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Written by Neil R. Gottehrer, DDS Wednesday, 01 January 2003 00:00
Management of periodontal disease is a dynamic and ongoing process. Only recently have we begun to understand what truly happens in the progression of the disease, thus making it easier and more predictable to treat. Risk factors suggest there is an increased chance for patients to develop periodontitis, yet the recognition of these risks and selective management of them can probably reduce the long-term chances of developing periodontal disease. With the advances in understanding the causes of periodontal disease, the opportunity to use combined therapies, systemic drugs to modify the host-destructive pathway, plus locally delivered antimicrobial drugs, better oral hygiene products (such as power brushes), and the inclusion of risk-reduction treatment for the identified risk factors, we finally have the opportunity to predictably and successfully manage this chronic disease. Korman1 (Figure 1) summarized the various host-derived inflammatory mediators present in both the gingival crevicular fluid (GCF) and periodontal tissue, which can contribute to periodontal tissue destruction in periodontitis. These mediators include cytokines, which can mediate inflammation and activate osteoclasts to destroy bone as well as matrix metalloproteinase enzymes (MMPs), eg, collagenase, which can break down the major structural tissue, collagen, in the periodontal complex.1 Understanding these potential causes for the disease led to the development of a new application for tetracycline as a host modulating drug, an adjunctive agent in managing periodontal disease. With knowledge of the role these enzymes (the MMPs) play in the breakdown of periodontal tissue, Golub et al2 used tetracycline not as a short-term antibiotic but as a host modulatory drug that requires a relatively long-term regimen, at least 3 months. He used sub-antimicrobial doses of doxycycline (SDD), often referred to as low-dosage doxycycline, delivered in 20-mg dosage tablets to prevent side effects of long-term usage of tetracycline. These include emergence of antibiotic-resistant microorganisms and gastrointestinal distress. This low-dose regimen or SDD was found to inhibit collagenase activity in the gingival tissues and GCF. This dosage of doxycycline also reduced the progression of periodontal disease in placebo controlled studies.3 As this host modulating drug was developed to aid in the successful nonsurgical management of periodontal disease, we have begun to have a better understanding of how risk factors contribute to periodontal breakdown and progression of the disease. Because enhanced severity of periodontitis can result from any of these factors, identification of these risks is very important if we are to achieve our goal of successful treatment of the disease. With large numbers of patients now being identified as suffering from some form of periodontal disease, it is obvious there is increased need for periodontal care. The new therapeutic modalities now available make it easier to manage periodontal disease and predictably treat sites of persistent periodontal inflammation.4 We must be prepared to provide this care, using systems such as the Stat-Ck Periodontal Record (Dynamic Dental Systems) that offer the patient the option of treating periodontal disease nonsurgically.5
Smoking has been known to be a risk factor in other major diseases, especially cancer and heart disease. From a survey of the health of the US population, Tomar7 reported that smoking increased the relative risk of the population to periodontitis almost four times. He calculates that smoking may be responsible for more than half of the adult periodontitis cases in the United States.7 Among current smokers, 75% of their periodontitis was attributable to smoking. They suggest that a large portion of adult periodontitis may be preventable through prevention and cessation of cigarette smoking.7 Smokers have a higher number of periodontal disease sites, greater loss of alveolar bone, and increased tooth loss.8 The severity of the disease increases with both the extent and duration of the smoking exposure.9 Nicotine and other toxic substances in tobacco smoke lead to increased periodontal breakdown by altering the host's ability to neutralize infection by inducing deleterious effects on various neutrophil functions that are vital to maintenance of gingival and periodontal health.10 In a position paper written by the American Academy of Periodontology11 on tobacco use and the periodontal patient, it was stated that smoking can exacerbate periodontal disease by altering the host's response to plaque, resulting in destruction of surrounding healthy periodontal tissue and possibly even causing direct local damage to tissue that appears cumulative.
