There has been a renewed and increased interest in conservative periodontal care with the introduction of safe, new drugs designed for the antimicrobial host response management of periodontal disease. These treatments show promise of possibly reducing the risk of serious systemic diseases with successful, long-term stabilization of the patient’s periodontal condition.
It has been estimated by MetLife that there are now 76 million aging baby boomers.1 The proportion of adults aged 55 to 64 with periodontal disease is estimated to exceed 90%, with those aged 35 to 44 exceeding 70%.2 The prevalence and severity of periodontitis is expected to increase as the life expectancy of the population retaining natural teeth increases.
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 process. This has made it easier for the dentist to treat the diseases with a more predictable and therefore more successful result.
With an increasing number of research studies examining the possible mechanisms linking inflammatory changes in the mouth to systemic diseases, we now realize that the successful treatment of gingivitis and periodontitis can affect a patientÌs total systemic health. Knowing this connection, major healthcare providers with disease management programs for cardiac care and diabetes now authorize reimbursement under their dental plans for nonsurgical periodontal care. In the future, we may even see direct coverage for this treatment in the healthcare plan.
With the recent advances in understanding the causes of periodontal disease, we now have the opportunity to use products to help us predictably and successfully manage these chronic conditions. For example, we can use systemic drugs to modify the host destructive pathway (response to disease), place oral site-specific antimicrobial drugs, and use better oral hygiene products including antimicrobial toothpastes and mouthrinses, irrigators, power toothbrushes, and power flossers.
It is truly a new direction in treatment. As Dr. Gordon Christensen wrote in the February 2006 issue of Dentistry Today, periodontal therapy is one of the most significant needs in dentistry. Successful treatments are now available for those patients who need them. We can enhance the probability that more patients can now be treated with the confidence that their oral health will improve and remain stable.
INFLAMMATION AND PERIODONTAL DISEASE
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Figure 1. Pathway of breakdown in response to bacterial insult. |
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Figure 2. Major inflammatory mediator leading to periodontal breakdown. |
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Figure 3. Problems that prevent complete removal of bacterial insult. |
In a 1990 article by Williams, gingival disease was described as an inflammatory process characterized by increasing redness, swelling, and bleeding of the gingiva on probing.3 Williams describes gingivitis as an inflammation of the gums caused by plaque and bacterial accumulation, which can progress to a more severe state when the inflammatory process extends into the periodontal ligament and alveolar bone. He describes periodontitis as one of the causes of connective tissue loss, resorption of alveolar bone, and formation of periodontal pockets, eventually leading to the loosening and loss of teeth. Periodontitis is one of the most common causes of tooth loss in adults.
Traditional periodontal treatment has been directed toward saving teeth and preventing bone loss. Until recently we had presumed that the only way to control chronic periodontal diseases was to eliminate the pathologic oral microbiota and inflammation with traditional methods of personal bacterial plaque control, scaling and root planing, and surgery, if necessary. In 1997 Kornman4 summarized the host response to the microbial challenge in periodontitis as a response to bacterial antigens, resulting in periodontal breakdown (Figure 1). As we better understand the causes of periodontal disease, we now have an elevated probability of predictably and successfully managing this chronic condition.
Kornman reviewed the various host-derived inflammatory mediators present in both the gingival crevicular fluid and periodontal tissue, which can contribute to periodontal tissue destruction in patients with periodontitis. These mediators include cytokines (Figure 2), which can mediate inflammation and activate osteoclasts to destroy bone, as well as matrix metalloproteinase enzymes (MMPs), such as collagenase, which break down the major structural protein in periodontal tissue. These host responses have evolved to protect the body from fulminating, systemic infection, yet a prolonged host response is largely responsible for the localized tissue destruction, namely, degradation of the periodontal ligament and resorption of alveolar bone.5 Because destructive MMPs and osteoclasts directly cause tissue breakdown, the objective of periodontal treatment is to reduce or eliminate their destructive activity, avoiding the clinical manifestations of the disease.6
Periodontitis has two distinct and interconnected etiologic components: (1) bacteria adjacent to the periodontal tissues and (2) host-mediated, connective tissue-destructive responses to the specific causative bacteria and their metabolic products. Although treatment focusing on the bacterial challenge has had impact on the disease, the bacterial insult can never be completely or permanently re-moved, especially at tooth sites that are difficult to access because of deep probing depths, problems of restrictive access, root morphology (Figure 3), and ineffective plaque control.7 Because mechanical and surgical interventions cannot completely eradicate the pathologic bacteria and arrest the disease process in the long term, alternative, additional forms of therapy have been developed.
