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White PapersO R A L I N F L A M M A T I O N

A Six-Part Review Series on theOral and Systemic Disease Relationship

Presented as a Service to Periodontists byThe Colgate-Palmolive Company

Note to Reader: The topics addressed in these White Papers were selected by Colgate-Palmolive.Each Paper was commissioned by Colgate. Each Paper reflects the views of its author regardingthe state-of-the-science on the topic addressed, and does not necessarily reflect the policy of theAcademy. THE AMERICAN ACADEMY OF PERIODONTOLOGY DOES NOT ENDORSEANY COMPANY OR PRODUCTS.

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Over the last 25 years, the field of periodontologyhas witnessed remarkable changes in theunderstanding of disease processes and theirrelationship to the body as a whole. The focus oninflammation of the gingiva and periodontium, asimportant solely for disease of the oral cavity, hasshifted to include significant associations with thehealth of other body systems.

BackgroundGingival disease is an inflammatory process

characterized by increased redness, swelling, andbleeding of the gingiva on probing.1 Gingivitis is aninflammation of the gums caused by plaque andbacteria accumulation. It can progress to a moresevere state when the inflammatory process extendsto the periodontal ligament and alveolar bone.1

Periodontitis is one of the causes of connective tissueloss, resorption of alveolar bone, and formationof periodontal pockets, eventually leading toloosening and the loss of teeth; periodontitis is oneof the most common causes of tooth loss in adults.1

The process is believed to be episodic rather thancontinuous, with alternating periods of diseaseprogression and remission.

According to a survey conducted in the UnitedStates in the mid 1980s, between 73% and 80% ofadults displayed some loss of periodontalattachment (2 mm or more), while 15% of adultsbetween the ages of 60 and 64 displayed advancedperiodontitis (i.e., loss of attachment ≥ 6 mm).1 Therisk of developing periodontal disease varies amongpatients based on factors including age, heredity,diabetes, poor oral hygiene, and smoking.2,3 Whilepreviously considered an inevitable consequenceof aging, it is now recognized that periodontaldisease can be prevented or treated once it develops.

Periodontal disease is bacterial in origin, andgingivitis and periodontitis are associated withextensive destruction of the collagen-proteoglycan-connective-tissue matrix.1 The development of

disease occurs through two separately mediatedmechanisms (see figure). In both the acute andchronic phases of infection, pathogenic mani-festations may result directly from the bacterialinvasion of the tissue and production of toxicsubstances that lead to inflammation, cell death,and tissue necrosis. Tissue damage results from theaction of major inflammatory and immuno-pathologic components activated by the hostresponse. These include alteration of fibroblastfunction, activation of macrophages that releasecollagenase and other lytic enzymes, activation oflymphocytes, modulation of fibroblast growth andcollagen synthesis, and stimulation of boneresorption.1 Prostaglandins and cytokines appearto be critically involved in the tissue destructioncaused by periodontitis.4

Prevention, Control, and TreatmentPrevention and treatment of periodontal disease

aims at slowing the progression of the diseaseprocess, increasing the regeneration of alveolarbone, periodontal ligament and root cementum,

Scientific Advisory Panel

Ray Williams, DMDChair, Department of PeriodontologyUniversity of North CarolinaSchool of DentistryChapel Hill, North Carolina

Maria Ryan, DDS, PhDAssociate Professor, Department ofOral Biology and PathologySUNY at Stony BrookSchool of Dental MedicineStony Brook, New York

Sara Grossi, DDSClinical Assistant Professor of OralBiologySUNY at BuffaloSchool of DentistryBuffalo, New York

Frank Scannapieco, DMD, PhDProfessor and Chair, Department ofOral BiologySUNY at BuffaloSchool of DentistryBuffalo, New York

Michael Reddy, DMDProfessor and Chair, Department ofPeriodontologyUniversity of Alabama atBirmingham School of DentistryBirmingham, Alabama

Rebecca Wilder, RDH, MSDirector, Graduate Dental HygieneEducation ProgramUniversity of North CarolinaSchool of DentistryChapel Hill, North Carolina

Overview of Oral InflammationRay C.Williams,DMD,Chair,Department of Periodontology

University of North Carolina School of Dentistry

Copyright © 2005 Colgate-Palmolive Company. All rights reserved.

Oral Inflammation �Periodontal Disease

Acute and Chronic Phase

• Bacterial invasion of tissue

• Production of toxic substances

• Inflammation, cell death and tissue necrosis

• Inflammatory/immunopathologic componentsactivated by host response

• Prostaglandins and cytokines involved

• Alteration of fibroblast function

• Activation of macrophages that release collagenase and other lytic enzymes

• Activation of lymphocytes

• Modulation of fibroblast growth and collagensynthesis

• Stimulation of bone resorptiondiabetes, poor oral hygiene, and smoking.23 Whilepreviously considered an inevitable consequenceof aging, it is now recognized that the onset ofperiodontal disease can be delayed or theseverity of the disease reduced once it develops.

Periodontal disease is bacterial in origin, andgingivitis and periodontitis are associated withextensive destuction of the collagen-proteoglycan-


Oral Inflammation �Periodontal Disease

Acute and Chronic Phase

• Bacterial invasion of tissue

• Production of toxic substances

• Inflammation, cell death and tissue necrosis

• Inflammatory/immunopathologic componentsactivated by host response

• Prostaglandins and cytokines involved

• Alteration of fibroblast function

• Activation of macrophages that release collagenase and other lytic enzymes

• Activation of lymphocytes

• Modulation of fibroblast growth and collagensynthesis

• Stimulation of bone resorption

connective-tissue matrix.1 The development ofdisease occurs through two separately mediatedmechanisms (see figure). In both the acute andchronic phases of infection, pathogenic mani-festations may result directly from the bacterialinvasion of the tissue and production of toxic substances that lead to inflammation, cell death,and tissue necrosis. Tissue damage results from theaction of major inflammatory and immuno-pathologic components activated by the hostresponse. These include alteration of fibroblastfunction, activation of macrophages that releasecollagenase and other lytic enzymes, activation oflymphocytes, modulation of fibroblast growthand collagen synthesis, and stimulation of boneresorption.1 Prostaglandins and cytokines appearto be critically involved in the tissue destructioncaused by periodontitis.4

Colgate White Papers #1Rev2:Layout 1 5/30/07 9:53 AM Page 1

WHITE PAPERS O R A L I N F L A M M A T I O N

and preventing recurrence after treatment.Elimination of gingival inflammation is a first step inreducing the risk for oral disease. Removal andcontrol of bacterial plaque are key componentstowards this end, and involve mechanicalinterventions adjusted to the stage and severityof disease. Early control of bacterial plaqueaccumulation is essential for the prevention ofperiodontal disease. Proper dental hygiene, withdaily mechanical removal of bacterial plaque bytooth brushing supplemented with flossing, isrecommended to control gingivitis.1

Antimicrobial agents can also play a role in theprevention and treatment of periodontal disease.Several antimicrobial agents have beenincorporated into mouthrinses or dentifricepreparations to inhibit plaque accumulation.Triclosan, a well known antibacterial agent, hasa wide spectrum of action against plaque-forming supragingival and subgingival bacteria,including many types of Gram-positive andGram-negative non-sporulating bacteria, somefungi, Plasmodium falciparum, and Toxoplasmagondii.5 The combination of triclosan with acopolymer allows the agent to remain on thetooth surface for a prolonged period of time,providing effective inhibition of plaque formationand of gingivitis.4 A dentifrice containingtriclosan/copolymer (Colgate® Total® Toothpaste)has been shown to effectively contribute to thecontrol of bacterial infection, reduce gingivalinflammation, and slow the progression ofperiodontitis.6

New avenues of treatment explore the use ofhistatins, histidine-rich proteins that are naturallyfound within parotid and submandibularsecretions, and contain antimicrobial peptidesthat can effectively inhibit plaque accumulation.Animal studies have shown that topicallyapplied synthetic histatins can significantlyreduce bleeding and the progression of gingivitis.7

While still being tested clinically, histatins holdpotential for the control of gingival inflammationbecause they are a natural component of humansaliva with no apparent adverse effect on hosttissue.8 Localized antibiotic treatments usingnovel delivery systems can also be used to controladvanced periodontitis and halt acute infection.4

For example, minocycline topically applied inmicrospheres (Arestin®) into periodontal pocketshas been shown to significantly reduce pocketdepth when combined with scaling and rootplaning.9

In parallel, the inflammatory nature ofperiodontitis suggests that blocking inflamma-

tory pathways and modulating host responsesvia pharmacological treatment may alsoattenuate periodontal tissue destruction.3,4 In thisresearch area, trials of topically appliedcyclooxygenase inhibitors (e.g., ketoprofen) havebeen shown to significantly reduce the rate ofalveolar bone loss compared to placebo in animalstudies.4

The Relationship Between Oral and Systemic Health

It has long been recognized that systemicconditions can contribute to the expression ofperiodontal disease; metabolic disorders (e.g.,diabetes), blood dyscrasias (e.g., leukemia),autoimmune disease (e.g., pemphigus),pregnancy, and puberty all increase the incidenceof periodontal disease.1 In recent years, increasingevidence has supported the concept that therelationship between systemic and oral health isbi-directional.10 Much research has documentedthe association between periodontitis and itseffects on preterm delivery and low birth weightnewborns.3,10-12 Studies have also indicated thatperiodontal disease can increase the risk forcardiovascular disease, respiratory diseases,osteoporosis, and accelerate the progression ofdiabetes (see figure).

The general mechanism behind the systemiceffects of periodontitis is thought to involve, inpart, a systemic inflammatory response throughblood-borne oral lipopolysaccharides and oralbacteria which provoke the release of thecytokines interleukin-6 and tumor necrosis factorα.10 These mediators activate a hepatic acutephase response with secretion and systemicrelease of C-reactive proteins, haptoglobin, α1-antitrypsin and fibrinogen.10 Understanding andmanaging the impact of oral infection on systemichealth is a challenge of periodontal medicine.10

For example, the identification and validation ofsystemic markers for periodontitis will providepowerful tools to diagnose, treat, and monitor

patients with periodontitis. These relationships,as well as management of the patient withperiodontal disease, will be the topics of futureissues of this Colgate White Papers series.

