Aug. 2, 2010
The amount of information that hygienists must analyze and interpret for their patients is extensive and continually evolving. Our ability to translate and apply timely research for our patients increases patient compliance and establishes the dental hygienist as an educated, competent, caring oral health care provider.

by Lois N. Dreyer, RDH, MS

Dental hygienists routinely assess their patients’ oral health by correlating their behaviors, habits, conditions, and diseases with current medical and dental data reported in the literature. However, informing patients of their status can be challenging, because most patients are neither able to decipher professional language and data nor apply it to themselves. Add to this the appointment time constraints that we face and it is easy to see why information critical to the success of offered treatment and increased patient compliance is often sketchy, or not as individualized as it could be.

Thanks to television, print, and radio advertisements, most patients have at least a passing acquaintance with plaque, the most predominant, local, environmental factor central to dental disease. However, they may not know that it is their own genetic mix of bacteria and/or individual body (host) response that predisposes them to caries or periodontal disease or both. User-friendly, evidenced-based resources that are readily available to consumers and practitioners are a good jumping-off point for patient/provider discussions. The 2000 U.S. Surgeon General’s report on oral health, available in its entirety at, “explores what the mouth and face can reveal about general health, describes the role the mouth plays as a portal of entry for infection, and concludes with studies that are associating oral infections with serious systemic diseases and conditions.” It states that “oral disease and disorders in and of themselves affect health and well-being throughout life, with some type of periodontal disease or gingivitis affecting 75% of the population.”1

Additionally, the American Academy of General Dentistry ( recognizes “that more than 90% of all systemic diseases have oral manifestations and that oral infection can affect major organs.”1 Used as opening statements, these sentences lend weight to the proposed treatment plan and strengthen the patient’s perception of the hygienist as an informed oral health provider. How technical the hygienist chooses to be when talking to patients is based upon basic communication skills as well as established patient/provider rapport.

Begin at the beginning

In the healthy mouth, there are more than 350 species of microorganisms. Periodontal infections are linked to fewer than 5% of these species2 and, for most cases, identification of specific disease organisms through saliva testing is expensive and unnecessary. But in cases that do not respond well or in a timely fashion to standard treatment, sophisticated data is critical. If testing is relevant, interpreting the data as it relates to the identified microorganisms is appropriate.

Periodontal disease is the result of a small number of Gram-negative bacteria. It is episodic and site-specific3 with the disease’s intensity a reflection of the host’s response to the inflammation process. In other words, the clinician may see one site that exhibits active disease of particular intensity in one patient and a completely different scenario in another patient or area of the same patient’s mouth. It is this low-level, persistent immune response of the body to bacterial overload that causes tissue destruction and damaging effects, not only in the gingiva but also in organs throughout the body, including the heart.2

Local factors (inadequate home care, decreased salivary function, tooth morphology, trauma from occlusal forces, poorly placed or maintained restorations) that increase plaque retention can be addressed generically.
• Explaining the systemic links — The relationship between periodontal disease and systemic diseases has been presented in professional journals and magazines for many years. Research has found that people with periodontal disease are almost twice as likely to suffer from coronary artery disease as those without, and that periodontal disease can exacerbate existing heart conditions.4 Diabetes and adverse pregnancy outcomes have also been identified as systemic conditions with strong links to poor oral health.

Until recently, the profession assumed that bacteria specific to periodontal disease was the singular cause of tissue breakdown and destruction. New findings are showing that although pathogens must be present, it is the body’s (the host) response that determines the onset and severity of the disease.3

The American Association of Periodontology offers a risk assessment test to rate an individual’s susceptibility to periodontal disease ( This easy-to-answer exam provides an immediate rating (low, medium, or high) response based upon the patient’s answers.

Explaining the oral health/systemic health link can become overwhelming to the patient when the conversation moves into the biological arena with terms such as inflammatory mediators, cytokines, Gram-negative bacteria, and C-reactive proteins. In addition, a number of theories can explain the body’s response to the migration of oral pathogens into other areas of the body.

Central to all theories is the fact that bacteria, normally residing in the oral cavity, enter the bloodstream through ulcerations at the base of the periodontal pocket. The more advanced and destructive the periodontal disease, the more surface area there is for the bacteria to enter the bloodstream.5 The body responds by initiating the process of inflammation. It is this response that scientists speculate is the causal link.

The majority of our patients understand that inflammation is a localized, protective bodily reaction, elicited by an injury or the destruction of tissue, intended to fight off infection, guard against injury, or shield against irritation.6 Inflammation is often characterized by swelling, redness, heat, and pain around the affected area. What patients may not know is that the inflammatory process destroys, dilutes, or walls off both the injurious agent and the injured tissue.7 Left unchecked, inflammation becomes a threat to healthy tissue. Over time, chronic inflammation leads to dysfunction of the infected tissues and, therefore, more severe health complications.

• Cardiovascular disease and stroke — As stated above, people with periodontal disease are almost twice as likely to suffer from coronary artery disease as those without, and periodontal disease can exacerbate existing heart conditions.