With knowledge of the role these enzymes (MMPs) play in the breakdown of periodontal tissue and the possible ineffectiveness of traditional mechanical and surgical interventions to stabilize a patientÌs periodontal condition, Golub, et al5 used tetracycline, not as a short-term antibiotic but as a host modulator drug that requires a relatively long-term regime (at least 3 months). Golub used sub-antimicrobial (no antibiotic activity) doses of doxycycline (SDD), often referred to as low-dosage doxycycline, delivered in 20-mg dosage tablets to prevent the side effects of long-term use of tetracycline. These side effects include gastrointestinal distress and emergence of antibiotic-resistant microorganisms. Golub found this low-dose regime to inhibit collagenase activity in the gingival tissues and gingival crevicular fluid. Caton, et al8 found this dosage of doxycycline to facilitate the reduction of periodontal disease progression in placebo controlled studies.
PERIODONTAL ASSOCIATION WITH SYSTEMIC DISEASE
Periodontitis has been identified as an important emerging risk factor for a number of major medical diseases, including cardiovascular disease, stroke, and type 2 diabetes, as well as for preterm, low-birthweight infants.9,10 Many studies have shown a connection between heart disease and periodontitis. Patients with severe periodontitis have been shown to be twice as likely to have a fatal heart attack and 3 times as likely to have a stroke compared to patients without periodontal disease, after adjusting for known cardiovascular risk factors,11,12 including blood lipids, cholesterol, body mass, diabetes, and smoking.
Gingivitis and periodontitis therefore can no longer be considered exclusively dental diseases or a localized infection, since they can now be associated with these other systemic diseases. Periodontal disease is now characterized by systemic inflammatory host responses that contribute to an elevation of C-reactive protein (CRP), a predictor of increased risk for cardiovascular disease. In 2001 Novak, et al showed that there was an increase in CRP levels in periodontitis patients when compared to healthy controls, after adjusting for age, smoking, body mass index, triglycerides, and cholesterol.13 There were also elevated levels of CRP associated with infection with subgingival organisms often associated with periodontal disease, including Porphy-romonas gingivalis, Prevotella intermedia, Campylobacter recta, and Bacteroides forsythus (now known as Tamerella forsythnensis). Re-cent data from cardiovascular research by Ridker has demonstrated that mild elevations in CRP, an inflammatory marker of acute phase response, appear to be associated with increased risk for both incident myocardial in-farctions and new diagnoses of peripheral artery disease in apparently healthy individuals.14
A clinical study by Genco, et al15 showed that treatment of periodontal disease caused a 65% reduction in the levels of CRP at 3 months, which remained reduced for 6 months. This suggests that periodontal disease induces CRP and possibly other in-flammatory mediators, which are known to be independent risk factors for heart disease. They postulated that periodontal disease results in bacteremias and stimulates production of factors such as TNF-alpha and IL-6, which likely stimulate the liver to make CRP. Thus, the periodontal infection can be a significant risk factor for cardiovascular disease linked through bacteremia and inflammatory mediators, and possibly immunologic factors.
Brown and Golub (2004)16 studied the clinical results of using low-dosage doxycycline in coronary syndrome patients. A double-blind study was performed, with controls receiving a placebo and the study patients, who had suffered episodes of angina or had previously documented coronary artery disease, receiving low-dosage doxycycline (20 mg) twice daily. CRP was reduced almost 50% (to almost normal levels) in the treatment group, with no change in the control patients.
