P E R I O D O N T OP LE OR G

I O
Y D O N T O L O G Y

Current Concepts in Periodontal

Pathogenesis
PHILIP M. PRESHAW, ROBIN A. SEYMOUR AND PETER A. HEASMAN

that, whilst gingivitis and mild-moderate

Abstract: Periodontal research over the last 40 years has been remarkably prolific. We periodontitis are relatively common in
now understand that severe periodontitis affects approximately 10–15% of the population
the population, severe periodontitis is
(representing a large number of individuals in the UK) and gingivitis and mild
periodontitis affect a majority of people. Microbiological research has identified some of less prevalent, despite plaque being a
the key pathogens that are implicated in periodontal disease. Plaque bacteria exist in common finding in a majority of people.
biofilms, which have evolved to protect individual organisms within the subgingival When considering periodontal
bacterial community. For this reason, root surface instrumentation (RSI) remains the pathogenesis, it is important first to
cornerstone of periodontal treatment, and is necessary to disrupt the subgingival biofilm consider how research into the
mechanically and reduce the bacterial bioburden. Although bacteria are necessary for epidemiology of periodontitis has
periodontal disease to occur, a susceptible host is also required. The immune- resulted in a changing understanding of
inflammatory response that develops in the gingival and periodontal tissues in response patterns of periodontitis over the years.
to the chronic presence of plaque bacteria results in destruction of structural components
of the periodontium leading, ultimately, to the clinical signs of periodontitis. The nature
of the host response is determined primarily by genetic factors and environmental and EPIDEMIOLOGY OF
acquired factors such as smoking. The host response is essentially protective in nature, PERIODONTITIS
but both under-activity (hypo-responsiveness) and over-activity (hyper-responsiveness) of
aspects of the host response can result in enhanced tissue destruction. The purpose of Epidemiology refers to the study of the
this paper is to review current thinking in periodontics with special reference to distribution of disease in human
periodontal epidemiology, microbiology, and pathogenesis. populations, with consideration of the
factors that influence this distribution.
Dent Update 2004; 31: 570-578 Two important concepts in periodontal
Clinical Relevance: A good understanding of periodontal disease processes and risk epidemiology are disease incidence and
factors is of clear benefit for those dentists engaged in the treatment of this condition. disease prevalence. Incidence refers to
the rate of occurrence of new disease in
a population over a given time interval,
whereas prevalence is the proportion of
persons affected by a disease at a given

T he pathogenesis of periodontal
disease involves a complex
interplay between plaque bacteria and a
susceptible host. Gingivitis precedes
periodontitis, but it is not inevitable that
periodontitis will follow gingivitis. In
gingivitis, the inflammatory lesion is
confined to the gingiva. By contrast, in
periodontitis, inflammatory processes
Philip M. Preshaw, BDS, FDS RCS(Edin.), PhD,
Robin A. Seymour, BDS, FDS RCS(Edin.),
FDS RCS, PhD and Peter A. Heasman, BDS,
FRCPS, PhD, School of Dental Sciences, University
of Newcastle upon Tyne, Framlington Place,
Newcastle upon Tyne, NE2 4BW, UK.
extend to affect all of the periodontal
support structures (gingiva, periodontal
ligament, cementum and alveolar bone),
leading to the clinical signs of
periodontitis. Breakdown of fibres of the
periodontal ligament (PDL) occurs,
resulting in clinical loss of attachment of
the tooth to its supporting structures,
and there is resorption of alveolar bone.
Pocket formation is evident, there is
radiographic alveolar bone loss, teeth
may become mobile, and may require
extraction.
Research into periodontal
pathogenesis has been driven, to a
significant degree, by the observation
point in time. Clearly, it would be very
difficult to identify accurately the
number of new cases of periodontitis
occurring within a given time period
and, for this reason, the prevalence of
periodontitis is routinely used in
periodontal epidemiology in preference
to incidence.
Assessing the prevalence of
periodontitis raises further difficulties.
For example, how is periodontitis
diagnosed or defined? The problem of
accurately identifying the presence of
periodontitis resulted, in the past, in an
overestimation of the prevalence of
disease. Many studies conducted in the

570 Dental Update – December 2004



Periodontal disease is inevitable following
gingivitis.

Periodontal disease is uniformly
distributed in the population.

Disease severity is correlated with plaque
levels.

There is a linear, progressive loss of
attachment over time.

