Relationship Between Oral Health and Systemic Disease - American ...

INFLAMMATION:The Relationship BetweenOral Health andSystemic DiseaseBy JoAnn R. Gurenlian, RDH, PhDspecial supplement toaccess april 2006sponsored by

Patients, dental hygienists, dentists,dental specialists and other healthcare providers should be aware ofthe consistent relationships betweenoral inflammation and systemicdiseases. They should value the needto modify assessment, prevention, andtreatment protocols to improve the oralhealth as well as total health of thepatients they treat in the officeeach day.

contentsAbstract . . . . . . . . . . . . . 1The InflammatoryProcess . . . . . . . . . . . . . . 1Inflammation &Oral Health. . . . . . . . . . . 2The Oral-SystemicRelationship . . . . . . . . . . 3Translating Scienceto Practice . . . . . . . . . . . 5Conclusion. . . . . . . . . . . 6A Case in Point . . . . . . . 7AbstractSince the mid 1990s, both the scientific community and thepublic have been inundated with articles addressing the associationbetween systemic diseases and oral health. It seems that almostmonthly there is an article in a fashion magazine reminding thepublic that tooth brushing and flossing can save their life. Somearticles point to the notion thatoral infection and bacteria maybe linked to heart attack andstroke. Others dispel the association,indicating that there is notenough research to determineany relationship between thetwo. The questions that havebeen raised focusing on the relationshipbetween periodontaldiseases and systemic conditionsnow extend beyond cardiovasculardisease and include diabetes,respiratory disease and adversepregnancy outcomes. ResearchResearch hasdemonstrated that theassociation between oralinflammation andsystemic inflammationmay be the key tounderstanding thedeleterious effects onmultiple organ systems.has demonstrated that the association between oral inflammationand systemic inflammation may be the key to understanding thedeleterious effects on multiple organ systems. However, is the relationshipso complex that it is like trying to crack the DaVinciCode, or can health care professionals and the public understandthe role of inflammation in oral and systemic health?The purpose of this article is to review how the inflammatoryprocess functions in the human body. The role of inflammation inoral and systemic health will be discussed. Translating this informationinto practical application for dental hygiene professionals willbe addressed so that both inquiring patients and astute clinicianswill capitalize on the opportunities for improving total health.The Inflammatory ProcessReferences. . . . . . . . . . . 8JoAnn R. Gurenlian, RDH, PhD, is the owner ofGurenlian & Associates. She provides consultingand continuing education programs for healthcare providers. She has experience in general,periodontic, pediatric and orthodontic practices,and works part-time in a medical practice.She is an internationally recognized speakeron the topics of oral pathology, oral medicine,diabetes, and women's health. Dr.Gurenlian volunteers with local cancer, healthand political organizations.Clinical cover image courtesy of Dr. Randy Valentine,www.gumsbleeding.com.What is inflammation? Isn’t this the process that is supposedto be good for our bodies? How can it now be something that causesharm to so many different aspects of the body? As we learn moreabout the biological mechanisms of inflammation, it becomes clearthat this process is more complicated than was once thought.Inflammation is the body’s response to cellular injury. Despitethe fact that the press has emphasized the harmful effects of inflammation,the fact remains that without this process, our bodiescould not survive. Inflammation represents a protective responsedesigned to rid the body of the initial cause of cell injury and theconsequences of that injury. Cell injury may occur due to trauma,genetic defects, physical and chemical agents, tissue necrosis, foreignbodies, immune reactions and infections.Inflammation is a local reactive change that involves therelease of antibacterial agents from nearby cells that defend the hostagainst infection. It also facilitates early tissue healing and repair. Itcontains—or “walls off”—the infectious or injurious agent andserves as a defense mechanism that the body can use to restore itselfto a normal morphological form and function.special supplemental issue—april 2006—access 1

