ArticlePDF AvailableLiterature Review

Prevalence of periodontal disease, its association with systemic diseases and prevention

Authors:

Abstract and Figures

Periodontal diseases are prevalent both in developed and developing countries and affect about 20-50% of global population. High prevalence of periodontal disease in adolescents, adults, and older individuals makes it a public health concern. Several risk factors such as smoking, poor oral hygiene, diabetes, medication, age, hereditary, and stress are related to periodontal diseases. Robust evidence shows the association of periodontal diseases with systemic diseases such as cardiovascular disease, diabetes, and adverse pregnancy outcomes. Periodontal disease is likely to cause 19% increase in the risk of cardiovascular disease, and this increase in relative risk reaches to 44% among individuals aged 65 years and over. Type 2 diabetic individuals with severe form of periodontal disease have 3.2 times greater mortality risk compared with individuals with no or mild periodontitis. Periodontal therapy has been shown to improve glycemic control in type 2 diabetic subjects. Periodontitis is related to maternal infection, preterm birth, low birth weight, and preeclampsia. Oral disease prevention strategies should be incorporated in chronic systemic disease preventive initiatives to curtail the burden of disease in populations. The reduction in the incidence and prevalence of periodontal disease can reduce its associated systemic diseases and can also minimize their financial impact on the health-care systems. It is hoped that medical, dental practitioners, and other health-care professionals will get familiar with perio-systemic link and risk factors, and need to refer to the specialized dental or periodontal care.
Content may be subject to copyright.
72 73
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
72 73
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
Prevalence of periodontal disease, its association with
systemic diseases and prevention
Introduction
Periodontal disease is a chronic inammatory disease of
periodontium and its advanced form is characterized by
periodontal ligament loss and destruction of surrounding
alveolar bone.1 It is the main cause of tooth loss and is
considered one of the two biggest threats to the oral health.1,2
There are approximately 800 species of bacteria identied in
the oral cavity3 and it is hypothesized that complex interaction
of bacterial infection and host response, modied by behavioral
factors such as smoking, can result in periodontal disease.4
The aim of the review is two-fold: (1) To evaluate the
prevalence of periodontal disease in different populations, risk
factors, and its association with systemic diseases and (2) to
discuss the strategies and measures to prevent and control
periodontal disease.
Prevalence of Periodontal Disease
Periodontal disease is the most common oral condition
of human population.5 The prevalence and incidence
statistics of periodontal diseases vary because of bias, case
misclassification, and the number of teeth and the sites
examined.6 According to the Canadian Health Measures Survey
2007-2009, the measurement of loss of periodontal ligament
attachment is considered the gold standard in reporting the
prevalence of periodontal disease.7 National Health and
Nutrition Examination Survey (NHANES) determined the
attachment loss (AL) and probing depth (PD) at six sites of all
teeth (excluding third molars) for the estimation of periodontal
disease in the U.S.8
The world Health Organization (WHO) has maintained global
oral health data bank using community periodontal index
(CPI).9 This global oral health data from large epidemiological
studies from different countries were gathered to show the
distribution of periodontal disease in adolescents, adults
and elderly populations (Figures 1-3).9 CPI index score
ranges from 0 to 4 and describes the periodontal condition
of individuals at population level. CPI score 0 represents
no periodontal disease; score 1 means gingival bleeding
on probing; score 2 shows the presence of calculus and
bleeding; score 3 indicates shallow periodontal pockets of
Periodontal diseases are prevalent both in developed and developing countries and
affect about 20-50% of global population. High prevalence of periodontal disease in
adolescents, adults, and older individuals makes it a public health concern. Several
risk factors such as smoking, poor oral hygiene, diabetes, medication, age, hereditary,
and stress are related to periodontal diseases. Robust evidence shows the association of
periodontal diseases with systemic diseases such as cardiovascular disease, diabetes,
and adverse pregnancy outcomes. Periodontal disease is likely to cause 19% increase
in the risk of cardiovascular disease, and this increase in relative risk reaches to 44%
among individuals aged 65 years and over. Type 2 diabetic individuals with severe form
of periodontal disease have 3.2 times greater mortality risk compared with individuals
with no or mild periodontitis. Periodontal therapy has been shown to improve glycemic
control in type 2 diabetic subjects. Periodontitis is related to maternal infection, preterm
birth, low birth weight, and preeclampsia. Oral disease prevention strategies should be
incorporated in chronic systemic disease preventive initiatives to curtail the burden of
disease in populations. The reduction in the incidence and prevalence of periodontal
disease can reduce its associated systemic diseases and can also minimize their nancial
impact on the health-care systems. It is hoped that medical, dental practitioners, and
other health-care professionals will get familiar with perio-systemic link and risk
factors, and need to refer to the specialized dental or periodontal care.
Keywords: Periodontal disease, epidemiology, risk factors, systemic disease,
preventive strategy
Muhammad Ashraf Nazir
Department of Preventive Dental Sciences,
University of Dammam College of Dentistry,
Dammam, Kingdom of Saudi Arabia
Address for correspondence:
Muhammad Ashraf Nazir,
Department of Preventive Dental Sciences,
University of Dammam College of Dentistry,
Dammam, Kingdom of Saudi Arabia.
E-mail: manazir@uod.edu.sa
Review Article
ABSTRACT
WEBSITE: ijhs.org.sa
ISSN: 1658-3639
PUBLISHER: Qassim University
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
72 73
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
72 73
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
4-5 mm; score 4 represents deep periodontal pockets of 6
mm or above.9
Compared with developed countries, developing nations have
higher prevalence of calculus and bleeding on probing among
adolescents (Figure 1). The proportion of adolescents with
calculus deposits ranged from 35% to 70% in developing countries
while it ranged from 4% to 34% in developed nations (Figure 1).
Similarly, 14-47% of adult populations in developed countries had
calculus deposits compared with 36-63% of adults in developing
nations. However, developed countries have higher percentage
of individuals with periodontal pockets of 4-5 mm (Figure 2).
Greater proportions of older individuals (65-74 years) exhibit
periodontal pockets of 6 mm or above compared with adult
populations in both developed and developing countries
(Figures 2 and 3).
Overall, periodontal disease affects about 20-50% of the
population around the globe.10
Risk Factors for Periodontal Disease
Several factors increase the risk of periodontal diseases. These
risk factors, modiable and non-modiable, contribute toward
the clinical signicance of periodontal diseases.
Figure 1: Proportions of adolescents (15-19 years) with and without periodontal conditions using community periodontal index in different
countries9 Pd: Pocket depth
Figure 2: Proportions of adults (35-44 years) with and without periodontal conditions using community periodontal index in different countries9
Pd: Pocket depth
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
74 75
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
Modiable Risk Factors
Smoking
Smoking is one of the most important risk factors for
periodontitis, and the reduction in periodontal disease prevalence
is related to the drop in smoking rates.11 Negative effects of
smoking cigarette, cigar, cannabis, and pipe on periodontal
tissues are similar.12 The smokers are 3 times more likely to
have a severe form of periodontal disease than non-smokers.13
The smokers also present signicantly increased the loss of
alveolar bone and higher prevalence of tooth loss compared
with non-smokers, and they have poor outcomes of all forms of
periodontal treatments.10,12,14,15 Evidence suggests that smoking
changes oral microbial ora increases the level of certain
periodontal microorganisms or affects host response.11 The
nicotine has been shown to cause periodontal tissue breakdown,
directly or indirectly through interaction with other factors.16
Poor oral hygiene
Poor oral hygiene is linked with periodontal disease, and lack
of proper tooth brushing and other measures of oral hygiene can
encourage bacterial deposition and build-up of dental plaque on
teeth and gums which can set a stage for inammatory changes
in periodontal tissues.17 There is pronounced relationship
between poor oral hygiene and increased accumulation of
dental plaque, high prevalence and increased severity of
periodontal disease.18 Axelsson et al. conducted a prospective
study of 15 years duration and found no further deterioration
of periodontal structure among the subjects who maintained
proper oral hygiene and took routine professional dental care.19
Hormonal changes in females
Hormonal changes in women increase the likelihood of
periodontal disease.20 Females may experience gingival
inammation before menstruation and during ovulation due to
a high level of progesterone which blocks the repair of collagen
bers and causes the dilatation of blood vessels.21 Similarly,
pregnant women most frequently exhibit gingival changes,
gingivitis, and sometimes localized growth of gingival tissues.