The severity of periodontitis increases
with age.
Table 1. The Old Theory of Periodontitis.
1950s and 1960s failed to distinguish
between gingivitis and periodontitis,
resulting in very high reported disease
prevalence. Data from research
conducted at that time suggested that
periodontitis began in early adulthood
and increased so that almost the entire
population was affected by the time
individuals reached their 40s.1 Tooth
loss was thought to increase gradually
with age, in a relatively linear fashion.1
Data gathered from studies conducted
around this time led to a theory of
disease that we might now refer to as the
Old Theory of Periodontitis (Table 1).
Dentists today recognize the
shortcomings of the old theory of
periodontitis. From careful, longitudinal
monitoring studies that have been
conducted more recently, we know that
the prevalence of severe periodontitis is
lower than previously thought. The
most recent UK Adult Dental Health
Survey reported that, whilst
approximately 43% of the adult
population have moderately advanced
chronic periodontitis (with attachment
loss > 4 mm), only 8% have severe
periodontitis (attachment loss > 6 mm).2
The same study found that over 70% of
adults have visible plaque and calculus
on their teeth. Similar data have been
reported in studies in different
populations. For example, a study of
7,447 dentate individuals in the USA
found that, whilst over 90% of people
aged 13 or older had experienced some
loss of attachment, only 15% exhibited
more severe destruction (attachment
loss > 5 mm).3 A study of Tanzanian
adults found that, whilst there were
abundant plaque and calculus deposits,
Dental Update – December 2004
P E R I O D O N T O L O G Y
with ubiquitous gingivitis, less than
10% of periodontal sites had pockets > 3
mm, and less than 10% of people had > 6
mm attachment loss.4
Research has also focused on the
nature of periodontitis progression.
Early studies considered that loss of
attachment and alveolar bone
destruction continued in a linear fashion
over time. These early studies were
based on repeated cross-sectional
evaluations of cohorts of patients, and
were primarily designed to monitor
periodontitis progression in
populations, rather than individuals.
More recent longitudinal monitoring
studies have revealed that, for the
majority of periodontitis patients, most
of their periodontal sites are stable at
any given time, and only a relatively
small proportion demonstrate disease
progression. Conversely, in a small
percentage of patients who are
susceptible to disease, periodontitis
progression occurs more frequently and
affects multiple sites.5
The data gathered from carefully
conducted, longitudinal monitoring
studies have resulted in a changed
understanding of the prevalence of
periodontal disease, and have led to the
development of a New Theory of
Periodontitis (Table 2). This theory
reveals that severe forms of
periodontitis are found in approximately
10–15% of the population of the
Western world (representing a very
large number of individuals in the UK
alone), and that these individuals are at
high risk for the disease.
MICROBIOLOGY
Evidence that periodontal diseases are
infectious diseases with a bacterial
aetiology was first demonstrated in
humans in experimental gingivitis
studies in the mid-1960s.6 Prior to this
time, the aetiology of periodontitis was
not known, although calculus was
considered to be an irritant to the
gingival tissues. As the pace of research
accelerated, the Specific Plaque
Hypothesis was proposed,7 which
suggested that specific bacterial species
are causative for periodontal disease.

Gingivitis and mild periodontitis are
common (seen in about 40–60% of
people).

Approximately 10–15% of the
population exhibit advanced
periodontitis.

Gingivitis precedes periodontitis, but not
all sites with gingivitis develop
periodontitis.

Periodontitis is not a natural
consequence of ageing.

In some patients, periodontitis may
progress with episodes of disease activity
and periods of quiescence, in a non-linear
manner.
Table 2. The New Theory of Periodontitis.
Putative periodontal pathogens include
Gram-negative species such as
Actinobacillus actinomycetemcomitans,
Porphyromonas gingivalis, Bacteroides
forsythus and Eikenella corrodens. An
alternative hypothesis, the Non-Specific
Plaque Hypothesis,8 stated that disease
results from the physical mass of
subgingival organisms present, and
occurs once a certain threshold has
been reached. In other words, it is the
quantity of plaque that is important
(rather than the quality).
More recently, cluster analysis of
subgingival plaque has demonstrated
that certain species frequently occur
together in ‘complexes’ (Figure 1).9
These complexes have been colour-
coded purple, yellow, green, orange and
red, representing a progression from
health (characterized by a predominantly
gram-positive, aerobic, non-motile
microflora) to disease (characterized by
a gram-negative, anaerobic, motile
microflora). The red complex of species
(P. gingivalis, B. forsythus and
Treponema denticola) is strongly
associated with the clinical signs of
periodontitis. The orange complex
(including Prevotella intermedia,
Fusobacterium nucleatum,
Peptostreptococcus micros and
Campylobacter rectus) is also
associated with periodontitis, but less
strongly than the red complex.9 Plaque
in patients with periodontitis tends to
contain an increased proportion of red
and orange complex species compared
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 P E R I O D O N T O L O G Y

