inflammation - adha

INFLAMMATION:The Relationship Between Oral Health andSystemic Disease

By JoAnn R. Gurenlian, RDH, PhD

special supplement toaccess april 2006

sponsored by

Patients, dental hygienists, dentists,

dental specialists and other health

care providers should be aware of

the consistent relationships between

oral inflammation and systemic

diseases. They should value the need

to modify assessment, prevention, and

treatment protocols to improve the oral

health as well as total health of the

patients they treat in the office

each day.

special supplemental issue—april 2006—access 1

Abstract

Since 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 associa-tion, indicating that there is notenough research to determineany relationship between thetwo. The questions that havebeen raised focusing on the rela-tionship between periodontaldiseases and systemic conditionsnow extend beyond cardiovascu-lar disease and include diabetes,respiratory disease and adversepregnancy outcomes. Researchhas demonstrated that the association between oral inflammationand systemic inflammation may be the key to understanding thedeleterious effects on multiple organ systems. However, is the rela-tionship so 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 informa-tion into 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 Process

What is inflammation? Isn’t this the process that is supposedto be good for our bodies? How can it now be something that caus-es harm 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 inflam-mation, 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, for-eign bodies, 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.

Research hasdemonstrated that theassociation between oralinflammation andsystemic inflammationmay be the key tounderstanding thedeleterious effects onmultiple organ systems.

contents

JoAnn 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 prac-tices, and works part-time in a medical prac-tice. She is an internationally recognized speak-er on the topics of oral pathology, oral medi-cine, 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.

Abstract . . . . . . . . . . . . . 1

The Inflammatory Process . . . . . . . . . . . . . . 1

Inflammation & Oral Health. . . . . . . . . . . 2

The Oral-Systemic Relationship . . . . . . . . . . 3

Translating Science to Practice . . . . . . . . . . . 5

Conclusion. . . . . . . . . . . 6

A Case in Point . . . . . . . 7

References. . . . . . . . . . . 8

2 access—special supplemental issue—april 2006

Table I: Physiologic Rationale for Cardinal Signs of Inflammation

Cardinal Signs of Inflammation

Rubor (redness)

Tumor (swelling)

Calor (heat)

Dolor (pain)

Functio laesa (loss of function)

Physiologic Rationale

Increased vascularity

Exudation of fluid

A combination of increased blood flow and therelease of inflammatory mediators

The stretching of pain receptors and nerves bythe inflammatory exudates, and by the releaseof chemical mediators

A combination of the above effects

The inflammatory response consists of a vascular and a cel-lular reaction. These reactions are mediated by chemical factorsderived from plasma proteins or cells. The classic signs ofinflammation are redness, swelling, heat, pain and loss of func-tion. The physiologic explanations for these signs appear inTable I. Other signs of inflammation include fever, leukocyto-sis or an increase in the number of circulating white blood cells,the presence of acute-phase proteins including C-reactive pro-teins (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 pro-teins, 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 sub-stances that tend to direct the inflammatory response. Theseinflammatory mediators come from plasma proteins or cellsincluding mast cells, platelets, neutrophils and monocytes/macro-phages. 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 activ-ity, 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 Health

The inflammatory process significantly affects the peri-odontium. 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 peri-odontitis. 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 gin-gival epithelium to produce chemical mediators includinginterleukin–1 beta (IL-1‚), prostaglandins, tumor necrosis fac-tor alpha (TNF-α), and matrix metalloproteinases.4 Theseproducts recruit neutrophils to the area and influence chemo-taxis, and can cause increased permeability of gingival vesselsthat permits plasma proteins to emigrate from the blood vesselsinto the tissue. As the inflammatory process progresses, addi-tional mediators are produced, and more cell types are recruit-ed to 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 exacerbate

McMahon RFT, Sloan P. Essentials of pathology for dentistry. Edinburgh: Churchill Livingstone; 2000, p. 26.


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 result-ing in 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.9

The Oral-Systemic Relationship

Although periodontal diseases are well known as an oralproblem, in the past decade, there has been a shift in perspec-tive. Research has been focusing on the potential impact ofperiodontal diseases on systemic health. The relationshipbetween periodontal inflammatory disease and systemic dis-eases such as cardiovascular disease, diabetes, respiratory disease

and adverse pregnancy outcomes has beenclosely investigated. The basis for the bio-logical mechanism 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 inflam-matory plaques that may cause throm-boses and 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 endothe-lium of elastic and muscular arterial tissue.One of the hallmarks of the early athero-sclerotic lesion is the presence of neu-trophils followed by monocytes and lym-phocytes.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 lipid-laden “foam cells.”11 The local inflamma-tion is sustained by secreting chemicalmediators, and the atherosclerotic lesionbegins to bulge within the luminal wall.As this lesion progresses, the extracellularmatrix is degraded by proteolytic enzymes

and 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 con-sistent markers of systemic inflammation and poor cardiovascu-lar prognosis is the acute-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.14-16

It has been proposed thatbacteria or viruses may direct-ly infect atherosclerotic lesionscontributing to the inflamma-tory process. 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 periodon-tal pathogens including Porphyromonas gingivalis, Tannerellaforsythensis, and Prevotella intermedia.18 In addition, P. gingi-

Figure 1: Mediators and cells present in established gingivitis

From: Scannapieco, FA: Periodontal inflammation: from gingivitis to systemic disease?Compend Cont Educ Dent. 2004; 25(7) (Suppl1): 16-24.

