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Dr. Nikhat Fatima PG ies

Dept of Periodontics
 Overview
 Classifying periodontal diseases – a long-standing dilemma.

 Noninflammatory destructive periodontal disease (NDPD).

 Beneficial bacteria of the periodontium

 Periodontitis–systemic disease associations in the presence of

smoking – causal or coincidental?

 In or out: the invasiveness of oral bacteria.

 Periodontal epithelium: a newly recognized role in health and disease.

 The role of stress in inflammatory disease, including periodontal

disease.

 Finding genetic risk factors for periodontal diseases.

 The periodontal–endodontic controversy.

 Introduction

“When a thing ceases to be a matter

of controversy, it ceases to be a
matter of interest.”

William Hazlitt (1778–1830).

“A civilization in which there is not a continuous
controversy about important issues is on the
way to totalitarianism and death” 
Robert Maynard Hutchins
 There are broad range of issues that
represent contemporary controversies in
the discipline of Periodontics and public
discussion of contending views is
essential for progression of any sphere of
thought.
 Three groups
First group of controversies on classification of
periodontal 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
invasion, periodontal epithelium, genetic factors,
and stress.

The third group includes clinical controversies.

Classification controversy
 “Crude classifications and false
generalizations are the curse of
organized life.”

George Bernard Shaw (1856-1950)

(Irish literary Critic, Playwright and Essayist.
1925 Nobel Prize for Literature.)
• G.C. Armitage says that classification
systems should be viewed as
dynamic works-in-progress that need
to be periodically modified.
 Classification of periodontal diseases can be placed
into three dominant paradigms:
(paradigm means “A set of assumptions, concepts,
values, and practices that constitutes a way of
viewing reality for the community that shares them,
especially in an intelluctual discipline.)

 Primarily based on the clinical

features of the diseases (1870–
1920).

 The concepts of classical pathology

(1920–1970).

 The infectious etiology of the

diseases (1970–present).
 Classification systems in the modern
era represent a blend of all three
paradigms since there is a certain
amount of validity to some of the
earliest thoughts about the nature of
periodontal diseases.
 As classification systems have
evolved, newer thoughts about
periodontal diseases have been
superimposed on a matrix of older
ideas that are still considered to be
valid.
 One of the interesting historical
features of classification systems is
the often intense resistance to their
modification.

 Unfortunately it seems that once

people learn and accept a given
classification, no matter how flawed it
may be, they are extremely reluctant
to accept revisions to their favorite
system of nomenclature.
 In fact, classification systems
should be viewed as dynamic works-
in–progress that needs to be
periodically modified based on
current thinking and new knowledge.
Classical pathology paradigm (1920–
1970)

 As the field of periodontology began to mature

scientifically in the first half of the 20th century,
many clinical scholars in both Europe and North
America began to develop, and argue about,
nomenclature and classification systems for
periodontal diseases.

 What emerged from this debate was the concept

that there were at least two forms of destructive
periodontal disease inflammatory and non
inflammatory (‘degenerative’ or ‘dystrophic’).
  Gottlieb, in particular, had a
significant influence on the field
when he postulated that certain
forms of destructive periodontal
disease were due to
degenerative changes in the
periodontium.

 He believed that he had

discovered histological evidence
of impairment in the continuous
deposition of cementum (i.e.
Bernhard Gottlieb
‘cementopathia’).
(1885-1950)
• In retrospect it is puzzling that Gottlieb’s
concept of cementopathia was so readily
accepted, and for such a long time.

• Although there has been an occasional

report that cemental abnormalities might be
associated with some forms of periodontal
disease there was never any convincing
evidence that Gottlieb’s hypothesis was
right.
• Most classification systems published
from 1920 to 1970 included a
degenerative disease category. At the
1966 World Workshop in Periodontics
serious questions were raised about the
existence of ‘periodontosis’ as a distinct
disease entity.