Approximately 300–500 bacterial species

have been identified as being able to
colonize a periodontal pocket but, of
these, only 20–30 are considered to be
pathogenic. Therefore, for periodontitis
to develop, not only is a susceptible
host required (an essential prerequisite),
but pathogenic species must develop in
sufficiently high quantities within the
subgingival plaque biofilm.

PATHOGENESIS OF
PERIODONTITIS
An awareness of the importance of the
host response in periodontal
pathogenesis began to develop in the
1970s and 1980s. For example, peripheral
blood neutrophils collected from
patients with what was then termed
localized juvenile periodontitis (now
called localized aggressive
Figure 1. Relationships of the bacterial species within microbial complexes. The red complex is most periodontitis14) were found to have a
strongly associated with periodontitis. (Adapted, with permission, from Socransky et al., 19989). defective response to chemotactic
stimuli, indicating that failure of a host
to plaque from periodontally healthy knowledge gained from the cluster protective mechanism led to increased
patients.10 In diseased patients, there is analyses of the periodontal microflora, susceptibility to disease.15 Throughout
also a decrease in the proportion of has led to the most current concept of the 1980s and 1990s, research focused
Actinomyces species, which are found in the role of bacteria in periodontitis, the on mediators of the periodontal
large numbers in periodontal health.10 Environmental Plaque Hypothesis.13 inflammatory response to the presence
A critical development in the This hypothesis suggests that the entire of plaque. In particular, these included
understanding of periodontal subgingival microbial environment is the the prostanoids (e.g. prostaglandin E2 –
microbiology was the concept that important determinant of the role of PGE2, which stimulates alveolar bone
plaque exists in biofilms,11 which can be bacteria in the development of disease. resorption) and the cytokines
defined as matrix enclosed bacterial
populations adherent to each other and/
or surfaces or interfaces.12 Biofilms are
complex bacterial communities that form
in aqueous environments where there is
a regular nutrient source. Within the
biofilm, there is primitive homeostasis, a
primitive circulatory system (for waste
elimination and nutrition supply) and a
degree of metabolic co-operation. The
biofilm has evolved to protect individual
bacteria, so that the bacteria are highly
resistant to killing by phagocytosis (and
also antimicrobial drugs) as a result of
the protective matrix in which they are
embedded. For this reason, mechanical
disruption of the biofilm by root surface
instrumentation (RSI) must always be
undertaken as part of periodontal
therapy. Figure 2. (a) Clinically healthy gingival tissues. (b) Histological appearance of clinically healthy
Realization of the importance of gingival tissues. OE, oral epithelium; SE, sulcular epithelium; JE, junctional epithelium; D, dentine; ES,
enamel space; CT, connective tissue.
plaque biofilms, together with

