Controversies in periodontics / /certified fixed orthodontic courses by Indian dental academy

CONTROVERSIES
IN
PERIODONTOLOGY

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com

CONTENTS:
Introduction.

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).

 Discussion of contending hypotheses on the nature
and treatment of diseases that adversely affect the
periodontium are no exception.
Controversies in three general areas are:
 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.

 Grouping periodontal diseases into a widely
accepted classification system has been difficult,
based primarily on disputes about the etiology and
pathogenesis of a clinically disparate disease
process.

 More recent classifications have been based on
relationships between an infecting pathogenic
microbiota, resulting inflammation, and a susceptible
host.

 The author notes that one of the constant
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
be periodically modified.


Classification of periodontal diseases
can be placed into three dominant
paradigms:
 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.

 Only those ideas that are believed to be
clearly outmoded or incorrect have been
discarded. In a sense, the newest or
dominant paradigm rests on a foundation of
the still valid components of the older or
previous paradigms.

 One of the interesting historical features of
classification systems is the often intense
resistance to their modification.

 Many people appear to believe that
classification systems are rigid and fixed
entities that should not be changed.

 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 noninflammatory
(‘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.
‘cementopathia’).


• Although most classification systems
published from approximately 1920 to 1970
included a degenerative disease category at
the 1966WorldWorkshop 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.


• 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.

• Distinguish between ‘Generalized Juvenile
Periodontitis’ and ‘Rapidly Progressive
Periodontitis’? Since there are no definitive answers
to these, and other similar questions, the
classification lost some of its clinical utility.


1999 CLASSIFICATION OF PERIODONTAL
DISEASES AND CONDITIONS
• Problems, inconsistencies, and deficiencies
associated with the 1989 classification led
many clinicians and investigators to call for
a revision of the currently used system.

• This resulted in a 1999 international
workshop on the classification of
periodontal diseases.

• One of the goals of this workshop was to
correct the problems associated with the
1989 system.


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.

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
dealt.

 Two basic questions have been raised and
continue to be matters of dispute.

 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.

• Most histological interpretations of the
past decades have suggested that the
dental pulp resides in a rather precarious
environment.

• Even some current texts list a litany of ills
which may befall a pulp from exposure to
periodontal disease and subsequent
periodontal treatment.

• Such projections, however, fail to
recognize more recent physiological data
which demonstrate that the pulp has a
quite sophisticated vasculature for such a
relatively primitive tissue.

• Vast networks of capillary beds have been
demonstrated as well as sophisticated
control systems including precapillary
sphincters and arteriovenous shunts have
been noticed.

• An active lymphatic system has also been
demonstrated.

• As the effectiveness of a tissue’s vasculature
is key to its adequate function, such
physiological observations suggest that the
dental pulp has mechanisms which provide a
significant capacity for survival.


The Effects of Periodontal Disease and Procedures on the
Dental Pulp:

• Over the years there has been a consistent stream of
speculation as to the effect of periodontal disease on the
dental pulp.

• Recent publications have suggested that ‘periodontal
disease’ is a ‘direct cause of pulpal atrophy and necrosis’
(Petka K 2001), ‘periodontal disease’ is ‘more deleterious
to the pulp than both caries and restorations combined’
(Petka K 2001), and ‘periodontal disease and periodontal
treatments should be regarded as potential causes of
pulpitis and pulpal necrosis’ (Wang et al 2002).

• Such interpretations have little basis in current scientific
fact, but do demonstrate the persistence of an often
repeated point of view in literature.

• A review of recent studies related to the ‘periodontal–
endodontic’ controversy therefore seems in order.


The pathways for communication and
extension of disease from a periodontal
pocket to the pulp are:
• Through patent dentinal tubules.
• Lateral canals.
• Apical foramen or foramina.

Demonstration of the presence of such
pathways is commonly identified as
evidence that specific periodontal disease
must have some effect on the health of
the dental pulp.


• The following histological and clinical studies
suggest, however, that such relationships rarely, if
ever, result in pulp necrosis.

• Kirkham BD (1975) examined 100 periodontally
involved teeth and found that only 2% had lateral
canals located in a periodontal pocket.
• Tagger M & Smukler H (1977) removed roots from
molar teeth so extensively involved with periodontal
disease that root amputation was required, and
found that none of the pulps of the resected roots
showed inflammatory changes.

• Haskell et al (1980) also removed roots from
maxillary molars with total or nearly total
periodontal involvement and found no inflammatory
cells or very few inflammatory cells present in the
pulps of the periodontally involved resected roots.