• Many recommended that the term be

discarded. It was not until 1977, that
meeting supported the conclusion that
‘periodontosis’ was actually an infection
and ‘juvenile periodontitis’ should
become the preferred term for this group
of diseases.
Infection/host response paradigm
(1970 to present)

1876 Robert Koch

provided experimental
proof of the germ theory
of disease, some
dentists began to
suggest that periodontal
diseases might be
caused by bacteria.

Robert Koch (1843-1910)

The next major discovery in
periodontal microbiology was the
preliminary demonstration in
1976–1977 of microbial specificity
at sites with periodontosis.

This finding, coupled with the

demonstration in 1977– 1979 that
neutrophils from patients with
juvenile periodontitis
(periodontosis) had defective
chemotactic and phagocytic
activities, marked the beginning of
the dominance of the
Infection/Host Response
paradigm.
• The next major landmark in the
classification of periodontal
diseases emerged from the 1989
World Workshop in Clinical
Periodontics where a new
classification of periodontitis based
on the Infection/ Host Response
paradigm was suggested by AAP.

• The classification was a refinement

of one that had been proposed by
Page & Schroeder in 1982 and a
similar one that had been adopted
by the AAP in 1986.
Five types of destructive periodontal
disease were listed:

• I Adult Periodontitis.
• II Early Onset Periodontitis.
• III Periodontitis Associated
with Systemic Disease.
• IV Necrotizing Ulcerative
Periodontitis.
• V Refractory Periodontitis.
Drawbacks:
• Depended heavily on the age of the
affected patients.
• Rates of progression.

Other important features:

• Periodontitis Associated with
Systemic Disease.
• Refractory Periodontitis category.
• Overlap exists among categories and
cases exist that do not clearly fit into any
single category.

• In addition, it was acknowledged that

considerable ‘heterogeneity’ existed within
the Refractory Periodontitis category
since, it includes patients who are
unresponsive to any treatment provided
whatever the thoroughness or frequency
as well as patients with recurrent disease
at few or many sites.
• Finally, different forms of periodontitis
proposed in the classification shared
many microbiologic and host response
features, which suggested extensive
overlap and heterogeneity among the
categories
• As a consequence of these
problems, the 1989 classification was
criticized shortly after it was
published and a different system was
proposed by Ranney(1993).
• Adult Periodontitis.
• Early Onset Periodontitis
• Necrotizing Ulcerative
Periodontitis.

• He suggested elimination of the

‘Refractory Periodontitis’ category
since it was a heterogeneous group
and it was impossible to standardize
the treatment that necessarily would
have to be given prior to making the
diagnosis.
• In addition, he recommended
elimination of the ‘Periodontitis
Associated with Systemic
Disease’ category.

• Since the, expression of all forms

of periodontitis can be modified
by some systemic diseases or
abnormalities, it is probably
better to consider them in that
specific context, rather than
treating them as a unique
category.
• Nevertheless, despite its
problems, the classification was
adopted by the world community
as reflected by its widespread use
in the periodontal literature.

• Its acceptance was facilitated by

the ease with which patients could
be placed into age-based
categories (i.e. adult vs. early
onset disease).
Drawbacks:

• The disease category of ‘Prepubertal

Periodontitis’ was the first to be seriously
questioned.

• The uncertainty about the proposal that ‘Rapidly

Progressive Periodontitis’ was a single entity,
and secondly, the questionable criteria used to
determine its presence.
 1999 classification of periodontal diseases and
conditions
There were six major problems with the
1989 classification that needed to be
addressed:

1) It did not include a gingivitis or

gingival disease category.

2) The periodontitis categories had

non validated age dependent
criteria.

3) There was extensive crossover in

rates of progression of the different
categories of periodontitis. Rapidly
Progressive Periodontitis was a
heterogeneous category.
4) There was extensive overlap in the
clinical characteristics of the different
categories of periodontitis.

5) Refractory Periodontitis was a

heterogeneous category.

6) Prepubertal Periodontitis was a

heterogeneous category.
• What emerged was a classification that
was even more firmly based on the
Infection/Host Response paradigm, but
without some of the inherent problems
of the 1989 classification.