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 P E R I O D O N T O L O G Y
Figure 3. (a) Clinical appearance of gingivitis. (b) Histological
appearance of inflamed gingival tissues. JE, proliferating, ulcerated
junctional epithelium; ICI, dense inflammatory cell infiltrate; BV, dilated
blood vessels. Contrast with histological appearance in Figure 2.
(including the interleukins and tumour
necrosis factor).16 An important family
of enzymes, the matrix
metalloproteinases (which includes
collagenases) was also identified as
having a key role in connective tissue
breakdown in inflamed periodontal
tissues. 17
HISTOLOGICAL CHANGES
In order to understand periodontal
pathogenesis, it is important to have an
appreciation of the histological
appearance of healthy (non-inflamed)
and inflamed gingival tissues. Figure 2
shows the clinical appearance of health
together with a buccal-lingual section
of clinically healthy gingiva. There is
continuity of the oral epithelium, the
sulcular epithelium and the junctional
epithelium. The connective tissue is
comprised of well ordered, densely
packed, collagen fibre bundles.
Occasional neutrophils can be
identified as small, dark-staining cells
present close to the junctional
epithelium. The free gingival margin is a
well-defined knife-edge facing the
enamel surface.
The appearance of the healthy
gingiva in Figure 2 contrasts sharply
with that of an established gingivitis
(Figure 3). Following plaque
574
Figure 4. (a) Clinical appearance of periodontitis. (b) Histological
appearance of periodontitis (note furcation involvement). D, dentine; AB,
alveolar bone; PE, pocket epithelium. Contrast with histological appearance
in Figures 2 and 3.
accumulation at the gingival margin,
there has been infiltration of the
connective tissues by numerous
defence cells, particularly neutrophils
(polymorphonuclear leukocytes or
PMNs), plasma cells, monocytes/
macrophages and lymphocytes. As a
result of the accumulation of these
defence cells, there has been disruption
of the normal anatomy of the
connective tissues, with breakdown of
collagen fibres to create space to
accommodate the infiltrating defence
cells. Blood vessels are dilated, there is
vascular proliferation, and further
collagen loss. The tissues are swollen
and the free gingival margin is rounded
and enlarged. When viewing a
histological section of inflamed tissues
(Figure 3), it is very easy to relate these
histological inflammatory changes to
the clinical changes seen in gingivitis,
such as redness (erythema), swelling
(oedema) and disruption of normal
anatomy.
The histological appearance of
periodontitis can be seen in Figure 4.
There is apical proliferation of the
junctional epithelium following
attachment loss and further destructive
events in the connective tissues in
response to plaque irritation. The
lesion is no longer localized, and the
inflammatory cell infiltrate extends
apically and laterally into the
underlying connective tissues,
including the periodontal ligament and
the alveolar bone. Alveolar bone loss is
evident and there is breakdown of
fibres of the periodontal ligament.
INFLAMMATORY RESPONSE
The accumulation of plaque bacteria in
the gingival sulcus results in the
release of microbial substances
(chemotactic factors such as
lipopolysaccharide – LPS, microbial
peptides) which cross the junctional
epithelium and enter the gingival
connective tissues. Epithelial and
connective tissue cells are thus
stimulated to produce inflammatory
mediators that result in an inflammatory
response in the tissues. Blood vessels
dilate (vasodilatation) and become more
permeable to fluid and cells. Fluid
accumulates in the tissues, and defence
cells migrate from the capillaries, up a
chemotactic concentration gradient
towards the source of the chemotactic
stimulus, bacteria and their products in
the gingival sulcus. Thus, there is
accumulation of fluid and cells in the
tissues, and the gingiva become
erythematous and oedematous. In early
stages of the gingival inflammation,
neutrophils predominate. These cells
Dental Update – December 2004