ConclusionOver recent years, we have increasingly begun

to focus on inflammation of the oral cavity, notonly as important for disease of the periodontaltissues, but also as a risk factor for systemicdiseases. It is evident that we can no longer viewgingivitis simply as a precursor of periodontitis, butwe should treat it as oral inflammation that needs tobe controlled and eliminated for the overall well beingof the individual. Any new treatment strategy thatcan help in controlling gingivitis should have abeneficial effect both on oral health and onsystemic health.

References1. Williams RC. Periodontal disease. N Engl J Med 1990;322(6):373-382.2. Williams RC. A century of progress in understandingperiodontal disease. Compend Cont Educ Dent 2002;23 5 (Suppl):3-10.3. Williams RC, Beck JD, Offenbacher SN. The impact of newtechnologies to diagnose and treat periodontal disease. A look tothe future. J Clin Periodontol 1996;23 (3 Pt 2):299-305.4. Williams RC, Paquette DW. Periodontal disease diagnosis andtreatment: An exciting future. J Dent Educ 1998;62 (10):871-881.5. Russell AD. Whither triclosan? J Antimicrob Chemother 2004;53(5):693-695.6. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effect of triclosanon mediators of gingival inflammation. J Clin Periodontol 1995;22(6):480-484.7. Paquette DW, Waters GS, Stefanidou VL, Lawrence HP, FridenPM, O’Connor SM, et al. Inhibition of experimental gingivitis inbeagle dogs with topical salivary histatins. J Clin Periodontol 1997;24(4):216-222.8. Kavanagh K, Dowd S. Histatins: Antimicrobial peptides withtherapeutic potential. J Pharm Pharmacol 2004;56 (3):285-289.9. Paquette DW, Hanlon A, Lessem J, Williams RC. Clinicalrelevance of adjunctive minocycline microspheres in patients withchronic periodontitis: Secondary analysis of a phase 3 trial. JPeriodontol 2004;75 (4):531-536.10. Williams RC, Offenbacher S. Periodontal medicine: Theemergence of a new branch of periodontology. Periodontol 20002000;23 (1):9-12.11. Scannapieco FA, Bush RB, Paju S. Periodontal disease as a riskfactor for adverse pregnancy outcomes. A systematic review. AnnPeriodontol 2003;8 (1):70-78.12. Lopez NJ, Smith PC, Gutierrez J. Higher risk of preterm birthand low birth weight in women with periodontal disease. J DentRes 2002;81 (1):58-63.

Diabetes

Cardiovascular Dise

ases

Res

pi

ratory

Diseases Osteoporosis

Oral Inflammation

Gingivitis

Periodontitis

Patient Management

This series is brought to you byColgate® Total® -

12-Hour Antibacterial plusAnti-inflammatory Protection.

This seriesis brought to you by

The Colgate-Palmolive Company

Brought to you through aneducational grant from

Colgate-Palmolive.

Brought to you through an educational grant from

Colgate-Palmolive.

References1. Caranza’s Clinical Periodontology 10th Edition. Newman MG,

Takai H, Klokkevold PR, eds. St. Louis, Saunders, 2006.2. Williams RC. A century of progress in understanding

periodontal disease. Compend Cont Educ Dent 2002;235(Suppl):3-10.

3. Caranza’s Clinical Periodontology10th Edition. Newman MG,Takai H, Klokkevold PR, eds. St. Louis, Saunders, 2006.

4. Williams RC, Paquette DW. Periodontal disease diagnosis andtreatment: An exciting future. J Dent Educ 1998;62 (10):871-881.

5. Russell AD. Whither triclosan? J Antimicrob Chemother2004;53 (5):693-695.

6. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM,Proskin HM: Advanced oral antibacterial/anti-inflammatorytechnology: A comprehensive review of the clinical benefits ofa triclosan/copolymer/fluoride dentifrice. J Clin Dent 2005; 16(Suppl):S1-S20.

7. Paquette DW, Waters GS, Stefanidou VL, Lawrence HP, FridenPM, O’Connor SM, et al. Inhibition of experimental gingivitis inbeagle dogs with topical salivary histatins. J Clin Periodontol1997;24 (4):216-222.

8. Kavanagh K, Dowd S. Histatins: Antimicrobial peptides withtherapeutic potential. J Pharm Pharmacol 2004;56 (3):285-289.

9. Paquette DW, Hanlon A, Lessem J, Williams RC. Clinicalrelevance of adjunctive minocycline microspheres in patientswith chronic periodontitis: Secondary analysis of a phase 3 trial.J Periodontol 2004;75 (4):531-536.

10. Williams RC, Offenbacher S. Periodontal medicine: Theemergence of a new branch of periodontology. Periodontol 20002000;23 (1:9-12.

11. Scannapieco FA, Bush RB, Paju S. Periodontal disease as a riskfactor for adverse pregnancy outcomes. A systematic review.Ann Periodontol 2003;8 (1):70-78.

12. Lopez NJ, Smith PC, Gutierrez J. Higher risk of preterm birthand low birth weight in women with periodontal disease. J DentRes 2002;81 (1):58-63.

Brought to you through an educational grant from

Colgate-Palmolive.

References1. Caranza’s Clinical Periodontology 10th Edition. Newman MG,

Takai H, Klokkevold PR, eds. St. Louis, Saunders, 2006.2. Williams RC. A century of progress in understanding

periodontal disease. Compend Cont Educ Dent 2002;235(Suppl):3-10.

3. Caranza’s Clinical Periodontology10th Edition. Newman MG,Takai H, Klokkevold PR, eds. St. Louis, Saunders, 2006.

4. Williams RC, Paquette DW. Periodontal disease diagnosis andtreatment: An exciting future. J Dent Educ 1998;62 (10):871-881.

5. Russell AD. Whither triclosan? J Antimicrob Chemother2004;53 (5):693-695.

6. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM,Proskin HM: Advanced oral antibacterial/anti-inflammatorytechnology: A comprehensive review of the clinical benefits ofa triclosan/copolymer/fluoride dentifrice. J Clin Dent 2005; 16(Suppl):S1-S20.

7. Paquette DW, Waters GS, Stefanidou VL, Lawrence HP, FridenPM, O’Connor SM, et al. Inhibition of experimental gingivitis inbeagle dogs with topical salivary histatins. J Clin Periodontol1997;24 (4):216-222.

8. Kavanagh K, Dowd S. Histatins: Antimicrobial peptides withtherapeutic potential. J Pharm Pharmacol 2004;56 (3):285-289.

9. Paquette DW, Hanlon A, Lessem J, Williams RC. Clinicalrelevance of adjunctive minocycline microspheres in patientswith chronic periodontitis: Secondary analysis of a phase 3 trial.J Periodontol 2004;75 (4):531-536.

10. Williams RC, Offenbacher S. Periodontal medicine: Theemergence of a new branch of periodontology. Periodontol 20002000;23 (1:9-12.

11. Scannapieco FA, Bush RB, Paju S. Periodontal disease as a riskfactor for adverse pregnancy outcomes. A systematic review.Ann Periodontol 2003;8 (1):70-78.

12. Lopez NJ, Smith PC, Gutierrez J. Higher risk of preterm birthand low birth weight in women with periodontal disease. J DentRes 2002;81 (1):58-63.

and preventing recurrence after treatment.Elimination of gingival inflammation is a firststep in reducing the risk for oral disease.Removal and control of bacterial plaque arekey components towards this end, andinvolve mechanical interventions adjustedto the stage and severity of disease. Earlycontrol of bacterial plaque accumu lation isessential to help slow the development ofperiodontal disease. Proper dental hygiene,with daily mechanical removal of bacterialplaque by tooth brushing supplementedwith flossing, is recommended to controlgingivitis.1

Antimicrobial agents can help to slow theprogression of periodontal disease. Severalantimicrobial agents have been incorporatedinto mouthrinses or dentifrice preparations toinhibit plaque accumulation. Triclosan, awell known antibacterial agent, has awide spectrum of action against plaque-forming supragingival and subgingivalbacteria, including many types of Gram-positive and Gram-negative non-sporulatingbacteria, some fungi, Plasmodium falciparum,and Toxoplasma gondii.5 The combination oftriclosan with a copolymer allows the agent toremain on the tooth surface for a prolongedperiod of time, providing effective inhibitionof plaque formation and of gingivitis.4 Adentifrice containing triclosan/copolymer(Colgate® Total® Toothpaste) has been shownto effectively contribute to the controlof bacterial infection, reduce gingivalinflammation, and slow the progression ofperiodontitis.4

New avenues of treatment explore the useof histatins, histidine-rich proteins that arenaturally found within parotid andsubmandibular secretions, and containantimicrobial peptides that can effectivelyinhibit plaque accumulation. Animal studieshave shown that topically applied synthetichistatins can significantly reduce bleedingand the presence of gingivitis.7 While stillbeing tested clinically, histatins hold potentialfor the control of gingival inflammationbecause they are a natural component ofhuman saliva withh no apparent adverseeffect on host tissue.8 Localized antibiotictreatments using novel delivery systems canalso be used to control advanced periodontitisand halt acute infection.4



Diabetes mellitus is a chronic metabolic disorderaffecting carbohydrate, fat, and protein metabolism.It is characterized by hyperglycemia (i.e., elevationof blood glucose concentration) caused by thedefective secretion of insulin (type I), or impairedinsulin action due to tissue resistance (type II). Whilethere is no known cure for diabetes, appropriatemeasures can be taken to control blood glucose levelsand prevent both acute and chronic complications.Poor glycemic control in diabetic patients has severalrepercussions, including some on oral health. Patientswith diabetes are prone to develop oral complicationssuch as gingivitis and periodontal disease, fungalinfections (oral candidiasis, lichen planus), dentalcaries, tooth loss, enlarged parotid glands, xerostomia,taste dysfunction, and burning mouth syndrome.1,2

