Copyright C Munksgaard 2000

Periodontology 2000, Vol. 23, 2000, 912

Printed in Denmark All rights reserved

PERIODONTOLOGY 2000
ISSN 0906-6713

Periodontal medicine:
the emergence of a new branch
of periodontology
R AY C . W ILLIAMS & S TEVEN O FFENBACHER

We are pleased to present this volume of PERIODONTOLOGY 2000, which focuses on the subject of periodontal medicine. In many ways, periodontal medicine is a fairly new term in periodontology and likely
new to many in dentistry and certainly to most outside of dentistry. What, then, does the term periodontal medicine mean or imply? If one defines
periodontal as pertaining to the periodontium, and
medicine as treating disease by nonsurgical means,
periodontal medicine could be used to describe the
treatments for periodontal disease that are nonsurgical. Thus, this volume of PERIODONTOLOGY 2000
would focus on the emerging use of antimicrobials
and antibiotics, as well as host-modulating agents,
as adjuncts to scaling and root planing in the management of the periodontal diseases. And clearly a
new branch or arm of periodontology is emerging to
include a medical approach, in addition to a mechanical or surgical approach, in managing disease.
But this definition of periodontal medicine, while
adequate, seems short of the mark. Another possible
definition of periodontal medicine could be the
science of the treatment of the diseases of the periodontium. But this definition would necessarily include mechanical or surgical approaches and would
defeat the purpose of focusing on medicine. Thus,
this definition also does not appear to reflect current
understanding of the term periodontal medicine.
What, then, do the editors of this volume of PERIODONTOLOGY 2000 mean by periodontal medicine?

Definition of periodontal medicine

We view the term periodontal medicine, as first suggested by Offenbacher (7), to be a broad term that
defines a rapidly emerging branch of periodontology
focusing on the wealth of new data establishing a

strong relationship between periodontal health or

disease and systemic health or disease. This means
a two-way relationship in which periodontal disease
in an individual may be a powerful influence on an
individuals systemic health or disease as well as the
more customarily understood role that systemic disease may have in influencing an individuals periodontal health or disease. Logically included in this
definition would be new diagnostic and treatment
strategies that recognize the relationship between
periodontal disease and systemic disease.
We are aware that, in many ways, certain aspects
of periodontal medicine have been part of dentistry
for a long time. The possible contribution of oral
bacteria in periodontal pockets to bacterial endocarditis has been acknowledged for decades. On the
complementary side, the contribution of systemic
diseases, such as diabetes, to the severity of periodontal disease has been recognized for many years
(5). In the last decade, studies of HIV infection and
AIDS have further pointed to the influence of systemic disease on the periodontium. But from our
perspective, it is the recent research that increasingly
substantiates a role for periodontitis in affecting systemic health that has brought the term periodontal
medicine to the forefront, and as such has fostered
a new branch of periodontology.
After reading the next chapter in this volume,
authored by Paul OReilly and Noel Claffey, the
reader will well note that the contribution of periodontitis, or the oral cavity, to systemic disease has
been written about since ancient civilization. And
certainly all students of dentistry are well familiar
with the proclamations of William Hunter in the first
part of this century, attesting to the influence of oral
sepsis on systemic health and disease. However, it is
important to note that, until very recently, all information on the effect of periodontal disease on sys-

Williams & Offenbacher

temic health was anecdotal at best, and all the writings through the ages were for the most part mythological musings by a diverse group of dentists and
physicians. Thus, it is in fact only very recently that
scientists and clinicians have begun to provide an
increasing body of scientific evidence suggesting
that moderate untreated periodontitis may affect an
individual systemically, and may contribute to cardiovascular disease, diabetes and pre-term low birth
weight. This is important new information indeed. It
appears that not just teeth are at stake in maintaining good oral health. Rather, oral health is an important component of general health, and individuals with periodontitis may be at risk for other diseases as well.