Table I: Physiologic Rationale for Cardinal Signs of InflammationCardinal Signs of InflammationPhysiologic RationaleRubor (redness)Increased vascularityTumor (swelling)Exudation of fluidCalor (heat)Dolor (pain)Functio laesa (loss of function)A combination of increased blood flow and therelease of inflammatory mediatorsThe stretching of pain receptors and nerves bythe inflammatory exudates, and by the releaseof chemical mediatorsA combination of the above effectsMcMahon RFT, Sloan P. Essentials of pathology for dentistry. Edinburgh: Churchill Livingstone; 2000, p. 26.The inflammatory response consists of a vascular and a cellularreaction. These reactions are mediated by chemical factorsderived from plasma proteins or cells. The classic signs ofinflammation are redness, swelling, heat, pain and loss of function.The physiologic explanations for these signs appear inTable I. Other signs of inflammation include fever, leukocytosisor an increase in the number of circulating white blood cells,the presence of acute-phase proteins including C-reactive proteins(CRP), fibrinogen and serum amyloid A protein (SAA),and sepsis.There are two types of inflammation: acute and chronic.Acute inflammation is characterized by a rapid onset and shortduration. It manifests with exudation of fluid and plasma proteins,and emigration of leukocytes, most notably neutrophils.Chronic inflammation is of prolonged duration and manifestshistologically by the presence of lymphocytes and macrophagesand results in fibrosis and tissue necrosis. When inflammationcontinues for prolonged periods of time, it can be thought of asthe healing process in overdrive, and deleterious changes canoccur to localized tissues as well as the entire body.In appreciating the inflammatory process, it is important tounderstand the role of chemical mediators. These are the substancesthat tend to direct the inflammatory response. Theseinflammatory mediators come from plasma proteins or cellsincluding mast cells, platelets, neutrophils and monocytes/macrophages.They are triggered by bacterial products or host proteins.Chemical mediators bind to specific receptors on target cells andcan increase vascular permeability and neutrophil chemotaxis,stimulate smooth muscle contraction, have direct enzymatic activity,induce pain or mediate oxidative damage. Most mediators areshort-lived but cause harmful effects. 1 Examples of chemicalmediators include vasoactive amines (histamine, serotonin),arachadonic acids (prostaglandins, leukotrienes) and cytokines(tumor necrosis factor and interleukin–1).Inflammation and Oral HealthThe inflammatory process significantly affects the periodontium.Plaque biofilm releases a variety of biologicallyactive products as gram-positive and gram-negative bacteriacolonize the tooth surface around the gingival margin andinterproximal areas. These products include endotoxins,cytokines and protein toxins. 2 These molecules penetrate thegingival epithelium and initiate a host response that eventuallyresults in gingivitis. Evidence of this can be seen clinically withchanges in tissue color from pink to red, swelling, and bleedingupon probing. 3 Because gingivitis is typically not painful, itmay remain untreated for years. Worse, it may be viewed bypractitioners as something that requires less concern than periodontitis.Nevertheless, chronic gingivitis that persists for yearsmay provide the basis for greater concern for systemic healththan a periodontitis condition that is more readily treated.As the biofilm continues to proliferate, soluble compoundspenetrate the sulcular epithelium. This, in turn, signals the gingivalepithelium to produce chemical mediators includinginterleukin–1 beta (IL-1‚), prostaglandins, tumor necrosis factoralpha (TNF-α), and matrix metalloproteinases. 4 Theseproducts recruit neutrophils to the area and influence chemotaxis,and can cause increased permeability of gingival vesselsthat permits plasma proteins to emigrate from the blood vesselsinto the tissue. As the inflammatory process progresses, additionalmediators are produced, and more cell types are recruitedto the area including neutrophils, T-cells, and monocytes.Continued inflammation results in signaling of fibroblasts andproduction of proinflammatory cytokines in the tissues.Antibodies specific to oral bacteria circulate in the peripheralblood. The acute-phase response becomes activated and CRP,fibrinogen and complement are produced both by local cellsand within the liver. 5,6 These proteins may further exacerbate2 access—special supplemental issue—april 2006

Figure 1: Mediators and cells present in established gingivitisFrom: Scannapieco, FA: Periodontal inflammation: from gingivitis to systemic disease?Compend Cont Educ Dent. 2004; 25(7) (Suppl1): 16-24.the local inflammatory response and may affect the initiation orprogression of systemic disease (i.e., atherosclerosis). 7,8 Thisprocess of chronic gingivitis is represented in Figure 1.It is important to note that even though an individual mayhave established or chronic gingivitis, the condition is stillreversible. Thorough dental hygiene debridement and regularhome oral hygiene care could return the gingival tissues to astate of health. In some individuals when the inflammatoryprocess continues and expands, the collagen of the periodontalligament breaks down and bone resorption occurs, thus resultingin periodontitis. Individuals with periodontitis have thesame increased levels of proinflammatory mediators as thosewith chronic gingivitis, including CRP, fibrinogen, and IL-1‚and 6. Fortunately, when periodontal treatment is performedand clinical inflammation decreases, the serum levels of theseinflammatory mediators also decrease. 