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Leonidas C. Batas DDS, Msc, PhD.
Dental Degree (DDS): Aristotle University of Thessaloniki Dental School, Greece.
Periodontology and Implant Dentistry: University of Minnesota Dental School
Department of Periodontology, USA.
Master of Science (Msc): University of Minnesota Dental School Department of
Periodontology, USA.
PhD: Aristotle University of Thessaloniki Dental School Department of
Periodontology, Greece
Abstract:
Periodontitis results in chronic inflammation of the soft tissue surrounding teeth.
The inflammation destroys the bone and soft tissue supporting the roots of the
teeth. Nowadays the literature evidence began to suggest a possible link between
chronic inflammatory periodontitis and a number of systemic diseases such as
cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease,
respiratory diseases, and low birth weight.
Periodontitis is a group of infectious diseases that result in chronic inflammation of
the soft tissue surrounding teeth. The inflammation destroys the bone and soft
tissue supporting the roots of the teeth. Periodontitis is associated with a variety
of bacteria species. The progression and severity of the disease depends on the
host’s response to the bacterial challenge (1). Chronic periodontitis is the most
common form of periodontitis. Clinical features of chronic periodontitis include
gingival inflammation, pocket formation, destruction of alveolar bone with
eventually tooth mobility and tooth loss (2). While periodontitis progresses at
various rates within individuals its accumulative advanced stage is usually seen in
the fifth and sixth decades of life (3,4). Host response factors normally include
functioning neutrophils and lymphocytes (5).
Microscopic observations of the subgingival organisms associated with adult
periodontitis demonstrate a high ratio of motile rods, curved rods, and spirochetes
(5,6). Plaque collected from periodontally diseased sites has been reported to
contain a higher proportion of cultivable Gram-negative anaerobic rods than
healthy gingival sites or gingival crevices associated with gingivitis(7). Gram-
negative bacteria may compose 75% of the total cultivable flora in advanced adult
periodontitis.
Many bacteriological and immunological studies have implicated specific
subgingival organisms in the pathogenesis of adult periodontitis. Tanner et al.
(1979) employed culture techniques to identify the subgingival bacteria associated
with progressing bone loss in 8 patients exhibiting advanced adult periodontitis.
They found a predominance of one or more of the following bacterial species in
each study patient: Bacteroides gingivalis (Porphyromonas gingivalis); Prevotella
intermedia; Bacteroides forsythus (Fusobacterium nucleatum; Eikenella
corrodens; Actinobacillus actinomycetemcomitans; Wolinella recta. (8)
The first signs of periodontal disease is plaque accumulation, calculus formation,
that leads to gingival redness and swelling, gingival bleeding and suppuration
which may occur either spontaneously or when subjected to probing, halitosis (bad
breath), and loss of alveolar bone. Others include: deepening of the gingival
crevice resulting in the formation of a pathological periodontal pocket, root
exposure due to gingival recession, and increased tooth mobility. Severe forms of
the disease may lead to tooth migration, compromised esthetics, impaired
masticatory function, and tooth loss ultimately (9,10).
In the United States alone, periodontitis affects approximately 65 million people
(11; 12), and represents the sixth-most prevalent diseasecondition worldwide (13).
Periodontitis is the leading cause of tooth loss in adults. In 2011, the total cost for
periodontal treatments in the US was approximately $50 billion (14).
Nowadays the literature evidence began to suggest a possible link between
chronic inflammatory periodontitis and a number of systemic diseases.(15-18) A
chronic oral infection such as periodontitis is a constant potential source of
infection and has been considered as a separate risk factor for cardiovascular
diseases, cerebrovascular diseases, peripheral arterial disease, respiratory
diseases, and low birth weight.(19) In addition, periodontitis has been described
as a potential risk for increased morbidity and mortality for diabetes, insulin
resistance, rheumatoid arthritis, obesity, osteoporosis, and complications of
pregnancy (16,17).
The concept that periodontal disease might influence systemic health is not new.
Miller originally published his focal infection theory in 1891 suggesting that
microorganisms or their waste products obtain entrance to parts of the body
adjacent to or remote from the mouth. The possible mechanisms or pathways
linking oral infections to secondary systemic effect are: metastatic spread of
infection from the oral cavity as a result of transient bacteremia, metastatic injury
from the effects of circulating oral microbial toxins, and metastatic inflammation
caused by immunological injury induced by oral micro-organisms. (18,20,21).