Periodontitis and systemic health

Recent research has established that periodontal infection is a probable risk factor for cardiovascular
disease, including atherosclerosis, myocardial infarction and stroke (13, 6, 12). For example, patients
with severe periodontitis are almost twice as likely
to have a fatal heart attack and three times as likely
to have a stroke as patients without periodontal disease, even after adjusting for known cardiovascular
risk factors such as blood lipids, cholesterol, body
mass, diabetes and smoking (1, 2). Furthermore, preliminary studies suggest that periodontitis may also
contribute to adverse pregnancy outcomes, diabetes
and other conditions (5, 8, 9, 13). Currently, the aims
of periodontal therapy are to prevent loss of the dentition, as well as restoration of periodontal form and
function. No periodontal treatment protocols are
available that are specifically designed to improve
systemic health. One might wonder therefore
whether the treatments used to prevent periodontal
attachment and bone loss are also optimal for preventing systemic risk. We do not know whether the
treatments to reduce the oral microbial and inflammatory burden of periodontitis and the clinical
end-points that are currently used to manage periodontitis are sufficient or even appropriate to manage these systemic problems. Optimal treatments
may be totally different for a high-risk individual. As
an example, current periodontal maintenance programs may prevent attachment loss but may not be
sufficient to prevent the inflammatory response
leading to a heart attack in the susceptible individual. The chapter by Ebersole & Capelli discusses the
effect of periodontal infection on systemic inflammation. New information suggests that periodontal

10

infection elicits a mild acute-phase response that

changes systemic blood chemistry. Hemocytology
data indicate that the dental profession must now
embrace traditional medical diagnostic tools to
manage the systemic sequela of oral infection. Dentists of the future will need to understand routine
medical diagnostic tests used to monitor patients
with systemic conditions that are modified by oral
infection. The impact of oral infection on systemic
health thus further defines the new branch of periodontology termed periodontal medicine.
Dentistry has an urgent need for new information
to enable the profession to identify who needs treatment and how to treat these individuals. Reducing
the systemic risk associated with periodontitis requires new diagnostic tools and a set of clinical
guidelines for treatment. In essence, a new standard
of care needs to be created. Dentists and periodontists are trained to save teeth, but clinical
guidelines to manage oral infection to protect systemic health represent a gap in knowledge. Although
the current therapies used to manage periodontitis
may be adequate to simultaneously manage systemic sequelae, there have been no studies to
measure the systemic impact of periodontal treatments.

New diagnostic and

monitoring tools
As already noted, periodontitis can no longer be
considered simply as a chronic localized infection
that places only the dentition at risk. Rather, periodontitis is also significantly associated with several
systemic conditions, including myocardial infarction, stroke and pre-term delivery. Although the
underlying mechanisms linking these conditions remain largely unknown, new data have indicated that
periodontitis can elicit a systemic inflammatory response by activating the hepatic acute phase response. This occurs presumably as a consequence of
the systemic appearance of transient and recurrent
bacteremia of oral origin, which has been a longrecognized characteristic of periodontal infections. It
is significant that periodontal infections are best
characterized as chronic and low-grade in nature but
can have short periods of acute activity. Cross-sectional evidence indicates that periodontitis elicits a
mild elevation in markers of the acute-phase response, including C-reactive protein, haptoglobin,
a1-antitrypsin and fibrinogen. The liver, in response