• In reality, the changes could be

characterized as a ‘course correction’
or ‘fine-tuning’ of the 1989
classification since no massive
alterations were made.
• A badly needed gingivitis or gingival
disease category was added.

• In addition, the heterogeneous disease

categories of prepubertal, refractory
and rapidly progressive periodontitis
were eliminated as distinct or stand-
alone entities.
• The ‘refractory’ designation remains in
the new classification, but not as a
single entity.

• Changing the names of ‘Adult

Periodontitis’ to ‘Chronic Periodontitis’
and ‘Juvenile Periodontitis’ to
‘Aggressive Periodontitis’ was made.

• These changes were specifically made

to eliminate the non validated age-
dependent designations.
Future challenges in the classification of periodontal
diseases

• As we enter the post genomic era with

our increased understanding of the
bacteria associated with periodontal
infections and the genetic factors
controlling host responses to these
infections, it would seem that a more
mechanistic or etiological classification
could be devised.
 Controversy on
Noninflammatory
destructive periodontal
disease (NDPD).
Noninflammatory destructive periodontal
disease (NDPD)

• Today the infectious nature of

periodontitis is no longer a
hypothesis but is a universally
accepted dogma.
• Experts agree that all forms of
periodontitis are infectious and are
characterized by chronic
inflammation, pocket formation
and deepening, and loss of
periodontal attachment and
alveolar bone.

• Although bacteria are thought to

be essential, bacteria alone are
insufficient; a susceptible host is
also required, and host
susceptibility is an important
determinant of disease status.
• It has been suggested that the existence
of at least one form of severe destructive
periodontal disease that is not
recognized in the recent classifications.

• In this form of periodontal disease, loss

of attachment, resorption of alveolar
bone and tooth loss occur, but gingival
inflammation and pocket formation and
deepening are not prominent features;
antimicrobial therapy is not effective in
arresting or slowing the progress of the
disease and bacteria may not be the
primary cause.
 Historical perspective
• A noninflammatory form of destructive
periodontal disease was first described by
Hunter in 1771 and subsequently confirmed
by Fox (1832), Gottlieb (1932) and Orban
(1942).

• A category of noninflammatory destructive

periodontitis was included in the first AAP
classification of periodontal diseases in 1942,
and was an integral part of virtually all
subsequent classifications published up to
about 1970.
• The disappearance of NDPD from the
literature occurred concurrently with
increasing documentation of the
important role of bacteria in the
etiology of periodontitis and the shift
in concepts about periodontal
diseases from the Classic Pathology
paradigm to the Infection/Host
Defense paradigm as described by
Armitage (2002).
• Under the latter paradigm, all forms of
destructive periodontal disease were
considered to be infectious and to be
characterized by inflammation, pocket
formation and loss of periodontal
attachment and alveolar bone.
NDPD has several distinct diagnostic
characteristics:

• Generalized loss of attachment.

• Resorption of alveolar bone.

• Extensive gingival recession, affecting many

teeth, without formation of deep periodontal
pockets or significant clinical manifestations
or history of gingival inflammation.
• Occurring in individuals with excellent
daily oral hygiene.

• The disease is recognized most frequently

in individuals in their 30s or 40s, although
it may begin in patients in their 20s.

• It may affect all of the teeth or it may be

more severe around the posterior or the
anterior teeth.
• Although the mechanisms underlying
NDPD have not been directly investigated,
its been suggested that they may be the
same as for periodontitis except that the
production of prostaglandins and MMP,
may be initiated and perpetuated by
factors other than bacterial infection.
• The mediators may be produced by cells
that are normally resident in the periodontal
tissues rather than infiltrating inflammatory
cells.

• Fibroblasts plus a few macrophages

(histiocytes) comprise the predominant cell
population present in noninflamed gingiva
(Schroeder HE 1973).
• In summary Page & Sturdivant
stated that over a period of more
than 30years of their practice, they
have encountered a large number
of cases of destructive periodontal
disease that do not fit the
diagnostic criteria of any form of
periodontal disease described in
the classifications published since
the 1970s.