Fortunately, these inammatory changes disappear within
few months after delivery without causing persistent damage
to periodontal tissues.22 Estrogen deciency reduces bone
density after menopause which can culminate in alveolar
bone loss and eventually falling of teeth. A longitudinal study
of 42,171 women at their postmenopausal stages showed that
the treatment of osteoporosis with estrogen hormonal therapy
resulted in reduced tooth loss.23
Diabetes mellitus
Literature consistently shows that diabetes mellitus is one
of the systemic risk factors for periodontal diseases which
can play a major role in initiation and progression of the
disease.24-26 Diabetes mellitus is associated with periodontal
ligament destruction which subsequently can lead to tooth
loss.27,28 Gingival crevicular uids and saliva have higher
concentrations of inammatory mediators including different
types of cytokines among diabetic patients with periodontitis
as compared to non-diabetic individuals with periodontal
disease.29 A report of a joint workshop of European Federation
of Periodontology and American Academy of Periodontology
identied dose-response relationship between the severity of
periodontal disease and adverse consequences of diabetes, and
periodontal treatment has been found as benecial as giving
an antidiabetic medication to the diabetic patients.29
Medications
Vulnerability to infections and periodontal diseases intensies
when there is diminished salivary flow due to certain
medications.20 The most common medications which can
Figure 3: Proportions of older adults (65-74 years) with and without periodontal conditions using community periodontal index in different
countries9 Pd: Pocket depth
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
74 75
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
minimize the ow of saliva and produce dryness of mouth
include tricyclic antidepressants, atropine, antihistamine, and
beta blockers.30 Some drugs (phenytoin, cyclosporine, and
nifedipine) can induce the abnormal growth of gingival tissues
which frequently complicates the appropriate removal of dental
plaque underneath the enlarged gingival mass, and thus, can
further aggravate the existing periodontal disease.20
Stress
It is clear from evidence that stress reduces the flow of
salivary secretions which in turn can enhance dental plaque
formation.15 Rai et al. observed a positive association between
stress scores and salivary stress markers (cortisol, salivary
CgA, b-endorphin, and a-amylase), tooth loss, clinical AL
(5-8 mm), and PD of 5-8 mm.31 A meta-analysis of about
300 empirical articles has indicated that stress is related to
immune system and different immunological changes occur
in response to different stressful events.32 The depressed
individuals have been shown to possess a higher concentration
of cortisol in gingival crevicular uid, and they respond poorly
to periodontal treatment. Academic stress also results in poor
oral hygiene and inammation of gingiva with increased
concentration of interleukin-1β.15
Non-modiable Risk Factors
Age
The risk of periodontal disease increases with the advancing
age that is why the high prevalence of periodontal disease
is seen among elderly population.23 Research identied that
age is associated with periodontal disease, and clinical AL
was signicantly higher among individuals aged 60-69 years
compared with group of adults 40-50 years.33
Hereditary
Hereditary is one of the factors associated with periodontitis
which makes some people more susceptible to the disease than
the others.24 The complex interplay of genetic factors with
environmental and demographic factors has been hypothesized
to demonstrate wide variations among different racial and
ethnic populations.34
Association of Periodontal Disease with
other Medical Conditions
Cardiovascular disease
Consistent body of evidence explains the relationship between
cardiovascular diseases and periodontal diseases. A systematic
review identied that periodontitis is a risk factor for coronary
heart disease, and the association is independent of other risk
factors such as diabetes, smoking, and socioeconomic status.35
In a meta-analysis of eight prospective and one retrospective
studies, it has been found that periodontal disease is likely to
cause a 19% increase in the risk of cardiovascular disease and
this increase in relative risk reaches to 44% among individuals
aged 65 years and over.36 Another systematic review and meta-
analysis of 11 studies (ve cohort and six cross-sectional studies)
found that periodontal disease with increased levels of systemic
bacterial markers was associated with coronary heart disease.37
Similarly, a meta-analysis of 29 studies (22 case–control and
cross-sectional studies, and seven cohort studies) reported
pooled odds ratio of 2.35 and pooled relative risk of 1.34 which
suggest that individuals with periodontal disease had greater
risk and higher odds of developing heart disease than those
without periodontal disease.38 Periodontal disease association
with stroke and peripheral artery disease is even stronger than
coronary heart disease (Figure 4).10
Metabolic disease
There are bi-directional relationship and synergism between
diabetes and periodontal disease.39 A prospective cohort study
of 628 subjects (35 years and older) with a follow-up of
11 years identied that type 2 diabetic individuals with severe
periodontal disease had 3.2 times the risk of mortality due to
ischemic heart disease compared to the individuals with no
or mild periodontal disease (Figure 4).40 Likewise, a meta-
analysis concluded that periodontal therapy improves glycemic
control for at least 3 months in type 2 diabetic subjects.41 A
systematic review provided the evidence to support the role
of periodontal disease in the development of type 2 diabetes
and its complications.42
Scientific literature consistently supports a relationship
between periodontitis and insulin resistance. It has been
argued that periodontal disease exacerbates insulin resistance,
a chronic condition implicated in the pathogenesis of metabolic
disease and type 2 diabetes mellitus.43 Lim et al. evaluated
data of 16,720 subjects from a national survey and identied
an association between insulin resistance and periodontitis in
postmenopausal Korean women.44 It has also been suggested
that periodontal intervention can reduce insulin resistance in
diabetic patients.45
Several systematic reviews have proposed an association between
obesity and periodontal disease and it has been identied as a risk
factor for the development of periodontitis.46-48 Recently, obesity
has been shown to increase oxidative stress in periodontal tissues
and cause their destruction.49,50 The prevalence of obesity is
increasing dramatically around the globe51 and its association
with periodontitis calls for the attention of health-care providers
to prevent these public health issues.
Adverse pregnancy outcomes
Periodontitis is related to adverse pregnancy outcomes which
include maternal infection, preterm birth, low birth weight,
preeclampsia, and microbiological and immunological
factors are implicated in the underlying mechanisms.52-55
Low socioeconomic status, smoking, and urinary tract
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
76 77
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
infection are already known to be associated with premature
birth; however, more recently it was found that periodontal
disease is also strongly linked with premature birth incidents
(Figure 4).56
Rheumatoid arthritis (RA)
Periodontal disease is prevalent among RA patients, and
the disease is thought to initiate autoimmune response in
RA (Figure 4).57 It is suggested that both periodontal disease
and RA have similar underlying pathogenic mechanisms.57
The individuals with RA have high prevalence of alveolar
bone destruction and tooth loss which are also sequelae of
periodontal disease.58
Respiratory diseases
The importance of maintaining optimum oral care among
patients with chronic obstructive pulmonary disease
(COPD) has been emphasized due to its association with
periodontitis. Chung et al. used data of 5,878 adults from
a Korean national survey and found signicantly higher
prevalence of periodontitis among COPD patients compared
with healthy individuals.59 In a large cohort study, about
22,332 patients with COPD were compared with individuals
without COPD and it was suggested that subjects with COPD
were at increased risk of developing periodontal disease.60
Similarly, a meta-analysis of 14 epidemiological studies
revealed a signicant association between periodontal disease
and COPD and periodontal disease was recognized as an
independent risk factor for COPD (Figure 4).61 It has also
been suggested that oral and periodontal microorganisms are
implicated in bacterial pneumonia.62
Chronic kidney disease (CKD)
There is a bidirectional relationship between periodontal
disease and CKD. Fisher and Taylor identied periodontitis
as a risk factor for CKD in an epidemiological study of
11,955 adults in the U.S.63 A systematic review of four
observational and three interventional studies found that
patients with periodontitis are at increased risk of CKD and
periodontal treatment results in positive outcomes in persons
with CKD.64 Ioannidou and Swede observed a dose-response
relationship between periodontal disease and different stages
of CKD, and they found that individuals with CKD were
30-60% more likely to develop moderate periodontitis.65
Later, in another study by Ioannidou et al., it was shown
that Mexican Americans with low kidney functions were
twice more likely to have periodontal disease compared with
subjects with normal kidney functions.66 Similarly, Iwasaki
et al. demonstrated a link between periodontitis and reduced
kidney functions in Japanese older individuals.67 In a recent
prospective cohort study with 14 years of follow-up, Ricardo
et al. found that CKD individuals with periodontitis had 35%
greater risk of mortality compared with CKD patients without
periodontal disease (Figure 4).68
Cancers
Increased cancer risk because of periodontal disease has
been demonstrated by Michaud and colleagues.69 The risk
of tongue cancer increases 5.23 times with each millimeter
loss of alveolar bone.70 Fitzpatrick and Katz observed that the