Periodontal medicine: the emergence of a new branch of periodontology

to the systemic challenge of organisms, secretes

acute phase proteins. This acute-phase response is
triggered by blood-borne oral lipopolysaccharide,
and oral bacteria which elicit the release of the cytokines interleukin-6 and tumor necrosis factor a.
These mediators act in the liver to induce the acutephase response and hepatic secretion of these serum
acute phase proteins. Recent data generated in cardiovascular research have demonstrated that mild
elevations in markers of the acute-phase response,
especially C-reactive protein appear to be associated
with increased risk for both incident myocardial infarction and new diagnoses of peripheral artery disease in apparently healthy individuals (10, 11). Until now, periodontitis has been viewed as a generally
asymptomatic disease that is not typically considered in medical physical evaluations. However, it
can be one potential trigger of a mild acute-phase
response, inducing a shift into the high-normal
range to a level similar in magnitude to that associated with increased cardiovascular risk. Thus, it is
not unreasonable to hypothesize that measures of
periodontal infection should be considered as one
of the potential underlying causes of both increased
levels of acute-phase response proteins and the attendant increase in cardiovascular risk; but this concept remains untested. It now appears that measures
of the acute-phase response should be considered in
the diagnosis and management of the periodontitis
patient if one wants to reduce risk of myocardial infarction or stroke.
The mild elevation in C-reactive protein is one example of the measures that are typically evaluated
by blood chemistry analyses. Other markers of the
acute-phase response that are associated with both
periodontitis and cardiovascular risk include elevations in white blood count, increased levels of a1antitrypsin and haptoglobin, increased levels of fibrinogen and decreases in albumin. Levels of C-reactive protein and haptoglobin have been shown to
decrease following scaling and root planing and
treatment with nonsteroidal anti-inflammatory
drugs (4). The fact that periodontitis progression and
resolution changes systemic blood chemistry and
hemocytology represents a critical new development
in periodontology and dentistry in general. Suddenly, the potential application of blood analyses to
diagnose, treat and monitor periodontitis patients
for assessing cardiovascular risk and the effects of
periodontal therapy truly represents the practice of
medical principles in periodontology. Furthermore,
the acute-phase response is only one dimension that
may provide diagnostic and prognostic information.

Infectious burden, cytokine responses, genetic cytokine polymorphisms, oxidative stress markers and
other tests are likely to be necessary in the armamentarium of the clinician of the future. Dentists are
not currently trained in applying these diagnostic
tools, because they have not done the necessary research to define the utility of these markers. It is
known that they are different in periodontitis patients, that they reflect increased risk, and that some
of them appear to change following periodontal
treatment with either mechanical or chemotherapeutic approaches. But the collective benefit of a historical empiricism gathered by master clinicians over
time to provide clinical guidance in periodontal
medicine is lacking. Dentists know how to diagnose
and treat periodontitis to save teeth but not how to
recognize periodontitis syndromes that have systemic involvement nor how to treat periodontitis to
alter systemic complications of periodontitis.

New therapies
Although multiple studies link periodontitis to systemic conditions such as cardiovascular disease (12),
no intervention studies have demonstrated the potential beneficial effects of periodontal therapy on
these systemic outcomes. Clinical scientists have no
experience to appreciate how to use this new information nor do they understand how the different
therapies may impact the surrogate markers of systemic diseases, such as monitoring C-reactive protein in cardiovascular disease. Some of the potential
microbial, cellular and molecular mechanisms
linking these conditions are being elucidated, but it
is not known whether the therapies designed to treat
periodontitis and retain the dentition are adequate
or appropriate to prevent systemic disease. For example, the pocket bacteria that are recognized
pathogens with regards to causing attachment, bone
or tooth loss may not be the same critical pathogens
for enhanced risk for myocardial infarction. Furthermore, the suppression of the oral microbial flora and
the local inflammatory response to prevent periodontal disease progression may not be sufficient to
prevent systemic complications in certain high-risk
patients. All of these uncertainties highlight the inability to counsel the dental profession on the optimal therapy for these patients. Nonetheless, the
challenge is clear. Understanding and managing the
impact that oral infection has on systemic health defines periodontal medicine. Filling this void in
knowledge would appear to be a timely and bold

11

Williams & Offenbacher

challenge to the profession as well as an unprecedented opportunity for the development of novel
therapies.