Periodontal disease has also been identified as being a complication of diabetes mellitus.12 It has been reported for many years that patients with diabetes mellitus have an increased susceptibility to periodontitis.13 Emrich and coauthors14 studied the Pima Indians residing in Arizona, who have the world's highest prevalence of type 2 diabetes. In this population, the onset of bone and attachment loss was early, and the rate of advance was almost three times that of nondiabetics. Proposed mechanisms for this association include the impaired neutrophil function found in diabetics, alterations in collagen metabolism including impaired collagen synthesis, and increased production of collagenase which degrades the collagen that makes up 90% of the organic matrix of bone. Bone formation has also been shown to be suppressed, which can promote osteopenia in the alveolar bone, with loss of crestal bone height as well as in the rest of the skeletal system. However, it has also been found that the relationship between diabetes and periodontal disease is bidirectional. While diabetes has been known to create a more severe periodontal condition, periodontal disease can also exacerbate the diabetic condition. It has been demonstrated that diabetic patients with severe periodontal disease are more likely to have poor glycemic control than patients without periodontal disease.15 From this study, it appears that the periodontal disease renders the diabetic condition more difficult to control.
Osteoporosis/osteopenia has also long been suspected as a risk factor for periodontal disease. Recently, Payne16 completed a 2-year longitudinal study of alveolar bone loss in postmenopausal osteoporotic/osteopenic women. None of the subjects were current smokers, all had a history of periodontitis, and all were participating in a 3- to 4-month periodontal maintenance program. The osteoporotic/osteopenic women in the study, compared with women with normal bone mineral density, exhibited a higher frequency of alveolar bone height loss and crestal and subcrestal density loss. Estrogen deficiency was associated with the increased frequency of alveolar bone crestal density loss. Osteopenia is reduced bone mass in the body, and represents an early stage of osteoporosis. Osteoporosis (porous bone) is a disease characterized by even greater loss of bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures of the hip, spine, and wrist. It is a major public health threat for more than 20 million Americans, 80% of whom are women. In the United States today, 10 million individuals have osteoporosis and 18 million more have low bone mass, placing them at increased risk for the disease. Combining medical care costs, lost activity, and other indirect factors, the costs of osteoporosis are estimated to reach $18 billion yearly.17
HEART DISEASE AND STROKE
Similar to the adverse systemic effects periodontal disease and its associated inflammation can have on diabetes, current information suggests that periodontal inflammation may also relate to increased risk of heart disease and stroke.18 (See Figure 3.) Beck19 confirmed this association. He hypothesized that periodontal diseases, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolitic events.19 Previous studies have demonstrated an association between periodontal disease severity and increased risk of coronary heart disease and stroke. Beck19 hypothesizes that this association may be because of an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. He further suggests that periodontal disease produces endotoxins and cytokines which initiate and exacerbate atherogenesis and thromboembolic events. Beck19 studied 1,147 men and found risk from periodontal disease for coronary heart disease, fatal coronary heart disease, and stroke to be as high as 2.8 times greater than for those without periodontal disease.19 One suspected mechanism involves periodontal bacteria gaining entry into the systemic circulation, with the bacteremia causing changes in blood vessel walls that lead to atherosclerosis. Recently, in a study of 50 human specimens removed from carotid arteries, periodontal pathogens were present in all specimens, with 26% being Porphyromonas gingivalis. It was suspected that these microorganisms may play a role in the development and progression of atherosclerosis, leading to coronary vascular disease.20 In a recent abstract presented to the 2002 Interscience Conference on Antimicrobial Agents, Dr. Caroline Genco et al21 studied the link between periodontal bacteria and heart attack. They placed P gingivalis into the mouths of mice. The bacterium were then traced as they spread from the mouth into the bloodstream and ultimately, the aorta, where they caused inflammation and accelerated atherosclerosis in 17 weeks. The results demonstrated oral infection exacerbated atherosclerotic plaque accumulation in the aorta.21 As previously described by Korman,1 cytokines are involved in the destruction of both periodontal tissue and alveolar bone. They can stimulate increased production of an important 'marker' of systemic inflammation, produced by the liner, called C-reactive protein (CRP). Genco22 recently performed a study on the relationship of cardiovascular disease (CVD), periodontal disease, and inflammatory mediators. A control group with neither CVD nor periodontal disease was studied versus patients with both diseases. The mean level of CRP in the diseased patients was almost eight times higher, a highly significant difference. The disease group was treated with scaling and root planing, resulting in a 