9The Oral-Systemic RelationshipAlthough periodontal diseases are well known as an oralproblem, in the past decade, there has been a shift in perspective.Research has been focusing on the potential impact ofperiodontal diseases on systemic health. The relationshipbetween periodontal inflammatory disease and systemic diseasessuch as cardiovascular disease, diabetes, respiratory diseaseand adverse pregnancy outcomes has beenclosely investigated. The basis for the biologicalmechanism of this relationship isbeginning to emerge and further studymay lead to an understanding of whetheror not a true causal relationship exists.Cardiovascular disease (CVD) ischaracterized by the build-up of inflammatoryplaques that may cause thrombosesand eventual myocardial infarction.Atherosclerosis is the term used for thethickening and hardening of the arteriesthat is produced by this plaque build-up.It represents a chronic inflammatoryresponse that causes injury to the endotheliumof elastic and muscular arterial tissue.One of the hallmarks of the early atheroscleroticlesion is the presence of neutrophilsfollowed by monocytes and lymphocytes.10 These leukocytes can affect thevascular endothelial lining and can causeoxidation of low-density lipoprotein(LDL) levels. Monocytes are induced tobecome macrophages, which take upmodified lipoproteins and become lipidladen“foam cells.” 11 The local inflammationis sustained by secreting chemicalmediators, and the atherosclerotic lesionbegins to bulge within the luminal wall.As this lesion progresses, the extracellularmatrix is degraded by proteolytic enzymesand becomes susceptible to rupture. Thromboses can occur,occluding blood flow to the heart, which may eventually leadto infarction.Since atherosclerosis is considered to be inflammatory innature, identifying inflammatory markers that correlate withdisease state is beneficial. One of the most recognized and consistentmarkers of systemic inflammation and poor cardiovascularprognosis is the acute-Cardiovascular disease(CVD) is characterized bythe build-up ofinflammatory plaquesthat may causethromboses and eventualmyocardial infarction.phase protein CRP. 12,13 It isproduced by the liver andreleased into the blood stream.It is positively correlated to IL-6, activates complement andaccounts for LDL uptake bymacrophages. 14-16It has been proposed thatbacteria or viruses may directlyinfect atherosclerotic lesionscontributing to the inflammatoryprocess. Further, distant infections may increase systemicinflammation through the release of toxins or the leakage ofchemical mediators into the circulation. 17 It has been reportedthat studies of atheromatous lesions in the carotid arteries havefound over 40% of atheromas contain antigens from periodontalpathogens including Porphyromonas gingivalis, Tannerellaforsythensis, and Prevotella intermedia. 18 In addition, P. gingi-special supplemental issue—april 2006—access 3

Figure 2: Connection between periodontal disease and atherosclerosisFrom: Dave S, Batista EL Jr, Van Dyke TE: Cardiovascular disease and periodontal diseases:commonality and causation. Compend Cont Educ Dent. 2004; 25(7) (Suppl 1):26-37.valis can induce platelet aggregation, a component of atheromaand thrombus formation. 19 This suggests a possible invasion ofatheromas by oral pathogens as well as a possible contributionto their development. However, causality has yet to be established.Animal model studies investigating the relationshipbetween CVD and periodontal disease have demonstrated thatclinically induced oral infection with P. gingivalis will increaseatheroma size and elevate CRP levels. 20 More recently, a studyof humans reported a positive independent association betweencarotid intima-media thickness (IMT) and bacterial burdenincluding P. gingivalis, Actinobacillus actinomycetemcomitans,Treponema denticola, and Tannerella forsythensis. 21 Figure 2represents the proposed connection between periodontal diseaseand atherosclerosis.It is also thought that an autoimmune response may beinvolved in the development of atherosclerosis. Most humanshave immune reactions against microbial heat-shock protein 60(HSP60). Antibodies against bacterial versions of this proteinmay cross-react with human HSP60, causing an autoimmuneresponse and stimulating athersosclerosis. 4Diabetes mellitus is another systemic condition with oralinflammatory connections. One of the major complications ofdiabetes is periodontitis. 22 While diabetes increases the probabilityof developing periodontal disease 22-24 , periodontitis alsoincreases the risk of poor glycemic control in people with diabeteswhen compared to those individuals with diabetes withoutperiodontitis. 25 Fortunately, periodontal treatment canimprove glycemic control by reducingthe bacterial burden and theinflammatory response. 26-28There are several biologicalmechanisms proposed to explain theincreased incidence and severity ofperiodontal disease in individualswith diabetes. Diabetes tends toincrease susceptibility to infection—including oral infection—and thedisease itself decreases the effectivenessof cells that kill bacteria.Another explanation is thatinflammation is enhanced in thosewith diabetes. Research has demonstratedelevated levels of inflammatorymediators in the gingival crevicularfluid of periodontal pockets of poorlycontrolled patients with diabetes ascompared to those without diabetesor those with diabetes who are wellcontrolled. These patients had significantperiodontal destruction with anequivalent bacterial challenge. 