Beck, et al,17 in their most recent appraisal of periodontal and coronary heart disease (2005), revisited a subset of participants in the Atherosclerosis Risk in Communi-ties Study (1996 to 1998). These patients had periodontal exams, and the exposures were periodontal status and serum IgG antibody levels against 17 periodontal organisms, with the outcome being prevalent coronary heart disease (CHD). They concluded that clinical signs of periodontal disease were not associated with CHD in both smokers and nonsmokers. However, they made a very significant conclusion: the findings indicate that the quality and quantity of the host response to oral bacteria may be an exposure more relevant to systemic athero-thrombotic coronary events than clinical measures, such as bleeding on probing and pocket depths.
We interpret this to mean that the mere presence of bacteria in the periodontal tissue, which stimulate an antibody response, can alone be a trigger to CHD, without clinical signs of periodontitis. New clinical tests are underway for a salivary test for antibody response to two major periodontal bacteria. This testing may make it possible to diagnose an increased risk for the beginning of periodontal diseases before they are clinically detectable with traditional clinical testing for bleeding on probing.
Periodontal disease, until now, has been considered exclusively an oral infectious disease, with its primary effects limited to the mouth and the periodontium. Phys-icians have not considered it in their physical exams or considered it in evaluating their patientsÌ cardiac condition. Based on this information, though, gingivitis and periodontitis should be considered for diagnosis and management of CHD if the physician wants to reduce the risk of heart attack or stroke.
DIABETES AND PERIODONTAL RISK
Periodontal disease has also been identified as being a complication of diabetes mellitus.18 It has been reported for many years that patients with diabetes mellitus have an increased susceptibility to periodontitis.19 Emrich, et al20 studied the Pima Indians residing in Arizona, who have the world’s highest prevalence of type 2 diabetes. In this population, the onset of alveolar bone and periodontal attachment loss was early, and the rate of advance was almost 3 times that of the nondiabetic patient. Proposed mechanisms for this association include the impaired neutrophil function found in patients with diabetes, 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 been shown to be suppressed, resulting in loss of alveolar bone.
However, it was also found in this population that the relationship between diabetes and periodontal disease is bidirectional. Periodontal disease can also exacerbate the diabetic condition. It has been demonstrated that diabetic patients with periodontal disease are more likely to have poor glycemic control than patients without periodontal disease.
We may presume, then, that appropriate, conservative periodontal care, supplemented with antimicrobial and host enzyme suppression management, will provide significant improvement in the patientÌs prognosis for any number of major diseases they previously had been diagnosed with. Clinical results have improved over time with continued, repeated administration, as documented in 2006 by Polson, Novak, et al.21 In our view, with conservative periodontal care, patients with diabetes may see an overall improvement in their diabetic condition.
IMPACT OF PERIODONTAL TREATMENT ON COST OF MEDICAL CARE
According to healthcare industry experts, the increased cost of care for diabetes was estimated at $132 billion for 2002, and for cardiovascular disease at $403.1 billion for 2006. Considering this, Aetna Insurance commissioned a study to assess the effects of periodontal treatment on medical costs; 144,225 insured persons were studied. The results were presented at the International Association for Dental Research meeting in March 2006. Expenditures were found to be lower for both diseases if periodontal treatment was completed for this group. No documentation was provided for use of antimicrobials with this periodontal treatment.
On May 23, 2006, CIGNA announced the expansion of its Oral Health Integration Program to include new initiatives that promote the treatment of periodontal disease for members with diabetes and cardiovascular disease. Under the new program, CIGNA Dental members who are also in the CIGNA Health Care disease management (“Well Aware”) program for diabetes and/or cardiac care may receive 100% reimbursement for out-of-pocket costs associated with periodontal scaling and root planing and periodontal maintenance.