65% reduction in CRP in 3 months, remaining at a reduced rate at 6 months. He concluded that periodontal disease induces CRP, known to be a risk factor for cardiac disease, possibly by contributing to atheroma formation, and that periodontal infection is a significant risk factor for CVD, linked through bacteremia and inflammatory mediators. Of significant interest is a study completed by Brown and coauthors23 this year. In an abstract presented as an oral presentation to the 75th Annual Meeting of the American Heart Association, they studied the effect of a 6-month regimen of low-dosage doxycycline (Periostat, Collagenex), a nonantimicrobial formulation known to decrease cytokines and MMPs, on patients with the acute coronary syndromes, which include acute myocardial infarction and unstable angina. Using low-dosage doxycycline twice/day, identical to the dosage and usage in managing periodontal disease, they observed a 60% reduction in CRP levels. There was no change seen in the placebo control group.23 These results closely parallel the responses seen by Genco in the previously mentioned clinical study where patients were treated for periodontal disease without taking the drug. In addition, in the same study Brown et al23 found that Interleukin 6 (IL 6) was significantly reduced. Increased levels of this pro-inflammatory cytokine are often detected in the acute myocardial infarction (heart attack) patient. Elevated levels of IL 6 stimulate the liver to again synthesize CRP, which correlates with reduced stability of plaque in the blood vessels, possibly resulting in thrombosis. Again, no change was seen in the placebo group. There was also a significant reduction in MMP 9 levels, which are also often increased in the acute condition. This proteolytic enzyme creates the breakdown of the collagen cap formed in the blood vessel over the atherosclerotic plaque. This 'cap' provides the body's defense to prevent thrombosis. When the cap is broken down, the plaque can rupture and result in an embolus and stroke, or heart attack. Again, there was no change in the placebo group. Additional clinical investigation studies are needed to determine the effects of periodontal treatment, in combination with use of low dosage doxycycline, on these inflammatory mediators, especially the level of CRP in the blood-stream. Recent years have seen an extension of the use of this dental medication, Periostat, in clinical studies on medical disorders such as dermatologic disorder, rosacea, and postmenopausal osteoporosis, in addition to acute coronary syndrome described previously.
ORAL BONE LOSS IN POST-MENOPAUSAL FEMALES
In a preliminary research study, Payne and Golub24 studied postmenopausal women with osteoporosis or osteopenia, presumed to be at greater risk of progressive alveolar bone loss associated with periodontitis. All of the postmenopausal patients underwent periodontal maintenance and half of them took Periostat, while the other group received placebo capsules over the 1-year time period. The group treated with the drug showed minimal loss of alveolar bone height (1.7%) and alveolar bone density (3.8%) versus the placebo group, in which the losses were almost four times greater. No sites in the treated group showed loss of attachment, and 2.4% of the sites showed a gain of greater than 2 mm, versus no sites in the placebo. The data indicated that Periostat can reduce the loss of alveolar bone height and density, and reduce attachment loss in the osteoporosis patients. A large scale clinical trial is underway now to further verify these results.
The Payne and Golub hypothesis is that sub-antimicrobial doxycycline may not only reduce bone loss supporting the teeth in these postmenopausal women, but may also increase bone density throughout their skeletons, thus reducing the severity of osteoporosis as well.
Adjunctive Management of Diabetes Mellitus
In previous studies mentioned, conducted by Genco,14 it has been suggested that advanced periodontitis in patients who suffer from diabetes mellitus can be a contributing factor to poor metabolic control of this systemic disease. A study by Grossi25 examined the effects of local debridement and systemic antibiotics on glycemic control in diabetic patients. The use of these antibiotics, along with periodontal therapy, was needed to significantly improve the metabolic controls.25 Improvement in the diabetic condition using low-dosage doxycycline, with no antibiotic activity, has been reported recently. In patients with diabetes mellitus who were administered the sub-antimicrobial 20-mg dose (Periostat), there was evidence of improved long-term glycosemic control based on reduced values of glycosylated hemoglobin (HbA1).26
Educating the diabetic patient to maintain a regular schedule of periodontal care for optimal periodontal health is a priority for these patients when discussing their treatment options with them. With more education provided to the patient regarding their condition and the options for them in managing their condition, the greater chance there is to improve their overall health.
Risks of Preterm Birth
The relationship of preterm birth to periodontal disease has also been studied. In a 1996 study, Offenbacher27 suggested that periodontal disease was associated with increased risk for preterm birth, and that as many as 18% of these births might be connected with periodontal disease. Clearly, pregnant women should be convinced by health professionals to maintain optimal periodontal condition throughout their pregnancies, through regular periodontal care, to prevent this serious risk.
