Why Is Periodontal Disease More Prevalent and More Severe in People with Down Syndrome?
James Morgan, BA, BDentSc
Co. Kildare, Ireland
Spec Care Dentist 27(5):197-202, 2007
Reprinted with the permission of Ronald L. Ettinger, BDS, MDS, DDSc, Editor|
Special Care Dentistry Association
Periodontal disease has been found to
be significantly more prevalent and more
severe in people with Down syndrome.
A series of studies have reported a
prevalence of between 58% and 96% for
persons younger than 35 years of age.
This phenomenon cannot simply be
attributed to poor oral hygiene. The etiology of periodontal disease in persons
with Down syndrome is complex. In
recent years, much focus has been
placed on the altered immune response
resulting from the underlying genetic
disorder. This paper presents an
overview of contemporary knowledge on
periodontal disease in patients with
KEY WORDS: Down syndrome, periodontal disease, preventive care
Down syndrome (DS) is an autosomal chromosomal disorder resulting from trisomy of
all or part of chromosome 21.1 Approximately 95% of people with DS have an extra
complete chromosome 21. The remaining 5% result from other chromosomal abnormalities including translocation in 3% of people and mosaicism in 2% of people.2,3 The
incidence of DS is generally cited as being between 1 in 600 to 1 in 1,000 live births.2
In Ireland, this condition affects approximately 1 in 580 live births, which is the highest incidence in Europe.4
Periodontal disease is defined as "an inflammatory disease of the supporting tissues
of the teeth caused by specific microorganisms, resulting in progressive destruction of
the periodontal ligament and alveolar bone with pocket formation, recession, or both."5
The pathogenesis of periodontal disease is complex. In response to microbial substances released from plaque bacteria in the gingival sulcus, epithelial and connective
tissue cells are stimulated to produce inflammatory mediators, leading to infiltration
of the connective tissue by numerous defense cells. In the early stages of the immune
response, neutrophils predominate. As further microbial substances enter the systemic circulation, committed lymphocytes return to the site of infection, and
antibodies specific to bacterial antigens are produced by plasma cells. This essentially
protective response is enough to control the infection in people who are not susceptible to periodontitis.6
In susceptible individuals, however,
the primary host defenses are unable to
control the microbial challenge, leading
to the epithelium becoming increasingly
permeable and ulcerated. There is
increased migration of neutrophils into
the tissues, which secrete a variety of
inflammatory mediators and proteolytic
enzymes. Once the concentration of
these inflammatory mediators and
enzymes becomes pathologically high,
histological destruction of the collagen
fibers, periodontal ligament, and alveolar
bone occurs.6 Preshaw et al.6 noted that
the majority of periodontal destruction is
the result of "collateral damage arising
from the activation of the host defenses
against the presence of bacteria".
In 2005, the World Health
Organization provided an overview of
periodontal disease worldwide and
reported that 10% to 15% of adults suffered from periodontal disease.7 Brown et
al.8 reported that the prevalence of periodontal disease among the general
population in the United States ranged
from 29% for persons aged 19 to 45
years, to 50% for persons aged 45 years
and older. An increased prevalence and
severity of periodontal disease has been
reported in people with DS compared
with age-matched subjects of similar
levels of intellectual impairment and
compared with the general population.9-15
Prevalence varies between 58% and 96%
for those under 35 years of age.11,14
The increased prevalence and severity
of periodontal disease in persons with
Down syndrome may be attributed to a
range of local factors associated with the
oral cavity, as well as systemic factors
associated with the genetic disorder itself.
Prevalence and severity of periodontal disease
Johnson and Young14 examined 70 children with DS (mean age 10.8 ± 3.0 years)
and compared them with 40 age-matched
subjects who did not have DS but had
similar learning disabilities. The presence
of periodontal disease was observed in
96% of persons in the group with DS and
it was much more severe than in the control group. Bone loss followed a horizontal
pattern and was most obvious in the lower
anterior segment. Agholme et al.,12 Cichon
et al.,16 and Saxén et al.17 also observed this
pattern of bone loss.