Figure 5. The pathogenesis of periodontitis. PMNs – polymorphonuclear leukocytes; MMPs – matrix
metalloproteinases; LPS – lipopolysaccharide. (Adapted, with permission, from Page and Kornman,
199718).
are capable of phagocytosis of plaque
bacteria and bacterial killing. Bacterial
killing by PMNs involves both
intracellular (following phagocytosis of
bacteria within membrane-bound
structures inside the cell) and
extracellular mechanisms (by release of
PMN enzymes and oxygen radicals
outside the cell). As bacterial products
enter the circulation, committed
lymphocytes return to the site of
infection, and B lymphocytes are
transformed to plasma cells, which
produce antibodies against specific
bacterial antigens. Antibodies are
released in the gingival tissues and, in
the presence of complement, facilitate
and enhance PMN phagocytosis and
bacterial killing.
Thus, as a result of the chronic
microbial challenge, the diffusion of
bacterial products (antigens,
lipopolysaccharide) across the
junctional epithelium results in a host
immune-inflammatory response in the
tissues. This response is essentially
protective in nature; defence cells are
recruited to the area (particularly
PMNs) and antibodies are produced
against the infecting bacteria. The
clinical signs of gingivitis develop. In
those patients who are not susceptible
to periodontitis, these primary defence
mechanisms control the infection and
Dental Update – December 2004
P E R I O D O N T O L O G Y
chronic inflammation (i.e. chronic
gingivitis) may persist indefinitely. A
schematic illustration of these events is
shown in Figure 5.18
In those individuals who are
susceptible to periodontitis, however,
the microbial challenge is not contained
by the primary host defences. There is
proliferation of the junctional
epithelium which becomes increasingly
permeable and ulcerated. This
accelerates the ingress of bacterial
products, and the inflammation
worsens. Further defence cells are
recruited to the area, including
macrophages and lymphocytes. Large
numbers of PMNs migrate into the
tissues, secreting large quantities of
destructive enzymes and inflammatory
mediators. These include matrix
metalloproteinases (MMPs), including
collagenases, which break down
collagen fibres in the gingival and
periodontal tissues. The infiltrating
inflammatory and immune cells are
accommodated by the breakdown of
structural components of the
periodontium. Further tissue damage
results from the extracellular release of
PMN enzymes and oxygen radicals,
which occurs when the PMN
encounters a bacterial mass that is too
large to be phagocytosed. Again, this
is primarily a protective response, but
the release of large quantities of
destructive enzymes into the
extracellular environment by the PMNs
results in significant damage to the
periodontal tissues.
Macrophages are also recruited to
the area, and are activated (by binding
to LPS) to produce prostaglandins (e.g.
PGE2), interleukins (e.g. interleukin-1),
tumour necrosis factor-Ȋ (TNF-Ȋ) and
MMPs. Interleukins and TNF-Ȋ bind to
fibroblasts, which are stimulated to
produce additional quantities of PGE2,
interleukins, TNF-Ȋ and MMPs. The
concentration of these enzymes and
inflammatory mediators becomes
pathologically high in the periodontal
tissues. MMPs break down collagen
fibres, disrupting the normal anatomy
of the gingival tissues, resulting in
destruction of the periodontal ligament
(PDL). As the inflammation extends
apically, osteoclasts are stimulated to
resorb alveolar bone to create yet more
space for the continuing inflammatory
cell infiltrate. Bone resorption by
osteoclasts is stimulated by the high
levels of prostaglandins, interleukins
and TNF-Ȋ in the tissues.
As the inflammation extends apically,
there is further breakdown of collagen
fibres in the PDL and resorption of
alveolar bone. These events occur as
part of a defence mechanism in which
defence cells are recruited to the area to
deal with the bacterial infection. The
breakdown of the tissues is occurring
to create space within the periodontium
to accommodate the defence cells. As
the epithelium is broken down, the
junctional epithelium regrows at a more
apical location, and a pocket is formed,
lined with an ulcerated, hyperplastic
pocket epithelium. Plaque bacteria then
migrate apically along the root surface
into the pocket where the physical
conditions allow gram-negative
anaerobic species to proliferate.
Bacterial products continue to
challenge the host, and the host
continues its frustrated response to
these products. Inflammation extends
further and further apically, more bone
is resorbed and PDL broken down to
accommodate infiltrating defence cells.
The pocket deepens, there is
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 P E R I O D O N T O L O G Y
attachment loss, bone loss, and the
clinical and radiographic signs of
periodontitis become apparent.
As is evident from Figure 5,
therefore, bacteria initiate the disease,
and bacterial antigens that cross the
junctional epithelium drive the
inflammatory process. Therefore,
bacteria are essential for periodontitis
to occur, but they are insufficient to
cause disease alone. For periodontitis,
a susceptible host is also required. The
majority of periodontal breakdown
(bone loss, attachment loss) is caused
by host-derived destructive enzymes
(MMPs) and inflammatory mediators
(prostaglandins, interleukins) that are
released during the inflammatory
response. That is, bacteria initiate
disease, but the key destructive events
in periodontitis are caused by host-
derived mediators and enzymes
released by inflammatory cells (and can
almost be considered as ‘collateral’
damage resulting from the inflammatory
response). It is paradoxical that the
inflammatory response to the plaque
bacteria, which is essentially protective
in design, is responsible for the
breakdown of the soft and hard
periodontal tissues. Periodontal
disease is characterized by high
concentrations of MMPs, cytokines
and prostanoids in the periodontal
tissues, whereas periodontal health is
characterized by the opposite.12
RISK FACTORS
Host susceptibility is also significantly
affected by risk factors (defined as any
factor that increases the probability
that disease will develop in an
individual19), including genetic risk
factors and environmental/acquired risk
factors.
Genetic factors have an important
role in determining risk for
periodontitis, and are only just
beginning to be understood. Genetic
factors may explain why certain
patients, despite good plaque control,
have advanced periodontitis, whereas
other patients with very poor oral
hygiene seem relatively resistant to
disease. Genetic factors that may
576
increase susceptibility to disease
include defects of phagocytosis
(resulting in a hypo-response to the
bacterial challenge), or enhanced
production (i.e. a hyper-response) of
cytokines (e.g. interleukins),
prostaglandins and/or MMPs for a
given bacterial challenge. The concept
of high- and normal-responders has
been postulated,20 in which high-
responders produce large quantities of
inflammatory mediators as part of their
host inflammatory response to the
presence of plaque (hyper-responsive
individuals). Consequently, these
individuals are susceptible to
periodontitis compared to normal-
responders who produce minimal levels
of inflammatory mediators for a given
bacterial challenge and do not
demonstrate significant periodontal
breakdown. There is clearly a fine
balance, therefore, in the nature of the
inflammatory response to the presence
of plaque, and both under-activity
(hypo-responsiveness) and over-
activity (hyper-responsiveness) of
components of the host response can
result in increased tissue damage, that
is, increased susceptibility to disease.
The interleukin-1 (IL–1) gene
polymorphism has also been
investigated for its role in periodontal
disease.21 The IL–1 gene is
polymorphic (can exist in more than one
distinct form), and early data suggest
that, when smokers are excluded, those
patients with one particular
polymorphism produce more IL–1 than
normal (hyper-responders), and are
more at risk for developing chronic
periodontitis than those individuals
who do not exhibit this polymorphism.
However, more recent genetic studies in
different population groups have
revealed some ambiguity with regards
to the relationship between the
presence of IL–1 polymorphisms and
clinical manifestations of
periodontitis.22 Genetics is a current
area of intense research in
periodontology, with the aim being to
identify those genetic traits that place
patients at risk for disease, so that they
can be identified and targeted for
intensive monitoring and preventive
treatment before advanced disease
develops.
Smoking is the most important
environmental risk factor for
periodontitis, and many studies have
shown that smokers have more
attachment loss, more bone loss and
more tooth loss than non-smokers.23-25
Indeed, a recent study of over 12,000
dentate adults concluded that smoking
may be responsible for more than half
of the cases of periodontitis in the
USA.26 Smoking has many effects on
the host immune-inflammatory
response, including:

