A Future for Periodontal Therapy

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Cardiovascular disease (CVD), the leading killer of men and women in the United States, is a major public health issue contributing to 2,400 deaths each day. Periodontal disease, a chronic inflammatory disease that destroys the bone and gum tissues that support the teeth, affects nearly 75% of Americans and is the major cause of adult tooth loss. And while the prevalence rates of these disease states seem grim, research suggests that managing one disease may reduce the risk for the other.

BACKGROUND: CONSENUS PAPER RECENTLY PUBLISHED
A consensus paper of the relationship between heart disease and gum disease was recently published concurrently in the online versions of 2 leading publications, the American Journal of Cardiology, a publication circulated to 30,000 cardiologists, and the Journal of Periodontology (JOP), the official publication of the American Academy or Periodontology (AAP).

DENTIST-PHYSICIAN COLLABORATION
This paper followed publication of an original paper authored by Drs. Marvin J. Slepian and Neil R. Gottehrer, “Oral-Body Inflammatory Connection,” published in Dentistry Today in January 2009.4 In that paper, the oral-systemic disease connection was clearly established. The connection hypothesis is logically extended for the physician, who is encouraged to work with the dentist to request his/her cardiac patient’s periodontal status. It allows them to work with the dentist in managing the patient at risk for CVD.

For the first time, a formal communication program between the patient’s dentist and the physician is established. The STAT-CK Periodontal Risk Assessment (STAT-CK PRA) is completed by the dentist. It is then faxed to the physician with a Physician Fax Transmittal Form, requesting key blood studies to be done by the physician, including a high-sensitivity C-reactive protein and hemoglobin A1C. With the physician ordering these tests for the patient at risk periodontally, it automatically involves the physician in the dental evaluation and establishes a friendly relationship for patient management with use of these standardized communication forms.

The consensus paper was developed in concert by cardiologists, the physicians specializing in treating diseases of the heart, and periodontists. The paper contains clinical recommendations for both medical and dental professionals to use in managing patients who have or are at risk for either disease. Cardiologists may now examine a patient’s mouth, and periodontists may begin asking questions about cardiac health and a familial history of heart disease.

In addition to the clinical recommendations, the consensus paper summarizes the scientific evidence that links periodontal disease and CVD and explains the underlying biologic and inflammatory mechanisms that may be the basis for the connection.

Informing the Patient
The clinical recommendations presented in the consensus paper suggest that periodontists inform their patients of the increased risk of CVD associated with periodontal disease and assess their risks and guide them to be evaluated for the major cardiac risk factors. The paper also recommends that physicians managing patients with CVD evaluate the mouth for the basic signs of periodontal disease such as tooth loss, visual signs of oral inflammation, and receding gums.

Hopefully, future research will be able to identify a direct relationship between periodontal disease and CVD. While recent research has been focused on the role of inflammation and the body’s immune response to combat infection, this inflammation initially can have a limited protective effect. If the inflammation is untreated, it can lead to increased disease in the protective, affected tissues and result in other health problems developing which may be more severe.

An Important First Step
According to Kenneth Kornman, DDS, PhD, editor of the JOP and a co-author of the consensus report, and David Cochran, DDS, PhD, president of the AAP and chair of the Department of Periodontics, University of Texas Health Science Center at San Antonio, “the cooperation between the cardiology and periodontal communities is an important first step in helping patients reduce their risk of these associated diseases.”

“Inflammation is a major risk factor for heart disease, and periodontal disease may increase the inflammation level throughout the body. Since several studies have shown that patients with periodontal disease have an increased risk for CVD, we felt it was important to develop clinical recommendations for our respective specialties. Therefore, you will now see cardiologists and periodontists joining forces to help our patients. Both periodontal disease and CVD are inflammatory diseases, and inflammation is the common mechanism that connects them. The clinical recommendations included in the consensus paper will help periodontists and cardiologists control the inflammatory burden in the body as a result of gum disease or heart disease, thereby helping to reduce further disease progression, and ultimately to improve our patients’ overall health, our common goal.”

Periodontitis (Figure 1), a bacterially induced, localized, chronic inflammatory disease, destroys connective tissue and bone that support the teeth. Periodontitis is common, with mild to moderate forms affecting 30% to 50% of adults and the severe generalized form affecting 5% to 15% of all adults in the United States. Periodontitis has even higher prevalence in developing countries and considerable global variation, although the prevalence of the severe generalized disease appears to be similar in most populations.

Periodontal Risk Assessment
PRA for cardiac disease has become a very important part of the process of managing oral systemic health. Demmer and Desvarieux, in 2006, reported that oral infection models have emerged as useful tools to study the hypothesis that infection is a CVD risk factor. After studying the reported associations between periodontal disease and CVD, they stated that periodontal infections are a leading culprit. They believe that an association exists between the 2 diseases, but indicate that it is unknown if it is causal or coincidental. They indicate that studies have enhanced the specific of infectious exposure definitions by measuring systemic antibodies to selected periodontal pathogens or by directly measuring and quantifying oral microbiota from subgingival dental plaque. They also indicate that results from these studies have shown positive associations between periodontal disease and CVD. They conclude that evidence supports an association between periodontal infections, atherosclerosis, and vascular disease.8

Because of the oral-body inflammatory connection and association, clinical treatment studies have been performed to evaluate the effect of aggressive treatment of periodontal disease on the degree of heart disease. In April 2009, Piconi, et al published a study showing that treatment of periodontal disease resulted in improvement in atherosclerosis and reduced narrowing of the carotid artery intimamedia thickness. The results clearly indicated a strict association existing between periodontal disease and atherosclerosis, suggesting that periodontal disease is an independent risk factor for the development of atherosclerosis and is a significant predisposition for the disease.