Cardiovascular disease(CVD) is characterized bythe build-up ofinflammatory plaquesthat may causethromboses and eventualmyocardial infarction.


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 estab-lished.

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 dis-ease and 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.4

Diabetes mellitus is another systemic condition with oralinflammatory connections. One of the major complications ofdiabetes is periodontitis.22 While diabetes increases the proba-bility of developing periodontal disease22-24, periodontitis alsoincreases the risk of poor glycemic control in people with dia-betes when compared to those individuals with diabetes with-out periodontitis.25 Fortunately, periodontal treatment can

improve glycemic control by reduc-ing the bacterial burden and theinflammatory response.26-28

There 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 effective-ness of cells that kill bacteria.

Another explanation is thatinflammation is enhanced in thosewith diabetes. Research has demon-strated elevated levels of inflammato-ry mediators 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 signifi-cant periodontal destruction with anequivalent bacterial challenge.24,29,30 Inparticular, the proinflammatorycytokine, TNF-α, plays a major rolein this process. TNF-α has a signifi-cant role in insulin resistance, the pri-mary cause of type 2 diabetes. It is

produced 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.31-33

It has also been hypothesized that diabetes interferes withthe capacity to form new bone after periodontal diseases havecaused bone resorption. Graves, et al., studied genetically dia-betic mice 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.34

As with CVD and diabetes mellitus, there is a relationshipbetween oral infection and respiratory disease. In particular,chronic obstructive pulmonary disease (COPD) and pneumo-nia have 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 facili-ties. These bacteria may be released into saliva and then aspirat-ed into the lower airway causing infection.4 Another vehicle bywhich bacteria from the oral cavity can be introduced into therespiratory system is intubation.

Figure 2: Connection between periodontal disease and atherosclerosis

From: 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.


Inflammatory mediators, such ascytokines produced by the periodon-tium, may be another mechanism bywhich respiratory disease are associatedwith oral health. These mediators pres-ent in 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 stimu-late the inflammatory process, whichleads to elevated amniotic levels ofprostaglandins, TNF-α, and IL-1 andIL-6. These mediators then lead to pre-mature rupture 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 biologi-cal mechanisms by which gingival inflammation effects sys-temic health appears in Figure 3.

Translating Science to Practice

As 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 opportu-nities for 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 cli-nicians to reframe their protocols. The process begins by prac-ticing oral medicine. First, comprehensive medical assessmentis needed for each patient. A review of systems and vital signs

evaluation should be part of that assessment process. Duringthese assessments, identifying risk factors for specific systemicdiseases is important, including age (over 40 years), hyperten-sion, dyslipidemia, smoking, obesity/overweight, CVD, dia-betes or symptoms of diabetes and women who are pregnantand have poor oral hygiene.

Comprehensive oral assess-ment is equally important. Thismay include thorough head andneck examination, radiographs(if clinically indicated), peri-odontal probing, bacterialmonitoring of periodontal andcarious pathogens, genetic test-ing for periodontal disease orother diagnostic tools that seemappropriate to each individualneed.

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 pur-pose of these assessments is to prevent problems from occurringor treat them as readily as possible. Patients are well acquaint-ed with 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 med-ical appointment and having certain assessments performed.They are even used to requesting certain tests or proceduresbased on their own education and experience. Thus, it is time

Figure 3: Model to explain oral inflammation-systemic disease association

From: Scannapieco, FA: Periodontal inflammation: from gingivitis to systemic disease?Compend Cont Educ Dent. 2004; 25(7) (Suppl1): 16-24.

Understanding theassociation betweenoral health andsystemic health doesprovide opportunitiesfor oral hygieneclinicians to reframetheir protocols.


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 chron-ic gingivitis or periodontitis condition may place them at riskfor CVD, poor glycemic control or an adverse pregnancy out-come.

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 pre-ventive oral 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 “clean-ing” 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 ques-tions about medicationsand products that have anti-inflammatory and/or anti-bacterial properties. Forexample, in the past decade,several engineered thera-peutic proteins and anti-bodies have been generatedand are either currently inuse or in the late stages of clinical trials. Patients may be famil-iar with:

• 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 disease

While these drugs are being used to treat systemic diseases,it is possible that they could be used to treat inflammation relat-ed to gingivitis and periodontal disease. Other engineered pro-teins under development may also be used to treat these oralinfections.43

Another anti-inflammatory medication that has beenshown to be effective for the treatment of periodontitis is low-dose doxycycline hyclate (Periostat). Periostat inhibits the colla-genase activity 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 have

demonstrated that Periostat improves the effectiveness of rou-tine scaling and root planing and that the progression of peri-odontitis is decreased.43

Optimal 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 dis-ease.45 In addition, triclosan has been shown to possess potentanti-inflammatory properties. In vitro studies have demonstrat-ed that triclosan has inhibited IL-1 stimulated prostaglandinproduction in human gingival fibroblast cells, inhibited theproduction of IL-1 by fibroblasts stimulated with TNF-α and

has inhibited the produc-tion of collagenases byhuman bone cells andfibroblasts stimulated withIL-1 and TNF-α.46,47 Theantibacterial and anti-inflammatory properties oftriclosan are reasons to rec-ommend Colgate Total®

toothpaste both for patientswith periodontal diseases aswell as for those whose sys-

temic health has been compromised.