Cigarette smoking has long been known to be a significant risk factor for both coronary heart disease and periodontal disease. Hyman28 conducted a study in an attempt to understand the role of smoking in the relationship between periodontal disease and heart attack history. His results suggested that cigarette smoking is a necessary cofactor in this relationship, and that the increase in risk appeared to be age dependent. However, he felt that further research was needed, particularly including longitudinal studies, to better understand the collaborating roles of smoking and periodontal disease in the etiology of coronary heart disease, including myocardial infarction.28
Because smoking cessation can slow the progression of periodontal disease, alerting dental patients who smoke about the need to quit, and making them aware of resources that can help them quit, is an important part of periodontal treatment. The severity of the periodontal disease increases with both the extent and duration of the smoking exposure. Because of staining and adverse cosmetic effects from smoking, these patients are often seen frequently in the dental practice for cleanings and stain removal, often unaware of their periodontal condition and the risk that smoking poses to their periodontal health. This is an appropriate time to alert and educate them. Most of these smoking patients want to quit. If they knew their dentist offered programs to help them stop, these would be accepted gladly by most patients. With proven smoking cessation products and a FREE QUITLINE (877-724-1090) available from the Pennsylvania Department of Health and the American Cancer Society (1-800-ACS-2345), the dentist can now help smokers quit and remain smoking free. Many states now have their own dedicated 'quit' lines.
An educational program on smoking cessation should be part of a nonsurgical periodontal treatment regime offered by the dental office. Not only can the dental staff educate the patients on the benefits of quitting, but they can also offer support for this behavioral change. One approach is to have a staff member call the patient once per week, while they are in the process of quitting, to promote compliance. A very good way to aid in quitting is to recommend to the patient that they use nicotine patches, known as nicotine replacement therapy. The dental office should purchase the patches and dispense them to the patients for the length of their program. By doing this, additional support is given and the office knows that the patient is making a genuine effort to quit.
According to the American Cancer Society publication, 'Information on Quitting Smoking,' available from the ACS, nicotine substitutes can treat the very difficult withdrawal symptoms and craving that 70% to 90% of smokers say is their only reason for not giving up cigarettes. By using the patches, a smoker's withdrawal symptoms are reduced, allowing the smoker to deal with the psychological aspects of quitting. Lack of success is often related to the onset of withdrawal symptoms. By using the patch, these symptoms are reduced and smokers who want to quit have a better chance of success.
Results of Nonsurgical Treatment
In a recent study by Dr. John Novak,29 treatment of aggressive periodontal disease by a regimen of repeated mechanical debridement plus adjunctive systemic therapy with Periostat resulted in average reductions in pocket depth of 3 mm or more; 70% of the patients who completed the study were current or past smokers.29 It seems clear from this study that the evidence presented provides good reason for all dentists to use this combined approach as part of their nonsurgical treatment for patients with advancing conditions of periodontitis, and in patients who are smokers and unable to stop their habit. Success with this treatment may stimulate quitting for the patient who previously thought there was no hope for their smoking-related condition to improve. With the recognition of the possible medical risks of periodontal disease, no longer is the patient with 4- to 6-mm pockets a candidate for 'watch and wait.' Early diagnosis is required. Use of newer systems, eg, the Stat-Ck5 for nonsurgical management, gives us direction in diagnosis, simplified documentation, and guidelines for treatment. With the use of this system, the decision to treat by the dentist/hygienist becomes much more systematic. Knowing the possible adverse affects of periodontitis on physical health, and recognizing that physicians may possibly be following dentists in prescribing low- dosage doxycycline to help treat these adverse physical conditions (medical risks), our patient population will find it much easier to accept the necessary periodontal nonsurgical treatment. They will want to have an early diagnosis and treatment of their periodontal condition because they want to remain healthy.
With new treatment combinations, and our knowledge of how best to manage the risk factors contributing to periodontal disease, we will be able to provide our patients with a better clinical outcome nonsurgically, and help our patients to improve and maintain their overall health.
The author would like to acknowledge the advice received from Dr. Lorne Golub, professor of oral biology and pathology, SUNY at Stonybrook School of Dental Medicine, while preparing this manuscript.
