implant

Possible diabetic disturbances in the


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Blood clot formation

Surgical implant

osteotomy

Bone resorption

phase

Matrix formation

phase

Bone

deposition/osteoid

mineralization

Maintenance of

osseointegration

Changes in wound healing proteins

Decreased number of osteoclasts

Inhibition of collagen formation

Decreased number of osteoblasts

Mineralization proteins reduced

Reduced bone turnover

Alterations in bone homeostasis

Change in diabetic status

Possible diabetic disturbances in the

implant wound-healing process


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Pinche JE 1998- (hemoglobin A1c)

measuresblood

glucoselevels overa period of

8 to 12weeks.

accurateand

relativelyinexpensive

one medicallaboratorytest andpatient

complianceis not

required

Long termglycemiccontrol

Provide anindication of

potential

response toperiodontal

therapy

4%-6% Normal

< 7% Good diabetes control

7%-8% Moderate diabetes control

>8% Action suggested to improve

diabetes control


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Home monitoring devices

test their blood glucose levels

four to six times daily.

simple, inexpensive and

reasonably accurate

used in dental offices as ascreening test

one or two-dropblood sample

reagentstrip

reflectormonitor


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Primary treatment goals for DM are achieving bloodglucose levels that are as close to normal as possibleand prevention of diabetic complications.Other goalsare normal growth and development, normal bodyweight, the avoidance of sustained hyperglycemia or

symptomatic hypoglycemia, the prevention of diabeticketoacidosis and nonketotic acidosis, and theimmediate detection and treatment of long-termdiabetic complications. Diet, exercise, weight control,and medications are the mainstays of diabetic care.

Obesity is very common in type 2 DM and contributesgreatly to insulin resistance. Weight reduction andexercise improve tissue sensitivity to insulin and allowits proper use by target tissues.


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Sulfonylureas stimulate pancreatic insulin secretion.The increased quantity of secreted insulin helpscounteract the qualitative decrease in tissuesensitivity to insulin, allowing greater glucose entryinto target cells and thereby lowering blood glucose

levels. Sulfonylureas have a relatively long duration ofaction (1224 hours), depending on the drug, and aretaken once or twice per day. Hypoglycemia is a majorside effect of sulfonylureas. In patients taking theseagents, food intake must be adequate to prevent

glucose levels from falling too low.


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Metformin is a biguanide agent that lowersplasma glucose mainly by preventingglycogenolysis in the liver. Metformin alsoimproves insulin use, counteracting the

insulin resistance seen with type 2 DM.Because metformin does not stimulateincreased insulin secretion, hypoglycemia ismuch less common with this drug.


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Insulin is taken via subcutaneous injection, most often with asyringe. Insulin infusion pumps deliver insulin through asubcutaneous catheter. There are a variety of insulinpreparations available; they vary in their onset, peak, andduration of activity and are classified as long-, intermediate-,

short-, or rapid-acting. Ultralente insulin is the longest-acting insulin. Commonly

called peakless insulin, Ultralente has a very slow onset ofaction, minimal peak activity, and a long duration of action.

The rapid-acting insulin (lispro insulin) is rapidly absorbed,becomes active about 15 minutes after injection, and is atpeak activity at 30 to 90 minutes.


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An emerging therapeutic option for type 1 DM istransplantation of the whole pancreas orpancreatic islet cells.Both are still complicated bymajor side effects and are thereby performed in

patients who have already developed significantmorbidity from DM.

With the development of continuous glucose-monitoring technology, it may now be possible to

use closed-loop pumps that infuse the correctamount of insulin in response to changing bloodglucose levels.


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Patients undergoing periodontal or oral surgeryprocedures other than single, simple extractionsshould be given dietary instructions after surgery;these instructions should be established with inputfrom the patients physician and nutritionist

Appointment scheduling is often determined by theindividuals medication regimen.

Traditionally, it was recommended that medicallycomplex patients, including those with DM, receive

dental treatment in the morning to reduce stress,. Thegreatest risk would occur in a patient who has takenthe usual amount of insulin or oral hypoglycemic agentbut has reduced or eliminated a meal prior to dentaltreatment.


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For example, if the patient takes the usual dose ofregular insulin before breakfast but then fails to eator eats less than the usual amount, the patient willbe at increased risk of hypoglycemia during a

morning dental appointment. the best time fordental treatment is either before or after periods ofpeak insulin activity. This reduces the risk ofperioperative hypoglycemic reactions, which occur

most often during peak insulin activity


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Treatment of oral fungal infections in the patient with DM issimilar to standard regimens except that topical antifungalmedications should be sugar free.

Studies conducted by (Williams & Mahan 1960; Grossi et al.1997; Miller et al. 1992)including antibiotics as an adjunct tomechanical therapy reported a limited, short-termimprovement in metabolic control.

Grossi et al. in 1997 reported a 10% improvement inglycated hemoglobin (HbA1c) at 3 months after the completionof non-surgical periodontal therapy combined with adjunctivesystemic doxycycline, although this effect was not sustainableat later time points.


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Whereas,Rodrigues et alin 2003randomlyassigned 30 type 2 patients to two treatmentgroups, one group receiving non-surgicalperiodontal therapy with amoxicillin/clavulanic acid

and the other receiving only mechanical therapy. At3 months, HbA1c levels were reduced in bothgroups, but the reduction was statisticallysignificant only in the group that received scalingand root planing alone.

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