relationship between periodontitis and oral, esophageal, gastric,
and pancreatic cancers have been reported more consistently
in literature than with lung and prostate cancers (Figure 4).71
Impairment of cognitive function
Older adults face decline in their cognitive abilities, which affect
their behaviors including oral hygiene habits.72 There is modest
evidence about an association between periodontal disease
and poor cognitive functions as periodontal inammation
has been shown to affect cognition in elderly populations.73,74
The analysis of data from Third NHANES-III identied high
levels of serum maker of periodontitis (P. gingivalis IgG) in
individuals with impaired cognitive performance.75 Further, a
recent study by Kamer and associates found that clinical AL
can promote amyloid β accumulation in the brain which can
cause cognitive dysfunction.76
Prevention of Periodontal Disease
WHO recommends employing integrated public health
preventive strategies which should be based on common risk
factor approach. Risk factors such as smoking, stress, and low
socioeconomic status are associated with periodontal disease as
well as other systemic chronic diseases; therefore, inclusion of
oral disease prevention strategies in chronic systemic disease
preventive initiatives can curtail the burden of disease at the
level of population.77
Oral hygiene practices
Proper mouth cleaning, regular tooth brushing, and dental
ossing are most effective in preventing oral disease and
periodontitis. Despite utmost signicance of tooth brushing,
about half of the population brush twice a day.78 There are
various sizes, shapes, and types of toothbrushes; however, two
more common types include powered toothbrushes and manual
toothbrushes. Powered toothbrushes offer more advantage over
the manual toothbrushes in reducing dental plaque.79
Diet
Although the role of diet in the prevention of dental caries is
more signicant compared with preventing periodontal disease;
nonetheless, poor diet can negatively affect periodontal tissues
causing rapid progression of disease.80 The vitamin C deciency
as a risk factor for periodontal disease has been discussed in
the literature. Nishida et al. used a sample of 12,419 adults and
showed that there was increased risk of periodontal disease due
to the poor dietary intake of vitamin C, and also observed a
dose-response relationship between vitamin C and the severity
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
76 77
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
of periodontal disease.81 A diet high in fruits, vegetables and
low in fat and sugars is required for the healthy periodontal
tissues. Vitamins C and E have antioxidant properties which
help to reduce the production of reactive oxygen radicals formed
during the inammatory process.80 Low-calorie intake has been
shown to reduce inammatory changes and diminish the tissue
damage in periodontal disease.82
Use of uoride
Stannous uoride has antiplaque and antigingivitis effects
and it reduces the proportion of bacteria and spirochetes
in subgingival areas, thus can help to promote gingival
health.83,84 He et al. conducted a randomized double-
blinded trial to investigate the antimicrobial role of stannous
fluoride dentifrice in periodontal disease and found a
signicant reduction in gingival bleeding over a period of
2-month.85
Use of antimicrobial agents
Chlorhexidine, triclosan, essential oils and zinc in
toothpastes, mouthwashes and gels are used to control
specific periodontal bacteria as well as plaque.86,87
Chlorhexidine reduces dental plaque (55% reduction in
dental plaque) and gingival inammation (30-45% decrease
in gingivitis) by lowering inflammatory mediators.88
Gunsolley compared the effectiveness of antiplaque and
antigingivitis mouthrinses with oral hygiene instructions
and adult prophylaxis and found great improvement in oral
hygiene due to antiplaque and antigingivitis mouth rinses.89
Moreover, research data from several clinical trials support
that antimicrobial mouth rinses have equal or greater efcacy
in controlling gingival disease than the use of interproximal
dental oss.90-92
Smoking cessation
Since smoking is a major risk factor for periodontal disease,
therefore smoking cessation can prevent a considerable
proportion of periodontitis cases.93 Smoking cessation not only
inhibits further progression of periodontal disease but can also
reduce the periodontal tissue destruction.94
Community and high risk approaches
Breast cancer and cervical cancer screening are considered
successful examples of screening for the prevention of
diseases, but the decision of oral screening should be based
on careful evaluation of nancial burden, ethical aspects, and
efcacy and adverse effects of the intervention.95 In addition,
implementation of oral health promotion policies at local,
national and international levels can help bring sustainable
reduction in periodontal disease burden and improve the
quality of life of people. Scaling is considered the most
common professional preventive measure for periodontal
disease. Because of the association between periodontal
disease and cardiovascular disease, scaling has recently been
shown to reduce the incidence of acute myocardial infarction
and stroke.96
Conclusion and Recommendations
Although periodontal disease is the most prevalent
infectious oral condition but is treatable and preventable.
The reduction in the incidence and prevalence of
Figure 4: Association between periodontal disease and various systemic conditions
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
78 79
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
periodontal disease can result in lowering its associated
systemic diseases and complications.
Decreased periodontal disease burden can minimize
treatment needs and can reduce nancial impact on health-
care systems.
High prevalence of periodontal disease also necessitates
the establishment of surveillance system for oral diseases
in the community.
Preventive programs for periodontal disease should utilize
common risk approaches to reduce the magnitude of other
chronic diseases.
Cost-effective strategies would also enhance
interdisciplinary collaborations among health-care
providers.
Health-care providers should be familiar with perio-
systemic link and should be able to diagnose and refer
the patients to specialized dental or periodontal care to
improve the quality of life of their patients.
Further research is needed to explore the underlying
mechanisms and risk factors of periodontal disease and develop
innovative preventive strategies.
References
1. de Pablo P, Chapple IL, Buckley CD, Dietrich T. Periodontitis in
systemic rheumatic diseases. Nat Rev Rheumatol 2009;5:218-24.
2. Benjamin RM. Oral health: The silent epidemic. Public Health Rep
2010;125:158-9.
3. Ashby MT, Kreth J, Soundarajan M, Sivuilu LS. Inuence of a model
human defensive peroxidase system on oral streptococcal antagonism.
Microbiology 2009;155:3691-700.
4. Fenesy KE. Periodontal disease: An overview for physicians. Mt Sinai
J Med 1998;65:362-9.
5. Raitapuro-Murray T, Molleson TI, Hughes FJ. The prevalence of
periodontal disease in a Romano-British population c 200-400 AD. Br
Dent J 2014;217:459-66.
6. Locker D, Slade GD, Murray H. Epidemiology of periodontal disease
among older adults: A review. Periodontol 2000 1998;16:16-33.
7. Health Canada. Report on the Findings of the Oral Health Component
of the Canadian Health Measures Survey; 2007-2009. Available from:
http://www.fptdwg.ca/assets/PDF/CHMS/CHMS-E-summ.pdf. [Last
accessed on 2014 Nov 07].
8. Eke PI, Dye BA, Wei L, Thornton-Evans GO, Genco RJ; CDC
Periodontal Disease Surveillance workgroup: James Beck
(University of North Carolina, Chapel Hill, USA), et al. Prevalence
of periodontitis in adults in the United States: 2009 and 2010. J Dent
Res 2012;91:914-20.
9. World Health Organization. WHO Global Oral Health Data; 2005.
Available from: http://www.who.int/oral_health/databases/niigata/en.
[Last accessed on 2014 Nov 07].
10. Sanz M, D’Aiuto F, Deaneld J, Fernandez-Avilés F. European
workshop in periodontal health and cardiovascular disease-scientic
evidence on the association between periodontal and cardiovascular
diseases: A review of the literature. Eur Heart J Suppl 2010;12 Suppl
B:B3-12.
11. Bergstrom J. Smoking rate and periodontal disease prevalence: 40-year
trends in Sweden 1970-2010. J Clin Periodontol 2014;41:952-7.
12. Underner M, Maes I, Urban T, Meurice JC. Effects of smoking on
periodontal disease. Rev Mal Respir 2009;26:1057-73.
13. Johnson GK, Hill M. Cigarette smoking and the periodontal patient.
J Periodontol 2004;75:196-209.
14. Albandar JM, Streckfus CF, Adesanya MR, Winn DM. Cigar, pipe, and
cigarette smoking as risk factors for periodontal disease and tooth loss.
J Periodontol 2000;71:1874-81.
15. Reners M, Brecx M. Stress and periodontal disease. Int J Dent Hyg
2007;5:199-204.
16. Nociti FH Jr, Nogueira-Filho GR, Tramontina VA, Machado MA,
Barros SP, Sallum EA, et al. Histometric evaluation of the effect of
nicotine administration on periodontal breakdown: An in vivo study.
J Periodontal Res 2001;36:361-6.
17. de Oliveira C, Watt R, Hamer M. Toothbrushing, inammation, and
risk of cardiovascular disease: Results from Scottish Health Survey.
BMJ 2010;340:c2451.
18. Albandar JM. Global risk factors and risk indicators for periodontal
diseases. Periodontol 2000 2002;29:177-206.
19. Axelsson P, Lindhe J, Nyström B. On the prevention of caries and
periodontal disease. Results of a 15-year longitudinal study in adults.
J Clin Periodontol 1991;18:182-9.
20. Güncü GN, Tözüm TF, Caglayan F. Effects of endogenous sex
hormones on the periodontium - Review of literature. Aust Dent J
2005;50:138-45.
21. Markou E, Boura E, Tsalikis L, Deligianidis A, Konstantinidis A. The
inuence of sex hormones on proinammatory cytokines in gingiva
of periodontally healthy premenopausal women. J Periodontal Res
2011;46:528-32.
22. Laine MA. Effect of pregnancy on periodontal and dental health. Acta
Odontol Scand 2002;60:257-64.
23. Grodstein F, Colditz GA, Stampfer MJ. Post-menopausal hormone use
and tooth loss: A prospective study. J Am Dent Assoc 1996;127:370-7.
24. Casanova L, Hughes FJ, Preshaw PM. Diabetes and periodontal
disease: A two-way relationship. Br Dent J 2014;217:433-7.