Saxén et al.17 used orthopantomograms to provide a more objective
method for evaluating periodontal disease. Bone loss was measured from the
cemento-enamel junction to the alveolar
bone margin. A tooth with bone loss of
5mm or more was regarded as affected. It
was reported that 69% of subjects with
DS aged 9 to 39 years had more than
5mm bone loss compared with 20% of
the control group, despite similar levels
of plaque and calculus. In a follow-up
study carried out five years later, the
prevalence of bone loss of 5mm or more
had increased to 75% in the subjects
In a longitudinal study carried out by
Agholme et al.,12 periapical and bitewing
radiographs were used to aid in the diagnosis of periodontal disease. It was
reported that 35% of subjects with DS
(mean age 16.6 years) had experienced
alveolar bone loss. Seven years later the
prevalence of alveolar bone loss had
increased to 74%.
Cutress19 reported that persons with
DS who were living in institutions had
poorer levels of plaque control,
increased calculus deposits, and an
increased prevalence of periodontal disease when compared to subjects living at
home with DS. Swallow20 came to the
Etiology of periodontal disease in Down syndrome
- Oral hygiene
Cohen et al.21 studied a group of 100 subjects with DS and found that oral
hygiene was generally poor. This was in
agreement with Sakellari et al.10 who
reported that people with DS had poorer
oral hygiene than healthy individuals. In
another study, Sakellari et al.22 found that
the mean plaque score was 100% in a
group of subjects with DS who were
between the ages of 26 and 37 years.
Sakellari22 also found that following oral
hygiene instruction, subjects with DS
had reduced ability to maintain adequate
plaque control. This could possibly be
associated with impairment of fine motor
function resulting in poor manual dexterity, as reported by Desai.2
Cohen et al.21 reported that calculus
deposits were abundant among children
with Down syndrome. This was in agreement with a similar study by Johnson
and Young.14 However, a less severe distribution of calculus was reported by
Barr-Agholme et al.23 (20%) and by Sasaki
et al.24 (14.8%), respectively.
- Open-mouth breathing
Persons with Down syndrome exhibit
characteristic phenotypical orofacial
anomalies including an underdeveloped
facial mid-third resulting in a hypoplastic
maxilla and mandibular prognathism.1
The hypoplastic maxilla, combined with
an enlarged tonsillar volume, causes
upper airway congestion and a tendency
for increased mouth-breathing.1,2
Swallow20 reported that 82.9% of children
with DS had their lips habitually apart.
- Tooth morphology
Several authors have discovered irregularities in the morphology of crowns and
roots in persons with DS.
Desai et al.2 reported that clinical
crowns were usually shorter and smaller
than normal in subjects with DS, and
that root length was reduced. Bajic et al.25
reported a significant reduction in root
length as well as an increased prevalence
of fused molar roots in persons with DS.
The prevalence of fused molar roots in the maxilla was 65.1%, and in the
mandible it was 40.5%, compared with
40.5% and 21.1%, respectively, in the
general population. Cutress19 also suggested that tooth morphology, including
short roots, could influence periodontal
disease in persons with Down syndrome.
- Microbiological plaque composition
Studies10,11,22,26-28 detailing the microbiological composition of plaque from subjects
with DS vary in reporting different types
of organisms involved in the periopathogenic process. Sakellari et al.10 reported
that subjects with DS in all age groups
had significantly higher levels of periodontopathic bacteria. In particular, a
significantly higher prevalence of P. gingivalis, A. actinomycetemcomitans (A.a.), T. forsythesis, and P. intermedia was
observed. These findings suggest that
colonization by significant periodontal
pathogens occurs frequently in subjects
with DS, even in adolescence. Amano et
al.26 observed that even in early childhood (age 2 to 4 years) significantly
higher levels of P. gingivalis, B. forsythis,
and T. denticola were detected in subjects
with DS. These are considered to be
important pathogens in severe types of
adult periodontitis.26 In particular, the
occurrence of P. gingivalis was found to
increase with age. No significant differences, however, were found in relation to A.a. between subjects with DS and
healthy age-matched controls. Morinushi
et al.27 measured the serum antibody titer
of subjects with DS to various periodontopathic bacteria and found that even in
subjects with DS under the age of 6
years, the average antibody titer to A.a., F. nucleatum, and P. intermedia exceeded
that of the normal adult reference pool.