The most prominent oral symptom associatedwith diabetes is the increased prevalence and severityof periodontitis; it is recognized as one of the majorcomplications of diabetes.3-5 Persistent poor glycemiccontrol has been associated with an increasedincidence and more rapid progression of gingivitisand periodontitis with associated alveolar bone loss.2

The degree of metabolic control and the duration ofdiabetes are closely associated with the severity ofperiodontal disease.6

The pathogenesis of periodontal disease involvestwo components: bacterial infection and the hostresponse. Bacteria present in periodontal pocketsinitiate an oral inflammatory response that can leadto the deterioration of the supporting periodontaltissues. When the host response is comprised of anexcess of pro-inflammatory mediators known ascytokines, prostanoids, and enzymes, the destructionof periodontal tissues occurs. This results in increasedpocket depths, loss of clinical attachment, andradiographic evidence of bone loss.7 In patients withpoorly controlled diabetes, periodontal destructionis exacerbated due to hyperglycemia.6

Hyperglycemia and Oral Health The effects of hyperglycemia on oral health are

two-fold. First, it causes an increase in theconcentration of glucose in the saliva and the gingivalcrevicular fluid of the periodontal pocket,

contributing to bacterial proliferation and oralinflammation. Second, hyperglycemia increases theformation of advanced glycation end-products(AGEs); the overexposure of proteins (such ascollagen) or lipids to aldose sugars induces non-enzymatic glycation and oxidation.6 Theseglycosylated products can create complex moleculararrangements, reducing collagen solubility andincreasing levels of pro-inflammatory mediatorsresponsible for the degradation of connective tissuesthroughout the body of the diabetic, including the

oral cavity. Changes to collagen metabolism result inaccelerated degradation of both non-mineralizedconnective tissue and mineralized bone.6 Researchhas demonstrated the presence of elevated levels ofpro-inflammatory mediators in the gingival crevicularfluid of periodontal pockets of poorly controlleddiabetics, compared to non-diabetics or well-controlled diabetics, resulting in significantperiodontal destruction with an equivalent bacterialchallenge.3,6,8 For clinicians and diabetic patients, thismeans that the oral hygiene of the diabetic must beoptimized to prevent further stimulation of an alreadyprimed and heightened host response.

The interaction of AGEs with target cells, such asmacrophages, via cell-surface polypeptide receptorsstimulates the production of cytokines and matrix



Maria Ryan, DDS, PhDAssociate Professor, Department of OralBiology and PathologySUNY at Stony BrookSchool of Dental MedicineStony Brook, New York

Sara Grossi, DDSClinical Assistant Professor of Oral BiologySUNY at BuffaloSchool of DentistryBuffalo, New York

Frank Scannapieco, DMD, PhDProfessor and Chair, Department of OralBiologySUNY at BuffaloSchool of DentistryBuffalo, New York

Michael Reddy, DMDProfessor and Chair, Department ofPeriodontologyUniversity of Alabama at Birmingham School of DentistryBirmingham, Alabama


This article was prepared with the assistance ofBioMedCom Consultants, inc., Montreal, Canada.

Oral Inflammation and DiabetesMaria Emanuel Ryan,DDS,PhD, Department of Oral Biology and Pathology

Stony Brook University School of Dental Medicine


Factors Accentuating PeriodontalDisease in Diabetic Patients• Duration of diabetes• Degree of metabolic control• Co-occurrence of complications

• Angiopathy (heart disease and stroke)• Delayed wound healing• Nephropathy (kidney disease)• Neuropathy• Retinopathy (eye disease)

• Concurrent risk factors• Hormonal variations

(e.g., adolescence, pregnancy, menopause)• Medications• Plaque• Smoking• StressFrom Ryan et al., 20036




metalloproteinases, including collagenases andother connective tissue-degrading enzymes.3 Thisexacerbation of the pro-inflammatory responsein diabetics can lead to delayed wound repairand amplify damage to connective tissues.6 Thisis important to consider when evaluating theresponse of poorly controlled diabetic patientsto periodontal therapy. The pro-inflammatoryresponse may be further heightened by thechemotactic properties of AGEs for humanmonocytes which differentiate into the chronicinflammatory macrophage cells.6

Degradation of newly synthesized collagenin connective tissues and alterations in theimmune response can both contribute topredisposition to periodontal disease andimpaired wound healing. The degree ofmetabolic control and the presence of othercomplications (e.g., retinopathy andnephropathy) can be predictive of the periodontalstatus. Concurrent risk factors (plaque, smoking,stress, medications, pregnancy, hormonalvariations) are cumulative and should beconsidered in the assessment of the periodontalstatus of a patient.6

The presence of AGEs has also been linkedto thickening of the basement membrane andaltered vasculature. These changes may beassociated with enlargement of the parotidglands and decreased salivary flow seen indiabetics, which facilitates plaque accumulationand increases the risk for caries, gingivitis,periodontitis, and candidiasis. Degenerativevascular changes may interfere with nutrient andleukocyte migration to gingival tissue, decreasingoxygen diffusion and elimination of metabolicwaste, thereby increasing the severity ofperiodontitis by decreasing dental healingcapacity.6 Collectively, diabetes creates specificconditions leading to enhanced oralinflammation associated with overproductionof inflammatory mediators and degradationenzymes, all of which participate in worseningperiodontal disease.

Oral-Systemic InteractionsWhile a systemic condition like diabetes can

affect oral health, there is growing evidence thatoral infections can also have systemicrepercussions.9 This bi-directional relationshipis especially important for the metabolic controlof diabetes. Studies of active inflammatoryconnective tissue disease have shown thatinflammation can trigger insulin resistance.10

Cytokines, such as tumor necrosis factor (TNF)-a, have been reported to interfere with lipidmetabolism and to cause insulin resistance, whileinterleukins (IL)-1b and IL-6 antagonize insulinaction.10 The host-mediated inflammatoryresponse can thus hinder glycemic control indiabetic patients, in turn creating a vicious cycleof events that compromises diabetes control and

further stimulates periodontal disease. Poormetabolic control of diabetes can also increasethe risk for other complications of diabetes, suchas angiopathy, nephropathy, retinopathy,neuropathy, and delayed wound healing.Prevention and control of oral infection andinflammation, i.e., periodontal disease, is essentialfor appropriate prevention and optimalmanagement of diabetic complications.11

It is also thought that elevations of AGEs ingingival tissue increase vascular permeability.11

An inflamed periodontium is highly vascularand may serve as a portal to the systemiccirculation for bacterial products (bacteremias)and host-produced local inflammatorymediators.10 Other connections between a poorperiodontal status and systemic health sequelaehave been studied; adverse pregnancy outcomesand cardiovascular disease are both knowncomplications in diabetics. Recent research hasshown that pregnant women with severeperiodontitis have a higher risk of giving birthto preterm low-birth-weight babies. Other studieshave shown that the risk of major cardiovascularevents, such as heart attack and stroke, issignificantly higher in those with severeperiodontal disease.9 It has become apparent thatprevention and treatment of periodontitis areessential to optimal systemic health, particularlyin the diabetic patient.

Management of Diabetes and Oral InflammationControl of blood glucose is the fundamental

aspect of diabetes management to minimizerelated complications. Adequate glycemic controlwill not only reduce glucose concentration inserum, gingival crevicular fluid, and saliva, butalso reduces AGE formation and limitsinflammation.11 Prevention and control ofperiodontal disease must be considered anintegral aspect of diabetes management, sinceimproved oral health can lead to improvementsin the overall health of diabetic patients.11

Given the increased susceptibility of diabeticpatients for oral inflammation, emphasis shouldbe placed on reduction of bacterial infection andgingivitis. An optimal prevention plan shouldinclude twice-daily brushing and flossing toremove bacterial plaque from teeth.12 Adentifricecontaining triclosan/copolymer (Colgate Total®

Toothpaste) has been shown to be very effectivein controlling bacterial infection, reducing plaqueand gingival inflammation, and preventing orslowing the progression of periodontitis.13

Restriction of oral infection and inflammation asmanifested in periodontitis contributes to themaintenance of normal blood glucose levels,which aids in the overall management of diabeticpatients.

For the treatment of periodontitis, a two-stepprocess aimed at the two components of thedisease offers the most favorable outcome.12 The

first step is reduction and control of bacteria, bothsupragingival and subgingival, in the toothpockets and spaces around teeth. Scaling androot planing helps remove bacterial plaque andassociated toxins from the tooth and root surfaces,and can help to prevent the bacterialaccumulation that is common on rough surfaces.The second step is inhibition of the enzymes thatdestroy periodontal tissue so that connectivetissue degradation is minimized (hostmodulation therapy). Clinical trials havedemonstrated the efficacy of some tetracyclineanalogs to inhibit a series of host-derived, tissue-destructive enzymes and inflammatorymediators,5,8 thereby reducing the connectivetissue damage associated with periodontitis.

ConclusionDiabetes is a complex disease with a wide

range of potential complications, including effectson oral health. Integrated strategies for theprevention and treatment of periodontal diseaseinvolving the removal of periodontal pathogensand host modulation therapy greatly reduce therisk for severe periodontitis, and can help in theoverall management of the diabetic patient. Adiabetic patient who maintains rigorous glycemiccontrol and good oral health has the same riskof severe periodontitis as a non-diabetic patient,emphasizing the importance of diabetes and oralhealth management.