24,29,30 Inparticular, the proinflammatorycytokine, TNF-α, plays a major rolein this process. TNF-α has a significantrole in insulin resistance, the primarycause of type 2 diabetes. It isproduced in large quantities by fat cells. Periodontitis has alsobeen associated with increased levels of TNF-α. Elevated levels ofTNF-α may lead to greater bone loss by killing cells that repairdamaged connective tissue or bone and may exacerbate insulinresistance and worsen glycemic control. 31-33It has also been hypothesized that diabetes interferes withthe capacity to form new bone after periodontal diseases havecaused bone resorption. Graves, et al., studied genetically diabeticmice with type 2 diabetes and nondiabetic littermates byinjecting them with P. gingivalis. The death of osteoblasts wasmeasured, and results indicated that there was a higher andmore prolonged rate of osteoblast cell death in the diabeticgroup. It was concluded that the capacity to repair a bonydefect by producing new bone would be severely limited whenosteoblasts died prematurely. Yet further study is needed in thisarea to refine this concept. 34As with CVD and diabetes mellitus, there is a relationshipbetween oral infection and respiratory disease. In particular,chronic obstructive pulmonary disease (COPD) and pneumoniahave been associated with poor oral health. 35-38 It is likelythat oral biofilm serves as a reservoir of infection for respiratorybacteria. Specifically, Pseudomonas aeruginosa, Staphylococcusaureus, and enteric bacteria that has been shown to colonize theteeth of patients admitted to hospitals or long-term care facilities.These bacteria may be released into saliva and then aspiratedinto the lower airway causing infection. 4 Another vehicle bywhich bacteria from the oral cavity can be introduced into therespiratory system is intubation.4 access—special supplemental issue—april 2006

Inflammatory mediators, such ascytokines produced by the periodontium,may be another mechanism bywhich respiratory disease are associatedwith oral health. These mediators presentin inflamed gingival tissues enter thegingival crevicular fluid and then thesaliva. Once aspirated, these mediatorscan have proinflammatory effects in thelower airway.Further, studies have demonstratedthat periodontal diseases have beenshown to increase the risk of adversepregnancy outcomes such as prematurebirth and low birth weight. 39-41 Uterinecontractions are stimulated by oxytocin,which is produced by the hypothalamus,and by prostaglandins produced by theplacenta. This process normally occursin the third trimester and leads to birth.However, chronic infection can stimulatethe inflammatory process, whichleads to elevated amniotic levels ofprostaglandins, TNF-α, and IL-1 andIL-6. These mediators then lead to prematurerupture of membranes andpreterm labor. Other work has suggestedthat periodontal pathogens may travelfrom the gingival sulcus to the placentaand stimulate preterm birth. Specifically, Han and colleaguesfound that periodontal bacteria, including Fusobacteriumnucleatum, entered the bloodstream from the oral cavity anddirectly affected the birth process. 42 A summary of the biologicalmechanisms by which gingival inflammation effects systemichealth appears in Figure 3.Translating Science to PracticeAs often occurs, research provides many answers anddrives more questions. Despite the knowledge obtainedthrough science, it is incumbent upon clinical practitioners totranslate the evidence into practical use. What does the aboveinformation mean for clinical practice? Does it offer opportunitiesfor changing dental hygiene interventions? How can weuse this information to answer patients’ questions when theyinquire about CRP levels, or ask if their periodontal conditionwill give them heart disease? Are we better prepared to addresstheir question when they say they read two conflicting articlesabout oral and systemic health in the same issue of Reader’sDigest, Prevention magazine, or Every Woman and wonderwhich one is accurate?Understanding the association between oral health andsystemic health does provide opportunities for oral hygiene cliniciansto reframe their protocols. The process begins by practicingoral medicine. First, comprehensive medical assessmentis needed for each patient. A review of systems and vital signsFigure 3: Model to explain oral inflammation-systemic disease associationFrom: Scannapieco, FA: Periodontal inflammation: from gingivitis to systemic disease?Compend Cont Educ Dent. 2004; 25(7) (Suppl1): 16-24.evaluation should be part of that assessment process. Duringthese assessments, identifying risk factors for specific systemicdiseases is important, including age (over 40 years), hypertension,dyslipidemia, smoking, obesity/overweight, CVD, diabetesor symptoms of diabetes and women who are pregnantand have poor oral hygiene.Comprehensive oral assessmentis