Periodontology 2000, Vol.
30, 2002, 7–8
Printed in Denmark. All rights reserved
Controversies in periodontology
P B. R & T A. DR
When a thing ceases to be a matter of controversy, it ceases
to be a matter of interest.
William Hazlitt (1778–1830)
This volume of Periodontology 2000 considers a
broad range of issues that represent contemporary
controversies in the discipline. Schopenhauer (12)
argues that public discussion of contending views is
essential for progression in any sphere of thought.
Discussion of contending hypotheses on the nature
and treatment of diseases that adversely affect the
periodontium are no exception. We present a series
of papers in three general areas. The first group of
papers deals broadly with the classification of peri-
odontal diseases and some aspects of microbial
colonization, inflammation and systemic factors,
upon which recent classifications have been based.
The second considers controversies in periodontal
pathogenesis, including the role of bacterial in-
vasion, periodontal epithelium, genetic factors, and
stress. The third group of papers explores clinical
controversies about changing practice patterns in
periodontics, implant treatment planning, and peri-
odontal–endodontic interrelationships. Regardless of
the reader’s orientation to periodontology, each of
these series of papers should provide at least one
controversy of interest.
Armitage (1) opens the first group of papers by de-
scribing the evolution of classification systems for
periodontal disease. Grouping periodontal diseases
into a widely accepted classification system has been
difficult, based primarily on disputes about the etiol-
ogy and pathogenesis of a clinically disparate dis-
ease process. More recent classifications have been
based on relationships between an infecting patho-
genic microbiota, resulting inflammation, and a sus-
ceptible host. The paper notes that one of the con-
stant historical features about classification systems
is the acrimony that accompanies their modification
and concludes that classification systems should be
viewed as dynamic works-in-progress that need to
Copyright C Blackwell Munksgaard 2002
PERIODONTOLOGY 2000
ISSN 0906-6713
be periodically modified. Page & Sturdivant (8) take
up that challenge by questioning the accepted
dogma that all forms of destructive periodontal dis-
ease are infectious and that all are characterized by
chronic inflammation. Illustrated by case reports,
they suggest the existence of at least one form of
non-inflammatory destructive periodontal disease
(NDPD), in which there is severe loss of attachment
but inflammation and pocket formation are not
prominent, and pathogenic bacteria may not be
causal. Roberts & Darveau (9) subsequently observe
that bacteria and their products are necessary com-
ponents of a healthy periodontium. The authors
postulate that while certain microorganisms appear
essential, if not sufficient, for the pathogenesis of
periodontal disease, commensal bacteria play an
equally important role in periodontal tissue develop-
ment, functional maturation, and state of health. To
complete this group of papers, Hujoel et al. (4) ad-
dress the power of smoking in confounding our
understanding of interactions between periodontitis
and systemic disease. The authors contend that
smoking spuriously causes many of the observed
periodontal–systemic disease interrelationships. The
challenge is to disentangle the effects of smoking on
periodontitis from the effects of smoking on coro-
nary heart disease, stroke, and other generalized dis-
eases.
Lamont & Yilmaz (5) begin the series on factors
critical to the pathogenesis of periodontal disease
with the misfortunes of Porphyry, a Greek philos-
opher in the third century. The chronicle naturally
leads to a discussion of invasion into periodontal
tissues by Porphyromonas gingivalis and other spe-
cies, including the ability of bacteria to invade, and
the pathogenic implications of such an invasive
event. Dale (2) follows with the observation that the
initial guardian of underlying supporting structures
is the periodontal epithelium. While long considered
a passive covering with disquieting periods of mi-
gration, she demonstrates that epithelium has an ac-
7
Robertson & DeRouen
tive role in maintaining periodontal health by pro-
ducing antimicrobial peptides, expressing chemo-
kines and cytokines in response to environmental
stimuli, and integrating innate and acquired im-
mune responses. Schenkein (11) reminds us that de-
spite the all but universal presence of factors fully
capable of provoking periodontal attachment loss,
not everyone is equally susceptible to periodontal
disease. He shows that there is considerable vari-
ation in individual susceptibility to periodontitis
even when known etiological factors are taken into
account. The paper explores the present status of
genetic profiles to determine periodontal risk, and
related optimum prevention and treatment ap-
proaches, for any particular patient. LeResche and
Dworkin (6) conclude this series by exploring per-
haps the least understood factor in periodontal dis-
ease: the role of psychosocial stress as a mediator of
physical illness. There is compelling evidence for the
importance of stress in conditions such as rheuma-
toid arthritis and inflammatory bowel disease, which
share a number of pathogenic features with peri-
odontitis. The authors propose an equally strong re-
lationship between parameters of periodontal dis-
ease, environmental factors, co-morbid diseases,
and psychosocial stressers.
Robertson et al. (10) introduce the series of papers
on clinical controversies by reporting a major shift in
patterns of periodontal care during the last decade,
particularly among procedures provided by peri-
odontists. Such shifts included the markedly de-
creased provision of periodontal surgery, which may
reflect a decline in the prevalence of periodontitis,
and concurrent increases in nonsurgical therapy,
crown-lengthening, and implant services. O’Neal &
Butler (7) examine the rapidly expanding advantages
of implants and consider the increasingly frequent
clinical quandary of maintaining an existing but un-
certain tooth vs. placing an implant. Finally, Harring-
ton et al. (3) return to a clinical aspect of evolving
periodontal disease classifications: the issue of peri-
odontitis associated with endodontic lesions. The
authors question whether the new combined peri-
odontal–endodontic lesion category clarifies which
lesion has coalesced, provides a foundation for diag-
nosis or treatment planning, or illuminates the
pathogenesis of either disease process. The paper
serves also to show that in controversy, one often
ends up where one started.
References
1. Armitage GC. Classifying periodontal diseases – a long-
standing dilemma. Periodontol 2000 2002: 30: 9–23.
2. Dale BA. Periodontal epithelium: a newly recognized role
in health and disease. Periodontol 2000 2002: 30: 70–7.
3. Harrington GW, Steiner DR, Ammons WF. The peri-
odontal–endodontic controversy. Periodontol 2000 2002:
30: 123–130.
4. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA.
Periodontitis–systemic disease associations in the pres-
ence of smoking. Causal or coincidental? Periodontol 2000
2002: 30: 51–60.
5. Lamont RJ, Yilmaz Ö. In or out: the invasiveness of oral
bacteria. Periodontol 2000 2002: 30: 61–69.
6. LeResche L, Dworkin SF. The role of stress in inflammatory
disease, including periodontal disease: review of current
concepts and current findings. Periodontol 2000 2002: 30:
91–103.
7. O’Neal RB, Butler BL. Restoration or implant placement: a
growing treament planning controversy. Periodontol 2000
2002: 30: 111–122.
8. Page RC, Sturdivant EC. Non-inflammatory destructive
periodontal disease. Periodontol 2000 2002: 30: 24–39.
9. Roberts FA, Darveau RP. Beneficial bacteria of the peri-
odontium. Periodontol 2000 2002: 30: 40–50.
10. Robertson PB, Anderson MA, del Aguila MA. Trends in
periodontal care. Periodontol 2000 2002: 30:104–110.
11. Schenkein HA. Finding genetic risk factors for periodontal
diseases: is the climb worth the view? Periodontol 2000
2002: 30: 79–90.
12. Schopenhauer A. Complete essays of Schopenhauer. Trans-
lated by Bailey Sanders T. New York: Wiley Book Company,
1942.