References1. Ship JA. Diabetes and oral health: An overview. JADA 2003;134:4S-10S.2. Vernillo AT. Dental considerations for the treatment of patients with

diabetes mellitus. JADA 2003;134:24S-33S.3. Ryan ME, Ramamurthy NS, Sorsa T, Golub LM. MMP-mediated events in

diabetes. Ann NY Acad Sci 1999;878:311-334.4. Selwitz RH, Pihlstrom BL. How to lower risk of developing diabetes and

its complications: Recommendations for the patient. JADA 2003;134:54S-58S.5. Ryan ME. Host response in diabetes-associated periodontitis: Effects of

tetracycline analogues. Dissertation Abstracts International 1999;59(8).6. Ryan ME, Carnu O, Kamer A. The influence of diabetes on the periodontal

tissues. JADA 2003;134:34S-40S.7. Ryan ME, Preshaw PM. Host modulation. In: Newman MG, Takei HH,

Carranza FA, Klokkevold PR, eds., Carranza’s Clinical Periodontology 10th ed. Elsevier, In press.

8. Ryan ME, Usman A, Ramamurthy NS, Golub LM, Greenwald RA. Excessive matrix metalloproteinase activity in diabetes: Inhibition by tetracycline analogues with zinc reactivity. Curr Med Chem 2001;8(3):305-316.

9. Li X, Kolltveit KM, Tronstad L, Olsen I. Systemic diseases caused by oral infection. Clin Microbiol Rev 2000;13(4):547-558.

10. Taylor GW. The effects of periodontal treatment on diabetes. JADA2003;134:41S-8S.

11. Matthews DC. The relationship between diabetes and periodontal disease. J Can Dent Assoc 2002;68(3):161-164.

12. Ryan ME. Non-Surgical Approaches for the Treatment of Periodontal Diseases. In: Scannapieco FA, ed., The Dental Clinics of North America. Elsevier, In press.

13. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effect of triclosan on mediators of gingival inflammation. J Clin Periodontol 1995;22(6):480-484.



Visit www. perio.org for moreinformation on periodontal disease and systemic health.

1. Ship JA. Diabetes and oral health: An overview. JADA 2003; 134:4S-10S.2. Caranza’s Clinical Periodontology 10th Edition. Newman MG, Takai H,

Klokkevold PR, eds. St. Louis, Saunders, 2006.3. Ryan ME, Ramamurthy NS, Sorsa T, Golub LM. MMP-mediated events

in diabetes. Am NY Acad Sci 1999; 878:331-334.4. Selwitz RH, Pihlstrom BL. How to lower risk of developing diabetes and its

complications: Recommendations for the patient. JADA 2003; 134:54S-58S.5. Ryan ME. Host response in diabetes-associated periodontitis: Effects of

teracycline analogues. Dissertation Abstracts International 1999;59(8).6. Ryan ME, Carnu O, Kramer A. The influence of diabetes on the perio -

dontal tissues. JADA 2003; 134:34S-40S.7. Ryan ME, Preshaw PM. Host modulation. In: Newman MG, Takei HH,

Carranza FA, Klokkevold PR, eds., Carranza’s Clinical Periodontology 10thed. Elsevier, In press.

8. Ryan ME, Usman A, Ramamurthy NS, Golub LM, Greenwald RA.Excessive matrix metalloproteinase activity in diabetes: Inhibition bytetracycline analogues with zinc reactivity. Curr Med Chem 2001;8(3)305-316.

9. Li X, Kolltveit KM, Tronstad L, Olsen I. Systemic diseases caused by oralinfection. Clin Microbiol Rev 2000;13(4):547-558.

10. Taylor GW. The effects of periodontal treatment on diabetes. JADA2003;134:41S-48S.

11. Matthews DC. The relationship between diabetes and periodontal disease. J Can Dent Assoc 2002;68(3):161-164.

12. Ryan ME. Nonsurgical approaches for the treatment of periodonal diseases. Dent Clin North Am 2005;49(3):611-636.

13. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM, ProskinHM. Advanced oral antibacterial/anti-inflammatory technology: Acomprehensive review of the clinical benefits of a triclosan/copolymer/fluoride dentifrice. J Clin Dent 2005;16 (Suppl)S1-S20.

essential to optimal systemic health, including

process aimed at the two components ofthe disease can be considered. The first step is

reduction and control of bacteria, bothsupragingival and subgingival, in the toothpockets and spaces around teeth. Scaling androot planing helps remove bacterial plaque andassociated toxins from the tooth and rootsurfaces, and can help to prevent the bacterialaccumulation that is common on roughsurfaces. The second step is inhibition of theenzymes that destroy periodontal tissue so thatconnective tissue degradation is minimized(host modulation therapy). Clinical trials havedemonstrated the efficacy of some tetracyclineanalogs to inhibit a series of host-derived,tissue-destructive enzymes and inflammatorymediators,5,8 thereby reducing the connectivetissue damage associated with periodontitis.

involving the reduction of periodontal pathogens

Colgate White Papers #2Rev2:Layout 1 5/31/07 1:05 PM Page 2


Cardiovascular Disease and AtherosclerosisAtherosclerosis, the thickening and hardening of

arteries produced by a build-up of plaque, is theunderlying cause of cardiovascular disease (CVD). Itis essentially an inflammatory disease, whereby aninitial lesion, in response to injury to the endotheliumof elastic and muscular arterial tissue, leads to acomplex chronic inflammatory process.1 There isaccumulating evidence of a role for infectious agentsin atherogenesis; by causing endothelial injury, theymay, in part, trigger the inflammatory response.2 Thelevels of inflammatory mediators in the systemiccirculation, such as C-reactive protein (CRP) andfibrinogen, are indicators of a general inflammatoryresponse and atherosclerosis.1 This link betweeninflammation and atherosclerosis suggests that chronicinfections, such as oral infections from periodontaldisease, may predispose to cardiovascular disease.3

Significant similarities in the pathogenesis ofatherosclerosis and periodontitis have suggested acommon underlying biological mechanism for the twoconditions. Based on this paradigm, several studieshave investigated the relationship betweenperiodontitis and cardiovascular disease.4

Indirect Evidence: Epidemiological StudiesMost of the evidence supporting a relationship

between periodontal disease and CVD comes fromepidemiological studies. In the late 1980s, pioneer workshowed that patients who had a history of myocardialinfarction (MI) generally had worse oral health thancontrol subjects.5 Subsequently, cross-sectional datafrom the Third National Health and Nutrition Survey(NHANES III) indicated that patients with severeclinical attachment loss were at greater risk for MI thansubjects with a healthy periodontium (odds ratio: 3.8).6

Since then, systematic literature reviews have indicatedthat most studies report a modest association betweenperiodontal disease and CVD, between a 1.3 and 2-foldincrease in the risk of CVD in people with periodontitis.7

Conversely, treatment of periodontitis was shown todecrease serum concentration of CRP, interleukin (IL)-6 and tumor necrosis factor (TNF)-a, indicating that

infection of the periodontium can influence systemicconditions. What remains unclear from these studies,however, is whether periodontitis can predispose toatherosclerosis.8

Direct Evidence: Experimental StudiesDirect evidence for the role of oral infection in

predisposing to atherosclerosis comes from severallines. The presence of predominant oral pathogens suchas Porphyromonas gingivalis, Tannerella forsythensis, andPrevotella intermedia was detected in atheroscleroticplaque, suggesting a possible invasion of atheromasby oral pathogens.9 In addition, P. gingivalis can invadeendothelial cells10 and can also induce plateletaggregation, a key process in atheroma and thrombusformation.11 Whether these pathogens activelycontribute to the development of atheroma, however,remains to be established.

Most of the experimental evidence supporting arelationship between CVD and periodontal diseasecomes from animal model studies. Usingapolipoprotein E-deficient mice, research has shownthat clinically induced bacteremia or oral infection withP. gingivalis increase atheroma size compared to non-



Maria Emanuel Ryan, DDS, PhD Professor and Director of Clinical Research Department of Oral Biology and Pathology SUNY at Stony Brook School of Dental Medicine Stony Brook, New York

Sara G. Grossi, DDS, MS,Clinical Assistant Professor of Oral BiologySUNY at BuffaloSchool of DentistryBuffalo, New York

Frank Scannapieco, DMD, PhDProfessor and Chair, Department of Oral BiologySUNY at BuffaloSchool of DentistryBuffalo, New York




Oral Inflammation and Cardiovascular DiseasesSara G.Grossi,DDS,MS,Senior Research Scientist,Department of Oral Biology,

State University of New York at Buffalo School of Dental Medicine

Copyright © 2005 Colgate-Palmolive Company. All rights reserved.Copyright © 2007 Colgate-Palmolive Company. All rights reserved.



infected mice.12 Similarly, pigs exposed orally to P.gingivalis had elevated CRP and increasedatheroma size compared to control animals,suggesting a role for this particular periodontalpathogen in the development of atherosclerosis.12

Arecent study in humans reported a positiveindependent association between periodontalbacterial burden and carotid intima-mediathickness (IMT).3 Results were adjusted for knownrisk factors for CVD (age, ethnicity, gender,education, body mass index, smoking, diabetes,systolic blood pressure, low-density and high-density lipoprotein cholesterol). A positiverelationship between carotid IMT and bacterialburden was especially strong in patientspredominantly infected by specific bacteriainvolved in the etiology of gingival disease,including P. gingivalis, Actinobacillusactinomycetemcomitans, Treponema denticola, andTannerella forsythensis (Figure 1).3

Biological Mechanism and PathogenesisGingival inflammation may influence

atherosclerosis in three distinct pathways (Figure2).13 Oral infection by periodontal pathogens initiatesthe formation of dental plaque which leads toinflammation of periodontal tissues. The formationof periodontal pockets increases subgingival space,which is conducive for bacterial growth anddeposits. Ensuing local inflammation processesproduce micro-ulcerations through the pocketepithelium, promoting risks for distant-site infectionand transient bacteremia. Moreover, bacteria releasea variety of biologically active molecules, includinglipopolysaccharides, endotoxins, chemotacticpeptides, proteins, and organic acids, that may thenenter the systemic circulation. These products cantrigger the host inflammatory response and elevateserum concentration of acute-phase reactants andinflammatory mediators (CRP, serum amyloid A,fibrinogen, haptoglobin, TNF-a, IL-6 and IL-8).3

Increased levels of circulating inflammatorymediators is thought to contribute to theinflammatory processes leading to atherosclerosis.2,13

Immunization against bacterial pathogens mayalso induce an autoimmune response involved inthe development of atherosclerosis. Homology ofsome bacterial and human proteins (e.g., heat-shock protein HSP60) raises the possibility thatantibodies against bacterial versions of the proteinmay cross-react with the human protein, inducingan autoimmune response. In the case of HSP60,disruption of arterial endothelial cells is thoughtto stimulate atherosclerosis.13 Proinflammatoryresponse may also be enhanced by cross-reactiveepitopes that stimulate T-cell response reactivewith host antigens, enhancing the effects ofbacterial pathogens on cardiovascular health.13

Establishing a direct link between periodontal diseaseand CVD is very difficult due to the multifactorialnature of both diseases with numerous confounding riskfactors common to the two.4,13 Nevertheless,epidemiological observations coupled with the biologicalplausibility of this association between two inflammatorydiseases warrant the need for further investigation andvalidation of the cardiovascular-periodontal link.