equally important. Thismay include thorough head andneck examination, radiographs(if clinically indicated), periodontalprobing, bacterialmonitoring of periodontal andcarious pathogens, genetic testingfor periodontal disease orother diagnostic tools that seemappropriate to each individualneed.Understanding theassociation betweenoral health andsystemic health doesprovide opportunitiesfor oral hygieneclinicians to reframetheir protocols.As these assessments are being performed, risk factors fororal and systemic diseases are being noted and explained to thepatient. It is essential that the patient understand that the purposeof these assessments is to prevent problems from occurringor treat them as readily as possible. Patients are well acquaintedwith the idea that physicians prefer to treat a stroke or aheart attack before it occurs by identifying possible risk factorsand trying to reduce them. They are used to attending a medicalappointment and having certain assessments performed.They are even used to requesting certain tests or proceduresbased on their own education and experience. Thus, it is timespecial supplemental issue—april 2006—access 5

that we incorporate these approaches into dental and dentalhygiene practice. Our patients need to become accustomed tothe same comprehensive assessment process. Clinicians canthen put together a picture for the patient that incorporates oraland systemic risk factor findings, and discuss how their chronicgingivitis or periodontitis condition may place them at riskfor CVD, poor glycemic control or an adverse pregnancy outcome.Once risks have been identified, those that can be modifiedare incorporated into the dental hygiene treatment plan andpatient education process. Just as a physician will recommend apatient lose weight or prescribe an antihypertensive agent, thedental hygiene therapist may make recommendations for thepatient to begin a smoking cessation program, use specific preventiveoral care products, monitor their blood sugar regularly orcomplete a nutrition counseling program, in addition to havingdebridement of plaque biofilm and calculus. Certainly, patientswill view the dental hygiene appointment as more than a “cleaning”if greater emphasis is placed on the patient’s total health, riskfactor assessment and risk factor modification.In addition, once risk factors have been identified andappropriate treatmentplanned, it is important tobe prepared to answer questionsabout medicationsand products that have antiinflammatoryand/or antibacterialproperties. Forexample, in the past decade,several engineered therapeuticproteins and antibodieshave been generatedand are either currently inuse or in the late stages of clinical trials. Patients may be familiarwith:• Etanercept (Embrel ® ), which binds TNF-α and preventsit from engaging its inflammatory functions• Recombinant Protein C, which helps the body dissolvesmall clots triggered during inflammation• Infliximab (Remicade), a monoclonal antibody thatbinds to TNF-α, and has been used to treat autoimmuneinflammatory diseases such as rheumatoid arthritis andCrohn’s diseaseWhile these drugs are being used to treat systemic diseases,it is possible that they could be used to treat inflammation relatedto gingivitis and periodontal disease. Other engineered proteinsunder development may also be used to treat these oralinfections. 43Another anti-inflammatory medication that has beenshown to be effective for the treatment of periodontitis is lowdosedoxycycline hyclate (Periostat). Periostat inhibits the collagenaseactivity by neutrophils, thus preventing the degradationof connective tissue and bone loss. Therefore, it is beneficial aspart of host modulation therapy. It is administered twice dailyat a dosage of 20 mg. Periostat is an antibiotic; however, thedose is too low to produce antibacterial effects. Studies haveJust as a physician will recommend a patient lose weight orprescribe an antihypertensive agent, the dental hygienetherapist may make recommendations for the patient tobegin a smoking cessation program, use specific preventiveoral care products, monitor their blood sugar regularly orcomplete a nutrition counseling program, in addition tohaving debridement of plaque biofilm and calculus.demonstrated that Periostat improves the effectiveness of routinescaling and root planing and that the progression of periodontitisis decreased. 43Optimal preventive education programs should includediscussion of twice-daily brushing, flossing and use of achemotherapeutic mouth rinse to reduce bacterial plaque andsusceptibility to gingivitis. 