• Czarnecki & Schilder (1979) performed a histological study
of intact, caries-free teeth and compared the pulps of teeth
which were periodontally within normal limits with teeth
which had periodontal disease.

• The pulps in the intact, caries-free, periodontitis group
were all histologically within normal limits regardless of
the severity of the periodontal disease.

• In the same study they found that only teeth with
extensive decay or extensive restorations showed evidence
of pulp pathosis.

• Jaoui et al (1995) studied patients with advanced
periodontal disease for 5–14years after completion of
active periodontal treatment.

• Of the 571 teeth that did not have root canal treatment at
the time of completion of periodontal treatment, only one
tooth (0.175%) required root canal treatment over the 5-
to 14-year recall period.


• The cause of pulp necrosis could be
identified by the clinicians in most cases.
Recurrent decay resulting in pulp exposure
was the primary cause.

• Extension of periodontal disease to involve
the root apices is also cited as a reason for
root canal treatment, but it is not known if
the pulps of these teeth were in fact necrotic
or whether root canal treatment was
accomplished to facilitate additional
periodontal treatment.

• But few of the teeth requiring root canal
treatment were listed as having unknown
cause.


 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 Effects of Endodontically Involved Teeth on
Periodontal Health and Healing:

• Historically the effect of periodontal disease on the
dental pulp has been a source of discussion for the
better part of the past century.

• Only in recent years has the reverse been discussed.

• The potential effect that a tooth with a necrotic pulp
or a tooth that has had root canal treatment may
pose as a risk factor:
• In the initiation and progression of periodontal
disease.
• Resolution of periodontal pockets.


• The projected negative effects of pulpless teeth
appear to be based on studies related to the
similarity of the microbial flora in root canals and
deep periodontal pockets, negative effects on
periodontal healing in replantation studies, and a
series of retrospective statistical studies by Jansson,
Ehnevid, Lindskog and Blömlof (1993).

• The presumed pathway is primarily through patent
dentinal tubules.

• The clinical consequences suggested by series of
studies are significantly deeper probing depths, more
bone loss, impaired periodontal healing following
nonsurgical periodontal treatment, and enhanced
progression of periodontal disease.


• Jansson et al (1993) conducted a study in a
smaller group to evaluate intraindividual
comparisons and reports a mean pocket
depth difference of 0.27mm to 0.66mm in
five tooth groups and 0.98mm in a sixth
group with or with out pulpal involvement.

• In a second paper Jansson et al (1993)
state, ‘Mean probing depths for each tooth
were approximately 0.2mm deeper in teeth
with the same degree of radiographic
attachment in the presence of angular
destructions when periapical pathology was
present compared to teeth without
periapical pathology’.


• Study, Jansson & Ehnevid (1998) evaluated the periodontal
status of mandibular molars.

• They reported that the mean periodontal probing depth of a
nonroot-filled molar with a periapical lesion was 0.7mm
deeper than corresponding teeth with no periapical lesions,
and that the mean probing depth difference at proximal
sites was 0.2mm.

• It is quite curious to note that they found that molars with
root canal fillings, but no evidence of periapical pathosis,
were not significantly correlated to periodontal probing
depth or to degree of furcation involvement.

• In summary, while it has been suggested that a pulpless
tooth may represent an etiological risk factor related to
periodontal disease, the comparative risk must be
considered negligible based on clinical outcomes.


NONINFLAMMATORY DESTRUCTIVE
PERIODONTAL DISEASE:
• Prior to the 1970s, the causes and pathobiology of
periodontitis in humans were not understood, and no
widely accepted system of nomenclature and
classification of periodontal diseases existed.

• The large number of suspected causes included local
irritation from calculus, rough or overhanging
restoration margins, or ill-fitting oral appliances,
systemic diseases and conditions, diet and nutrition,
abnormal occlusal forces, were considered.

• By the 1970s, the central role of bacteria in causing
periodontitis had been documented, and concepts
about the nature of periodontal disease had begun to
shift from those of classical pathology to the
infectious/host defense paradigm.

• Destructive periodontal disease is infectious, and
they are all characterized by chronic inflammation,
pocket formation and progressive deepening, and
loss of attachment and alveolar bone.

• Author suggest 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.


• 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.


• NDPD may be a noninfectious form of
periodontal destruction.

• Analysis of the plaque flora fails to reveal
the presence of expected putative
periodontal pathogens such as P.
gingivalis, B. forsythus, A.
actinomycetemcomitans, and T. denticola
or enteric bacterial species.