According to Miles Hall, DDS, national dental director for CIGNA, the programs are designed to help eliminate cost as a barrier to seeking appropriate treatment. The Oral Health Integration Di-abetes and Cardiovascular Programs were created to address the emerging evidence of a connection between dental health and other systemic health conditions as a benefit for its members.
As discussed in the Au-gust 2006 Dentistry Today Viewpoint editorial, it is now our obligation to review our patientsÌ medical histories carefully to determine if they have medical conditions that may place them at elevated risk for systemic disease if they also have gingivitis or periodontitis. Clinical probing and x-ray examinations must be done for every patient to evaluate for periodontal diseases. If disease is present, it is our obligation to advise patients of their condition, its possible risk to their health, and to treat the disease as described. With recognition of the possible medical risks of periodontal disease, no longer is the patient with 4 to 6 mm of pockets and with bleeding on probing a candidate for Ïwatch and wait.Ó Early diagnosis is required. Use of newer systems for nonsurgical antimicrobial host response management, eg, the Stat-Ck,22 available on Pat-terson Dental EagleSoft Version 13.00, gives us the direction for diagnosis, simplified documentation, and guidelines for treatment. With the use of such systems, the decision to treat becomes more systematic for the dentist/hygienist (Figure 4).
Knowing the possible ad-verse affects of periodontitis/gingivitis on physical health, and recognizing that cardiologists and family physicians may be leading dentists in prescribing low-dosage doxycycline to help treat these adverse physical conditions/medical risks, the patient population will find it much easier to undertake the necessary, conservative periodontal treatment. They will want to have an early diagnosis made for their condition, with the necessary treatment provided, so they can remain healthy.
FUTURE CLINICAL OUTCOME ASSESSMENT STUDIES
In a 2005 study, Beck17 concluded that systemic exposure to more than one oral organism was related to a higher prevalence of CHD, especially in never smokers. His findings suggest that the quality and quantity of an individualÌs host response to oral pathogens, which results in clinical expression of periodontal diseases, may also be a more direct measure of periodontal disease as an exposure for CHD. Beck and his colleagues concluded that the findings of this study are relevant for future research in that they indicate that clinical measures of periodontitis may not adequately represent the systemic burden of infection and inflammation associated with periodontal diseases. Instead, they felt future researchers may want to use measures that better capture the interplay of the infection, the host immune and inflammatory responses, and the resulting clinical signs of this complex exposure that may affect general health.
The Institute for Advanced Oral/Physical Health, a nonprofit group in suburban Philadelphia, is answering this challenge. They are in the process of conducting an outcome assessment study, “Cumulative Periodontal Bac-terial Burden: The Role it Plays in Cardiovascular Disease and Diabetic Control.” Lessening the cumulative periodontal burden in patients who have had cardiac stents placed will be evaluated for its effect on inflammatory biomarkers and patient mortality.
Challenges like this must be answered if we are to treat these serious, life-threatening diseases effectively. And with our antimicrobial host response treatment necessitated by condition, not only may we save many teeth but we may also save lives!
Note: This article is the first of a 4-part series on nonsurgical periodontal therapy and its importance in periodontal as well as systemic health. Part 2 will be published in January 2007.
References
l. A Profile of American Baby Boomers. MetLife Mature Market Institute Analysis Population Projections Program. US Census Bureau. 2000. Available at: www.metlife.com/WPSAssets/ 34442486101113318029V1FBoomer%20Profile%202005.pdf. Accessed August 7, 2006.
2. Position paper: epidemiology of periodontal diseases. American Academy of Periodontology. J Periodontol. 1996;67:935-945.
3. Williams RC. Periodontal disease. New Engl J Med. 1990;332:373-382.
4. Kornman KS, Page RC, Tonetti MS. The host response to the microbial challenge in periodontitis: assembling the players. Periodontol 2000. 1997;14:33-53.
5. Golub LM, Wolff M, Roberts S, et al. Treating periodontal diseases by blocking tissue-destructive enzymes. J Am Dent Assoc. 1994;125:163-171.