• Recognition of this disease as a

specific entity is important as it is a
significant cause of tooth mortality
at a relatively young age, and it
fails to respond to the usual
periodontal therapies.
• Goal is to bring the disease to the
attention of practitioners and
periodontal investigators in order
to develop better diagnostic criteria
and discover successful means of
prevention and treatment.

• To distinguish the disease from

various forms of periodontitis, Page
& Sturdivant suggest the name
Non-inflammatory Destructive
Periodontal Disease.
 Controversy on

Beneficial bacteria of the periodontium

Beneficial bacteria of the periodontium

Commensal bacteria of the oral cavity

• The term commensal is defined as a relationship

between organisms of two different species in
which one derives nutrients or other benefits
from the association while the other remains
unharmed and unaffected.
(Encarta Dictionary)
•Symbiosis of Vibrio
fischeri and the Hawaiian
sepiolid squid Euprymna
scolopes.

•The luminous bacterium

V. fischeri colonizes the
light-emitting organ in
the mantle of the bobtail
squid providing a
defence camouflage
during nocturnal
feeding.
• Classifying oral bacteria into
commensal and pathogenic
organisms is an anathema to
some in the oral microbiology
arena.

• This stems largely from the

argument that there are no actual
pathogenic oral bacteria, only
opportunistic commensal
bacteria. While this may seem to
be a trivial matter, it nonetheless
can be problematic.
• The term commensal is designated to
all bacteria of the oral cavity, with the
caveat that where evidence suggests a
beneficial role for some of these
organisms in the oral cavity, they will be
referred to as beneficial commensals,
while those found to harm the oral cavity
will be referred to as periodontopathic
bacteria.
• Extensive culture studies by Moore
et al found certain species,
including Actinomyces,
Streptococcus, and Veillonella to
be associated with health while
more gram-negative species,
Treponemes, and higher numbers
of Fusobacterium nucleatum were
associated with disease.

• Socransky et al found that many of

the bacterial taxa appeared to
cluster together including those
associated with gingival health.
• Certain periodontal pathogens, such
as P. gingivalis, are adapted to
survival in the pocket.

• Their outer membrane

lipopolysaccharide is capable of
downregulating E-selectin and
interleukin-8.
• Thus potentially interrupting the local
inflammatory response.

• This helps the bacteria to avoid

elimination while maintaining deeper
inflammation that provides the
organism with needed nutrients in the
form of increased crevicular fluid flow
and blood products from the ulcerated
pocket epithelium.
• In summary human beings generally do
well with regards to their periodontal
status because we have co-evolved with
the commensal bacteria that serve to
protect us through promotion of a
beneficial host response.

• However, this host-bacterial balance is

dependent on the specific genetic
markers of each individual (major
histocompatibility complex type, gene
polymorphisms, etc.), environmental
factors (smoking, stress, etc.), and the
continually evolving microbial
community.
• A more thorough understanding
of these factors should lead to
improved periodontal health in
the twenty-first century.
 Controversy on

Periodontitis–systemic disease associations

in the presence of smoking –
causal or coincidental?
• No current issue in periodontal
research is more visible or
controversial than the relationship
between periodontitis and
systemic diseases.

• Although there is some awareness

that the observed associations
could be coincidental, as a result
of confounders such as age and
smoking, the full impact such
confounding can have, especially
without adequate statistical
adjustment, does not seem to be
appreciated.
 Four lines of evidence
• First, no periodontitis–systemic disease
associations have been identified among
never smokers.
• Second, periodontitis and smoking mimic
one another with respect to the types of
diseases with which they are associated
(e.g. lung cancer and Parkinson’s
disease).
• Third, only studies with inadequate
adjustment for smoking report significant
periodontitis–systemic disease
associations.
• Lastly, elimination of dental infection,
unlike smoking cessation, does not
reduce coronary heart disease risk.
Periodontitis and smoking are associated with
similar health risk
• Smoking is most strongly
associated with lung cancer,
followed by COPD, CHD and stroke.
Smoking is associated with a
decreased risk for Parkinson’s
disease.