• Furthermore, serum antibody analyses
generally fail to reveal evidence for prior
periodontal infection.


• There is abundant evidence that periodontitis, as the
disease is traditionally defined, is caused by specific
bacteria that extend apically between the gingiva
and tooth surface to cause inflammation, formation
of periodontal pockets with a pocket epithelium and
destruction of the periodontal ligament, the gingival
connective tissue and the alveolar bone.

• Inflammatory macrophages and granulocytes which
become activated to produce large quantities of
cytokines, especially interleukin-l (IL-1), tumor
necrosis factor-a (TNF-a) and prostaglandins, and
members of a large family of enzymes known as the
matrix metalloproteinases (MMP).


• Although the mechanisms underlying NDPD
have not been directly investigated, author
suggest that they may be the same as for
periodontitis except that the production of
prostaglandins and MMP, as described
above, 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).

• These cells could become activated to produce,
cytokines, prostaglandins and MMP by application of
abnormal forces as well as by binding of IL-l, TNF-α,
or bacterial substances.

• Such forces could originate from enduring, frequently
applied aggressive oral hygiene.

• The resident fibroblasts could therefore serve as a
source of molecules that mediate resorption of the
alveolar bone and destruction of gingival and
periodontal ligament connective tissues.

• Based on the above hypothesis, author have focused
on the idea that soft tissue trauma resulting from
aggressive daily oral hygiene combined with a
possible genetically determined enhanced
susceptibility could account for the pathobiology of
NDPD.


• In summary, over a period of more than 30years of
practice, author 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.

• The primary diagnostic features of the disease
include progressive gingival recession and loss of
periodontal attachment and alveolar bone, the
absence of gingival inflammation and microbial
deposits and periodontal pocket formation, and
failure of the disease to respond to traditional
antimicrobial periodontal treatments.

• In addition, the disease appears to be noninfectious.

• To distinguish the disease from various forms of
periodontitis, author suggests the name Non-
inflammatory Destructive Periodontal Disease.

BENEFICIAL BACTERIA OF THE
PERIODONTIUM:
• Author proposes that bacteria and their
products are a necessary and beneficial
component of a healthy periodontium.

• The primary evidence for their hypothesis is
that clinically healthy periodontal tissue
contains a highly orchestrated gradient of
selected inflammatory mediators that plays
a key role in the defense of this tissue and
the overall health of the individual.


• 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.

• His green cluster included Capnocytophaga
species, Campylobacter concisus, Eubacteria
nodatum and Streptococcus constellatus.


• The yellow cluster was formed by a group of
streptococci, and the purple cluster included
Actinomyces odontolyticus and Veillonella
parvula.

• These species tended to occur together in the
periodontal crevice and did not associate
with increasing pocket depth or gingival
bleeding.

• Interestingly, in other studies the species
from those clusters associated with
periodontal health were found to be
unaffected or even increased following
scaling and root planing and periodontal
maintenance procedures.


• Recently, Ximenez-Fyvie et al (2000) examined supra
and subgingival plaque in clinically healthy subjects
and in periodontitis patients for the same 40
bacterial taxa in a DNA checkerboard analysis and
found similar species in both supra and subgingival
plaque samples from healthy and diseased sites.

• However, they observed a higher mean prevalence of
the Actinomyces species in health, with the diseased
(deeper) sites tending to have higher counts of
bacteria overall as well as greater proportions of the
more pathogenic ‘orange’ and ‘red’ complexes of
bacteria including Bacteroides forsythus,
Porphyromonas gingivalis, Treponema denticola, and
Prevotella intermedia.


• 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.


PERIODONTITIS–SYSTEMIC DISEASE ASSOCIATIONS IN THE
PRESENCE OF SMOKING – CAUSAL OR COINCIDENTAL?

• Individuals with periodontitis are more likely to be
current or past cigarette smokers than individuals
without periodontitis (Hujole PP et al 2002).

• Therefore, when individuals with and without
periodontitis are compared it is to be expected that
individuals with periodontitis will have more
smoking-related diseases, such as coronary heart
disease, lung cancer, low-birth weight babies etc.,
than individuals without periodontitis.

• The comparison between individuals with and
without periodontitis with respect to the occurrence
of systemic diseases is said to be biased because of
the unequal distribution of smoking in the two
groups.


• In epidemiological terminology, smoking is referred
to as a confounder factor.