Medical and dental specialists tend to see patient management from regional
rather than systemic point of view, not taking under consideration the role of oral
infections like periodontitis on multifarious systemic disorders, it has become
necessary to undertake a literature review on the subject. The literature has
provided information about the potential association of oral infections like
periodontitis on multifarious systemic disorders. This fact should have the attention
of health practitioners to the impact of oral health care on the general well-being;
and to emphasize the need for a deeper interaction between medical and dental
trainings.
Cardiovascular disease
In the literature there is a cumulative evidence supports a causal association
between periodontal infection and artherosclerotic cardiovascular disease or its
sequelae.(22) The possible link may involve direct and indirect effects of the
periodontal infection; an alternative pathway may be related to genetic and other
host factors that increase the susceptibility to both atherosclerosis/thrombosis and
chronic periodontitis.(23-26) Studies have shown that periodontitis results in higher
systemic levels of C-reactive protein, interleukin (IL)-6, and neutrophilsThese
elevated inflammatory factors may increase inflammatory activity in atherosclerotic
lesions, potentially increasing the risk for cardiac or cerebrovascular
events(27,28)These systemic markers of inflammation are also said to serve as
predictors of present and future cardiovascular events and disease. (29) In
addition, oral bacteria have been found in carotid atheromas and it is reported that
some oral bacteria may be associated with platelet aggregation, an event
important for thrombosis.(27,28) Evidence that suggests an association between
chronic oral infections and myocardial infarction had also been presented.(30)
Premature and low-birth-weight births (PLBW).
Infection is now considered one of the major causes of Premature and low birth
weight (PLBW) deliveries, responsible for somewhere between 30% and 50% of
all cases, and periodontitis and periodontal diseases are true infections of the oral
cavity(31) Research has shown that the bacteria that cause inflammation in the
gums can actually get into the bloodstream and target the fetus, potentially leading
to PLBW babies. One possible mechanism begins with endotoxins resulting from
Gram-negative bacterial infections (such as periodontal disease). These
endotoxins stimulate the production of cytokines and prostaglandins (IL-1β, IL-6,
and TNF-α) and in appropriate quantities stimulate labor,(32) and proinflammatory
mediators may cross the placenta barrier and cause fetal toxicity resulting in
preterm delivery and low-birth-weight babies (33,34). High concentrations of these
cytokines, in pregnant women, are responsible for rupture of the uterine
membranes causing premature birth and retardation. Several animal and clinical
studies clearly indicate an association between periodontal infection and adverse
pregnancy outcomes. Although no definitive causal relationship has been
established, and other explanations for the correlation might be offered, a model
can nevertheless be envisaged wherein chronic periodontal infection could
mediate this systemic effect through one or more of the following mechanisms (35)
Translocation of periodontal pathogens to the fetoplacental unit, Action of a
periodontal reservoir of LPS on the fetoplacental unit, Action of a periodontal
reservoir of inflammatory mediators (IL-1, IL-6, TNF-α, PGE2) on the fetoplacental
unit.
Respiratory system
There is a fair evidence of an association of pneumonia with oral health and that a
good evidence exists that improved oral hygiene and frequent professional oral
health care reduce the progression or occurrence of respiratory diseases among
the high-risk elderly living in nursing homes, especially those in intensive care
units.(36) The oral cavity has long been considered a potential reservoir for
respiratory pathogens. The mechanism of infection could be aspiration of oral
bacteria capable of causing pneumonia into the lungs, colonization of dental
plaque by respiratory pathogens, followed by aspiration.(38) Other mechanisms
include: alteration of the mucus surface by salivary enzymes in periodontitis,
leading to an increase in adhesion and colonization of respiratory pathogens;
destruction of salivary pellicles on pathogenic bacteria by periodontal disease-
associated enzymes; and alteration of respiratory epithelium by cytokines from
periodontal disease, facilitating the infection of the epithelium by respiratory
pathogens.(39) that a potential association between periodontitis and chronic
pulmonary diseases like chronic obstructive pulmonary disease (COPD) may
exist.(37) In one of the studies by Scannapieco et al., they found a nearly fivefold
increase in chronic respiratory diseases in subjects that had poor oral hygiene
when compared to those with good oral hygiene. Poor oral hygiene and
periodontitis influence the incidence of pulmonary infections, especially
nosocomial pneumonia episodes in high-risk subjects. (37)
Conclusion.