25. Chávarry NG, Vettore MV, Sansone C, Sheiham A. The relationship
between diabetes mellitus and destructive periodontal disease: A meta-
analysis. Oral Health Prev Dent 2009;7:107-27.
26. Preshaw PM, Bissett SM. Periodontitis: Oral complication of diabetes.
Endocrinol Metab Clin North Am 2013;42:849-67.
27. Grossi SG, Zambon JJ, Ho AW, Koch G, Dunford RG, Machtei EE,
et al. Assessment of risk for periodontal disease. I. Risk indicators for
attachment loss. J Periodontol 1994;65:260-7.
28. Patel MH, Kumar JV, Moss ME. Diabetes and tooth loss: An analysis
of data from the national health and nutrition examination survey,
2003-2004. J Am Dent Assoc 2013;144:478-85.
29. Chapple IL, Genco R; Working group 2 of the joint EFP/AAP
workshop. Diabetes and periodontal diseases: Consensus report of the
Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases.
J Periodontol 2013;84 4 Suppl:S106-12.
30. Scully C. Drug effects on salivary glands: Dry mouth. Oral Dis
2003;9:165-76.
31. Rai B, Kaur J, Anand SC, Jacobs R. Salivary stress markers, stress, and
periodontitis: A pilot study. J Periodontol 2011;82:287-92.
32. Segerstrom SC, Miller GE. Psychological stress and the human
immune system: A meta-analytic study of 30 years of inquiry. Psychol
Bull 2004;130:601-30.
33. Rheu GB, Ji S, Ryu JJ, Lee JB, Shin C, Lee JY, et al. Risk assessment
for clinical attachment loss of periodontal tissue in Korean adults.
J Adv Prosthodont 2011;3:25-32.
34. Albandar JM, Rams TE. Global epidemiology of periodontal diseases:
An overview. Periodontol 2000 2002;29:7-10.
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
78 79
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
35. Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M. Periodontal
disease and coronary heart disease incidence: A systematic review and
meta-analysis. J Gen Intern Med 2008;23:2079-86.
36. Janket SJ, Baird AE, Chuang SK, Jones JA. Meta-analysis of
periodontal disease and risk of coronary heart disease and stroke. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95:559-69.
37. Mustapha IZ, Debrey S, Oladubu M, Ugarte R. Markers of systemic
bacterial exposure in periodontal disease and cardiovascular
disease risk: A systematic review and meta-analysis. J Periodontol
2007;78:2289-302.
38. Blaizot A, Vergnes JN, Nuwwareh S, Amar J, Sixou M. Periodontal
diseases and cardiovascular events: Meta-analysis of observational
studies. Int Dent J 2009;59:197-209.
39. Kinane DF, Marshall GJ. Periodontal manifestations of systemic
disease. Aust Dent J 2001;46:2-12.
40. Saremi A, Nelson RG, Tulloch-Reid M, Hanson RL, Sievers ML,
Taylor GW, et al. Periodontal disease and mortality in Type 2 diabetes.
Diabetes Care 2005;28:27-32.
41. Teeuw WJ, Gerdes VE, Loos BG. Effect of periodontal treatment on
glycemic control of diabetic patients: A systematic review and meta-
analysis. Diabetes Care 2010;33:421-7.
42. Borgnakke WS, Ylöstalo PV, Taylor GW, Genco RJ. Effect of
periodontal disease on diabetes: Systematic review of epidemiologic
observational evidence. J Periodontol 2013;84 Suppl 4:S135-52.
43. Gurav AN. Periodontitis and insulin resistance: Casual or causal
relationship? Diabetes Metab J 2012;36:404-11.
44. Lim SG, Han K, Kim HA, Pyo SW, Cho YS, Kim KS, et al. Association
between insulin resistance and periodontitis in Korean adults. J Clin
Periodontol 2014;41:121-30.
45. Sun WL, Chen LL, Zhang SZ, Wu YM, Ren YZ, Qin GM. Inammatory
cytokines, adiponectin, insulin resistance and metabolic control after
periodontal intervention in patients with Type 2 diabetes and chronic
periodontitis. Intern Med 2011;50:1569-74.
46. Chaffee BW, Weston SJ. Association between chronic periodontal
disease and obesity: A systematic review and meta-analysis.
J Periodontol 2010;81:1708-24.
47. Nascimento GG, Leite FR, Do LG, Peres KG, Correa MB,
Demarco FF, et al. Is weight gain associated with the incidence
of periodontitis? A systematic review and meta-analysis. J Clin
Periodontol 2015;42:495-505.
48. Keller A, Rohde JF, Raymond K, Heitmann BL. Association between
periodontal disease and overweight and obesity: A systematic review.
J Periodontol 2015;86:766-76.
49. Atabay VE, Lutoglu M, Avci B, Sakallioglu EE, Aydogdu A. Obesity
and oxidative stress in patients with different periodontal status: A
case-control study. J Periodontal Res 2017;52:51-60.
50. Dursun E, Akalin FA, Genc T, Cinar N, Erel O, Yildiz BO. Oxidative
stress and periodontal disease in obesity. Medicine (Baltimore)
2016;95:e3136.
51. WHO. Global Health Observatory (GHO) Data. Obesity. Available
from: http://www.who.int/gho/ncd/risk_factors/obesity_text/en. [Last
accessed on 2015 Jan 21].
52. Ide M, Papapanou PN. Epidemiology of association between maternal
periodontal disease and adverse pregnancy outcomes-systematic
review. J Clin Periodontol 2013;40 Suppl 14:S181-94.
53. Bobetsis YA, Barros SP, Offenbacher S. Exploring the relationship
between periodontal disease and pregnancy complications. J Am Dent
Assoc 2006;137 Suppl:7S-13.
54. Polyzos NP, Polyzos IP, Mauri D, Tzioras S, Tsappi M, Cortinovis I,
et al. Effect of periodontal disease treatment during pregnancy on
preterm birth incidence: A metaanalysis of randomized trials. Am J
Obstet Gynecol 2009;200:225-32.
55. Azarpazhooh A, Tenenbaum HC. Separating fact from ction: Use
of high-level evidence from research syntheses to identify diseases
and disorders associated with periodontal disease. J Can Dent Assoc
2012;78:c25.
56. Piscoya MD, Ximenes RA, Silva GM, Jamelli SR, Coutinho SB.
Maternal periodontitis as a risk factor for prematurity. Pediatr Int
2012;54:68-75.
57. Mercado FB, Marshall RI, Bartold PM. Inter-relationships between
rheumatoid arthritis and periodontal disease. A review. J Clin
Periodontol 2003;30:761-72.
58. Detert J, Pischon N, Burmester GR, Buttgereit F. The association
between rheumatoid arthritis and periodontal disease. Arthritis Res
Ther 2010;12:218.
59. Chung JH, Hwang HJ, Kim SH, Kim TH. Associations between
periodontitis and chronic obstructive pulmonary disease: The
2010-2012 Korean National Health and Nutrition Examination Survey.
J Periodontol 2016;25:1-11.
60. Shen TC, Chang PY, Lin CL, Chen CH, Tu CY, Hsia TC, et al. Risk
of periodontal diseases in patients with chronic obstructive pulmonary
disease: A nationwide population-based cohort study. Medicine
(Baltimore) 2015;94:e2047.
61. Zeng XT, Tu ML, Liu DY, Zheng D, Zhang J, Leng W. Periodontal
disease and risk of chronic obstructive pulmonary disease: A meta-
analysis of observational studies. PLoS One 2012;7:e46508.
62. Paju S, Scannapieco FA. Oral biolms, periodontitis, and pulmonary
infections. Oral Dis 2007;13:508-12.
63. Fisher MA, Taylor GW. A prediction model for chronic kidney disease
includes periodontal disease. J Periodontol 2009;80:16-23.
64. Chambrone L, Foz AM, Guglielmetti MR, Pannuti CM, Artese HP,
Feres M, et al. Periodontitis and chronic kidney disease: A systematic
review of the association of diseases and the effect of periodontal
treatment on estimated glomerular ltration rate. J Clin Periodontol
2013;40:443-56.
65. Ioannidou E, Swede H. Disparities in periodontitis prevalence among
chronic kidney disease patients. J Dent Res 2011;90:730-4.
66. Ioannidou E, Hall Y, Swede H, Himmelfarb J. Periodontitis associated
with chronic kidney disease among Mexican Americans. J Public
Health Dent 2013;73:112-9.
67. Iwasaki M, Taylor GW, Nesse W, Vissink A, Yoshihara A, Miyazaki H.
Periodontal disease and decreased kidney function in Japanese elderly.
Am J Kidney Dis 2012;59:202-9.
68. Ricardo AC, Athavale A, Chen J, Hampole H, Garside D, Marucha P,
et al. Periodontal disease, chronic kidney disease and mortality: Results
from the third national health and nutrition examination survey. BMC
Nephrol 2015;16:97.