decreased wound healing;

suppression of antibody
production;

reduced fibroblast function
(resulting in increased collagen
breakdown and decreased collagen
repair);

reduced PMN phagocytosis and
bacterial killing;

reduced vascularity.
Smoking therefore inhibits the defence
mechanisms against the microbial
challenge, and reduces the
opportunities for healing in the
periodontal tissues.
OPTIONS FOR TREATMENT
Periodontal treatment primarily
involves reducing the bacterial
bioburden, by the mechanical removal
of plaque and calculus (either by a non-
surgical approach, or in combination
with periodontal surgery). This is
undertaken by root surface
instrumentation (RSI) of affected tooth
roots, which can be performed using
both manual and ultrasonic
instruments. RSI involves the
mechanical disruption of the
subgingival plaque biofilm, together
with removal of plaque, calculus and
necrotic cementum. The term RSI is
used in preference to ‘scaling and root
planing’ (SRP), which implies a
requirement to achieve a smooth and
glassy-hard root surface, neither of
which is necessary to permit
periodontal healing.27,28
Dental Update – December 2004

RSI is an effective procedure and
studies have shown that treatment
outcomes (pocket reduction,
attachment gain) following RSI are
remarkably consistent on a population
basis.29 Our improved understanding of
the microbiology of periodontitis,
including the concept of biofilms,
underscores the importance of
mechanical disruption of subgingival
plaque in periodontal treatment. Well-
executed and thorough RSI will
continue to be the cornerstone of
periodontal treatment for the
foreseeable future.
Research into the pathogenesis of
periodontal disease, particularly the
role of the host response, has also
introduced other possibilities for
adjunctive pharmacotherapies in the
management of periodontitis. A variety
of drug categories are under research
for their ability to modulate destructive
components of the host response (such
drugs are termed Host Modulatory
Therapies, HMTs) so that periodontal
breakdown is reduced. These include:

non-steroidal anti-inflammatory
drugs (NSAIDs), which block the
production of prostaglandins; 30

doxycycline, which downregulates
MMPs (collagenases) in inflamed
periodontal tissues; 31 and the