6. Golub LM, Sorsa T, Lee HM, et al. Doxycycline inhibits neutrophil (PMN)-type matrix metalloproteinases in human adult periodontitis gingiva. J Clin Periodontol. 1995;22:100-109.
7. Pihlstrom BL, Ammons WF. Treatment of gingivitis and periodontitis. Research, Science and Therapy Committee of the American Academy of Periodontology. J Periodontol. 1997;68:1246-1253.
8. Caton JG, Ciancio SG, Blieden TM, et al. Treatment with subantimicrobial dose doxycycline improves the efficacy of scaling and root planing in patients with adult periodontitis. J Periodontol. 2000;71:521-532.
9. Offenbacher S. Periodontal diseases: pathogenesis. Ann Periodontol. 1996;1:821-878.
10. Page RC. The pathobiology of periodontal diseases may affect systemic diseases: inversion of a paradigm. Ann Periodontol. 1998;3:108-120.
11. Beck JD, Garcia R, Heiss G, et al. Periodontal disease and cardiovascular disease. J Periodontol. 1996;67(suppl):1123-1137.
12. Beck JD, Offenbacher S, Williams R, et al. Periodontitis: a risk factor for coronary heart disease? Ann Periodontol. 1998;3:127-141.
13. Noack B, Genco RJ, Trevisan M, et al. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol. 2001;72:1221-1227.
14. Ridker PM, Cushman M, Stampfer MJ, et al. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation. 1998;97:425-428.
15. 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. 1999;19(suppl 1):40-45.
16. Brown D, Desai KK, Vakili BA, et al. Clinical and biochemical results of the metalloproteinase inhibition with subantimicrobial doses of doxycycline to prevent acute coronary syndromes (MIDAS) pilot trial. Arterioscler Thromb Vasc Biol. 2004;24:733-738.
17. Beck JD, Eke P, Heiss G, et al. Periodontal disease and coronary heart disease: a reappraisal of the exposure. Circulation. 2005;112:19-24.
18. Loe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care. 1993;16:329-334.
19. Belting CM, Hiniker JJ, Dummett CO. Influence of diabetes mellitus on the severity of periodontal disease. J Periodontol. 1964;35:476-480.
20. Emrich J, Shlossman M, Genco RJ. Periodontal disease in nonÒinsulin-dependent diabetes mellitus. J Periodontol. 1991;62:123-131.
21. Polson AM, Novak MJ, Ryan ME, et al. Effects of combination Periostat, Atridox, and SRP on surgical needs. Presented at: IADR/AADR/CADR 83rd General Session. Abstract 2631. Baltimore, Md; March 9-12, 2005.
22. Gottehrer NR, Shirdan TA. A new guide to nonsurgical management of periodontal disease. Dent Today. 2002;21:54-59.
Dr. Gottehrer has maintained a private practice in aesthetics, periodontics, and implant dentistry in Havertown and Abington, Pa, since 1975. He is a graduate of the University of Maryland Dental School and received a certificate in periodontics from the University of Pennsylvania. He is a board-certified diplomate of the American Academy of Periodontology, a former assistant clinical professor of oral medicine at the New York University College of Dentistry, and is a staff periodontist at Abington Memorial Hospital. He can be reached at (610) 449-9500 or dr.neilg@verizon.net.
Dr. Berglund has maintained a private practice limited to periodontics and dental implants in Hyannis, Mass, since 1972. He is a graduate of the University of Oregon School of Dentistry, where he also received a MS in bacteriology. He worked at NIDR-NIH as a research associate for 3 years, received a certificate in periodontology from the University of Pennsylvania, and was a member of the board of trustees of the American Academy of Periodontology from 1997 to 2003. He is on the advisory board of the Cape Cod Community College School of Dental Hygiene and serves as a consultant to the Council on Dental Practice Massachusetts Dental Society. He can be reached at (508) 771-2606 or sebx@comcast.net.