It was also found that these titers
increased significantly with age. These
findings suggest that A.a., F. nucleatum,
and P. intermedia are probably present in
significant numbers in subjects with DS,
even in those under the age of 6 years.
Hanookai et al.28 investigated the
prevalence of herpes virus species in
periodontally involved subgingival sites
in subjects with DS. It was found that
32% of patients had Epstein-Barr virus-1, 26% human cytomegalovirus, and 16%
herpes simplex virus. Herpes virus
species may cause periodontal pathology
by suppressing the activity of B- and T-
lymphocytes as well as up-regulating
certain pro-inflammatory mediators such
as IL-1 and TNF-alpha.28
- Acute necrotizing ulcerative gingivitis (ANUG)
Cohen et al.29 reported that of 100 subjects with DS examined, 29% had
experienced ANUG. In a later study,
Brown et al.30 compared 149 subjects
with DS with 657 normal subjects and
found that at least 35.6% of patients with
DS had experienced at least one episode
of ANUG compared with 4.1% of the
control group. Of the affected subjects
with DS, 49.1% had experienced recurrent episodes. The mean age at the time
of the first recorded episode was 9.4 ± 4.4 years, even though ANUG typically
affects young adults.31 Dissimilarities in
the diagnostic criteria for ANUG have
led to confusion in the literature as to its
prevalence among the general population. These values range from less than
1% to 6.9%.32
- Neutrophil dysfunction
"Neutrophils are the primary cells
involved in the first line of host defense
against bacterial infection."33
"Neutrophils have multiple surface
receptors that enable them to bind to and
phagocytize bacteria once they reach the
site of infection."34 In the different stages
of periodontal disease, accumulation of
neutrophils in the connective tissue,
junctional epithelium, and gingival
sulcus are characteristic morphological
Izumi et al.33 reported that neutrophil
chemotaxis was significantly impaired in
subjects with DS when compared with
healthy controls. The authors found that
50% of subjects with DS had defective
neutrophil chemotaxis. They also found
that the prevalence of bone loss in subjects with DS was inversely proportional
to the neutrophil chemotactic index of
the patient. These findings are in agreement with Yavuzyilmaz et al.,35 who found a reduction in neutrophil chemotaxis, in neutrophil phagocytosis, and in
the mean random migration of neutrophils. The relatively short half-life of
neutrophils in people with DS (3.7 hours
compared with 6.6 hours in healthy individuals) may account for their neutrophil
- T-lymphocyte dysfunction
Cichon et al.16 reported that peripheral T-lymphocytes in subjects with DS have a diminished ability to recognize and
respond to specific antigens. This study
demonstrated a quantitative and qualitative deficiency of T-lymphocytes.
Clee-Sohoel et al.36 observed that the
number of T-cell receptor-bearing lymphocytes in marginal periodontitis in
subjects with DS was less than in otherwise healthy individuals. Shaw and
Saxby37 stated that the percentage of circulating T-cells is low from birth and
suggested that T-cell maturation may be
an integral part of Down syndrome.
Whittingham et al.38 demonstrated an
atypical immunodeficiency of the T-lymphocyte system. The authors reported
that the T-cell pattern included hypo-responsiveness to antigenic stimulus, a
low mitotic activity, and an increase in
immature T-lymphocytes. Björkstén et al.39 reported a link
between depressed neutrophil chemotaxis and depressed lymphocyte
responsiveness in patients with DS who
had low serum zinc levels. Following a
two-month course of treatment with zinc
phosphate, an increase in serum zinc
levels as well as enhanced neutrophil and
T-lymphocyte function was observed.
Zinc is involved in numerous metabolic
pathways and is essential for synthesizing RNA and DNA.40
- Inflammatory mediators and proteolytic enzymes
Komatsu et al.41 found that tissue
destruction related to progressive periodontitis was due to actions of both the
host and bacterial-derived proteolytic
enzymes. Barr-Agholme et al.42 reported
that the mean level of Prostaglandin E2
(PGE2) in the gingival crevicular fluid
(GCF) of subjects with DS was significantly higher than in the healthy controls. This finding was in agreement with
a similar study carried out by
Tsilingaridis et al.43 PGE2 was present in
inflamed periodontal tissue and was a
potent mediator of bone resorption.44
Barr-Agholme et al.42 also proposed that
the enhanced levels of PGE2 found in
the GCF of patients with Down syndrome might be related to the altered
composition of the subgingival
microflora. This suggestion was based on
the fact that lipopolysaccharide from A.a.