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6. Genco R. Current view of risk factors for periodontal diseases. J Periodontol. 1996;67:1041-1049.
7. Tomar SL, Asma S. Smoking- attributable periodontitis in the United States: Findings from NHANES III. J Periodontol. 2000;71:743-751.
8. Axelsson P, Paulander J, Linde J. Relationship between smoking and dental status in 35-, 50-, and 75-year-old individuals. J Clin Periodontol. 1998;25:297-305.
9. Bergstrom J, Eliasson S, Doch J. Exposure to tobacco smoking and periodontal health. J Clin Periodontol. 2000;27:61-68.
10. Haber J, Wattles J, Crowley M, et al. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol. 1993; 64:16-23.
11. American Academy of Periodontology Position Paper: Tobacco Use and the Periodontal Patient. J Periodontol. 1996;67:51-56.
12. Loe H. Periodontal disease. The sixth complication of Diabetes Mellitus. Diabetes Care. 1993;16:329-334.
13. Belting CM, Hiniker JJ, Dummett CO. Influence of diabetes mellitus on the severity of periodontal disease. J Periodontol. 1964;35:476-480.
14. Emrich J, Shlossman M, Genco RJ. Periodontal disease in non insulin dependent diabetes mellitus. J Periodontol. 1991;62:123-130.
15. Taylor GW, Burt BA, Becker MP, Genco RJ, et al. Severe periodontitis and risk for poor glycemic control in patients with non-insulin dependent diabetes mellitus. J Periodontol. 1996;67(vol. 10 suppl.):1085-1093.
16. Payne JB. Reinhardt RA, Nummikoski PV, et al. Longitudinal alveolar bone loss in postmenopausal osteoporitic/osteopenic women. Osteoporos Int. 1999;10:34-40.
17. Wactawshi-Wende J, Grossi SG, Trevisan M, et al. The role of osteopenia in oral bone loss and periodontal disease. J Periodontol. 1996;67
18. Loesche WJ. Periodontal disease as a risk factor for heart disease. Compend Contin Educ Dent. 1994;15:976-992.
19. Beck J, Garcia R, Heiss G, Vokonas PS, et al. Periodontal Diseases and Cardiovascular Disease. J Periodontol. 1996;67(suppl.):1123-1137.
20. Haraszthy VI, Sambon JJ, Trevisan M, et al. Identification of periodontal pathogens in Atheromatous plaques. J Periodontol. 2000;71:1554-1561.
21. Gibson FC, Hong C, Wang J, Genco C. Oral infection with invasive P gingivalis stimulates accelerated atherosclerotic plaque formation in ApoE Mice. Abstract presentation. Interscience Conference on Antimicrobial Agents, San Diego, 2002.
22. Genco RJ, Glurich I, Haraszthy V, et al. Overview of risk factors for periodontal disease and implications for diabetes and cardiovascular disease. Compend Contin Educ Dent. 1998;19(suppl):40-46.
23. Brown DL, Desai K, Vakili BA, et al. Clinical and biochemical results of the metalloproteinase inhibition with low dose doxycycline to prevent acute coronary syndromes (MIDAS). Pilot trial. 2002. American Heart Association Annual Meeting, Abstract Oral presentation 2253.
24. Payne JB, Reinhardt RA, Nummikoski PV, Golub LM. Doxycycline effects on oral bone loss in postmenopausal women. J Dent Res. 2001:80:55.
25. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatment of periodontal disease diabetics reduces glycated hemoglobin. J Periodontol. 1997;68:713-719.
26. Ryan M. Clinical applications for host modulatory therapy. Comp Cont Dent Educ. 2002;23:1-12.
27. Offenbacher S. Katz V, Fertik G, et al. Periodontal disease as a possible risk factor for preterm low birth weight. J Periodontol. 1996;67:1103-1113.
28. Hyman J, Winn D, Reid B. The result of cigarette smoking in the association between periodontal disease and coronary heart disease. J Periodontol. 2002;73:988-994.
29. Novak, MJ, Johns LP, Miller C, et al. Adjunctive benefits of subantimicrobial dose doxycycline in the management of severe generalized chronic periodontitis. J Periodontol. 2002;73:762-769.
Disclosure: Dr. Gottehrer is chief medical officer of Dynamic Dental Systems, Inc, which developed the Stat-Ck System.
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