• Statistical adjustment or control for confounding is
possible using different statistical methods such as
stratification or covariance adjustment in statistical
models.

• Such statistical adjustment can be used to eliminate
some but not all of the bias caused by the higher
prevalence of smokers among individuals with
periodontitis.

• The goal of statistical adjustment is to make the two
compared groups (individuals with and without
periodontitis) similar with respect to the true lifelong
exposure to any form of tobacco smoking.


Periodontitis and smoking are associated with similar
health risks:

• 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.


IN OR OUT: THE INVASIVENESS OF ORAL BACTERIA
INVASION OBSERVED IN VIVO:
The concept that oral bacteria can penetrate the gingiva extends
back to at least the beginning of the twentieth century when
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.

In 1965 Listgarten used electron microscopy to observe gingival
tissue from cases of acute necrotizing ulcerative gingivitis, there
by beginning a new era of research into tissue invasion.

Listgarten reported the presence of spirochetes and fusiforms in
the necrotic zone overlying ulcerated lesions and also observed a
deeper zone beneath the surface of the ulcerated region that
contained only spirochetes.


• The application of immunofluorescence and immunohistochemical
staining provided a means to identify the invading bacteria. P.g,
P.intermedia, A.a and A. naeslundii were all recorded within
gingival tissues, with their presence being a characteristic of
diseased sites.

• Up to this juncture the term ‘invasion’ was taken to mean
intercellular penetration, i.e. bacteria locating between the host
cells.

• Although as early as 1974 Takarada et al noted that invasion ‘into
the superficial epithelial cells was occasionally encountered’, 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.

• Rudney et al. (2001) employed fluorescent in situ hybridization
(FISH) in combination with CSLM to examine buccal epithelial
cells. Both A.a and P.g, along with other unidentified species,
were found in high numbers within these cells taken from 23 of 24
healthy subjects.


Porphyromonas gingivalis:
• Is a gram-negative anaerobe.

• Strongly associated with severe manifestations of
periodontal disease and possesses a vast array of
virulence factors.

• In terms of invasion of epithelial cells, two invitro
models have been used extensively, namely
primary cultures of gingival epithelial cells (GEC)
and transformed oral epithelial cells such as the
KB cell.

• Invasion of GEC by P. gingivalis is swift and
profuse. Within 15min of exposure, high numbers
of P. gingivalis cells are located intracellularly,
predominantly in the perinuclear area.


• The bacteria are not constrained by
membranous vacuoles and can remain
viable for extended periods.

• The invasive process, represented
schematically, begins with the proximal
association between P. gingivalis cells and
GEC.

• Under these conditions P. gingivalis is
induced to secrete a novel set of
extracellular proteins, including homologs
of a phosphoserine phosphatase and a
polysaccharide biosynthesis enzyme.

Actinobacillus actinomycetemcomitans:

 Predominant pathogen in localized juvenile periodontitis, the
invasive properties of the gram negative capnophile A.a are under
active investigation. Bacterially driven internalization within KB
cells was first reported by Taylor’s group in 1991 and uptake is
now understood to be a dynamic multistep process, as
schematically represented.

 Initial adhesion to the epithelial cell transferrin receptor
appears to be the primary stimulus for invasion, although binding
to integrins may constitute a secondary entry pathway.

 Attachment induces effacement of the microvilli and the
bacteria enter through ruffled apertures in the cell membrane.


PERIODONTAL EPITHELIUM: A NEWLY RECOGNIZED ROLE IN
HEALTH AND DISEASE:

• The epithelium has an active role in keeping the
periodontium healthy, as shown by its effective barrier
function, its production of antimicrobial peptides, and its role
in chemokine and cytokine expression in response to
environmental stimuli.

• In a state of health, our epithelial barriers and our innate
defenses are extremely effective. When these first-line
defenses are impaired, the acquired immune system serves
as the back-up mode of defense.

• In the past, research has focused on the destruction of
connective tissue and on the acquired immune response in
periodontal disease.

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.


FINDING GENETIC RISK FACTORS FOR
PERIODONTAL DISEASES:


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.


• Machtei et al (1992) conducted one year
follow up study who demonstrated further
periodontal attachment loss after 1-year.

• Immune system response was examined for
level of serum IgG antibody to three
periodontal pathogens, Bacteroides
forsythus, P. g, and A.a.

• Significantly elevated odds ratios (OR) for
cases was associated with IgG for
Bacteroides forsythus, P. g, and A.a.


REFERENCE:
• Periodontology 2000, Vol. 30, 2002, 7–8


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