It is thought that the resulting infection causes a buildup of fatty deposits inside the arteries of the heart, which restricts the amount of nutrients and oxygen required for the heart to function properly.3,4 Advanced heart disease may be as great a risk factor as cholesterol.

Additional studies have pointed to a relationship between periodontal disease and stroke. In a study that looked at oral infection as a risk factor for stroke, people diagnosed with acute cerebrovascular ischemia were found more likely to have an oral infection compared to those in the control group.4 In addition, bacteria in the bloodstream may cause blood clots that contribute to clogged arteries, leading up to heart attacks or strokes.8

• Diabetes — Diabetes, a condition that results in the body’s inability to produce or properly use insulin, affects approximately 16 million Americans (5.9% of the population). More than half of these people do not know that they are affected.3 A review of the literature did not differentiate between Type 1 and Type 2 diabetes in regard to periodontal disease; however, diabetic patients who control their condition, either through diet or medications, are no more vulnerable to periodontal disease than healthy patients. It is the uncontrolled or undiagnosed diabetic patient who faces a twofold threat from this systemic condition.3

Diabetes is an immune system dysfunction, so patients are more prone to infection and delayed wound healing due to decreased peripheral circulation. This translates into a higher susceptibility to periodontal disease.9 Periodontal disease affects patients’ ability to control their blood sugar levels. As a result, these patients have an increased likelihood of developing acute periodontal abscesses, a greater degree of attachment loss, and periodontal destruction. Increased glucose levels have been found in the crevicular fluid of diabetics. Because numerous bacteria flourish in a glucose-rich environment, this may increase the development of periodontal disease.3 Simply put, these two conditions — diabetes and periodontal disease — potentiate each other.

• Tobacco — Nicotine and other toxic substances alter the host’s ability to neutralize infection by reducing the effectiveness of neutrophils. Neutrophils, the most common type of white blood cell, are present in the bloodstream until signaled to a site of infection by chemical cues in the body. They are fast-acting, arriving at the site of infection within an hour, plentiful, and responsible for the bulk of the immune response. As such, they are an important part of the immune response; a lowered neutrophil count can result in a compromised immune system.10

The use of any tobacco product raises the level of the patient’s oral health risk. Smoking may be the etiology of more than half the cases of periodontal disease among adults here in the United States, and tobacco has also been strongly linked to aggressive periodontal disease in adults in their 20s and 30s. Refractory periodontal disease (periodontitis that does not respond to professional treatment coupled with excellent home care) seems to be directly affected by smoking; 90% of patients with refractory periodontitis are smokers.3

It has been reported that probing depth is correlated to “packyears” (i.e., packs of cigarettes smoked per day multiplied by the number of years the subject has smoked). Furthermore, years of exposure to tobacco products have been shown to be a statistically significant risk factor for periodontal disease. Gingival recession, pocket depth, and probing attachment levels are related to smoking status and are proportionate to the quantity of cigarettes smoked. Smoking one cigarette per day increased probing attachment levels by 0.5%, up to 10 mm (5%), and up to 20 mm (10%). Alveolar bone height has been shown to be significantly lower in individuals smoking more than 5 g of tobacco per day. Moderate to heavy smoking (10 or more cigarettes per day) is associated with severe periodontitis. Because nicotine may cause a vasoconstriction in the peripheral blood vessels, there may be a reduction in the clinical signs of gingivitis; i.e., chronic inflammation in response to plaque. Therefore, patients may think their gingiva is healthy.11

Smokers lose more teeth than nonsmokers, and the degree of periodontal disease is directly related to the number of packs smoked per year and the number of years of smoking.3 Cigar and pipe smokers have nearly three times greater risk of having moderate to severe periodontal disease than nonsmokers. The cigar smoker is 1.3 times more likely to suffer tooth loss than nonsmokers, and pipe smokers have 1.6 times greater risk of losing teeth than nonsmokers.3

Patients who smoke do not respond well to periodontal debridement; there is a smaller reduction in probing depth and fewer gains in attachment levels compared to nonsmokers. Data shows that smokers harbor higher levels of pathogens (Bacteroides forsythus and Porphyromonas gingivalis) after treatment than former or nonsmokers. And even after five or more years of treatment, smokers are twice as likely to suffer tooth loss. Success rates for implants are also lower for smokers.

It has been reported that cigarette smoke contains 55 carcinogens that could harm a developing embryo. Researchers are looking into how genetics and the toxic chemicals found in cigarette smoke, direct or secondhand, affect tissue development, specifically how it may be linked to orofacial clefts. One study suggests that if the fetus lacks the ability to genetically produce enzymes that detoxify toxins found in smoke, the risk of cleft development is almost three times greater than average when the mother smokes fewer than 20 cigarettes a day. The risk rises to seven times greater if the mother is considered a heavy smoker, having more than 20 cigarettes a day. A 2001 published study stated that an embryo’s response to cigarette smoke is threefold and dependent upon the mother’s ability to biotransform toxins. First, the oxygen-poor environment created by the toxins damages the embryo.