69. Michaud DS, Liu Y, Meyer M, Giovannucci E, Joshipura K. Periodontal
disease, tooth loss, and cancer risk in male health professionals: A
prospective cohort study. Lancet Oncol 2008;9:550-8.
70. Tezal M, Sullivan MA, Reid ME, Marshall JR, Hyland A, Loree T, et al.
Chronic periodontitis and the risk of tongue cancer. Arch Otolaryngol
Head Neck Surg 2007;133:450-4.
71. Fitzpatrick SG, Katz J. The association between periodontal disease
and cancer: A review of the literature. J Dent 2010;38:83-95.
72. Brennan LJ, Strauss J. Cognitive impairment in older adults and oral
health considerations: Treatment and management. Dent Clin North
Am 2014;58:815-28.
73. Kamer AR, Morse DE, Holm-Pedersen P, Mortensen EL, Avlund K.
Periodontal inammation in relation to cognitive function in an older
adult Danish population. J Alzheimers Dis 2012;28:613-24.
74. Kaye EK, Valencia A, Baba N, Spiro A 3rd, Dietrich T, Garcia RI. Tooth
Nazir: Prevalence of periodondal disease, its associations with systemic diseases and prevention
80 PB
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
International Journal of Health Sciences
Vol. 1, Issue 2, April‑June 2017
loss and periodontal disease predict poor cognitive function in older
men. J Am Geriatr Soc 2010;58:713-8.
75. Noble JM, Borrell LN, Papapanou PN, Elkind MS, Scarmeas N,
Wright CB. Periodontitis is associated with cognitive impairment
among older adults: Analysis of NHANES-III. J Neurol Neurosurg
Psychiatry 2009;80:1206-11.
76. Kamer AR, Pirraglia E, Tsui W, Rusinek H, Vallabhajosula S,
Mosconi L, et al. Periodontal disease associates with higher brain
amyloid load in normal elderly. Neurobiol Aging 2015;36:627-33.
77. Petersen PE, Ogawa H. Strengthening the prevention of periodontal
disease: The WHO approach. J Periodontol 2005;76:2187-93.
78. Bhardwaj VK. Tooth brushing behaviours and dental abrasion among
the population in Shimla, Himachal Pradesh in India: A cross-sectional
study. J Cranio Maxillary Dis 2014;3:89-94.
79. Niederman R. Moderate quality evidence nds statistical benet in
oral health for powered over manual toothbrushes. Evid Based Dent
2014;15:77-8.
80. Moynihan PJ. The role of diet and nutrition in the etiology and
prevention of oral diseases. Bull World Health Organ 2005;83:694-9.
81. Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ.
Dietary vitamin C and the risk for periodontal disease. J Periodontol
2000;71:1215-23.
82. Branch-Mays GL, Dawson DR, Gunsolley JC, Reynolds MA,
Ebersole JL, Novak KF, et al. The effects of a calorie-reduced diet on
periodontal inammation and disease in a non-human primate model.
J Periodontol 2008;79:1184-91.
83. Gunsolley JC. A meta-analysis of six-month studies of antiplaque and
antigingivitis agents. J Am Dent Assoc 2006;137:1649-57.
84. Mazza JE, Newman MG, Sims TN. Clinical and antimicrobial effect of
stannous uoride on periodontitis. J Clin Periodontol 1981;8:203-12.
85. He T, Barker ML, Goyal CR, Biesbrock AR. Anti-gingivitis effects
of a novel 0.454% stabilized stannous uoride dentifrice relative to a
positive control. Am J Dent 2012;25:136-40.
86. Axelsson P. Current role of pharmaceuticals in prevention of caries and
periodontal disease. Int Dent J 1993;43:473-82.
87. García-Caballero L, Quintas V, Prada-López I, Seoane J, Donos N,
Tomás I. Chlorhexidine substantivity on salivary ora and plaque-like
biolm: An in situ model. PLoS One 2013;8:e83522.
88. Puig Silla M, Montiel Company JM, Almerich Silla JM. Use of
chlorhexidine varnishes in preventing and treating periodontal
disease. A review of the literature. Med Oral Patol Oral Cir Bucal
2008;13:E257-60.
89. Gunsolley JC. Clinical efcacy of antimicrobial mouthrinses. J Dent
2010;38 Suppl 1:S6-10.
90. Sharma N, Charles CH, Lynch MC, Qaqish J, McGuire JA,
Galustians JG, et al. Adjunctive benet of an essential oil-
containing mouthrinse in reducing plaque and gingivitis in patients
who brush and oss regularly: A six-month study. J Am Dent Assoc
2004;135:496-504.
91. Mythri H, Ananda SR, Prashant GM, Subba Reddy VV, Chandu GN.
The efcacy of antiseptic mouth rinses in comparison with dental oss
in controlling interproximal gingivitis. J Int Soc Prev Community Dent
2011;1:31-5.
92. Bauroth K, Charles CH, Mankodi SM, Simmons K, Zhao Q, Kumar LD.
The efcacy of an essential oil antiseptic mouthrinse vs. Dental oss in
controlling interproximal gingivitis: A comparative study. J Am Dent
Assoc 2003;134:359-65.
93. Tomar SL, Asma S. Smoking-attributable periodontitis in the United
States: Findings from NHANES III. National health and nutrition
examination survey. J Periodontol 2000;71:743-51.
94. Hodge P, Binnie V. Smoking cessation and periodontal health - A missed
opportunity? Evid Based Dent 2009;10:18-9.
95. Deep P. Screening for common oral diseases. J Can Dent Assoc
2000;66:298-9.
96. Chen ZY, Chiang CH, Huang CC, Chung CM, Chan WL, Huang PH, et al.
The association of tooth scaling and decreased cardiovascular disease: A
nationwide population-based study. Am J Med 2012;125:568-75.
... Even though most of the patients visited the dentist on a regular base, a high percentage (44.3%) of patients had an oral focus prior to the start of the chemotherapy, although lower than reported in the literature [13,15,32]. In most cases, asymptomatic chronic dental foci seem not to cause infectious problems in healthy individuals [12]. ...
Article
Full-text available
Introduction Febrile neutropenia (FN) is a potential life-threatening complication of myelosuppressive chemotherapy, particularly when induced by infection. There is evidence that FN can originate from the oral cavity, but its contribution to FN is largely understudied in patients treated for solid tumors. The aim of this study was to assess the prevalence of FN in these patients and to evaluate its relation with dental foci and oral mucositis. Material and Methods A prospective longitudinal observational study was conducted. Patients diagnosed with solid tumors and lymphoma scheduled to be treated with myelosuppressive chemotherapy with an intermediate risk of developing FN were included. A pre-chemotherapy dental examination was performed and patients were followed during and after chemotherapy regimen. During subsequent hospital visits for chemotherapy administration, the oral cavity was inspected and oral mucositis (OM) was scored using the CTC-AE version 3.0. When patients presented with fever, a comprehensive full body examination including laboratory/microbiological/imaging investigation was performed. Results Eighty-eight patients were included. Pre-chemotherapy, 39 patients (44.3%) were diagnosed with a dental focus. During chemotherapy, 46 patients developed OM (53.4%), of which 15 patients had a maximum score of grade II (ulcerative mucositis). Ten patients developed FN during the follow-up period. Patients with FN more often suffered from ulcerative OM compared to patients without FN; both FN and mucositis risk was associated with the myelotoxicity of chemotherapy. However, no relation could be established between the presence of dental foci prior to chemotherapy and the development of FN ( p > 0.05). Conclusion A significant relation was identified between ulcerative OM and FN, but no robust conclusions could be drawn with respect to a relationship between the presence of dental foci and FN.
... As previously stated peridontitis is caused by a range of etiological and risk factors. Poor dental hygiene can be one of the causes of periodontal diseases, which can contribute to neuro-inflammation and ADHD [68]. ...
Article
Full-text available
Periodontitis is a condition caused mostly by the creation of a biofilm by the bacterium P. gingivalis, which releases toxins and damages the tooth structure. Recent research studies have reported association between dental health and neuropsychiatric illnesses. Neuroinflammation triggered by the first systemic inflammation caused by the bacterium present in the oral cavities is a plausible explanation for such a relationship. Substantial amount of evidence supports the role of neuroinflammation and dysfunction of the dopaminergic system in the pathology of ADHD (Attention deficit hyperactivity disorders). Recent epidemiological, microbiological and inflammatory findings strengthen that, periodontal bacteria, which cause systemic inflammation can contribute to neuroinflammation and finally ADHD. Although both diseases are characterized by inflammation, the specific pathways and crosslink’s between periodontitis and ADHD remain unknown. Here, the authors describe the inflammatory elements of periodontitis, how this dental illness causes systemic inflammation, and how this systemic inflammation contributes to deteriorating neuroinflammation in the evolution of ADHD. Therefore, the aim of this review is to present possible links and mechanisms that could confirm the evidence of this association.