Historically, diseases of the oral cavity have been viewed separately from those of
the rest of the body. In recent years, however, efforts have been made to recognize
oral health as an integral part of overall health. The concept that periodontal
disease might influence systemic health is not new. Nowadays the literature
evidence strongly suggest a link between chronic inflammatory periodontitis and a
number of systemic diseases (15-18). A chronic oral infection such as periodontitis
is potential and constant source of infection and has been considered as a risk
factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial
disease, respiratory diseases, and low birth weight.(19). The fact that there is an
impact of oral health care on the general well-being, points out and emphasizes
the need for a deeper interaction between medical and dental trainings.
References :
1. Socransky, S. S., A. D. Haffajee, M. A. Cugini, C. Smith, and R. L. Kent, Jr.
1998. Microbial complexes in subgingival plaque. J Clin Periodontol 25:134.
2. Kornman, K. S. 1987. Nature of periodontal diseases: assessment and
diagnosis. J Periodontal Res 22:192.
3. Glickman, F. R. 1984. Ergonomics in occupational health and safety. Fam
Community Health 7:64.
4. Suzuki, J. B. 1988. Diagnosis and classification of the periodontal diseases.
Dent Clin North Am 32:195.
5. Listgarten, M. A. 1976. Structure of the microbial flora associated with
periodontal health and disease in man. A light and electron microscopic
study. J Periodontol 47:1.
6. Wolff, L. F., C. Bandt, B. Pihlstrom, and L. Brayer. 1982. Phase contrast
microscopic evaluation of subgingival plaque in combination with either
conventional or antimicrobial home treatment of patients with periodontal
inflammation. J Periodontal Res 17:537.
7. Robertson, M. R., F. R. Saglie, F. A. Carranza, Jr., and M. G. Newman.
1985. [Bacterial invasion and disease activity in human periodontitis (I)]. Av
Odontoestomatol 1:200.
8. Tanner, A. C., C. Haffer, G. T. Bratthall, R. A. Visconti, and S. S. Socransky.
1979. A study of the bacteria associated with advancing periodontitis in
man. J Clin Periodontol 6:278.
9. Newman MG. Classification and epidemiology of periodontal diseases. In:
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WS, Taylor GW, Page RC, Beck JD, Genco RJ. Update on Prevalence of
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W. Global burden of severe periodontitis in 1990-2010: a systematic review
and meta-regression. J Dent Res. 2014 Nov;93(11):1045-53
14.Flemmig TF, Beikler T. 2013 Economics of periodontal care: market
trends, competitive forces and incentives.Periodontol
2000. Jun;62(1):287-304.
15.Paquette DW. The periodontal infection-systemic disease link: A review of
the truth or myth. J Int Acad Periodontol. 2002;4:101–9.
16.Moutsopoulos NM, Madianos PN. Low-grade inflammation in chronic
infectious diseases: Paradigm of periodontal infections. Ann N Y Acad
Sci. 2006;1088:251–64.
17.Fowler EB, Breault LG, Cuenin MF. Periodontal disease and its
association with systemic disease. Mil Med. 2001;166:85–9.
18. DeBowes LJ. The effects of dental disease on systemic disease. Vet Clin
North Am Small Anim Pract.1998;28:1057–62
19.Ohyama H, Nakasho K, Yamanegi K, Noiri Y, Kuhara A, Kato-Kogoe N, et
al. An unusual autopsy case of pyogenic liver abscess caused by
periodontal bacteria. Jpn Infect Dis. 2009;62:381–3.
20.Taylor GW. Bidirectional interrelationships between diabetes and
periodontal diseases: An epidemiologic perspective. Ann
Periodontol. 2001;6:99–12.
21.Loos BG. Systemic markers of inflammation in periodontitis. J
Periodontol. 2005;76:2106–15.
22.Genco R, Offenbecker S, Beck J. Periodontal disease and cardiovascular
disease: Epidemiology and possible mechanisms. J Am Dent
Assoc. 2002;133:145–25.
23. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal
disease and coronary heart disease risk. J Am Dent
Assoc. 2000;284:1406–10.
24. Danesh J, Collins R, Peto R. Chronic infections and coronary heart
disease: Is there a link? Lancet.1997;350:430–6.
25. Madianos PN, Bobetsis GA, Kinane DF. Is periodontitis associated with
an increased risk of coronary heart disease and preterm and/or low birth
weight births? J Clin Periodontol. 2002;29:22–36.
26. Geismar K, Stoltze K, Sigurd B, Gyntelberg F, Holmstrup P. Periodontal
disease and coronary heart disease. J Periodontol. 2006;77:1547–54.
27. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of
periodontal pathogens in atheromatous plaques. J
Periodontol. 2000;71:1554–60.
28. Chiu B. Multiple infections in carotid atherosclerotic plaques. Am Heart
J. 1999;138:534–6.
29.Fong IW. Infection and their role in artherosclerotic vascular disease. J Am
Dent Assoc. 2002;133:7–3.
30.Willershausen B, Adrian K, Willershausen I, Zahorka D, Briseňo B,
Blettner M, et al. Association between chronic dental infection and acute
myocardial infarction. J Endod. 2009;35:626–30.
31.Saini R, Marawar PP, Shete S, Saini S. Periodontitis a true infection. J Glob
Infect Dis. 2009;1:149–51.
32.Madianos PN1, Lieff S, Murtha AP, Boggess KA, Auten RL Jr, Beck
JD, Offenbacher S.Maternal periodontitis and prematurity. Part II: Maternal
infection and fetal exposure. Ann,Periodontol. 2001 Dec;6(1):175-82.
33.McGaw T. Periodontal diseases and pre-term delivery of low birth weight
infants. J Can Dent Assoc.2002;68:165–9.
34.Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC.
Periodontal infection and preterm birth: Results of a prospective study. J
Am Dent Assoc. 2001;132:875–80
35.Yeo BK, Lim LP, Paquette DW, Williams RC. Periodontal disease – the
emergence of a risk for systemic conditions: Pre-term low birth weight. Ann
Acad Med Singapore Azarpazhooh A, Leake JL. Systematic review of the
association between respiratory diseases and oral health. J
Periodontol. 2006;77:1465–82.
36.Scannapieco FA. Potential associations between chronic respiratory
disease and periodontal disease: Analysis of National Health and Nutrition
Examination Survey III. J Periodontol. 2000;71:1528–34.[
37.Scannapieco FA, Bush RB, Paju S. Associations between periodontal
disease and risk for nosocomial bacterial pneumonia and chronic
obstructive pulmonary disease. A systematic review. Ann
Periodontol.2003;8:54–69.
38.Mion P. Oral health and respiratory infection. J Can Dent
Assoc. 2002;68:340–5.
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periodontitis and systemic diseases. Acta Stomatol Croat. 2001;35:267–71.

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Periodontitis

  • 1. Leonidas C. Batas DDS, Msc, PhD. Dental Degree (DDS): Aristotle University of Thessaloniki Dental School, Greece. Periodontology and Implant Dentistry: University of Minnesota Dental School Department of Periodontology, USA. Master of Science (Msc): University of Minnesota Dental School Department of Periodontology, USA. PhD: Aristotle University of Thessaloniki Dental School Department of Periodontology, Greece Abstract: Periodontitis results in chronic inflammation of the soft tissue surrounding teeth. The inflammation destroys the bone and soft tissue supporting the roots of the teeth. Nowadays the literature evidence began to suggest a possible link between chronic inflammatory periodontitis and a number of systemic diseases such as cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease, respiratory diseases, and low birth weight.