bisphosphonates, which reduce
osteoclast activity and bone
resorption. 32
The future will see the development
of new HMTs for the treatment of
periodontitis, such as chemically
modified tetracyclines (CMTs) (in
which the tetracycline molecule is
altered to remove all antibiotic
properties, retaining only the
collagenase inhibition capabilities of
the compound), antioxidant
preparations, and anti-cytokine drugs
(which may have a role in the
modulation of excessive cytokine
activity in periodontal tissues).
SUMMARY
The dental profession now has a much
better understanding of the
Dental Update – December 2004
P E R I O D O N T O L O G Y
microbiology of periodontitis and the
importance of the host response in
periodontal pathogenesis. We know
that a susceptible host, together with
the emergence of periodontal
pathogens within the subgingival
biofilm, are required for periodontitis to
develop. In health, PMNs are the
predominant defence cell-type in the
gingival tissues, and these
phagocytose and kill bacteria without
significant damage occurring to the
periodontal tissues. In susceptible
patients, periodontitis develops
following chronic exposure of the host
to bacterial products that diffuse
across the junctional epithelium,
resulting in the development of an
immune-inflammatory response. This is
characterized by an increased fluid and
cellular infiltrate in the gingival tissues.
Pro-inflammatory mediators
(interleukins, prostaglandins) are
released within the tissues. More
PMNs are recruited to the area,
together with macrophages and
lymphocytes. Tissue damage results
from extracellular release of destructive
host-derived enzymes, and the large
numbers of infiltrating defence cells are
accommodated by breakdown of
structural components of the
periodontium. The majority of the
tissue breakdown occurs as collateral
damage arising from the activation of
the host defences against the presence
of bacteria leading, ultimately, to the
clinical signs of periodontitis,
attachment loss and alveolar bone
resorption.
A CKNOWLEDGEMENTS
Permission for the use of the following images is
gratefully acknowledged:
Figures 2b and 4b from Heasman PA, Preshaw PM,
Smith DG (1997). Colour Guide: Periodontology.
Elsevier.
Figure 3b from Rateitschak KH, Rateitschak EM, Wolf
HF, Hassell TM (1989). Colour Atlas of Dental
Medicine – Periodontology, 2nd edn.Thieme.
R EFERENCES
1. Marshall-Day CD, Stephens RG, Quigley LF.
Periodontal disease: prevalence and incidence.
J Periodontol 1955; 26: 185–203.
2. Kelly M, Steele J, Nuttall N, et al.The condition of
supporting structures. In: Adult Dental Health
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3. Brown LJ, Brunelle JA, Kingman A. Periodontal
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Comparison of the microbiota of supra- and
subgingival plaque in health and periodontitis.
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Korber DR, Lappin-Scott HM. Microbial biofilms.
Annu Rev Microbiol 1995; 49: 711–745.
12. Page RC. Milestones in periodontal research and
the remaining critical issues. J Periodont Res 1999;
34: 331–339.
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system for periodontal diseases and conditions.
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juvenile and rapidly progressing periodontitis.
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and prostaglandins in immune homeostasis and
tissue destruction in periodontal disease.
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3: 85–96.
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Modulation of host PGE2 secretion as a
determinant of periodontal disease expression.
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BOOK REVIEW
A Colour Handbook of Oral Medicine. By
M.A.O. Lewis and R.C.K. Jordan. Manson
Publishing Ltd, London, 2004 (192pp.,
£48.00h/b; £29.95p/b). ISBN 1-84076-032-
Xh/b; 1-84076-033-8p/b.
This book uses a symptom-based
approach to the diagnosis and initial
treatment of oral medical conditions.
Such an approach to the subject matter
makes this book a genuinely practical
source of reference and will be
welcomed by clinicians, particularly
those in the primary care setting.
The first chapter provides a useful
reminder of the diagnostic process,
briefly addressing history, examination
and investigative methods. Importantly,
it details some normal oral mucosal
features that may be mistaken for
COCHRANE SYNOPSES
Al-Ani MZ, Davies SJ, Gray RJM, Sloan P,
Glenny AM. Stabilisation splint therapy
for temporomandibular pain dysfunction
