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PERIODONTOLOGY 2000
mentioned that practitioners of obstetrics, cardiovascular disease and periodontics are collaborating in
scientific progress in ways not previously imagined.
Recently, it has been suggested that herpesviruses
comprise an important source for triggering periodontal tissue destruction. Herpesvirus infections may
initiate or accelerate periodontal breakdown via their
ability to stimulate cytokine release from host cells,
or they might impair host defense mechanisms,
resulting in heightened virulence of resident periodontopathic bacteria (24). In the light of the potential
importance of mammalian viruses in periodontal
diseases (2325), a discussion of virally induced host
responses is also included in this volume.
Microbial antigens and virulence factors elicit an
immediate inflammatory and immune response from
the host. The host reacts to microbial insults by
producing cytokines, eicasonoids, kinins, complement activation products and matrix metalloproteinases. Some of these inflammatory mediators
participate in periodontal ligament and bone
destruction. In turn, the inflammatory response is
regulated by genetic and environmental modifiers. As
reported by Page et al. (17), bacteria are essential in,
but not sufficient to cause, periodontitis, and host
factors, such as heredity, and environmental factors,
such as smoking, are important determinants of
periodontal disease occurrence and severity. Bacteria
may cause periodontal tissue destruction indirectly
by activating various components of the host defense
system. When activated, these host systems may
provide protection at the cost of some level of
periodontal destruction. Periodontal researchers
have extensively studied this double-edged sword
phenomenon, and the concepts thus derived consider the involvement of intrinsic and induced host
factors. In addition, cell-specific receptors and their
pathways have been identified. In this volume of
Periodontology 2000 we have compiled the latest
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kappa B ligand and its decoy receptor, osteoprotegerin, in osteoblasts. Receptor activator of nuclear
factor kappa B ligand is thought to be a major
mediator of alveolar bone resorption in periodontitis.
Nagasawa et al. (12) have discussed the role of
receptor activator of nuclear factor kappa B, receptor
activator of nuclear factor kappa B ligand and osteoprotegerin in periodontal bone resorption. The
potential importance of differences in receptor
activator of nuclear factor kappa B ligand and
osteoprotegerin expression among human gingival
fibroblasts, periodontal fibroblasts and osteoblasts is
also addressed. In addition, Nagasawa et al. (12)
review recent concepts of antibodies against periodontopathic bacteria, especially the diagnostic value
of antibacterial antibodies, which are becoming
important not only in periodontal diagnosis but also
in the risk assessment of coronary heart disease and
peripheral vascular disease (4,18). New insights into
the classic axis of neutrophilsantibodiescomplement in periodontal diseases are also summarized.
Prostaglandin E2 is an important mediator of tissue destruction in periodontitis. Prostaglandin E2
stimulates pro-inflammatory responses, including
osteoclastogenesis, by enhancing the expression of
receptor activator of nuclear factor kappa B ligand.
However, prostaglandin E2 also has anti-inflammatory effects, including inhibiting the production of
pro-inflammatory cytokines, such as tumor necrosis
factor-a, and can elicit anabolic actions on bone. An
article by Noguchi & Ishikawa (15), discussing the
periodontal roles of prostaglandin E2 and cyclooxygenase-2, has been included. The authors suggest
that prostaglandin E2 has the ability to down-regulate
hyper-inflammation occurring in periodontal lesions,
and to stimulate wound healing.
Similarly to environmental factors, host factors,
such as heredity, are a major determinant of infectious disease occurrence and severity. With recent
advances in the science of genetics, genes responsible for various diseases have been identified
and mapped. Genetic traits that may be associated
with an increased risk for periodontitis include
abnormal phagocyte function, a reduced capacity
to produce immunoglobulin G2, hFc-gamma-RIIa
polymorphism, tumor necrosis factor-a polymorphism, interleukin-1a polymorphism and prostaglandin
endoperoxide synthase 1 gene polymorphism (17). In
this volume of Periodontology 2000, Yoshie et al. (29)
have reviewed the possible role of genetic polymorphisms in periodontitis. In addition to listing the
evidence linking genetics and aggressive and chronic
forms of periodontitis, the authors have discussed the
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References
1. Beck JD, Eke P, Heiss G, Madianos P, Couper D, Lin D,
Moss K, Elter J, Offenbacher S. Periodontal disease and
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