... Si tratta di una correlazione di tipo bidirezionale, caratterizzata dall'esacerbazione di entrambe le patologie quando presenti nello stesso individuo (Figura 3). Diversi studi hanno mostrato infatti una maggiore prevalenza di parodontite nei pazienti diabetici, così come una maggiore gravità della malattia parodontale nei pazienti affetti da diabete 16,17 . L'elemento in comune è la presenza di risposta infiammatoria: il diabete, come la malattia parodontale, induce un'alterazione della produzione e regolazione di molti mediatori infiammatori. ...
Article
Full-text available
Alcune condizioni sistemiche possono correlarsi alla salute orale rendendo necessaria un’adeguata gestione del paziente al fine di consentire una diagnosi precoce, intercettare l’insorgenza e migliorare il decorso di alcune patologie organiche. L’importanza di questi temi è dimostrata da una recente dichiarazione della WHO, nella quale viene riconosciuta la salute orale come parte integrante della salute generale e pertanto, degna di un approccio globale. Non ultimo, nel manifesto ufficiale della EFP, viene posta attenzione sulla diagnosi e trattamento della malattia parodontale come mezzo per contrastare gli effetti negativi dell’infiammazione sia a livello orale che sistemico. L’elemento che accumuna la patologia generale a quella orale è la presenza di infiammazione in seguito a iperattivazione delle difese immunitarie dell’organismo. Attraverso l’approfondimento di alcune patologie sistemiche (come diabete di tipo 2, malattie cardiovascolari e sindrome metabolica, malattie neurodegenerative, neoplasie e Sars-COV2) e condizioni fisiologiche particolari (come la gravidanza) emerge come la presenza di malattia parodontale, con le specie batteriche che la caratterizzano, possa contribuire ad aumentare l’infiammazione sistemica, con conseguente peggioramento delle condizioni di salute del paziente. Le terapie parodontali non chirurgiche e integrative (air-polishing, fotodinamica, probiotici, ozono-terapia, profilazione batterica e analisi salivare) con lo scopo di ridurre la quantità di batteri parodonto-patogeni, rappresentano uno strumento per ripristinare lo stato di salute, funzionalità ed estetica del parodonto.
... Furthermore, no edentulous patients were included in the current study, while edentulism is still prevalent, despite the current increased focus on preventive dentistry [34,35]. Periodontitis still affects 20-50% of the world population [36] and it is the most important reason for tooth loss after caries [37]. Moreover, teeth might get lost PM if the patient suffered from periodontitis during the last months of his/her life. ...
Article
Full-text available
The current study aimed to select the best mandibular morphological identifiers. One-hundred eighty-five panoramic radiographs were retrospectively collected, in which four landmarks were located on the mandible: the most superior point of the condyle right/left (CONR/L), of the coronoid right/left (CORR/L), of the mandibular lingula right/left (LINR/L), and the most mesial point of the mental foramen right/left (MMFR/L). Five linear measurements, 6 angles, and 10 ratios were measured bilaterally. Three groups of statistics were considered: (1) mean potential set; (2) inter-observer agreement quantified by intra-class correlation (ICC) and within-subject coefficient of variation (WSCV); and (3) Spearman correlation. Parameters were selected for a step-by-step cascade. In a univariate approach, the following parameters proved to have the best identifying capacity: ratio 3 right (between lines CONR — CORR and LINR — MMFR) with mean potential set 13%, ICC 0.90, and WSCV 4.8%; ratio 4 (between lines CONR/L — CORR/L and MMFR — MMFL) with mean potential set 13%, ICC 0.92, and WSCV 8.9%; and angle 4 left (between landmarks LINL, MMFL, and MMFR) with mean potential set of 18%, ICC 0.91, and WSCV 1.2%. The correlation coefficients ranged from 0.01 to 0.33. In a multivariate approach, the identifying capacity improved drastically, with all ratios combined as the strongest identifier (mean potential set 1.29%). In conclusion, a single ratio or a single angle already narrows down the set of potential matches, but the mean potential set remains relatively large. Combining all ratios drastically increases the certainty of the match.
... 48 The spread of these infectious agents from dental plaque and inflammatory mediators from periodontal tissues to other organs of the body across the junctional epithelium is believed to cause different systemic diseases like; Alzheimer's disease, 49 diabetes, cardiovascular disease, feto-maternal complications, rheumatoid arthritis, and chronic obstructive pulmonary disease. [50][51][52][53][54][55][56] Despite the World Health Organization (WHO) recommending the inclusion of oral health in a political declaration on universal health coverage in 2019, the periodontal disease remained disproportionately affecting poor and socially disadvantaged group of society. 57 Due to the nature of the disease also, the early stages of periodontitis usually remain asymptomatic, 58 and so that most women are complicated by feto-maternal complications associated with severe periodontitis. ...
Article
Full-text available
Background: Periodontal disease is characterized by the inflammation of all tissues that surround and support the teeth, and it is the most common public health problem worldwide. It has many different contributing factors, such as poor oral hygiene, smoking, anemia, bacterial plaque, poor economic status, and nutritional deficiency. It also causes different feto-maternal complications like preeclampsia, gestational diabetes, preterm labor, low birth weight, and early abortion. Thus, this study aimed to assess the prevalence and associated factors of periodontal disease among pregnant women. Methods: A cross-sectional study was conducted among 618 women at public hospitals in the Southwest Ethiopia. Data were collected using a systematic random sampling method and a structured interviewer administered questionnaire. The data were entered into Epi-Data Manager 4.2 and then transferred to a statistical package for social science (SPSS) version 21 for analysis. The logistic regression analysis was done to see the significant association between each predictor with periodontal disease by considering a p-value of <0.05 and a CI of 95%. Results: A total of 618 women attending ANC with a 100% response rate were enrolled in this study. The mean and standard deviation of the age of the study participants was 31.07 ± 7.8 years. The periodontal disease was observed among 240 (38.8%) of the total participants with 95% C.I of (35%, 43%). Predictors like rural residency, women who could not read and write, women with poor wealth index, nutritional status of underweight, had no information about periodontal disease, depression, history of diabetes mellitus, self-perceived halitosis, no history of ANC, and lower gestational age were found to be significantly associated with periodontal disease. Conclusion: In this study, the prevalence of periodontal disease was found to be significantly higher. Therefore, in order to minimize the burden of periodontal disease among pregnant women, oral, medical, and mental health education should be promoted.
Article
Periodontal disease is a common worldwide oral inflammation/infection affecting tissues that surround and support teeth. This study aims to evaluate the prevalence, extent and severity of periodontal diseases and its risk factors, according to the most recent periodontal classification, in an adult population of Northern Portugal. This observational study collected data from clinical records of patients who attended the University Clinic of Gandra between April 2021 and April 2022. Of a total of 941 patients included, 457 (48.6%) had periodontitis, 253 (26.9%) had gingivitis and the remaining 231 (24.5%) were healthy patients. The prevalence of stage III severe periodontitis was 51.2%, more prevalent in males, and in the age group of 61–70 years. Gingivitis was more prevalent in females, and in the age group of 31–40 years; in both diseases, the most prevalent extension was the generalized one. Using a binary logistic regression, we observe a significant relation of the risk of periodontitis with age (p = 0.019; OR 1.033; 95% CI 1.005–1.062), tooth brushing (p = 0.002; OR 0.25; 95% CI 0.105–0.599) and dental flossing (p = 0.015; OR 0.63; 95% CI 0.09–0.768). This study revealed a high prevalence of periodontitis. Increased age, lack of tooth brushing and flossing were identified as potential risk factors for periodontitis in the investigated Portuguese population.
Article
Background: Periodontal disease diagnosis and its stability after treatment are still a field of interest for both researchers and clinicians. Aims: First aim of this study was to implement the new periodontal classification for the reflection of periodontitis severity in private practice. Second, periodontal stability and tooth loss were observed in patients who attended supportive periodontal therapy (SPT). Patients and methods: A total of 454 patients were classified according to the new classification. To define periodontitis, patients were staged according to the clinical attachment level, and tooth and bone loss. Grading was also assessed by bone loss to age ratio, smoking, and/or presence of diabetes. Associations between periodontitis and age, gender, presence of diabetes, and smoking were also analyzed. Additionally, periodontal stability, tooth loss, and adherence to oral hygiene were recorded for those who attended SPT. Results: One hundred five patients were diagnosed as generalized gingivitis and 349 patients as periodontitis. Among them, 166 suffered from severe periodontitis (stage 3 or 4). Most of the patients had stage 3 grade C periodontitis (40.4%). Out of the 344 patients who attended SPT at least once, no treatment was needed in 57 (16.6%) patients who were accepted periodontally stable. Twenty-nine patients lost at least one tooth due to periodontal reason. Conclusions: According to the new periodontal classification, 47.6% of the patients had severe periodontitis (stage 3 or 4). Periodontal stability was observed in 16.6% of patients who attended SPT.