has been reported to stimulate the production of PGE2 in monocytes.42
Komatsu et al.41 reported that the
production of matrix metalloproteinases
was significantly higher in subjects with
DS than in the control group. These findings were in agreement with Tsilingaridis
et al.43 "Matrix metalloproteinases comprise a family of proteolytic enzymes that
collectively degrade the extra-cellular
matrix in chronic inflammatory diseases
such as periodontitis."44
- Hyper-innervation of the gingiva
Barr-Agholme et al.45 observed that the
gingivae of subjects with DS display profound inflammatory reactions alongside
hyper-innervation of what was assumed
to be the sensory part of the innervation
of the gingiva. This "hyper-innervation"
may not be particular to Down syndrome
but may be a reaction brought on by
inflammation. Alternatively, chemical
transmitters released from these nerves
may be responsible for the inflammatory
reaction observed.45 This phenomenon
may explain results obtained from two
studies on experimental gingivitis, which
showed that despite identical plaque
accumulation, the gingivae of subjects
with DS had more extensive inflammation when compared to age-matched
healthy individuals.46,47 However, functional defects of neutrophils and
lymphocytes have also been proposed as
possible explanations for the difference
in gingival response to plaque.47
Barriers to dental services
Kaye et al.48 reported that while most
adults with DS regularly attended their
dentist, little treatment was actually provided. Allison et al.49 observed that parents of children with Down syndrome
frequently encounter problems with
access to oral care for their children.
Children with DS were significantly less
likely to receive dental treatment than
their non-DS siblings. Although some
authors16,18 have reported that preventive
programs have little effect on the progression of periodontal disease in
patients with Down syndrome, more
recent studies9,24 have shown the effectiveness of frequent preventive care.
Yoshihara et al.9 demonstrated the usefulness of periodic preventive care in
suppressing the severity and progression
of periodontal disease in subjects with
DS. In their study, patients were divided
into two groups: those who had received
frequent preventive care, and those who
had not been treated professionally in
more than a year. Significant reductions
were noted in mean pocket depth
(2.5mm and 3.1mm, respectively), mean
frequency of periodontal pockets (46%
and 91% respectively), and frequency of
the prevalence of pathological alveolar
bone loss (62% and 100% respectively),
when the "managed group" was compared to the "interrupted group." Sasaki et al.24 showed the efficacy of monthly
preventive care, which consisted of
mechanical plaque control and oral
hygiene instruction over a period of two
and a half years. Significant reduction in
gingival inflammation and probing
pocket depths were noted at that time
(mean pocket depth at baseline was
2.9mm and after 2.5 years was 1.3mm).
The use of chlorhexidine mouthwash to
compensate for ineffective plaque
removal has also been advocated.50
People with Down syndrome experience
more prevalent and severe periodontal
disease.9-15 It has been reported16,37 that the
progression of the disease in persons with
DS was similar to aggressive periodontal
disease. A multi-factorial etiology
accounting for this prevalence and severity has been proposed. People with DS
have poorer levels of oral hygiene,2,10,21,22 and increased calculus.14,17,21,23,24 However, most authors agree that the amount of
plaque and calculus present was not commensurate with the severity of
periodontal disease observed.16,17,19,21,47,51
Open-mouth breathing reduces the
cleansing action of the saliva and encourages the accumulation of plaque; it also
dehydrates the gingival tissues, which
may impair the individual's resistance to
infection.52 Shorter root lengths and an
increased prevalence of fused roots may
also influence periodontal disease.2,19,25 It
has been suggested that the fused molar
roots favor the progression of periodontal
disease because occlusal forces have a
greater effect on these than on teeth with
Subgingival plaque in people with DS harbors increased amounts of suspected
periodontal pathogens.10,26-28 Gram-negative bacteria contain lipopolysaccharide
in their cell wall. Among other effects,
lipopolysaccharide has the potential to
activate the complement system, produce
inflammation, and stimulate bone resorption.53 Herpes virus can also influence
periodontal disease. Hanookai et al.28
suggested that periodontal herpes virus
and bacterial co-infections might favor
destructive periodontal disease. However,
few studies have been carried out on this
ANUG is more prevalent in Down
syndrome.29,30 ANUG can result in the
formation of characteristic gingival
craters, which encourages plaque stagnation, and can favor the progression of
any underlying periodontal disease.31
Neutrophils and T-lymphocyte function is impaired in people with DS.16,33,35,36 Neutrophils play an intimate role in the
periodontal disease process because they
have the ability to detect and migrate
toward infection and phagocytose
microorganisms.34 Van Dyke et al.54 suggested that because of this close
involvement in periodontal disease, a
decrease in neutrophil function might
result in more severe periodontal breakdown. They also suggested that in
diseases where neutrophil function was
impaired (for example, neutropenia,
Papillon-Lefèvre syndrome, and Down
syndrome), an increase in periodontal
disease was usually seen.54 The immune system can be further compromised by
the T-cell dysfunction in Down syndrome. Whittingham et al.38 proposed
that the T-cell dysfunction "might be
explained by failing immuno-competence
due to accelerated ageing". He further
proposed that it might even be caused
"by a heavy load of infections early in life
because of an incapacity to maintain adequate standards of personal hygiene".