Management and PreventionOral inflammation and periodontal disease are

generally chronic and can persistasymptomatically for many years in the absenceof appropriate treatment. This results in chronicexposure to local and systemic inflammation,which may induce or enhance already existinginflammatory disease, including atherosclerosis.For this reason, appropriate oral preventive careis important not only to preserve oral health, butalso systemic health. Management and preventionstrategies must sensitize both dental care providersand patients to the importance of good oral healthon systemic burden and chronic diseases.

Early control of bacterial plaque accumulationis essential for the prevention of oral inflammationand periodontal disease, with daily mechanicalremoval of bacterial plaque by tooth brushingsupplemented with flossing. Utilization of adentifrice with antibacterial and anti-inflammationproperties will help in achieving this goal. Such adentifrice, that contains the antibacterial agenttriclosan in a copolymer to prolong adherence tothe tooth (Colgate® Total® Toothpaste), has beenshown to effectively contribute to the control oforal inflammation14 and to slow the progression

of periodontitis.15 This is due to its 12- hourantibacterial action coupled with its ability todirectly inhibit potent inflammatory mediators.16

Control of periodontal infection andinflammation will improve the oral health ofpatients, decrease the systemic chronic inflammationburden caused by oral inflammation, improvegeneral health, and may ultimately contribute to thereduction of cardiovascular disease.

References1. Ross R. Atherosclerosis — An inflammatory disease.

N Engl J Med 1999;340(2):115-126.2. Genco R, Offenbacher S, Beck J, Rees T. Cardiovascular diseases

and oral infections. In: Rose LF, Genco R, Cohen DW, Mealey BL,eds. Periodontal Medicine. BC Decker Inc.; 2000. pp. 63-82.

3. Desvarieux M, Demmer RT, Rundek T, Boden-Albala B, Jacobs DR, Jr., Sacco RL, et al. Periodontal microbiota andcarotid intima-media thickness: The oral infections and vasculardisease epidemiology study (INVEST). Circulation2005;111(5):576-582.

4. Meurman JH, Sanz M, Janket SJ. Oral health, atherosclerosis, and cardiovascular disease. Crit Rev Oral Biol Med2004;15(6):403-413.

5. Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesaniemi YA, Syrjala SL, et al. Association between dental health and acute myocardial infarction. BMJ 1989;298(6676):779-781.

6. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. BMJ 1993;306(6879):688-691.

7. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann Periodontol2003;8(1):38-53.

8. Jin LJ, Chiu GK, Corbet EF. Are periodontal diseases risk factors for certain systemic disorders—What matters to medical practitioners? Hong Kong Med J 2003;9(1):31-37.

9. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol 2000;71(10):1554-1560.

10. Desphande RG, Kahn MB, Genco CA. Invasion of aortic and heart endothelial cells by Porphyromonas gingivalis. Infect Immun1998;66:5337-5343.

11. Herzberg MC, Meyer MW. Effects of oral flora on platelets: Possible consequences in cardiovascular disease. J Periodontol1996;67(10 Suppl):1138-1142.

12. Paquette DW. The periodontal-cardiovascular link. Compend Cont Educ Dent 2004;25(9):681-692.

13. Scannapieco FA. Periodontal inflammation: From gingivitis to systemic disease? Compend Cont Educ Dent 2004;25(7 Suppl 1):16-25.

14. Davies RM, Ellwood RP, Davies GM. The effectiveness of a toothpaste containing triclosan and polyvinyl-methyl ether maleic acid copolymer in improving plaque control and gingival health: A systematic review. J Clin Periodontol 2004;31(12):1029-1033.

15. Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ, Seymour GJ. The effect of a triclosan-containing dentifrice on the progression of periodontal disease in an adult population. J Clin Periodontol 2003;30(5):414-419.

16. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effect of triclosan on mediators of gingival inflammation. J Clin Periodontol1995;22(6):480-484.



Visit www. perio.org andwww.AmericanHeart.org for

more information on periodontal disease and cardiovascular health.

References1. Haffner SM. The metabolic syndrome. Inflammation, diabetes

mellitus, and cardiovascular disease. Am J Cardiol 2006;97(2A):3A-11A.

2. Genco R, Offenbacher S, Beck J, Rees T. Cardiovascular diseasesand oral infections. In: Rose LF, Genco R, Cohen DW, MealeyBL, eds. Periodontal Medicine. BC Decker Inc.; 2000. pp. 63-82.

3. Desvarieux M, Demmer RT, Rundek T, Boden-Albala B, JacobsDR, Jr., Sacco RL, et al. Periodontal microbiota and carotidintima-media thickness: The oral infections and vascular diseaseepidemiology study (INVEST). Circulation2005;111(5):576-582.

4. Meurman JH, Sanz M, Janket SJ. Oral health, atherosclerosis,and cardiovascular disease. Crit Rev Oral Biol Med 2004;15(6):403-413.

5. Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesaniemi YA,Syrjala SL, et al. Association between dental health and acutemyocardial infarction. BMJ 1989;298(6676):779-781.

6. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM.Dental disease and risk of coronary heart disease and mortality.BMJ 1993;306(6879):688-691.

7. Scannapieco FA, Bush RB, Paju S. Associations betweenperiodontal disease and risk for atherosclerosis, cardiovasculardisease, and stroke. A systematic review. Ann Periodontol 2003;8(1):38-53.

8. Jin LJ, Chiu GK, Corbet EF. Are periodontal diseases risk factorsfor certain systemic disorders—What matters to medicalpractitioners? Hong Kong Med J 2003;9(1):31-37.

9. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco R.Identification of periodontal pathogens in atheromatousplaques. J Periodontol 2000;71(10):1554-1560.

10. Desphande RG, Kahn MB, Genco CA. Invasion of aortic andheart endothelial cells by Porphyromonas gingivalis. Infect Immun1998;66:5337-5343.

11. Herzberg MC, Meyer MW. Effects of oral flora on platelets:Possible consequences in cardiovascular disease. J Periodontol1996;67(10 Suppl):1138-1142.

12. Paquette DW. The periodontal-cardiovascular link. CompendCont Educ Dent 2004;25(9):681-692.

13. Scannapieco FA. Periodontal inflammation: From gingivitis tosystemic disease? Compend Cont Educ Dent 2004;25(7 Suppl 1):16-25.

14. Davies RM, Ellwood RP, Davies GM. The effectiveness of atoothpaste containing triclosan and polyvinyl-methyl ether maleicacid copolymer in improving plaque control and gingival health:A systematic review. J Clin Periodontol 2004;31(12):1029-1033.

15. Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ,Seymour GJ. The effect of a triclosan-containing dentifrice onthe progression of periodontal disease in an adult population.J Clin Periodontol 2003;30(5):414-419.

16. Panagakos FS, Volpe AR, Petrone ME, Devizio W, Davies RM,Proskin HM: Advanced oral antibacterial/anti-inflammatorytechnology: A comprehensive review of the clinical benefitsof a triclosan/copolymer/fluoride dentifrice. J Clin Dent 2005;16 (Suppl):S1-S20.

Visit www. perio.org andwww.AmericanHeart.org for

more information on periodontal disease and cardiovascular health.



Periodontal disease has been linked to an increasedrisk of respiratory diseases, such as pneumonia andchronic obstructive pulmonary disease (COPD). Thisarticle briefly describes evidence for this association,and the mechanisms by which oral bacteria maypromote colonization of the lungs by pathogens.

PneumoniaPneumonia is defined as inflammation of the lungs

resulting from infection, usually bacterial or viral.Pneumonia cases can be divided into two major types:community-acquired and hospital-acquired (nosocomial).About 1.1 million cases of community-acquiredpneumonia require hospitalization annually in theUnited States, with a mortality in hospitalized patientsof 12%.1 Bacteria that often colonize the oropharynx andupper airway, such as Streptococcus pneumoniae,Haemophilus influenzae and Mycoplasma pneumoniae,usually cause community-acquired pneumonia.1,2

Nosocomial pneumonia represents 13-18% ofhospital-acquired infections and occurs in 0.4-0.7% ofhospitalizations; mortality is about 30%.3 Nosocomialpneumonia is usually caused by bacteria acquired fromthe environment, such as Pseudomonas aeruginosa,Staphylococcus aureus and enteric Gram-negativebacteria.2,3

Association Between Oral Bacteria and PneumoniaSeveral lines of evidence indicate that people with

poor oral health are at higher risk for nosocomialpneumonia. First, a number of oral health factorsincrease the risk of pneumonia, including having teethor dentures (versus being edentulous without wearingdentures), being dependent on others for oral care(which leads to higher amounts of plaque), andinfrequent tooth brushing.2

Second, microbiological studies reveal a directassociation between pneumonia risk and colonizationof the teeth and oral cavity by enteric Gram-negativebacteria and respiratory pathogens in intensive carepatients.2

Third, in controlled clinical trials, interventions thatinhibited dental plaque, such as treatment with oral or

topical antibiotics, chlorhexidine, or povidone-iodineplus tooth brushing, reduced the risk of pneumonia (seeTable).2 When data from the five trials in the Table werecombined in a meta-analysis, oral hygiene interventionreduced the risk of pneumonia by a factor of 3.0(p < 0.001; 95% confidence interval: 2.1-4.4).2 The varietyof interventions that reduce respiratory disease suggeststhat other antibacterial treatments could have similareffects. The antibacterial Colgate® Total® Toothpaste, forexample, uses a copolymer to improve retention of thebactericide triclosan on oral surfaces, providing 12-hourantibacterial action and direct inhibition of potentinflammatory mediators.4 Although its effects onrespiratory disease have not been tested, this dentifricemay provide protection because it reduces the growthof oral bacteria and formation of plaque.