44 Products recommended should bethose that have been well-researched and demonstrated safetyand efficacy. For example, Peridex ® and Listerine ® AntisepticMouthrinse are the only two chemotherapeutic mouth rinsesthat have been approved by the American Dental AssociationCouncil on Scientific Affairs. Their effectiveness has been wellestablished. Similarly, a dentifrice containing triclosan/copolymer(Colgate Total ® Toothpaste) has been shown to be effective inreducing plaque and gingivitis, controlling bacterial infectionand preventing or slowing the progression of periodontal disease.45 In addition, triclosan has been shown to possess potentanti-inflammatory properties. In vitro studies have demonstratedthat triclosan has inhibited IL-1 stimulated prostaglandinproduction in human gingival fibroblast cells, inhibited theproduction of IL-1 by fibroblasts stimulated with TNF-α andhas inhibited the productionof collagenases byhuman bone cells andfibroblasts stimulated withIL-1 and TNF-α. 46,47 Theantibacterial and antiinflammatoryproperties oftriclosan are reasons to recommendColgate Total ®toothpaste both for patientswith periodontal diseases aswell as for those whose systemichealth has been compromised.ConclusionResearch suggests that there is an interrelationship betweenoral infection, inflammation and systemic health. Patients, dentalhygienists, dentists, dental specialists and other health careproviders should be aware of the consistent relationshipsbetween oral inflammation and systemic diseases. They shouldvalue the need to modify assessment, prevention, and treatmentprotocols to improve the oral health as well as total health of thepatients they treat in the office each day.Take Advantage of the Opportunity toEarn CE PointsBased on the information presented in Inflammation: TheRelationship Between Oral Health and Systemic Disease,you can earn 2 CE points by visiting www.adha.org andselecting “Continuing Ed” on the left-hand navigational bar.Then simply click on ADHA Continuing Education Coursesand select this course.6 access—special supplemental issue—april 2006

A Case in PointMrs. White, a 45-year-old Hispanic female, presents toyour practice for an initial dental hygiene appointment.She is new to the area, but reports that she faithfully haddental and dental hygiene care every six months. Mrs.White’s medical history is significant for the following:• Myopia for which she wears corrective lenses• Borderline hypertension—no medications prescribed• Prediabetes—diet and exercise recommendationsmade by nurse practitioner• Overweight—diet and exercise recommendationsmade by nurse practitioner, advised to lose 20pounds• Smokes 1/2 pack of cigarettes daily for over 20yearsOral history is significant for the following:• Generalized gingivitis with moderate plaque presenton lingual surfaces of mandibular premolar andmolar teeth and supragingival calculus and plaquenoted on the lingual surfaces of mandibular incisors• No evidence of current or recurrent decay, previoushistory of decay with occlusal restorations presenton all first molars, and a crown on tooth #31• Presence of nicotine stomatitisMrs. White reports that she has been advised previouslyto quit smoking and has attempted to do so on threeoccasions without success. She states that she was toldthat she had gingivitis by her previous dentist and dentalhygienist, but that it was not serious and that she shouldbrush and floss more. Mrs. White admits that she does notfloss regularly, but brushes twice daily with a manual toothbrush.Given this information about Mrs. White, take amoment and imagine her sitting in the operatory. She isready for her appointment. What is your next step? Do youneed more information or are you ready to proceed withtreatment? Have you mentally picked up your cureteagerly anticipating removing the debris from themandibular region? If your answer is “Yes, let’s get started,”read this paper again. Mrs. White does not need theplaque and calculus removed yet nearly as much as sheneeds to know about her risk factors for oral and systemichealth. Mrs. White needs you to take time out to reviewyour findings from assessments and speak frankly with herabout her health status. This is the perfect moment to discusssymptoms of diabetes that Mrs. White may not realizeshe has, to educate her about the links between smoking,hypertension, diabetes and CVD. Mrs. White is 45, overweightand Hispanic, placing her at greater risk for convertingfrom prediabetes to diabetes. Nevertheless, withsome effort, she can avoid that step through a concertedeffort of diet and exercise. She may not realize that amodest weight loss will benefit her greatly in terms ofimproved general health. In addition, now is when you canbegin discussing the link between her oral health and generalhealth. The presence of chronic gingivitis coupled withprediabetes and borderline hypertension places Mrs.Whiteat risk for further health issues. Also, she presents with nicotinestomatitis, another reason to incorporate smoking cessationas part of your education discussion and treatmentplan. Mrs. Whitehas known shehas gingivitis, admitsshe does notfloss regularly, butdoes brush daily.What recommendationswould youmake to help improveher oralIn the course of reviewing thisinformation, it is possible to see howthe traditional dental hygieneappointment can be reframed. That45-minute “cleaning” just does not fitthe profile of needs for Mrs. White.home care regimen? Would you switch her to a poweredtoothbrush, have her use a mouth rinse, recommendColage Total ®toothpaste? How often would you want tosee Mrs. White for follow-up?In the course of reviewing this information, it is possibleto see how