  • 2. Periodontitis is a group of infectious diseases that result in chronic inflammation of the soft tissue surrounding teeth. The inflammation destroys the bone and soft tissue supporting the roots of the teeth. Periodontitis is associated with a variety of bacteria species. The progression and severity of the disease depends on the host’s response to the bacterial challenge (1). Chronic periodontitis is the most common form of periodontitis. Clinical features of chronic periodontitis include gingival inflammation, pocket formation, destruction of alveolar bone with eventually tooth mobility and tooth loss (2). While periodontitis progresses at various rates within individuals its accumulative advanced stage is usually seen in the fifth and sixth decades of life (3,4). Host response factors normally include functioning neutrophils and lymphocytes (5). Microscopic observations of the subgingival organisms associated with adult periodontitis demonstrate a high ratio of motile rods, curved rods, and spirochetes (5,6). Plaque collected from periodontally diseased sites has been reported to contain a higher proportion of cultivable Gram-negative anaerobic rods than healthy gingival sites or gingival crevices associated with gingivitis(7). Gram- negative bacteria may compose 75% of the total cultivable flora in advanced adult periodontitis. Many bacteriological and immunological studies have implicated specific subgingival organisms in the pathogenesis of adult periodontitis. Tanner et al. (1979) employed culture techniques to identify the subgingival bacteria associated with progressing bone loss in 8 patients exhibiting advanced adult periodontitis. They found a predominance of one or more of the following bacterial species in each study patient: Bacteroides gingivalis (Porphyromonas gingivalis); Prevotella intermedia; Bacteroides forsythus (Fusobacterium nucleatum; Eikenella corrodens; Actinobacillus actinomycetemcomitans; Wolinella recta. (8) The first signs of periodontal disease is plaque accumulation, calculus formation, that leads to gingival redness and swelling, gingival bleeding and suppuration which may occur either spontaneously or when subjected to probing, halitosis (bad breath), and loss of alveolar bone. Others include: deepening of the gingival
  • 3. crevice resulting in the formation of a pathological periodontal pocket, root exposure due to gingival recession, and increased tooth mobility. Severe forms of the disease may lead to tooth migration, compromised esthetics, impaired masticatory function, and tooth loss ultimately (9,10). In the United States alone, periodontitis affects approximately 65 million people (11; 12), and represents the sixth-most prevalent diseasecondition worldwide (13). Periodontitis is the leading cause of tooth loss in adults. In 2011, the total cost for periodontal treatments in the US was approximately $50 billion (14). Nowadays the literature evidence began to suggest a possible link between chronic inflammatory periodontitis and a number of systemic diseases.(15-18) A chronic oral infection such as periodontitis is a constant potential source of infection and has been considered as a separate risk factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease, respiratory diseases, and low birth weight.(19) In addition, periodontitis has been described as a potential risk for increased morbidity and mortality for diabetes, insulin resistance, rheumatoid arthritis, obesity, osteoporosis, and complications of pregnancy (16,17). The concept that periodontal disease might influence systemic health is not new. Miller originally published his focal infection theory in 1891 suggesting that microorganisms or their waste products obtain entrance to parts of the body adjacent to or remote from the mouth. The possible mechanisms or pathways linking oral infections to secondary systemic effect are: metastatic spread of infection from the oral cavity as a result of transient bacteremia, metastatic injury from the effects of circulating oral microbial toxins, and metastatic inflammation caused by immunological injury induced by oral micro-organisms. (18,20,21). Medical and dental specialists tend to see patient management from regional rather than systemic point of view, not taking under consideration the role of oral infections like periodontitis on multifarious systemic disorders, it has become necessary to undertake a literature review on the subject. The literature has provided information about the potential association of oral infections like
  • 4. periodontitis on multifarious systemic disorders. This fact should have the attention of health practitioners to the impact of oral health care on the general well-being; and to emphasize the need for a deeper interaction between medical and dental trainings. Cardiovascular disease In the literature there is a cumulative evidence supports a causal association between periodontal infection and artherosclerotic cardiovascular disease or its sequelae.(22) The possible link may involve direct and indirect effects of the periodontal infection; an alternative pathway may be related to genetic and other host factors that increase the susceptibility to both atherosclerosis/thrombosis and chronic periodontitis.