Dental-hygiene therapy is no longer limited to maintaining healthy teeth and periodontal tissues.
Trisha E. O`Hehir, RDH, BS
Good oral health is desirable, not only for the teeth and gums, but also for general health and longevity. Periodontal disease has been linked to preterm, low-birthweight babies, heart disease, lung disease, diabetes, and peptic ulcers.
Your patients may have asked about these links, if they`ve read any of the articles appearing in newspapers and magazines lately. If they haven`t asked, you may want to be sure they`re aware of these new findings. The following information is taken from the "Oral Health Update," Vol. 1, #2, which is produced by Perio Reports for dental office patients. For more information, call (800) 374-4290.
Preterm, low-birthweight babies
Pregnant women with periodontal disease are 7 1/2 times more likely to have a premature, low-birthweight baby. Alcohol and smoking also are risk factors, but they increase the risk by only 1 to 2 1/2 times.
Prostaglandin, an enzyme produced during periodontal disease, is the same enzyme that pregnant women produce to dilate the cervix and induce labor. When prostaglandin enters the blood stream from the gingival tissues, before the baby is due, it can induce premature delivery. Oral bacteria also can enter the blood stream, traveling to the uterus and potentially creating problems for the fetus.
Babies born early are often of low birthweight, weighing less than 5 pounds, 8 ounces. Low-birthweight babies are prone to severe physical problems. If controlling periodontal disease in pregnant women proves to reduce the incidence of preterm, low-birthweight babies, the high financial and emotional burden of these problems also would be reduced.
Heart disease took nearly a half million lives in the United States in 1997. It is the largest, single killer of Americans, responsible for 20 percent of all deaths. Periodontal disease is linked to cardiovascular disease, although it has not been demonstrated as a direct cause of heart attacks.
Several theories have been suggested to explain this link. For example, oral bacteria may enter the blood stream and directly infect the lining of blood vessels, leading to heart attack or stroke. The toxins associated with periodontal disease are linked to the accumulation of fatty deposits on blood-vessel walls and may trigger blood-clot formation. Another theory suggests that greater quantities of pro-inflammatory substances are secreted as a result of gum disease, causing not only bone loss around the teeth, but also the inflammation associated with atherosclerosis.
An analysis of survey data on nearly 6,000 adults found heart attacks reported by 4 percent of the group. Missing from this group were those who had a heart attack and died as a result, suggesting that perhaps the incidence of heart attacks and any estimates of association between periodontal disease and heart disease may be higher than predicted. Based on these figures, people with the greatest amount of attachment loss were 3 times more likely to have been told they had a heart attack.
Studies have demonstrated that a short-term, high-fat diet compromised the antibacterial function of white blood cells (PMNs, polymorphonuclear leukocytes) and increased release of superoxide. Altered PMNs are associated with damage to periodontal tissues, heart valves, lungs, and kidneys. Host resistance may be impaired by an ongoing state of hyperlipidemia.
Laboratory studies on rats demonstrated that elevated serum lipids and the systemic presence of periodontal pathogens can trigger the release of pro-inflammatory cytokines. These cytokines can alter fat metabolism, resulting in elevated triglyceride levels. Poorly controlled diabetics with high cholesterol levels also have higher levels of gingival inflammation.
Long-term changes in fat metabolism linked to periodontal pathogens may add adult periodontitis to the list of risk factors for coronary artery disease. As more research is provided, we may be advising patients of the importance of good periodontal health to reduce cholesterol and triglyceride levels.
Billions of dollars are spent each year in the U.S. treating respiratory infections. Bacteria from the oropharyngeal mucosa cause bacterial pneumonia. Pneumonia acquired during a hospital stay often is caused by bacteria from the hospital environment. More than 5 percent of hospital patients will develop an infection of some sort, and 20 percent of those infections will be pneumonia. Acquiring infections will prolong hospital stays, increase costs, result in significant illness, and, in some cases, death. It is estimated that 30 percent of the 300,000 hospital-acquired pneumonia cases each year lead to death.
Healthy adults have a pulmonary defense system to keep the airway sterile. Infection results from a defect in the host response, introduction of a virulent pathogen, and/or an overwhelming number of bacteria. A critical factor is colonization of mucosa in the mouth and throat by respiratory pathogens. As mucosal cells shed, these pathogens, now in the saliva, are aspirated into the lungs.
Several theories are suggested to explain how respiratory pathogens adhere to the mucosal surfaces of the oral cavity. Enzymes produced by periodontal pathogens may change respiratory pathogens or receptor sites on the mucosa to allow colonization. Products from the periodontal pocket also may play a role.
Oral pathogens, such as Aa and P. gingivalis, are known to cause lung infections. Plaque biofilm in the mouth provides an environment for respiratory bacterial colonization. Teeth and periodontal tissues may serve as reservoirs for respiratory infection, with poor oral hygiene as a risk factor for aspiration of bacteria. Good oral hygiene is a key factor in reducing the incidence of respiratory infection in high-risk subjects. For patients and caregivers of those at risk, oral-hygiene techniques and instructions need to be improved to ensure effectiveness. Professional deplaquing every 48 hours may be a cost-effective means of preventing respiratory infection for hospitalized and other at-risk patients.
We see the two-way street effect with diabetes and periodontal disease. Periodontal disease in diabetics makes controlling the diabetes more difficult. and uncontrolled diabetes leads to more periodontal disease. Due to a compromised immune system, diabetics are twice as likely as nondiabetics to have periodontal disease.
Bacteria that cause ulcers are called helicobacter pylori. This bacteria is found in saliva and bacterial-plaque biofilm. The mouth may be a prime breeding ground for the bacteria that cause ulcers. If ulcers have been treated, and then return, it may be that periodontal pockets are harboring helicobacter pylori bacteria.
Dental-hygiene therapy is no longer limited to maintaining healthy teeth and periodontal tissues. It may be a key factor in maintaining general health and longevity. Be sure you and your patients understand these links and keep an eye on the research to learn more.
Trisha E. O`Hehir, RDH, BS, is a senior consulting editor of RDH. She also is editor of Perio Reports, a newsletter for dental professionals that addresses periodontics. The Web site for Perio Reports is www.perioreports.com. She can be reached by phone at (800) 374-4290 and by e-mail at trisha@