A periodontal exam is recommended for every dental patient and should be conducted on follow up care as indicated by the condition of the mouth. An abbreviated exam, the STAT-CK PRA Periodontal Record, has been developed for screening and probing by Dr. Neil Gottehrer (Figure 2). All the teeth are probed circumferentially, with formal recording postponed for a future visit. The patient status is then graded A to F, A being no risk and F being a failing condition with major risk for disease as well as loss of teeth. The mouth is examined in quadrants with a risk grade given for each quadrant.9 The implementation of the STAT-CK PRA in the dental practice is described in Evaluation and Management of the Oral Body Inflammatory Connection: Resource Guide, published by ChaseHealthAdvance in 2009. The form can be forwarded to the physician, with a copy given to the patient, to establish a connection with the physician, presumably helping to improve the patient’s long term health as a result of the communication and combined treatment of the patient.
TREATMENT
All appropriate treatment strategies for periodontitis focus on the resolution of gingival inflammation and healing of the soft- and hard-tissue attachment of the teeth to the alveolar process by removal of the bacterial biofilm attached to the tooth roots and reinforcement of patient oral hygiene to reduce bacterial regrowth. Antibiotics locally delivered into the periodontal pockets, eg, Atridox (TOLMAR) (Figure 3), have been approved by the United States Food and Drug Administration (FDA) as an adjunct to conventional bacterial removal in the management of periodontitis. Antibiotics markedly reduce the bacterial load but taken alone do not usually eliminate periodontal pathogens in the oral cavity. Antibiotics may transiently improve sites of periodontitis when combined with mechanical debridement to disrupt the subgingival biofilm.

Golub and associates developed the host-modulating, subantimicrobial dose Periostat (low dose doxycycline) drug that reduces the clinical signs and symptoms and progression of periodontitis. Periostat (CollaGenex Pharmaceuticals) (Figure 4) is a matrix metalloproteinase inhibitor, the only FDA-approved host-modulating drug for the treatment of periodontitis.

A 6-month, randomized, multicenter, placebo-controlled, examiner-masked study was undertaken by Novack, et al to evaluate the clinical usefulness of a combination treatment of systemically delivered HMT (low-dose doxycycline hyclate; 20 mg, twice a day) plus locally delivered TAT (doxycycline gel, 10%) in combination with SRP (experimental group) versus SRP + placebo (control group) on clinical measures of periodontal disease. The results of the randomized, multicenter study support the use of a combination of adjunctive therapies for the nonsurgical management of chronic periodontitis. This study was the first to report the use of a combination of SRP, TAT, and HMT in the treatment of chronic periodontitis. At 6 months, 3 times as many subjects in the combination therapy group had no residual pockets less than 5 mm compared to the SRP + placebo group. Pocket depth reduction to less than 5 mm occurred more rapidly and more extensively with combination therapy.

In the Novak13 study, the endpoint of nonsurgical therapy is an important clinical question that was not addressed. Although this study continued for 6 months, with test and control treatments provided at baseline and at 3 months, it was clear from the observed reductions in pocket depth, bleeding on probing and gains in clinical attachment that a continuation of the intervention protocol may have resulted in further improvements.

Advanced periodontitis (moderate to severe bone loss and gingival probing depth less than 5 mm) may require surgery to gain adequate access for removal of the bacterial biofilm and residual calculus on the root surfaces. In some instances, surgical approaches include bone and soft tissue regeneration to regain at least some support for the teeth and to facilitate bacterial control. Excessive tissue can now be easily achieved with a bipolar BIDENT Surgical System (Figure 5). It can also be used to prevent tissue bleeding following periodontal treatment for patients who are on anticoagulant therapy.

CONCLUSION

The future of periodontal therapy is very promising and appears to have the opportunity to reduce medical risk. With periodontal assessment and screening exams done for those patients who require treatment, and combined management from the physician and dentist for these chronically inflammed conditions, reduction of medical risk can be possible, with benefit to everyone and an anticipated healthier population.

        

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[Anonymous]

Long-term low-dose use of antimicrobials for periodontal therapy does not produce drug resistance. The guidelines for prescribing antibiotics in dentistry have changed significantly in recent years. Today, the American Dental Association has drastically reduced the number and types of patients who require prophylactic antibiotics before dental procedures to avoid producing oral bacteria with drug resistance. However, periodontists are currently prescribing long-term low doses of doxycycline for many of their recalcitrant periodontal patients. Does long-term doxycycline create resistant strains of bacteria? This issue was evaluated in the Journal of Periodontolgy (2000;71:1472–1483). This article compared 4 previous studies by the authors(Thomas J, Walker C, Bradshaw M.) in which subantimicrobial doses of doxycycline were given to adult periodontitis patients. In all studies, up to 20 mg of doxycycline were given 4 times a day to these patients. Then the resistance of oral microbes was evaluated with a variety of tests. The results of this study show that there were no statistically significant differences in the proportion of doxycycline-resistant bacteria among the treatment groups and no evidence of multiantibiotic resistance. In conclusion, long-term subantimicrobial doses of doxycycline do not alter or contribute to alterations in the antibiotic susceptibility of the subgingival microflora compared with a placebo.

        

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