Article
Periodontal disease is a major threat to oral health and would further contribute to systemic diseases without timely control. We aimed to evaluate the relation between periodontal disease, periodontal treatment and carotid intima–media thickness (CIMT) based on available epidemiological and clinical evidence. PubMed and Scopus were searched for relevant studies through May 2021. Observational studies reporting risk estimates with 95% confidence intervals (95% CIs) for the association between periodontal disease (including periodontitis and gingivitis) and risk of increased CIMT (defined as CIMT value that exceeded the cut‐off value of clinical and prognostic significance), as well as interventional studies providing mean values with standard deviations of CIMT before and after periodontal intervention, were included. Random‐effect models for meta‐analysis were used to calculate the summary effect estimates with 95% CIs. A total of 406 citations were retrieved from electronic databases and 45 full‐text articles were screened, leaving 11 articles using ultrasound to measure CIMT with 8744 participants included. Pooled results of seven cross‐sectional studies involving 8558 participants indicated that compared to those without periodontitis, patients with periodontitis and those with severe periodontitis had an odds ratio of 1.42 (95% CI: 1.16, 1.75) and 1.70 (95% CI: 1.24, 2.33) for increased CIMT, respectively. Although publication bias was detected in these results, odds ratios corrected by the trim‐and‐fill method were still statistically significant. Results of four non‐randomized controlled trials with 186 patients suggested that periodontal intervention may help reduce CIMT in patients with periodontal disease in the short term. Periodontitis, especially severe periodontitis, was significantly associated with the risk of increased CIMT. Periodontal intervention might help slow the progression of carotid intima–media thickening in patients with periodontal disease in the short term.
Article
Diabetes and periodontal disease are highly prevalent conditions around the world with a bilateral causative relationship. Research suggests that interprofessional collaboration can improve care delivery and treatment outcomes. However, there continues to be little interprofessional management of these diseases. DiabOH research aims to develop an interprofessional diabetes and oral health care model for primary health care that would be globally applicable. Community medical practitioners (CMPs), community health nurses (CNs), and dentists in Shanghai were recruited to participate in online quantitative surveys. Response data of 76 CMPs, CNs, and dentists was analysed for descriptive statistics and compared with Australian data. Health professionals in China reported that, while screening for diabetes and periodontitis, increasing patient referral and improving interprofessional collaboration would be feasible, these were not within their scope of practice. Oral health screening was rarely conducted by CMPs or CNs, while dentists were not comfortable discussing diabetes with patients. Most participants believed that better collaboration would benefit patients. Chinese professionals concurred that interprofessional collaboration is vital for the improved management of diabetes and periodontitis. These views were similar in Melbourne, except that Shanghai health professionals held increased confidence in managing patients with diabetes and were more welcoming to increased oral health training.
Article
Full-text available
Periodontal disease is a chronic inflammatory disease of the jaws and is more prevalent in obesity. Local and systemic oxidative stress may be an early link between periodontal disease and obesity. The primary aim of this study was to detect whether increased periodontal disease susceptibility in obese individuals is associated with local and systemic oxidative stress. Accordingly; we analyzed periodontal status and systemic (serum) and local (gingival crevicular fluid [GCF]) oxidative status markers in young obese women in comparison with age-matched lean women. Twenty obese and 20 lean women participated. Periodontal condition was determined by clinical periodontal indices including probing depth, clinical attachment level, gingival index, gingival bleeding index, and plaque index. Anthropometric, hormonal, and metabolic measurements were also performed. Blood and GCF sampling was performed at the same time after an overnight fasting. Serum and GCF total antioxidant capacity (TAOC), and total oxidant status (TOS) levels were determined, and oxidative stress index (OSI) was calculated. Clinical periodontal analyses showed higher gingival index and gingival bleeding index in the obese group (P = 0.001 for both) with no significant difference in probing depth, clinical attachment level, and plaque index between the obese and the lean women. Oxidant status analyses revealed lower GCF and serum TAOC, and higher GCF and serum OSI values in the obese women (P < 0.05 for all). GCF TOS was higher in the obese women (P < 0.05), whereas there was a nonsignificant trend for higher serum TOS in obese women (P = 0.074). GCF TAOC values showed a negative correlation with body mass index, whereas GCF OSI was positively correlated with fasting insulin and low-density lipoprotein-cholesterol levels (P < 0.05 for all). Clinical periodontal indices showed significant correlations with body mass index, insulin, and lipid levels, and also oxidant status markers. Our results suggest that young obese, otherwise healthy, women show findings of early periodontal disease (gingival inflammation) compared with age-matched healthy lean women, and that local/periodontal oxidative stress generated by obesity seems to be associated with periodontal disease.
Article
Full-text available
Several studies have reported an association between chronic obstructive pulmonary disease (COPD) and periodontal diseases. However, a large-scale population-based cohort study was previously absent from the literature. Therefore, we evaluated the risk of periodontal diseases in patients with COPD in a nationwide population. From the National Health Insurance claims data of Taiwan, we identified 22,332 patients with COPD who were newly diagnosed during 2000 to 2010. For each case, two individuals without COPD were randomly selected and frequency matched by age, sex, and diagnosis year. Both groups were followed up till the end of 2011. The overall incidence of periodontal diseases was 1.19-fold greater in the COPD group than in the comparison group (32.2 vs 26.4 per 1000 person-years; 95% confidence interval [CI] 1.15–1.24). Compared with non-COPD patients, the adjusted hazard ratios of patients with COPD increased with the number of emergency room visits (from 1.14 [95% CI 1.10–1.19] to 5.09 [95% CI 4.53–5.72]) and admissions (from 1.15 [95% CI 1.10–1.20] to 3.17 [95% CI 2.81–3.57]). In addition, the adjusted hazard ratios of patients with COPD treated with inhaled corticosteroids (1.22, 95% CI 1.11–1.34) and systemic corticosteroids (1.15, 95% CI 1.07–1.23) were significantly higher than those of patients not treated with corticosteroids. Patient with COPD are at a higher risk of developing periodontal diseases than the general population. Our results also support that the risk of periodontal diseases is proportional to COPD control. In addition, patients who receive corticosteroid treatment are at a higher risk of developing periodontal diseases.
Article
Full-text available
Periodontal disease is associated with increased mortality in the general population, however its prognostic significance in chronic kidney disease (CKD) is not known. We evaluated the joint effect of periodontal disease and CKD on all-cause and cardiovascular mortality. Prospective observational study of 10,755 adult participants in the National Health and Nutrition Examination Survey, 1988-1994 (NHANES III). CKD was defined as estimated glomerular filtration rate < 60 ml/minute/1.73 m(2) or albumin-to-creatinine ratio ≥ 30 mg/g. Periodontal disease was defined as moderate (> 4 mm attachment loss in ≥ 2 mesial sites or 5 mm pocket depth in ≥ 2 mesial sites), or severe (> 6 mm attachment loss in ≥ 2 mesial sites and > 5 mm pocket depth in ≥ 1 mesial site). All-cause and cardiovascular mortality were evaluated using Cox proportional hazards models. There were 1,813 deaths over a median follow-up of 14 years. In multivariate analyses, as compared to participants with neither periodontal disease nor CKD, those with periodontal disease only or CKD only had increased all-cause mortality (HR 1.39; 95 % CI, 1.06 - 1.81 and 1.55; 1.30 - 1.84, respectively). The presence of both periodontal disease and CKD was associated with HR (95 % CI) 2.07 (1.65 - 2.59) for all-cause mortality, and 2.11 (1.52 - 2.94) for cardiovascular mortality. We found no evidence of multiplicativity or additivity between periodontal disease and CKD. In stratified analyses limited to individuals with CKD, periodontal disease (vs. not) was associated with adjusted HR (95 % CI) 1.35 (1.04 - 1.76) for all-cause, and 1.36 (0.95 - 1.95) for cardiovascular mortality. These findings confirm the well-established association between periodontal disease and increased mortality in the general population, and provide new evidence of this association among individuals with CKD.
Article
Full-text available
Background: Periodontitis and obesity are among the most common chronic disorders affecting the world's populations, and recent reviews suggest a potential link between overweight/obesity and periodontitis. However, because of the scarcity of prospective evidence, previous reviews were primarily based on cross-sectional studies, with only a few longitudinal or intervention studies included. This study's objective is to examine the time-dependent association between obesity and periodontitis and how weight changes may affect the development of periodontitis in the general population. Therefore, longitudinal and experimental studies that assessed the association among overweight, obesity, weight gain, waist circumference, and periodontitis are reviewed. Methods: Intervention and longitudinal studies with overweight or obesity as exposure and periodontitis as outcome were searched through the platforms PubMed/Medline and Web of Knowledge. Results: Eight longitudinal and five intervention studies were included. Two of the longitudinal studies found a direct association between degree of overweight at baseline and subsequent risk of developing periodontitis, and a further three studies found a direct association between obesity and development of periodontitis among adults. Two intervention studies on the influence of obesity on periodontal treatment effects found that the response to non-surgical periodontal treatment was better among lean than obese patients; the remaining three studies did not report treatment differences between obese and lean participants. Among the eight longitudinal studies, one study adjusted for C-reactive protein (CRP) and biologic markers of inflammation such as CRP, interleukin-6, and tumor necrosis factor-α, and inflammation markers were analyzed separately in three of the five intervention studies. Conclusion: This systematic review suggests that overweight, obesity, weight gain, and increased waist circumference may be risk factors for development of periodontitis or worsening of periodontal measures.