Second, carcinogens are passed on to the embryo binding DNA, and third, combinations of biotransformation pathways can result in tissue exposure and damage.12

Smokeless tobacco (chewing and snuff) is popular with athletes, young adults, and older women residing in the rural South. In 25% to 30% of users, clinical attachment loss of alveolar mucosa develops adjacent to the oral site where the product is held. At least 28 cancer-causing chemicals have been identified in smokeless tobacco products.13 Holding an average-size dip in your mouth for 30 minutes gives the user as much nicotine as smoking two to three cigarettes.14

• Respiratory diseases — Patients with respiratory infections such as COPD (chronic obstructive pulmonary disease), asthma, and pneumonia have decreased lung function, making it difficult to eliminate bacteria from the lungs. Both pulmonary and periodontal pathogens have been identified in dental plaque. Aspirated from the mouth and throat into the lungs, these pathogens, along with dental decay and cariogenic bacteria, have been linked to lower-airway infections and aspiration pneumonia.15 COPD and asthma, traditionally associated with long-term smoking, are now suspected to be impacted upon by poor oral hygiene.15,16

• Medications used in treatment — There are more than 400 prescribed and over-the-counter drugs that cause xerostomia (dry mouth) as a side effect.3 Drugs, such as antidepressants, can alter the patient’s oral environment as well as the enthusiasm and ability to sustain necessary oral home care.

• Pregnancy — The American Academy of Periodontology recommends that women considering pregnancy have a periodontal evaluation. All infections are cause for concern among pregnant women because of the risk they pose to the health of the baby. Risk factors such as smoking, alcohol use, and drug use contribute to premature low-birth-weight babies. Evidence suggests that pregnant women who have periodontal disease may be seven times more likely to have a preterm low-birth-weight baby. It appears that periodontal disease triggers increased levels of biological fluids that induce labor. Furthermore, data suggests that women whose periodontal condition worsens during pregnancy have an even higher risk of having a premature baby.7 However, in the 2006 New England Journal of Medicine,17 researchers concluded that there was not a correlation between periodontal disease and an increased incidence of preterm low-weight births. This is the first article to cast doubt on information oral care professionals have been sharing with their patients since 1996. Despite this possible refutation of the previously reported data, it would seem prudent to continue to encourage oral health in pregnant women.

Clearly, the amount of information that hygienists must analyze and interpret for their patients is extensive and continually evolving. Our ability to translate and apply timely research for our patients increases patient compliance and establishes the dental hygienist as an educated, competent, caring oral health care provider.

Lois N. Dreyer, RDH, MS, is an associate professor in the Department of Dental Hygiene, New York City College of Technology.

1. 2000 Surgeon General’s Report, oralhealth/
2. University of Maryland Medical Center
3. Nield-Gehrig J, Willmann D., Foundations of Periodontics for the Dental Hygienist, Lippincott Williams & Wilkins, 2003
4. American Academy of Periodontology, “The mouth/body connection”,
5. Kimbrough V, Henderson K,. Oral Health Education, Pearson Prentice Hall, 2006
6. Miller-Keane, Encyclopedia and Dictionary of Medicine, Nursing and Allied Health, 6th edition, Saunders
8. AAP,
9. Daniel & Harfst, Mosby’s Dental Hygiene Concepts, Cases and Competencies, 2004. Mosby Publishing
10 Logothetis D. Success in Dental Hygiene, Pearson, 2009
11. Kinane DF, Chestnutt IG,. “Smoking and periodontal disease”. Crit. Rev. Oral Biol. Med. 2000; 11; 356
12. de la Torre M, Thurman M., “Cigarette smoking and Orofacial Cleft Development”. Access Magazine, Jan. 2008
13. ( American Dental Association)
15. Gulch J. “Exploring the connection: the relationship between respiratory diseases and oral health”. Dimensions of Dental Hygiene, Oct. 2009; 7(10)
16. Andrews E., Practice Management for Dental Hygienists, Lippincott Williams & Wilkins, 2007
17. Michalowicz B, et al. “Treatment of Periodontal Disease and the Risk of Preterm Babies”, N Engl J Med, 2006; 355:1885-1894

Additional references
Wilkins E., Clinical Practice of the Dental Hygienist, Ninth Ed. Lippincott Williams & Wilkins, 2005.
Axelesson P,. An Introduction to Risk Prediction and Preventive Dentistry, Quintessence Publishing Co., Inc., 1999.
Slade GD, Ghezzi EM, Heiss G, Beck JD, Riche E, Offenbacher S. “Relationship Between Periodontal Disease and C-Reactive Protein Among Adults in the Atherosclerosis Risk in Communities Study”.
MedlinePlus, www.
The American Academy of Periodontology, June 22, 2004; Journal of Periodontology Study Abstract*.
Arch Intern Med. 2003; 163:1172-1179.