the traditional dental hygiene appointmentcan be reframed. That 45-minute “cleaning” just does notfit the profile of needs for Mrs. White. She deserves aschedule that allows for assessment and education, treatmentand education, and re-evaluation and education. Isall this necessary for a simple case of gingivitis? Perhapsthe real question we should be asking is, do we ever seesimple cases of gingivitis? What have we been missing bynot allowing adequate time to perform comprehensiveassessment and risk factor analysis?This case and the questions posed provide the dentalhygiene reader an opportunity to reflect on the prospectof incorporating oral medicine into dental hygiene practice.Continually reviewing the literature related to oral andsystemic health – and discerning relevant components –will enable dental hygienists to refine practice and continueto provide quality care to their patients.special supplemental issue—april 2006—access 7

References1. Mariotti A. A primer on inflammation. CompendCont Educ Dent 2004; 25 (7) (Suppl 1):7-15.2. Kornman KS, Page RC, Tonetti MS. The host responseto the microbial challenge in periodontitis: assemblingthe players. Periodontol 2000 1997; 14:33-53.3. Armitage GC. Diagnosis of periodontal diseases. JPeriodontol 2003; 74; 1237-47.4. Scannapieco FA: Periodontal inflammation: fromgingivitis to systemic disease? Compend Cont EducDent 2004; 25 (7) (Suppl 1): 16-25.5. Ebersole JL, Machen RL, Steffen MJ, et al. Systemicacute-phase reactants, C-reactive protein andhaptoglobin, in adult periodontitis. Clin ExpImmunol 1997; 107: 347-52.6. Loos BG, Craandijk J, Hoek FL, et al. Elevation ofsystemic markers related to cardiovascular diseasein the peripheral blood of periodontitis patients. JPeriodontol 2000; 71: 1528-34.7. Danesh J, Collins R, Appleby P, et al. Association offibrinogen, C-reactive protein, albumin, or leukocytecount with coronary heart disease: metaanalysesof prospective studies. J Am Med Assoc.1998; 279: 1477-82.8. Ridker PM, Buring JE, Shih J, et al. Prospective studyof C-reactive protein and the risk of future cardiovascularevents among apparently healthywomen. Circulation. 1998;98:731-33.9. D’Aiuto F, Parkar M, Andreou G, et al. Periodontitisand systemic inflammation: control of the localinfection is associated with a reduction in seruminflammatory markers. J Dent Res 2004; 83:156-60.10. Schwartz CJ, Valente AJ, Sprague EA, et al. Thepathogenesis of atherosclerosis: an overview. ClinCardiol 1991; 14 (2 suppl 1): 11-6.11. Paigen B, Morrow A, Holmes PA, et al. Quantitativeassessment of atherosclerotic lesions in mice.Atherosclerosis. 1987; 68: 231-40.12. Ridker PM, Hennekens CH, Buring JE, et al. C-reactiveprotein and other markers of inflammation inthe prediction of cardiovascular disease in women.N Engl J Med. 2000; 342: 836-43.13. Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognosticvalue of C-reactive protein and serum amyloidA protein in severe unstable angina. N Engl JMed 1994; 331: 417-24.14. Ruderman NB, Williamson JR, Brownlee M. Glucoseand diabetic vascular disease. FASEB J. 1992; 6:2905-14.15. Bhakdi S, Torzewski M, Klouche M, et al.Complement and atherogenesis: binding of CRP todegraded, nonoxidized LDL enhances complementactivation. Arterioscler Thromb Vasc Biol.1999; 19: 2348-54.16. Zwaka TP, Hombach V, Torzewski J. C-reactive protrein-mediatedlow density lipoprotein uptake bymacrophages: implications for atherosclerosis.Circulation 2001; 103: 1194-7.17. Epstein SE. The multiple mechanisms by whichinfection may contribute to atherosclerosis developmentand course. Circ Res 2002; 90: 2-4.18. Haraszthy VI, Zambon JJ, Trevisan M, et al.Identification of periodontal pathogens in atheromatousplaques. J Periodontol. 2000; 71 (10): 1554-60.19. Herzberg MC, Meyer MW: Effects of oral flora onplatelets: possible consequences in cardiovasculardisease. J Periodontol. 1996; 67 (10Suppl): 1138-42.20. Paquette DW. The periodontal-cardiovascular link.Compend Cont Educ Dent. 2004; 25 (9):681-92.21. Desvarieux M, Demmer RT, Rundek T, et al.Periodontal microbiota and carotid intima-mediathickness: the oral infections and vascular diseaseepidemiology study (INVEST). Circulation. 2005; 111(5): 576-82.22. Löe H. Periodontal disease. The sixth complicationof diabetes mellitus. Diabetes Care. 1993; 16: 329-34.23. Nishimura F, Takahshi K, Kurihara M, et al.Periodontal disease as a complication of diabetesmellitus. Ann Periodontol. 1998;3:20-29.24. Ryan ME, Carnu A, Kamer A. The influence of diabeteson the periodontal tissues. J Am Dent Assoc2003; 134: 34S-40S.25. Taylor GW, Burt BA, Becker MP, et al. Severe periodontitisand risk for poor glycemic control in8 access—special supplemental issue—april 2006