Article
Background and objective: Obesity has become an important global health concern as obesity-associated adiposity is supposedly related to systemic immunologic and inflammatory alterations. The aim of this study was to evaluate the effects of obesity on periodontally healthy and diseased tissue according to the changes in malondialdehyde (MDA), protein carbonyl (PC) and total antioxidant capacity (TAOC) levels in gingival crevicular fluid as biomarkers of oxidative stress (OS). Material and methods: The study sample comprised systemically healthy normal-weight (n = 45) and obese (n = 48) adults. Obesity was diagnosed according to body mass index, waist circumference and waist/hip ratio. Periodontal status was evaluated according to plaque index, gingival index, bleeding on probing, probing depth and clinical attachment level. Participants were distributed among six groups according to obesity and periodontal status, as follows: normal weight+periodontally healthy (NH); normal weight+gingivitis (NG); normal weight+generalized chronic periodontitis (NCP); obese+periodontally healthy (OH); obese+gingivitis (OG); and obese+generalized chronic periodontitis (OCP). MDA, PC and TAOC levels were measured using ELISA. Results: The MDA and PC levels in gingival crevicular fluid varied among groups, as follows: NCP > NG > NH (p < 0.01) and OCP > OG > OH (p < 0.01). Conversely, the levels of TAOC in gingival crevicular fluid varied as follows: NCP < NG < NH (p < 0.01) and OCP < OG < OH (p < 0.01). Paired comparisons conducted according to periodontal status showed MDA and PC levels to be higher, and TAOC levels to be lower, in the OCP group than in the NCP group, in the OG group than in the NG group and in the OH group than in the NH group. However, only the differences between the OCP and NCP groups were significant (p < 0.01). In both obese and normal-weight individuals, clinical assessments showed significant, positive correlations with MDA and PC levels and negative correlations with TAOC levels (p < 0.01). Conclusion: Obesity may influence periodontal tissue destruction and disease severity by increasing the level of oxidative stress in the presence of periodontal disease.
Article
Objectives: To examine whether the oral hygiene and self care especially in periodontal health are associated with chronic obstructive pulmonary disease (COPD) in a Korean population. Methods: Using data from the Korean National Health and Nutrition Examination Survey (KNHANES) between 2010 and 2012, we included 5,878 participants (normal lung function: 5181, obstructive spirometric pattern: 697) aged ≥40 years who underwent spirometry and assess the community periodontal index (CPI). Results: Participants with COPD brushed their teeth less frequently, used less frequently dental floss and / or interdental brush, mouthwash and electric toothbrush (p<0.001). The prevalence of periodontitis in COPD (58.1%) was significantly higher than without COPD (34.0%, p<0.001). The number of teeth was significantly lower in COPD patients when compared to the controls. DMF (decayed+missing+filled teeth) index is significantly lower in COPD patients. Table 3 showed risk of COPD by periodontal severity. Periodontitis (CPI 3 and 4) was associated in male COPD after adjustment for age, income, education, smoking, alcohol consumption, exercise, BMI, tooth brushing frequency, diabetes and number of teeth (CPI 3, RR 1.38; 95% confidence interval [CI], 1.12-2.05: CPI 4, RR 1.23; 95% CI, 1.06-1.56) . Conclusions: Findings of this cross-sectional study suggest that male COPD may be associated with the severe periodontitis and indicate the importance of promoting dental care in COPD patients.
Article
This study aimed to conduct a systematic review assessing the effects of weight gain on the incidence of periodontitis in adults. Electronic searches in four databases were performed up to and including September 2014. Only prospective longitudinal studies assessing the association between weight gain and the incidence of periodontitis in adults were eligible to be included in this study. All studies should state a clear description of nutritional status (Body Mass Index; Waist Circumference) as well as the case definition of periodontitis. Pooled relative risks (RR) for becoming overweight and obese on the incidence of periodontitis were estimated by meta-analysis. Quality was assessed with the Newcastle-Ottawa scale for cohort studies. Five articles were included in this review and meta-analysis with 42,198 subjects enrolled. Subjects who became overweight and obese presented higher risk to develop new cases of periodontitis (RR 1.13; 95%CI 1.06-1.20 and RR 1.33 95%CI 1.21-1.47, respectively) compared with counterparts who stayed in normal weight. A clear positive association between weight gain and new cases of periodontitis was found. However, these results are originated from limited evidence. Thus, more studies with longitudinal prospective design are needed. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
Article
The accumulation of amyloid ?? plaques (A??) is a central feature of Alzheimer's disease (AD). First reported in animal models, it remains uncertain if peripheral inflammatory/infectious conditions in humans can promote A?? brain accumulation. Periodontal disease, a common chronic infection, has been previously reported to be associated with AD.Methods Thirty-eight cognitively normal, healthy, community residing elderly (mean age 61; 68% female) were examined in an Alzheimer’s Disease research center and a University-based Dental School. Linear regression models (adjusted for age, ApoE and smoking) were used to test the hypothesis that periodontal disease assessed by clinical attachment loss was associated with brain A?? load using 11C-PIB PET imaging.ResultsAfter adjusting for confounders, clinical attachment loss (≥ 3mm), representing a history of periodontal inflammatory/infectious burden, was associated with increased 11C-PIB uptake in A?? vulnerable brain regions (p=0.002).Conclusion We show for the first time in humans an association between periodontal disease and brain A?? load. These data are consistent with prior animal studies showing that peripheral inflammation/infections are sufficient to produce brain A?? accumulations.
Article
Data sourcesThe Cochrane Oral Health Group's Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL), Medline, Embase, CINAHL, National Institutes of Health Trials Register and the WHO Clinical Trials Registry Platform for ongoing trials. Reference lists of identified articles were also scanned for relevant papers. Identified manufacturers were contacted for additional information.Study selectionOnly randomised controlled trials comparing manual and powered toothbrushes were considered. Crossover trials were eligible for inclusion if the wash-out period length was more than two weeks.Data extraction and synthesisStudy assessment and data extraction were carried out independently by at least two reviewers. The primary outcome measures were quantified levels of plaque or gingivitis. Risk of bias assessment was undertaken. Standard Cochrane methodological approaches were taken. Random-effects models were used provided there were four or more studies included in the meta-analysis, otherwise fixed-effect models were used. Data were classed as short term (one to three months) and long term (greater than three months).ResultsFifty-six trials were included with 51 (4624 patients) providing data for meta-analysis. The majority (46) were at unclear risk of bias, five at high risk of bias and five at low risk. There was moderate quality evidence that powered toothbrushes provide a statistically significant benefit compared with manual toothbrushes with regard to the reduction of plaque in both the short and long-term. This corresponds to an 11% reduction in plaque for the Quigley Hein index (Turesky) in the short term and a 21% reduction in the long term. There was a high degree of heterogeneity that was not explained by the different powered toothbrush type subgroups.There was also moderate quality evidence that powered toothbrushes again provide a statistically significant reduction in gingivitis when compared with manual toothbrushes both in the short and long term. This corresponds to a 6% and 11% reduction in gingivitis for the Löe and Silness indices respectively. Again there was a high degree of heterogeneity that was not explained by the different powered toothbrush type subgroups. The greatest body of evidence was for rotation oscillation brushes which demonstrated a statistically significant reduction in plaque and gingivitis at both time points.Conclusions Powered toothbrushes reduce plaque and gingivitis more than manual toothbrushing in the short and long term. The clinical importance of these findings remains unclear. Observation of methodological guidelines and greater standardisation of design would benefit both future trials and meta-analyses. Cost, reliability and side effects were inconsistently reported. Any reported side effects were localised and only temporary.
Article
Periodontitis and diabetes are common, complex, chronic diseases with an established bidirectional relationship. That is, diabetes (particularly if glycaemic control is poor) is associated with an increased prevalence and severity of periodontitis, and, severe periodontitis is associated with compromised glycaemic control. Periodontal treatment (conventional non-surgical periodontal therapy) has been associated with improvements in glycaemic control in diabetic patients, with reductions in HbA1c of approximately 0.4% following periodontal therapy. For these reasons, management of periodontitis in people with diabetes is particularly important. The dental team therefore has an important role to play in the management of people with diabetes. An emerging role for dental professionals is envisaged, in which diabetes screening tools could be used to identify patients at high risk of diabetes, to enable them to seek further investigation and assessment from medical healthcare providers.