The association between oral bacteria andpneumonia has implications for the institutionalized,









Oral Inflammation and Respiratory DiseasesFrank A. Scannapieco,DMD,PhD,Professor and Chair,Department of Oral Biology,

State University of New York at Buffalo School of Dental Medicine

Copyright © 2005 Colgate-Palmolive Company. All rights reserved.Copyright © 2007 Colgate-Palmolive Company. All rights reserved.

may provide some protection because it reducesthe growth of oral bacteria and formation of plaque.

The association between oral bacteria andpneumonia has implications for the institutionalized,



including those living in nursing homes orhospitals for extended periods of time. People inthese situations have a higher exposure topathogens, are less likely to pay close attention tooral health, and are more likely to have poorgeneral health.10 In descriptive studies,institutionalized subjects have more dental plaqueand are more prone to colonization by respiratorypathogens than controls.2 Therefore,institutionalized people represent a high-risk groupfor pneumonia related to oral bacteria.

Chronic Obstructive Pulmonary DiseaseChronic obstructive pulmonary disease (COPD)

was the sixth leading cause of death worldwide in1990.11 COPD includes chronic bronchitis, in whichirritation of the bronchial airway causes increasedmucous production and persistent cough, andemphysema, in which dilation of small air passagesleads to lung damage.10

Risk factors for COPD include smoking, chronicexposure to atmospheric pollutants, such assecond-hand smoke, and genetic conditions.10

COPD patients experience periodic exacerbationsfor unknown reasons, and bacterial infectionscaused by H. influenzae, S. pneumoniae, andMoraxella catarrhalis may contribute to theseepisodes.10

Association Between Periodontal Disease and COPD

Epidemiological studies have revealed anassociation between periodontal disease andCOPD.2 For example, among 13,792 participantsin a national health survey who received astandardized dental examination, subjects with ahistory of COPD had a greater mean periodontalattachment loss (p = 0.0001).12 Those with a meanattachment loss of at least 2.0 mm were more likelyto have COPD than those with a mean attachmentloss of less than 2.0 mm (odds ratio 1.35, 95%confidence interval = 1.07-1.71). However, thisassociation has been reported in epidemiologicalstudies only. To date, no prospective studies haveinvestigated the link between periodontal diseaseand COPD.2

Potential Mechanisms by which Oral BacteriaInfluence Respiratory Disease

At least four mechanisms have beenenvisioned10 to explain the role of oral bacteria inthe pathogenesis of respiratory disease (see Figure).

First, oral pathogens may be directly inhaled.Organisms living in dental plaque are shed intosaliva, and small droplets may be aspirated intothe lungs. Normally, the defense mechanisms ofthe lungs prevent infection. However, bacterialcolonization of the lower airway can occur if the

immune system is suppressed or defective, if anunusually virulent pathogen is aspirated, or if anoverwhelming number of organisms are aspiratedsimultaneously.

Second, the action of bacterial enzymes on oralepithelial cells may promote colonization byrespiratory pathogens. Ordinarily, molecules onthe surface of epithelial cells protect againstbacterial adhesion, but oral bacteria releaseenzymes that may degrade these molecules. Poororal health results in high protease activity in salivathat may damage epithelial cell surfaces and causeincreased susceptibility to colonization bypathogenic bacteria.

Third, bacterial enzymes may reduce theprotection against colonization provided bymucosal secretions. Proteins in mucosal secretionsappear to bind to invading bacteria, inhibiting theiradherence to epithelial cells and promoting theirelimination from the host. Enzymes from oralbacteria can modify these protective proteins,preventing them from binding to invadingpathogens.

Fourth, cytokines may contribute tocolonization of the respiratory epithelium.Periodontitis stimulates gum tissue to releasecytokines, which may induce changes on theepithelial cell surface. Cytokines also recruitneutrophils to the site of inflammation; neutrophilsproduce proteases and oxygen radicals that maydamage the epithelium. Either of these actions mayincrease the susceptibility of tissue to bacterialcolonization. Contamination of the respiratoryepithelium by orally released cytokines, or releaseof cytokines by the respiratory epithelium itself inresponse to contact with oral bacteria, may promote

respiratory infection.Conclusion

Regardless of the mechanism, large numbersof respiratory pathogens in the oral cavity appearto promote respiratory diseases, such aspneumonia and COPD. Although further study isneeded to define the relationships betweenperiodontitis and respiratory disease, inhibitinggrowth of oral bacteria reduces the risk ofpneumonia. Therefore, proper attention to oralhygiene, including brushing with an antibacterialdentifrice such as Colgate® Total® and regularflossing, may help prevent respiratory illness,especially in vulnerable populations, such ashospitalized patients and institutionalized elders.

References1. Niederman MS, Mandell LA, Anzueto A, Bass JB, Broughton WA,

Campbell GD, et al. Guidelines for the management of adults with community-acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention. Am J Respir Crit Care Med 2001; 163(7): 1730-1754.

2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for nosocomial bacterial pneumoniaand chronic obstructive pulmonary disease. A systematic review.Ann Periodontol 2003; 8(1): 54-69.

3. Craven DE, Steger KA. Hospital-acquired pneumonia: Perspectives for the healthcare epidemiologist. Infect Control Hosp Epidemiol1997; 18(11): 783-795.

4. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effect of triclosan on mediators of gingival inflammation. J Clin Periodontol 1995; 22(6): 480-484.

5. Pugin J, Auckenthaler R, Lew DP, Suter PM. Oropharyngeal decontamination decreases incidence of ventilator-associated pneumonia. A randomized, placebo-controlled, double-blind clinical trial. JAMA 1991; 265(20): 2704-2710.

6. DeRiso AJ, Ladowski JS, Dillon TA, Justice JW, Peterson AC. Chlorhexidine gluconate 0.12% oral rinse reduces the incidence of total nosocomial respiratory infection and nonprophylactic systemic antibiotic use in patients undergoing heart surgery. Chest 1996; 109(6): 1556-1561.

7. Fourrier F, Cau-Pottier E, Boutigny H, Roussel-Delvallez M, Jourdain M, Chopin C. Effects of dental plaque antiseptic decontamination on bacterial colonization and nosocomial infections in critically ill patients. Intensive Care Med 2000; 26(9): 1239-1247.

8. Bergmans DC, Bonten MJ, Gaillard CA, Paling JC, van der GS, van Tiel FH, et al. Prevention of ventilator-associated pneumonia by oral decontamination: A prospective, randomized, double-blind, placebo-controlled study. Am J Respir Crit Care Med 2001; 164(3): 382-388.

9. Yoneyama T, Yoshida M, Ohrui T, Mukaiyama H, Okamoto H, Hoshiba K, et al. Oral care reduces pneumonia in older patients in nursing homes. J Am Geriatr Soc 2002; 50(3): 430-433.

10. Scannapieco FA. Role of oral bacteria in respiratory infection.J Periodontol 1999; 70(7): 793-802.

11. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global burden of disease study. Lancet 1997; 349(9061): 1269-1276.

12. Scannapieco FA, Ho AW. Potential associations between chronic respiratory disease and periodontal disease: Analysis of national health and nutrition examination survey III. J Periodontol 2001; 72(1): 50-56.



This seriesis brought to you by

The Colgate-Palmolive Company

Brought to you through aneducational grant from

Colgate-Palmolive.

Visit www. perio.org for moreinformation on periodontaldisease and systemic health.




2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for nosocomial bacterial pneumonia and chronic obstructive pulmonary disease. A systematic review. Ann Periodontol 2003; 8(1): 54-69.


4. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM, ProskinHM: Advanced oral inflammatory technology: A comprehensivereview of the clinical benefits of a triclosan/copolymer/fluoridedentifrice. J Clin Dent 2005; 16 (Suppl):S1-S20.






10. Scannapieco FA. Role of oral bacteria in respiratory infection. J Periodontol 1999; 70(7): 793-802.



Fourth, cytokines may contribute to colonizationof the respiratory epithelium. Periodontitisstimulates gum tissue to release cytokines,which may induce changes on the epithelialcell surface. Cytokines also recruit neutrophilsto the site of inflammation; neutrophils produceproteases and oxygen radicals that may damagethe epithelium. Either of these actions may increasethe susceptibility of tissue to bacterial colonization.Contamination of the respiratory epithelium byorally released cytokines, or release of cytokines bythe respiratory epithelium itself in response to contactwith oral bacteria, may promote respiratory infection.

ConclusionRegardless of the mechanism, large numbers

of respiratory pathogens in the oral cavity appearto promote respiratory diseases, such aspneumonia and COPD. Although further study isneeded to define the relationships betweenperiodontitis and respiratory disease, inhibitinggrowth of oral bacteria reduces the risk ofpneumonia. Therefore, proper attention to oralhygiene, including brushing with an antibacterialdentifrice such as Colgate® Total® and regularflossing, may help prevent respiratory illness,especially in vulnerable populations, such ashospitalized patients and institutionalized elders.



2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for nosocomial bacterial pneumoniaand chronic obstructive pulmonary disease. A systematic review.Ann Periodontol 2003; 8(1): 54-69.


4. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effect of triclosan on mediators of gingival inflammation. J Clin Periodontol 1995; 22(6): 480-484.






10. Scannapieco FA. Role of oral bacteria in respiratory infection.J Periodontol 1999; 70(7): 793-802.





2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for nosocomial bacterial pneumonia and chronic obstructive pulmonary disease. A systematic review. Ann Periodontol 2003; 8(1): 54-69.


4. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM, ProskinHM: Advanced oral inflammatory technology: A comprehensivereview of the clinical benefits of a triclosan/copolymer/fluoridedentifrice. J Clin Dent 2005; 16 (Suppl):S1-S20.






10. Scannapieco FA. Role of oral bacteria in respiratory infection. J Periodontol 1999; 70(7): 793-802.



growth of oral bacteria may reduce the risk of



Bone loss is a central, common feature of bothperiodontal disease and osteoporosis. Osteopenia,or low bone mineral density (BMD), results whenbone metabolism becomes unbalanced, with boneresorption by osteoclast cells occurring at a fasterrate than bone production by osteoblast cells.1 Awoman with a BMD 2.5 standard deviations belowthe mean peak density for young women hasosteoporosis, according to the definition of theWorld Health Organization.2 Prevalence is higherin women than men and increases with age. About35% of post-menopausal white women haveosteoporosis of the hip, spine, or distal forearm;prevalence in Asian women is similar.3

Increased risk of fracture associated withosteoporosis is a serious concern. After age 50, 50%of women and 25% of men will have anosteoporosis-related fracture, and the financialimplications are significant. In 2002, for example,the direct cost of treating hip fractures was $18billion in the US alone.4

In periodontal disease, oral inflammation dueto chronic infection of the tissue around the teethresults in destruction of oral bone and periodontalligament (Figure 1), ultimately leading to tooth loss.Oral inflammation increases production ofcytokines, such as interleukin-6, that stimulateosteoclast activity and promote bone resorption.5

A similar mechanism may contribute toosteoporosis, raising the question of whetherpeople with low skeletal BMD are at increased riskof oral osteopenia (Figure 1). Several lines ofevidence indicate that there is an associationbetween osteoporosis and periodontal disease.

Common Risk FactorsFirst, there are risk factors common to both

conditions. Both osteoporosis and periodontaldisease become more prevalent with advancingage, and individuals with a family history are athigher risk.5 In women, estrogen deficiencyincreases the risk of both oral and systemic

osteopenia.6 Smoking is a risk factor for, and hastensprogression of, both conditions.5,6

Cross-Sectional and Longitudinal StudiesSecond, many studies have reported an

association between systemic BMD andperiodontal disease, regardless of whether themeasure of periodontal status is clinical (e.g.,attachment loss, probing pocket depth), orradiographic (alveolar crestal height loss).5

Although studies of osteoporosis and clinicalattachment level have produced mixed results,larger cross-sectional studies and at least twoprospective studies support an association.5 Forexample, in a three-year longitudinal study, 70-year-old subjects were divided into osteopenia andnon-osteopenia groups based on BMD of the heelat baseline.

7The number of sites with at least 3 mm

of additional attachment loss after three years wassignificantly higher in the osteopenia group (p =









Oral Inflammation and OsteoporosisElizabeth A. Krall, MPH, PhD, Professor, Director of Epidemiology Division

Boston University School of Dental Medicine


Figure 1. Relationship between Oral Inflammation, Systemic Osteoporosis,

and Oral Osteopenia

Adapted from Chesnut, 20016

Oral inflammation• chronic periodontal infection

Oral osteopenia• loss of alveolar bone

Systemic osteopeniaor osteoporosis

• decreased bone strength ?




0.043).7 This study indicates that, in this olderpopulation, systemic BMD may be one factorin predicting periodontal disease progression.7

A positive association between low BMD andtooth loss has also been reported in manystudies, and studies that found no associationhave generally been in younger populations.5

The relationship is not firmly established,however, because some studies report noassociation, and of those that do, most arecross-sectional, many have small sample sizes,and most do not control adequately forpossible confounding factors, such as smokingstatus, postmenopausal hormone use, ortreatment for periodontal disease.5 Moreprospective studies are needed.

Therapies Affecting Both Osteoporosis andPeriodontal Disease

Third, some interventions that improvesystemic BMD also improve measures ofperiodontal disease.8 Improvement of the twoconditions by the same therapies suggests anunderlying connection. The three classes oftherapy that have been implicated in thisregard are 1) hormone replacement therapy(HRT), 2) diet supplementation with calciumand vitamin D, and 3) bisphosphonates.

HRT appears to improve oral bone density,and also leads to less bleeding on probing, lessfrequent clinical attachment loss, and less toothloss.8 These effects are consistent with thebenefit of HRT for systemic BMD.

Sufficient dietary calcium is essential formaintaining BMD, and low calcium intakemay increase the risk of periodontal diseaseor hasten disease progression.8 Vitamin D aidscalcium absorption from the intestine andregulates calcium metabolism. A three-yearprospective, placebo-controlled trial of calciumand vitamin D supplementation in men andwomen over age 65 found that fewer subjectswho received supplements lost at least onetooth (Figure 2, odds ratio for tooth loss = 0.4,p < 0.05).9 In a two-year follow-up period,fewer subjects consuming at least 1000 mg ofcalcium per day lost one or more teeth thanthose who consumed less calcium (Figure 2,odds ratio for tooth loss = 0.4, p < 0.03).9 Theseresults support a potential benefit of calciumand vitamin D for improving periodontaldisease.

Few studies have examined the impact ofbisphosphonate therapy on periodontaloutcomes. One prospective, double-blind trialin women aged 55–65 years who were notreceiving HRT found greater improvement inprobing depth and gingival bleeding insubjects receiving bisphosphonate alendronatethan in those receiving placebo.10 SystemicBMD and alveolar crestal height increased in

the alendronate group but worsened in theplacebo group.10 More studies ofbisphosphonates are needed to confirm theirimpact on periodontal disease.

Possible MechanismsThe above evidence supports an association

between systemic BMD and periodontaldisease. The mechanisms underlying thisassociation, however, are unknown. Patientswith low systemic BMD may also have loworal BMD, allowing periodontal disease toprogress more rapidly because there is simplyless oral bone present.5 A second possibility isthat osteoporosis and bone loss due toperiodontal disease both proceed by the samecellular mechanism, namely increasedproduction of cytokines, such as interleukin-6,that stimulate osteoclast activity.1 Genetics mayalso play a role, in that patients predisposed toBMD loss may also be more likely to sufferperiodontal damage.5 Finally, certain lifestylefactors may increase a patient’s risk of bone lossand periodontal disease.5

Regardless of the mechanism, patients withlow systemic BMD appear to be at higher riskfor progression of periodontal disease.Therefore, it is especially important for patientswho have osteoporosis or who are at high riskfor systemic bone loss to prevent oralinflammation through good oral hygiene,including daily brushing with an antibacterialdentifrice, such as Colgate® Total® Toothpaste.Colgate® Total® uses a copolymer to improveretention of the antibacterial agent triclosan onoral surfaces, resulting in antibacterial andantiplaque activity for as long as 12 hours afterbrushing.11 Colgate® Total® also directly inhibitspotent inflammatory mediators,12 helping tokeep oral inflammation under control.13

ConclusionAlthough mechanisms explaining the

association between periodontal disease and

osteoporosis have been suggested, it isunknown if one of these conditions helps causethe other, if they are independently caused bythe same factors, or if the association iscoincidental. More prospective longitudinalstudies, ideally intervention trials, are neededto understand this relationship. Given theincreasing worldwide prevalence of osteopeniaand osteoporosis, a full understanding of theprecise relationship between these two diseasesis necessary. Measures commonly used toprevent and treat systemic bone loss may havea beneficial impact on the oral health of thepopulation as well.

References1. Mundy GR. Cellular and molecular regulation of bone

turnover. Bone 1999;24(5 Suppl):35S-38S.2. Assessment of fracture risk and its application to screening

for postmenopausal osteoporosis. Geneva: World HealthOrganization; 1994. Report No. WHO Technical ReportSeries No. 843.

3. Melton LJ, III. Epidemiology worldwide. Endocrinol MetabClin North Am 2003;32(1):1-13, v.

4. Fast facts on osteoporosis. National Osteoporosis Foundationwebsite (updated 2005; cited 2005 Jul 22). Availablefrom:http://www.nof.org/osteoporosis/diseasefacts.htm.

5. Wactawski-Wende J. Periodontal diseases and osteoporosis:Association and mechanisms. Ann Periodontol 2001;6(1):197-208.

6. Chesnut CH, III. The relationship between skeletal andoral bone mineral density: An overview. Ann Periodontol2001;6(1):193-196.

7. Yoshihara A, Seida Y, Hanada N, Miyazaki H. Alongitudinal study of the relationship between periodontaldisease and bone mineral density in community-dwellingolder adults. J Clin Periodontol 2004;31(8):680-684.

8. Krall EA. The periodontal-systemic connection: Implicationsfor treatment of patients with osteoporosis and periodontaldisease. Ann Periodontol 2001;6(1):209-213.

9. Krall EA, Wehler C, Garcia RI, Harris SS, Dawson-HughesB. Calcium and vitamin D supplements reduce tooth lossin the elderly. Am J Med 2001;111(6):452-456.

10. Rocha ML, Malacara JM, Sanchez-Marin FJ, Vazquez dela Torre CJ, Fajardo ME. Effect of alendronate onperiodontal disease in postmenopausal women: Arandomized placebo-controlled trial. J Periodontol 2004;75(12):1579-1585.

11. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, DaviesRM, Proskin HM: Advanced oral inflammatory technology:A comprehensive review of the clinical benefits of a triclosan/copolymer/fluoride dentifrice. J Clin Dent2005; 16 (Suppl):S1-S20.

12. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, DaviesRM, Proskin HM: Advanced oral antibacterial/anti-inflammatory technology: A comprehensive review of theclinical benefits of a triclosan/copolymer/fluoridedentifrice.J Clin Dent 2005; 16 (Suppl):S1-S20.

13. Davies RM, Ellwood RP, Davies GM. The effectiveness of atoothpaste containing triclosan and polyvinyl-methyl ethermaleic acid copolymer in improving plaque control andgingival health: A systematic review. J Clin Periodontol2004;31(12):1029-1033.

Figure 2. Effect of Calcium Intakeon Tooth Loss9

0%

10%

20%

30%

40%

50%

60%

70%

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enta

ge o

f sub

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s w

ho lo

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3-year randomized trial

13%

27%

40%

59%

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Lowcalciumintake

Highcalciumintake

PlaceboCalcium andvitamin D

supplements






The effects of oral inflammation are not limitedto oral health.1 The previous five installments inthis series of articles have addressed various aspectsof the relationship between oral inflammation andsystemic conditions,2-6 including cardiovasculardisease,4 respiratory diseases,5 osteoporosis,6 anddiabetes.3 In this respect, it is critical to manage oralinflammation not only for oral health, but also tomaintain the general health of patients.

Oral InflammationOral inflammation is the basis of gingivitis and

periodontitis; it is caused by bacteria that initiatethe destruction of gingival tissue and compromiseperiodontal attachment.7,8 Bacteria adhere to oralsurfaces and aggregate to produce plaque, ordental biofilm, that are complex and physicallystructured microbial communities able to supportthe growth of several pathogenic species in largenumbers.9,10 Dental biofilm is largely composed ofpolysaccharides that form a physical barrier whichprotects bacteria from the effects of antibiotics,antiseptics, and host defense mechanisms.10

The pathogenic bacteria in the periodontiumhave the ability to evade the host defensemechanisms that would routinely control suchinfections and prevent disease.8 This breakdownin the host defense mechanism appears as aninflammatory response, which can itself contributeto tissue pathology, promoting the release of tissue-derived enzymes that destroy the extracellularmatrix and bone.8 Antigens released by bacterialcells stimulate the production of antibodies whichare not effective at killing bacteria within biofilm,but may form immune complexes that furtherdamage surrounding tissues.9

The main underlying concepts for the treatmentof oral inflammation are summarized in the figureat right. Therapy is targeted at three interdependentcomponents to prevent initiation or halt progressionof oral inflammation. Treatment requirements andeffectiveness are modulated by genetic and

environmental factors. The first component is toremove dental biofilm and reduce the levels ofbacteria, which also changes the composition of theoral microflora. The second component involves themodulation of the host response (inflammation) bylimiting the production of antibodies and the releaseof proteinase caused by bacterial tissue invasion. Thelast component involves alteration of the oralmicrohabitat by modifying the physical features thatfacilitate the growth and accumulation of bacteria.

Several factors can contribute to oralinflammation (see table overleaf). Some factorscan be modified to minimize the risk of oraldiseases and improve control of oral inflammation,while others will help to define an individualtreatment plan for optimal oral health.11

Management of the Patient with OralInflammation

The optimal strategy to eliminate dental biofilmfrom the oral cavity has four dimensions: physicalremoval of dental biofilm; destruction of theremaining bacteria using antimicrobial agents;routine oral hygiene habits; and patient education.10









Oral Inflammation and Patient ManagementRebecca S. Wilder, RDH, MS, Associate Professor, Department of Dental Ecology

University of North Carolina School of Dentistry


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Instrumentation and Physical Removal ofBiofilm

Dental biofilm offers remarkable resistanceto host defense mechanisms and antibacterialagents. The most effective method to disruptdental biofilm is through mechanical means,such as the use of power and handinstrumentation, and oral physiotherapy aidssuch as toothbrushes, floss, and other interdentaldevices.7,10 Mechanical alteration of dental biofilmdisrupts the bacterial structure and is essentialin dislodging bacteria, reducing plaque,preventing dental calculus, and maintainingsubgingival bacteria at a level below that whichis capable of initiating inflammation.7

Alteration of the microenvironmentsurrounding the subgingival microbiota canaffect numbers, proportions, and prevalence ofbacterial species present in the oral cavity. Somephysical features predisposing to theaccumulation of plaque, such as over-contouredcrowns, open or overhanging margins, narrowembrasure space, open contacts, caries, or toothmalposition, should be preventively corrected toimprove the patient’s ability to remove thebiofilm.11 Gingival deformities hindering biofilmcontrol should be corrected by adequate surgeryto reduce the potential for plaque accumulation.10,11

Daily removal of supragingival plaque reducesgingival inflammation and also controls theamount of subgingival plaque. It also cansignificantly reduce the proportion of knownperiodontal pathogens such as B. forsythus,P. gingivalis, and A. actinomycetemcomitans.10

Antibacterial Agents Despite frequent mechanical cleaning, the

rapid multiplication rates of bacteria warrantconsistent efforts to decrease these pathogens tobaseline levels.10 Use of topical oral rinsescontaining antibacterial agents, such aschlorhexidine (Peridex®, PerioGard®) or essential

oils (Listerine®), or of an antibacterial dentifrice(Colgate® Total®), will help to prevent or delaybacterial accumulation and dental biofilmformation.8 Daily brushing with Colgate Totalhas been shown to reduce the growth of oralbacteria and the formation of plaque.12 It is theonly toothpaste in the United States that containsthe antibacterial agent triclosan, and uses apatented copolymer to improve retention of thebactericide triclosan to oral surfaces, providing12-hour antibacterial action. In addition, itprovides direct inhibition of potent inflammatorymediators, thus affecting the inflammationprocess as well.10,12 Topical agents improve thecontrol of supragingival plaque, which will alsohave indirect effects on subgingival plaque.7

Individualized Patient Oral Hygiene Program A long-term treatment plan for managing

chronic oral inflammation should includeregular maintenance care by an oral healthcareprofessional for thorough elimination of dentalbiofilm and calculus, and to perform periodicevaluation of the periodontal status.7 Frequencyof visits—every three to six months—dependson the patient’s condition and risk factors, andthe extent of bacterial infection, oralinflammation, and periodontal disease.Diagnosis of the periodontal condition is basedon traditional clinical assessments, including thepresence of clinical signs of inflammation(gingival bleeding), probing depth, loss of clinicalattachment, radiographic findings and varioussymptoms such as pain, ulceration, and amountof observable plaque and calculus.13 An accuratediagnosis of periodontal disease severity isessential for selecting an appropriate treatmentand maintenance strategy for a given patient.For the patient with gingivitis, a combination ofroutine personal plaque control in combinationwith professional removal of plaque, calculus,and local contributing factors may be needed toreduce inflammation. At-home use of anantimicrobial toothpaste containing triclosan/copolymer (Colgate Total) has been shown toimprove the outcome of a gingivitis treatmentregimen and reduce oral inflammation.8,12

Self-Care Communication and Education Control of oral inflammation essentially relies

on preventive measures to inhibit dental biofilmaccumulation, and can be achieved bymaintaining good oral hygiene involving dailyflossing and brushing with an antibacterialantiplaque toothpaste. Patient education andsupport are essential for successful preventionor treatment of gingivitis and oral inflammation,and personalized oral hygiene instruction shouldbe provided, taking into account each patient’sprofile. Patient non-compliance to treatment is

a frequent cause of failure to preventinflammation and periodontal disease.11

Consequences of a lack of attention to the dailytreatment regimen should be explained topatients to reinforce their motivation to performthe required daily preventive measures.11

An individualized treatment plan is neededto monitor the maintenance of the oralenvironment and the progression of oralinflammation. Frequent follow-up evaluation ofa patient’as condition to determine the need forfurther treatment is recommended.11

Communication between practitioners andpatients is an essential aspect of oralinflammation management. Oral healthcareprofessionals should advise patients on how tomodify risk factors to reduce oral inflammation.Cessation of smoking, a key risk factor for oraldisease, should be advocated.

A good plaque control program, coupled withregular periodontal maintenance by an oralhealthcare professional and reduction of riskfactors, can effectively manage oral inflammationin the majority of patients.

References1. Caranza’s Clinical Periodontology 10th Edition. Newman MG, Takai H,

Klokkevold PR, eds. St. Louis, Saunders, 2006.2. Williams R. Overview of oral inflammation. White Papers on Oral

Inflam mation 2005;1(1):1-2.3. Ryan M. Oral inflammation and diabetes. White Papers on Oral

Inflam mation. 2005; 1(2):1-2.4. Grossi S. Oral inflammation and cardiovascular diseases. White Papers

on Oral Inflammation. 2005; 1(3):1-2.5. Scannapieco F. Oral inflammation and respiratory diseases. White Papers

on Oral Inflammation. 2005; 1(4):1-2.6. Krall E. Oral inflammation and osteoporosis. White Papers on Oral

Inflammation. 2005; 1(5):1-2.7. American Academy of Periodontology. Treatment of plaque-induced

gingivitis, chronic periodontitis, and other clinical conditions. J Periodontol2001;72(12):1790-1800.

8. American Academy of Periodontology. The pathogenesis of periodontaldiseases. J Periodontol 1999;70(4):457-470.

9. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: Acommon cause of persistent infections. Science1999;284(5418):1318-1322.

10. Socransky SS, Haffajee AD. Dental biofilms: Difficult therapeutic targets.Periodontol 2000 2002;28:12-55.

11. American Academy of Periodontology. Parameter on plaque-inducedgingivitis. J Periodontol 2000;71(5 Suppl):851-852.

12. Panagakos FS, Volpe AR, Petrone ME, DeVizio W, Davies RM, Proskin HM:Advanced oral antibacterial/anti-inflammatory technology: A com -prehensive review of the clinical benefits of a triclosan/copolymer/fluoride dentifrice. J Clin Dent 2005; 16 (Suppl)LS1-S20.

13. Armitage GC. Diagnosis of periodontal diseases. J Periodontol 2003;74(8):1237-1247.


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