syndrome (Cochrane Review). In: The
Cochrane Library, Issue 1, 2004.
Chichester, UK: John Wiley & Sons, Ltd.
'Not enough evidence about whether
stabilisation splints can reduce pain
caused by painful temporomandibular
(jaw) disorders.
Pain dysfunction syndrome (PDS) is
the most common TMD (temporo-
mandibular disorder, from the joint
between the lower jaw and base of the
skull). PDS is also called facial
arthromylagia, myofacial pain
dysfunction syndrome and
578
NHANES III. National Health and Nutrition
Examination Survey. J Periodontol 2000; 71: 743–
751.
27. Khatiblou F, Ghodssi A. Root surface
smoothness or roughness in periodontal
treatment.A clinical study. J Periodontol 1983; 54:
365–367.
28. Oberholzer R, Rateitschak KH. Root cleaning or
root smoothing: an in vivo study. J Clin Periodontol
1996; 23: 326–330.
29. Cobb CM. Clinical significance of non-surgical
periodontal therapy: an evidence-based
pathology. The remaining eight chapters
each deal with a particular clinical sign
or symptom and include ulceration,
blisters, white patches, erythema,
swelling, pigmentation, pain and dry
mouth. These chapters are arranged in a
similar, accessible format, namely a list
of differential diagnoses, and then a
brief paragraph relating to the topic area
under discussion. Subsequently, each
clinical entity is discussed under the
headings of ‘aetiology and
pathogenesis’, ‘clinical features’,
‘diagnosis’ and ‘management’. The text
is lavishly illustrated with some 342
illustrations in total. The majority of
these are high quality colour clinical
photographs that often helpfully depict
a variety of presentations of the same
condition, so facilitating its easier
identification.
Inevitably, as with all books, there are
certain aspects of the text that may be
craniomandibular dysfunction. One
option is a splint (a type of bite plate) at
night when people otherwise may grind
their teeth more. The stabilisation splint
(SS) is one type, also known as the
Tanner appliance, the Fox appliance, the
Michigan splint or the centric relation
appliance. The review found there is not
enough evidence from trials to show
whether or not stabilisation splints can
reduce PDS.'
Marinho VCC, Higgins JPT, Sheiham A,
Logan S. One topical fluoride
(toothpastes, or mouthrinses, or gels, or
varnishes) versus another for
preventing dental caries in children and
adolescents (Cochrane Review). In: The
Cochrane Library, Issue 1, 2004.
Chichester, UK: John Wiley & Sons, Ltd.
perspective of scaling and root planing. J Clin
Periodontol 2002; 29(Suppl. 2): 6–16.
30. Higgs GA,Vane JR. Inhibition of cyclo-oxygenase
and lipoxygenase. Br Med Bull 1983; 39: 265–270.
31. Caton JG, Ciancio SG, Blieden TM, et al.
Treatment with subantimicrobial dose
doxycycline improves the efficacy of scaling and
root planing in patients with adult periodontitis.
J Periodontol 2000; 71: 521–532.
32. Reddy MS, Weatherford TW, Smith CA, West
BD, Jeffcoat MK, Jacks TM. Alendronate
treatment of naturally-occurring periodontitis in
beagle dogs. J Periodontol 1995; 66: 211–217.
deemed a little controversial or out of
date, but these are minor in nature. For
example, the use of stimulated parotid
flow rates is cited as an investigation for
..
Sjogren’s syndrome. However, the
revised EU-USA consensus criteria,
which are now broadly adopted, require
the use of unstimulated whole saliva
flow rates.
In summary, this book details the
salient features of a wide range of both
common, and also some less common,
orofacial pathologies, in a practical and
accessible fashion. Although principally
aimed at clinicians, this book will also
appeal to dental undergraduates who are
sure to find its well-planned layout and
wealth of colour images of real value in
their studies.
John Hamburger
University of Birmingham School of
Dentistry
'Topical fluorides such as mouthrinses
and gels do not appear to be more
effective at reducing tooth decay in
children and adolescents than fluoride
toothpaste.
Tooth decay (dental caries) is painful,
expensive to treat and can seriously
damage teeth. Fluoride is a mineral that
prevents tooth decay. Fluoride is added
to the water supply in many areas. It can
also be applied in the form of
toothpastes, mouthrinses, gels or
varnishes. The review of trials found that
fluoride toothpastes, mouthrinses and
gels reduce tooth decay in children and
adolescents to a similar extent. However,
toothpastes are more likely to be regularly
used. There is no strong evidence that
varnishes are more effective than other
types of topical fluoride.'
Dental Update – December 2004