Conclusion

Research suggests that there is an interrelationship betweenoral infection, inflammation and systemic health. Patients, den-tal hygienists, 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.

Just 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.

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.


Mrs. 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 pre-

scribed• Prediabetes—diet and exercise recommendations

made by nurse practitioner• Overweight—diet and exercise recommendations

made by nurse practitioner, advised to lose 20pounds

• Smokes 1/2 pack of cigarettes daily for over 20years

Oral history is significant for the following:

• Generalized gingivitis with moderate plaque pres-ent on 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 stomatitis

Mrs. White reports that she has been advised previous-ly to 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 tooth-brush.

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 her

about her health status. This is the perfect moment to dis-cuss symptoms 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, over-weight and Hispanic, placing her at greater risk for con-verting from 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 gen-eral health. The presence of chronic gingivitis coupled withprediabetes and borderline hypertension places Mrs.Whiteat risk for further health issues. Also, she presents with nico-tine stomatitis, another reason to incorporate smoking ces-sation as part of your education discussion and treatmentplan. Mrs. Whitehas known shehas gingivitis, ad-mits she does notfloss regularly, butdoes brush daily.What recommen-dations would youmake to help im-prove her oralhome 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, treat-ment and 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 prac-tice. Continually reviewing the literature related to oral andsystemic health – and discerning relevant components –will enable dental hygienists to refine practice and contin-ue to provide quality care to their patients.

A Case in Point

In 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.


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26. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatmentof periodontal disease in diabetics reduces glycat-ed hemoglobin. J Periodontol 1997; 68: 713-9.

27. Miller LS, Manwell MA, Newbold D, et al. The rela-tionship between reduction in periodontal inflam-mation and 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. MMP-mediated events in diabetes. Ann NY Acad Sci1999; 878: 331-4.

30. Ryan ME, Usman A, Ramamurthy NS, et al.Excessive matrix metalloproteinase activity in dia-betes: 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 dia-betes mellitus: a two-way relationship. AnnPeriodontol 1998; 3: 51-61.

34. Graves DT, Al-Mashat H, Liu, RL. Evidence that dia-betes mellitus 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 respirato-ry infection. J Periodontol. 1999; 70: 793-802.

36. Scannapieco FA, Bush RM, Paju S. Associationsbetween periodontal disease and risk for nosoco-mial bacterial pneumonia and chronic obstructivepulmonary disease: a systematic review. AnnPeriodontol. 2003; 8: 54-69.

37. Hayes C, Sparrow D, Cohen M, et al. The associa-tion between alveolar bone loss and pulmonary

function: the VA Dental Longitudinal Study. AnnPeriodontol. 1998; 3: 257-61.

38. Scannapieco FA, Ho AW. Potential associationsbetween chronic respiratory disease and peri-odontal disease: 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 pro-viding comprehensive 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 microbiologi-cal and 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.

Only Colgate Total® contains triclosan, and only triclosan

fights oral inflammation in 2 important ways1-3,5,6

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.

Visit colgateprofessional.com for free patient samples. Colgate Total® is the only FDA-approved toothpaste for plaque and gingivitis.

“Recent evidence suggests a strong relationship between periodontal inflammatory disease and systemic diseases such as cardiovascular disease. It is now generally accepted that inflammation plays an important role…”7

—Sheilesh, et al. Compendium. 2004.

Think all toothpastes

work the same?

Take a deeper look.

Colgate Total® is proven to fight oral

inflammation. Scientific evidence has

linked oral inflammation to systemic

health diseases such as cardiovascular

and other diseases throughout the body1-4

12-Hour Antibacterial plus Anti-inflammatory Protection for Better Oral and Overall Health

Reduces the level of inflammatory mediatorsthat may play a role in systemic health3,4

70% Reduction in PGE2—a Key Mediator6†

Kills plaque bacteria for a full 12 hours5

Up to 98% More Plaque Reduction1,2*;up to 88% More Gingivitis Reduction1,2*

-10

-20

-30

Plaque

-40

-50

-60

-70

-80

-90

-100

Gingivitis

% R

educ

tion

Com

pare

d

With

Con

trol

Control

PG

E 2 (

pg/1

03 C

ells

)

Triclosan(1 g/mL)

0.0

1.0

2.0

3.0

70%

Reduction

©2005 Colgate-Palmolive Company C53248 7/05

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