Preshaw et al.6 highlighted the important role played by both inflammatory
mediators and proteolytic enzymes in the
pathogenesis of periodontal disease. Both
PGE2 and matrix metalloproteinases
have been shown to be present in significantly higher levels in people with DS.41-43
PGE2 is a vasodilator, which is "involved
in the increased vascular permeability
occurring at sites of inflammation, and a
mediator of bone demineralization".44
Matrix metalloproteinases can degrade
type I-V collagens, laminin, gelatin,
fibronectin, and elastin.44
Institutionalization has been
shown19,20 to be associated with an
increased prevalence and severity of periodontal disease. Swallow20 proposed that
this may be a reflection of the quality of
oral hygiene practiced, whereby aid given
to non-institutionalized children by their
parents may slow the disease's process.
Cutress19 suggested that fecal-oral transmission of contagious microorganisms in
institutionalized patients may account
for the increased prevalence of periodontal disease.
Recent studies9,22,24 have reported the
effectiveness of frequent preventive care
in slowing the progression and reducing
the severity of periodontal disease.
Therefore, any barriers that hinder the
access of people with DS to dental services could have detrimental effects on
their oral health. Fiske and Shafik3 recommended the development and
instigation of a realistic preventive program that would include regular scaling
and root planing, and advice regarding
anti-microbial agents. The results
obtained by Yoshihara et al.9 suggest that
to combat the severity and progression of
periodontal disease in persons with DS, a
more frequent treatment interval than
the six months suggested by Hennequin et al.1 should be employed. In their study,
the mean interval between dental visits
in the managed group was 3.7 (± 1.3
months). Sakellari et al.21 also recommended a three-month treatment
interval. It has been suggested that an
oral hygiene regime that includes
chlorhexidine — as a mouthwash, a gel,
or as a professionally applied varnish —
may be beneficial in reducing oral
plaque, and may help compensate for
The increased prevalence and severity of
periodontal disease in persons with Down
syndrome is due partly to an inability to
adequately maintain oral hygiene. Other
contributing factors include an earlier
and more extensive colonization with
known periodontal pathogens along with
other local factors such as open-mouth
breathing, tooth morphology, altered
microbial plaque composition, and acute
necrotizing ulcerative gingivitis.
Increasing evidence, however, supports
the theory that an impaired immunity
due to a reduction in neutrophil chemotaxis, neutrophil phagocytosis, and
T-lymphocyte function, as well as an
increased production of inflammatory
mediators and proteolytic enzymes, may
contribute most to the prevalence and
severity of periodontal disease in persons
with Down syndrome.
Down syndrome is the most commonly diagnosed intellectual disability in
Ireland.4 In recent years, trends toward
de-institutionalizing people with Down
syndrome and placing them in community settings have emerged.15 Therefore, it
is increasingly likely that most dental
practitioners will encounter a patient
with Down syndrome. Every effort must
be made to encourage the implementation of frequent preventive care in order
to decrease the severity and progression
of periodontal disease in their patients.
The author acknowledges Prof. June Nunn for her advice and encouragement
in writing this article.
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