• Periodontitis mimics this pattern

step by step: periodontitis is most
strongly associated with lung
cancer, followed by COPD, CHD and
stroke.
• If periodontitis–systemic disease
associations are a result of
incomplete adjustment for smoking,
other periodontitis–systemic
disease associations should
become predictable. Because
smoking is negatively associated
with Parkinson’s disease,
periodontitis should be also.
• There have been a total of
nine cohort studies
published on the
periodontitis–CHD
associations.

• Four of the nine studies

had poor smoking
adjustment, while five had
good smoking adjustment.
• Periodontitis was not
significantly associated with
CHD (HR 1.05; 95% confidence
interval 0.96–1.15) among those
studies that provided a good
adjustment for smoking dose.

• In contrast, periodontitis was

significantly associated with
CHD in the four studies that
either did not adjust for smoking
or adjusted crudely (HR 1.25;
95% confidence interval 1.15–
1.37).
• Lack of control for smoking dose
provides a plausible explanation for
why small, but statistically significant,
periodontitis– CHD associations are
only present for studies that poorly
adjust for smoking.

• In summary the possibility of

smoking–periodontitis interactions
cannot be excluded.
• Periodontitis may cause
systemic diseases only in
the presence of smoking;
or, periodontitis may
worsen the ill effects of
smoking on systemic
health.
 Controversy on
In or out: the invasiveness of oral bacteria
• The concept that oral bacteria
can penetrate the gingiva
extends back to at least the
beginning of the twentieth
century when KW Goadby
(1907) proposed that bacteria
can invade oral tissues.

• Later cultural and histological

studies provided experimental
support; however, being
sustained only by sporadic
reports in the literature the idea
fell into abeyance.
• This was to change in
1965 when Listgarten
unleashed the power
of electron microscopy
to observe gingival
tissue from cases of
acute necrotizing
ulcerative gingivitis,
ushering in the
modern era of
research into tissue
invasion.
• The application of
immunofluorescence and
immunohistochemical
staining provided a means
to identify the invading
bacteria. Porphyromonas
gingivalis, Prevotella
intermedia, Actinobacillus
actinomycetemcomitans
and Actinomyces
naeslundii were all
recorded within gingival
tissues.
• Up to this juncture the term ‘invasion’
was taken to mean intercellular
penetration, i.e. bacteria locating
between the host cells.
• It was not until intracellular
invasion (i.e. bacteria locating
within epithelial cells) became
established as an important
property of enteropathogens,
that researchers seriously
considered this possibility for
oral pathogens.
Fluorescence microscopy image of a 0.2-mm
optical section through gingival epithelial cells
(green) exposed to Porphyromonas gingivalis
(red) for 15min. Internalized P. gingivalis
(orange/yellow) accumulate in the perinuclear
region.
Immunofluorescence micrograph of Actinobacillus
actinomycetemcomitans (green) within KB cells (red)
connected by intercellular protrusions. Internalized
bacteria appear yellow.
 Potential relevance of invasion
• There is strong evidence to support
a role for both inter- and intracellular
invasion in the initiation and
progression of disease.

• Perhaps the broader question with

which we should concern ourselves
is: under what circumstances is the
outcome of the molecular dialog
between bacterial and eukaryotic
cells detrimental or beneficial to the
host?
 Controversy on

Periodontal epithelium:
a newly recognized role in health and disease
The problem
• Periodontal epithelium is the oral
surface and covering of the
periodontal attachment. It serves to
cover and protect the underlying
tissues. It has a critical function in
serving to seal the site of
penetration of the teeth.

• This unique function imparts special

challenges to the tissue and leads
to certain vulnerabilities associated
with periodontal disease.
• Historically, the approach of
periodontists has been to consider
the epithelium as a passive covering.
When active disease is present, the
epithelial barrier function fails and
the epithelium has been breached.

• The problem is amplified by apical

epithelial migration resulting in a
deepening pocket.