patients with non-insulin-dependent diabetes mellitus.J Periodontol 1996; 67 (10 Suppl): 1085-93.26. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatmentof periodontal disease in diabetics reduces glycatedhemoglobin. J Periodontol 1997; 68: 713-9.27. Miller LS, Manwell MA, Newbold D, et al. The relationshipbetween reduction in periodontal inflammationand diabetes control: a report of 9 cases. JPeriodontol 1992; 63: 843-8.28. Mealey DL, Rethman MP: Periodontal disease anddiabetes mellitus. Bidirectional relationship. DentToday 2003; 22: 107-13.29. Ryan ME, Ramamurthy NS, Corsa T, Golub LM. MMPmediatedevents in diabetes. Ann NY Acad Sci1999; 878: 331-4.30. Ryan ME, Usman A, Ramamurthy NS, et al.Excessive matrix metalloproteinase activity in diabetes:inhibition by tetracycline analogues withzinc reactivity. Curr Med Chem 2001; 8 (3): 305-16.31. Salvi GE, Yalda B, Collins JG, et al. Inflammatorymediator response as a potential risk marker forperiodontal diseases in insulin-dependent diabetesmellitus patients. J Periodontol 1997; 68: 127-35.32. Lalla E, Lamster IB, Feit M, et al. Blockade of RAGEsuppresses periodontitis-associated bone loss indiabetic mice. J Clin Invest 2000; 105: 1117-24.33. Grossi SG, Genco RJ. Periodontal disease and diabetesmellitus: a two-way relationship. AnnPeriodontol 1998; 3: 51-61.34. Graves DT, Al-Mashat H, Liu, RL. Evidence that diabetesmellitus aggravates periodontal diseasesand modifies the response to an oral pathogen inanimal models. Compend Cont Educ Dent. 2004;25 (7) (Suppl 1): 38-45.35. Scannapieco FA. Role of oral bacteria in respiratoryinfection. J Periodontol. 1999; 70: 793-802.36. Scannapieco FA, Bush RM, Paju S. Associationsbetween periodontal disease and risk for nosocomialbacterial pneumonia and chronic obstructivepulmonary disease: a systematic review. AnnPeriodontol. 2003; 8: 54-69.37. Hayes C, Sparrow D, Cohen M, et al. The associationbetween alveolar bone loss and pulmonaryfunction: the VA Dental Longitudinal Study. AnnPeriodontol. 1998; 3: 257-61.38. Scannapieco FA, Ho AW. Potential associationsbetween chronic respiratory disease and periodontaldisease: analysis of National Health andNutrition Examination Survey III. J Periodontol. 2001;72: 50-6.39. Offenbacher S, Katz V, Fertik G, et al. Periodontalinfection as a possible risk factor for preterm lowbirth weight. J Periodontol. 1996; 67 (10 suppl):1103-13.40. Jeffcoat MK, Guers NC, Reddy MS, et al.Periodontal infection and preterm birth: results of aprospective study. J Am Dent Assoc. 2001; 132:875-80.41. Scannapieco FA, Bush RP, Paju S. Periodontal diseaseas a risk factor for adverse pregnancy outcomes. Asystematic review. Ann Periodontol 2003; 8: 70-8.42. Han YW, Redline RW, Li M, et al. Fusobacteriumnucleatum induces premature and term stillbirth inpregnant mice: implication of oral bacteria inpreterm birth. Infect Immun. 2004; 72: 2272-9.43. Panagakos FS. Inflammation: its role in health andits mediation by chemotherapeutic agents.Continuing Education for the HealthcareProfessional (CEHP), distributed by Sullivan-Schein,a Henry Schein Company, course reference#05AS2906B, 2005.44. Gurenlian JR. Diabetes mellitus: strategies for providingcomprehensive care. Continuing Educationfor the Healthcare Professional (CEHP), distributedby Sullivan-Schein, a Henry Schein Company,course reference # 05AS2904, 2005.45. Gaffar A, Scherl D, Afflitto J, Coleman EJ. The effectof triclosan on mediators of gingival inflammation.J Clin Periodontol. 1995; 22(6): 480-4.46. Xu T, Deshmukh M, Barnes VM, et al. Effectiveness ofa triclosan/copolymer dentifrice on microbiologicaland inflammatory parameters. Compend ContEduc Dent 2004; 25 (7) (Suppl 1): 46-53.47. DeVizio W, Davies R. Rationale for the daily use of adentifrice containing triclosan in the maintenanceof oral health. Compend Cont Educ Dent 2004; 25(7) (Suppl 1): 54-7.

Think all toothpasteswork the same?Take a deeper look.Colgate Total ® is proven to fight oralinflammation.Scientific evidence haslinked oral inflammation to systemichealth diseases such as cardiovascularand other diseases throughout the body 1-4Only Colgate Total ® contains triclosan, and only triclosanfights oral inflammation in 2 important ways 1-3,5,6Kills plaque bacteria for a full 12 hours 5Up to 98% More Plaque Reduction 1,2 *;up to 88% More Gingivitis Reduction 1,2 *% Reduction ComparedWith Control-10-20-30-40-50-60-70-80-90-100PlaqueGingivitisReduces the level of inflammatory mediatorsthat may play a role in systemic health 3,470% Reduction in PGE 2 —a Key Mediator 6†PGE 2 (pg/10 3 Cells)3.02.01.00.0Control70%ReductionTriclosan(1 g/mL)“Recent evidence suggests a strong relationship between periodontal inflammatory disease and systemic diseasessuch as cardiovascular disease. It is now generally accepted that inflammation plays an important role…” 7—Sheilesh, et al. Compendium. 2004.12-Hour Antibacterial plus Anti-inflammatory Protection for Better Oral and Overall HealthVisit colgateprofessional.com for free patient samples.Colgate Total ® is the only FDA-approved toothpaste for plaque and gingivitis.1. Volpe AR, et al. J Clin Dent. 1996;7(suppl):S1-S14. 2. Davies RM, et al. J Clin Periodontol. 2004;31:1029-1033. 3. Gaffar A, et al. J Clin Periodontol. 1995;22:480-484. 4. Scannapieco FA. Compendium. 2004;7(suppl 1):16-25. 5. Amornchat C, et al.Mahidol Dent J. 2004;24:103-111. 6. Modéer T, et al. J Clin Periodontol. 1996;23:927-933. 7. Sheilesh D, et al. Compendium. 2004;7(suppl 1):26-37.*vs ordinary fluoride toothpaste. † in vitro.©2005 Colgate-Palmolive Company C53248 7/05