New educational responsibilities

It appears highly likely that the new knowledge being
gained in the discipline of periodontal medicine will
serve as an impetus to further coalesce medicine
and dentistry. Dentists will need to assume a larger
responsibility for the overall health of patients, and
eventually periodontal care may become a medical
necessity. Knowledge of relevant systemic conditions
needs to be more extensive to enable dentists to interact more meaningfully with their medical colleagues. This will place new educational goals on the
profession. Hopefully, this volume of PERIODONTOLOGY 2000 will lead to the creation of a new body of
clinical information specifically for the dental profession to meet this need. Dental clinicians are likely
to have different diagnostic criteria and therapeutic
end-points than physicians. For example, how much
of a drop in glycosylated hemoglobin represents a
reasonable therapeutic outcome following periodontal medicine therapy in a diabetic patient? Periodontitis also contributes to the metabolic dysregulation associated with the development of non-insulin-dependent (type 2) diabetes, as evidenced by
impaired fasting glucose. What therapeutic benefit
should be expected in measures of fasting glucose
following therapy in a pre-diabetic patient? Over the
next decade answers can be found to these questions through the area of periodontal medicine, and
educators and clinicians can be trained.
Clearly, dentistry has much to do. As the many
authors in this volume carefully point out, these initial observations of an association between periodontitis and systemic disease need to be confirmed
and extended. In fact, it is not yet known whether
the relationship between periodontal infection and
systemic disease is a casual or a causal relationship
(14). Other authors look at possible mechanisms
whereby periodontitis would affect an individual or
whereby systemic disease would affect the periodontium. Still other authors in this volume offer new
prevention and treatment considerations for the
periodontal medicine patient. Much needs to be researched about this new branch of periodontology,

12

periodontal medicine, but this is a start and there is

no turning back. We hope you will enjoy the chapters
presented by our extraordinary group of clinicians
and scientists. And we hope you will join in the exciting era of discovery and development of periodontal
medicine.

References
1. Beck JD, Garcia RG, Heiss G, Volconos P, Offenbacher S.
Periodontal disease and cardiovascular disease. J Periodontol 1996: 67(suppl): 11231137.
2. Beck JD, Offenbacher S, Williams RC, Gibbs P, Garcia R.
Periodontitis: a risk factor for coronary heart disease? Ann
Periodontol 1998: 3: 127141.
3. DeStefano F, Anda LF, Kahn HS, Williamson DF, Rasell CM.
Dental disease and risk of coronary heart disease and mortality. BMJ 1993: 306: 688691.
4. Ebersole JL, Machen RL, Steffen MJ, Willman DE. Systemic
acute phase reactants, C-reactive protein and haptoglobin
in adult periodontitis. Clin Exp Immunol 1997: 107: 347
352.
5. Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: a two-way relationship. Ann Periodontol 1998: 3: 51
61.
6. Mattila KJ, Niemeier MS, Valtonen VV, Rasi VP, Kesaniemi
YA, Syrjala SL, Jungell PS, Isoluoma M, Hietaniemi K, Jokinen MJ. Association between dental health and acute myocardial infarction. BMJ 1989: 298: 779782.
7. Offenbacher S. Periodontal diseases. Pathogenesis. Ann
Periodontol 1996: 1: 821878.
8. Offenbacher S, Beck JD, Lieff S, Slade G. Role of periodontitis in systemic health: Spontaneous preterm birth. J
Dent Ed 1998: 62: 852858.
9. Offenbacher S, Katz V, Fertik G, Collins J, Boyd D, Maynor
G, McKaig R, Beck J. Periodontal disease as a possible risk
factor for preterm low birth weight. J Periodontol 1996:
67(suppl): 11031113.
10. Ridker P, Cushman M, Stampfer M, Tracy R, Hennekens C.
Inflammation, aspirin and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997: 336:
973979.
11. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens
CH. Plasma concentration of C-reactive protein and risk of
developing peripheral vascular disease. Circulation 1998:
97: 425428.
12. Scannapieco FA. Position paper. Periodontal disease as a
potential risk factor for systemic diseases. J Periodontol
1998: 69: 841850.
13. Soskolne WA. Epidemiological and clinical aspects of periodontal diseases in diabetics. Ann Periodontol 1998: 3: 3
12.
14. Slots J. Casual or causal relationship between periodontal
infection and non-oral disease? J Dent Res 1998: 77: 1764
1765.