• This results in bacterial invasion,

inflammation and destruction of the
connective tissue, with subsequent
bone loss and possible tooth loss.
• We now have quite a
different perspective. While
the epithelial compartment
does provide a physical
barrier to infection, it also
has an active role in innate
host defence.
• Epithelial cells also respond to
bacteria by altering cell signalling
events. Langerhans cells function as
antigen-presenting cells and serve
as one of the connecting links
between the epithelium and acquired
immunity.

• A family of pathogen pattern

recognition receptors, the Toll-like
receptors, have been identified as
critical in mediating responses to
bacteria. These receptors can be
anticipated to be a key to the
molecular events of innate host
defense in the epithelial cell
compartment.
The epithelium signals other cell types in response to bacteria for
contributions to the microbial barrier. Chemokines (i.e. IL-8), cytokines, and
adhesion molecules (i.e. intercellular adhesion molecule-1) are expressed by
keratinocytes and Langerhans cells (purple). Langerhans cells also migrate
out of the tissue for antigen presentation and to elicit the acquired immune
response. Epithelial antimicrobial peptides are up-regulated; these have both
direct action on bacteria and signal immature dendritic cells and
macrophages which then further upregulate epithelial responses.
• In summary with emerging
evidence of the role of innate
immunity, it is time to look at the
other side of the story and to
understand the periodontal
epithelium and its important role in
maintaining health and
communicating environmental
dangers before they get out of
hand.
 Controversy on

The role of stress in inflammatory disease,

including periodontal disease
Stress and periodontal disease
Stress, a term
continually being
redefined in the
scientific study of
disease and illness,
is nevertheless a
confirmed and
important factor in
the etiology and
maintenance of
many inflammatory
diseases, including
periodontal disease.
 Evidence for the role of stress in periodontal
disease
• In a review of psychosocial factors
in inflammatory periodontal
disease reported in 1995 Monteiro
da Silva et al distinguish between
acute necrotizing ulcerative
gingivitis and adult periodontitis,
concluding that the evidence is
strong for stress as a predisposing
factor to acute necrotizing
ulcerative gingivitis, while the
evidence for psychosocial factors
as etiological agents in
periodontitis is not as substantive.
• Evidence for a relationship between
psychosocial stress, coping in
response to stress, and periodontal
disease was also observed in a
cross-sectional epidemiological
study of 1426 adults, aged 25–
74years by (Genco RJ 1999).

• Results indicated a significant role

for financial strain in relation to
greater alveolar bone and
periodontal attachment loss, after
adjusting not only for age and
gender, but also for smoking.
• Interestingly, those
individuals with a problem-
solving coping style for
managing the stressors of
daily living fared better than
those who exhibited a more
emotionally focused and
less adequate coping
response to psychosocial
strain.
• Deinzer et al (1999) report an
experiment to assess the relationship
between academic stress and gingival
inflammation, assessing changes in
IL- 1β, a component of the immune
system thought to play a role in
periodontal tissue destruction.

• Using a split mouth design, medical

students voluntarily neglected oral
hygiene of two quadrants for 21days,
to induce an experimental gingivitis in
those quadrants, while maintaining
high levels of oral hygiene in the
remaining two quadrants.
• It was observed that examination
students showed significantly higher
levels of IL-1β at both the
experimental gingivitis sites than the
sites of good oral hygiene.

• Indicating that stress may affect

periodontal health through
suppressed immune system activity,
and that such a relationship would be
more pronounced when oral hygiene
was not maintained.
• Major dependent variables across studies
– dental plaque levels, gingival bleeding
on probing, pocket depth, attachment
loss, loss of alveolar bone, etc. – makes
comparisons across studies difficult and
limits the ability to generalize about the
specificity of the relationship between
psychosocial stress and periodontal
disease.
• Not withstanding these shortcomings as
well as the inherent difficulties in
assessing the relationship between
physical disease status and the quality
and quantity of psychosocial stress, it is
clear that findings are almost
universally in the hypothesized
direction of a meaningful relationship
between parameters of periodontal
disease.
 Controversy on

Finding genetic risk factors for periodontal diseases:

Is the climb worth the view?
• Despite the fact that
environmental factors
appear to provide
sufficient disease-
provoking factors, the
fact remains that not
everyone appears to be
equally susceptible to
periodontal disease.
 What advantage is there in knowing the
genes involved in periodontitis?

• At least for the time being, genes

are unalterable; as clinicians we
cannot treat or modify them.

• Secondly, it is likely that there are

multiple genes that will be found to
be associated with periodontitis
risk, and the effects of these genes
may not be independent of each
other.
 Diagnostic tests
• Most clinicians would agree that
current routine diagnostic methods
for detecting periodontitis are
nothing more than recordings of
the history of previous destructive
disease.

• A great deal of research has been

performed in an attempt to detect
active disease or subclinical
initiation of disease but no
universally accepted test has
emerged for clinical application.
• Most importantly, identifying
specific genetic risk factors may
be academically appealing but is
of little use unless it leads to
improvements in the prevention or
treatment of disease.
The periodontal–endodontic
controversy
Periodontic _ Endodontic Relationship

1 Complicate the Diagnosis

2 Complicate the Treatment Plan

3 Affect the Sequence of Care

The periodontal–endodontic
controversy
• Over the past century the dental
literature has consistently
reflected a controversy related to
the effect of periodontal disease
on the dental pulp and more
recently the effect of pulpal
necrosis on the initiation and
progression of marginal bone
loss.
• Is periodontal disease a
cause of pulp necrosis? Can
a pulpless tooth be the cause
of periodontal disease? The
answers to these basic
questions are of utmost
clinical importance. The
appropriateness of treatment
planning hangs in the
balance.
• Should root canal
treatment be carried out
prophylactically for a
tooth associated with
moderate or advanced
periodontal disease?

• Should a pulpless tooth

be retained or should it
be removed and replaced
with an osseointegrated
implant?
• The periodontium and the pulp have
embryonic, anatomic and functional
interrelationship.

endo

Embryonic , anatomic , functional

perio
•They are ectomesenchymal in
origin, from which the cells
proliferate to form the dental papilla
and follicle, which are the
precursors of the pulp and the
periodontium respectively.
• Three main avenues for communication
are,

• 1) Dentinal tubules.

• 2) Lateral and accessory canals and

• 3) The apical foramen

 Apical
Foramen

Perio-Endo
Relationship

Dentinal
Tubules
Lateral & Accessory
canals
• From studies in the
periodontics literature, it
appears that periodontal
treatment, as well as
periodontal disease, has a
negligible effect on the dental
pulp.
• In summary, unless
periodontal disease extends
all the way to the tooth
apex, the weight of evidence
in the literature suggests
that the dental pulp is
capable of surviving
significant insults and that
the effect of periodontal
disease as well as
periodontal treatment on the
dental pulp is negligible.
• It also appears that the clinical
significance of the relationship
between periodontal disease and
the dental pulp has been greatly
exaggerated in historical and
much of the current periodontal–
endodontic literature.
• The terminology currently
used in our literature adds to
the confusion ‘Periodontitis
Associated With Endodontic
Lesions’ and a subcategory of
‘combined periodontic–
endodontic lesions.’
• Combined lesions are
defined as ‘those cases
where there is any
coalescence of endodontic
and periodontal lesions.

• The definition opens the

door for a very broad
interpretation of
‘periodontal–endodontic
lesions.’
• Inclusion of ‘combined
periodontic and endodontic
lesions’ in a periodontal
classification seems not very
helpful in concept, confusing
as to which lesion has
‘coalesced’ and which has not,
and certainly not helpful in
diagnosis and treatment
planning.
 In conclusion

• In controversy, one often

ends up where one started.
 References

•Periodontology 2000,
• Vol 30, 7–8, 9–23,
24–39, 40–50, 51–60,
61–69, 70–78, 79–90,
91–103, 123–130.

•Carranza’s clinical periodontology