(23-26) Studies have shown that periodontitis results in higher systemic levels of C-reactive protein, interleukin (IL)-6, and neutrophilsThese elevated inflammatory factors may increase inflammatory activity in atherosclerotic lesions, potentially increasing the risk for cardiac or cerebrovascular events(27,28)These systemic markers of inflammation are also said to serve as predictors of present and future cardiovascular events and disease. (29) In addition, oral bacteria have been found in carotid atheromas and it is reported that some oral bacteria may be associated with platelet aggregation, an event important for thrombosis.(27,28) Evidence that suggests an association between chronic oral infections and myocardial infarction had also been presented.(30) Premature and low-birth-weight births (PLBW). Infection is now considered one of the major causes of Premature and low birth weight (PLBW) deliveries, responsible for somewhere between 30% and 50% of all cases, and periodontitis and periodontal diseases are true infections of the oral cavity(31) Research has shown that the bacteria that cause inflammation in the gums can actually get into the bloodstream and target the fetus, potentially leading to PLBW babies. One possible mechanism begins with endotoxins resulting from Gram-negative bacterial infections (such as periodontal disease). These
  • 5. endotoxins stimulate the production of cytokines and prostaglandins (IL-1β, IL-6, and TNF-α) and in appropriate quantities stimulate labor,(32) and proinflammatory mediators may cross the placenta barrier and cause fetal toxicity resulting in preterm delivery and low-birth-weight babies (33,34). High concentrations of these cytokines, in pregnant women, are responsible for rupture of the uterine membranes causing premature birth and retardation. Several animal and clinical studies clearly indicate an association between periodontal infection and adverse pregnancy outcomes. Although no definitive causal relationship has been established, and other explanations for the correlation might be offered, a model can nevertheless be envisaged wherein chronic periodontal infection could mediate this systemic effect through one or more of the following mechanisms (35) Translocation of periodontal pathogens to the fetoplacental unit, Action of a periodontal reservoir of LPS on the fetoplacental unit, Action of a periodontal reservoir of inflammatory mediators (IL-1, IL-6, TNF-α, PGE2) on the fetoplacental unit. Respiratory system There is a fair evidence of an association of pneumonia with oral health and that a good evidence exists that improved oral hygiene and frequent professional oral health care reduce the progression or occurrence of respiratory diseases among the high-risk elderly living in nursing homes, especially those in intensive care units.(36) The oral cavity has long been considered a potential reservoir for respiratory pathogens. The mechanism of infection could be aspiration of oral bacteria capable of causing pneumonia into the lungs, colonization of dental plaque by respiratory pathogens, followed by aspiration.(38) Other mechanisms include: alteration of the mucus surface by salivary enzymes in periodontitis, leading to an increase in adhesion and colonization of respiratory pathogens; destruction of salivary pellicles on pathogenic bacteria by periodontal disease- associated enzymes; and alteration of respiratory epithelium by cytokines from periodontal disease, facilitating the infection of the epithelium by respiratory pathogens.(39) that a potential association between periodontitis and chronic
  • 6. pulmonary diseases like chronic obstructive pulmonary disease (COPD) may exist.(37) In one of the studies by Scannapieco et al., they found a nearly fivefold increase in chronic respiratory diseases in subjects that had poor oral hygiene when compared to those with good oral hygiene. Poor oral hygiene and periodontitis influence the incidence of pulmonary infections, especially nosocomial pneumonia episodes in high-risk subjects. (37) Conclusion. Historically, diseases of the oral cavity have been viewed separately from those of the rest of the body. In recent years, however, efforts have been made to recognize oral health as an integral part of overall health. The concept that periodontal disease might influence systemic health is not new. Nowadays the literature evidence strongly suggest a link between chronic inflammatory periodontitis and a number of systemic diseases (15-18). A chronic oral infection such as periodontitis is potential and constant source of infection and has been considered as a risk factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease, respiratory diseases, and low birth weight.(19). The fact that there is an impact of oral health care on the general well-being, points out and emphasizes the need for a deeper interaction between medical and dental trainings. References : 1. Socransky, S. S., A. D. Haffajee, M. A. Cugini, C. Smith, and R. L. Kent, Jr. 1998. Microbial complexes in subgingival plaque. J Clin Periodontol 25:134. 2. Kornman, K. S. 1987. Nature of periodontal diseases: assessment and diagnosis. J Periodontal Res 22:192. 3. Glickman, F. R. 1984. Ergonomics in occupational health and safety. Fam Community Health 7:64.
  • 7. 4. Suzuki, J. B. 1988. Diagnosis and classification of the periodontal diseases. Dent Clin North Am 32:195. 5. Listgarten, M. A. 1976. Structure of the microbial flora associated with periodontal health and disease in man. A light and electron microscopic study. J Periodontol 47:1. 6. Wolff, L. F., C. Bandt, B. Pihlstrom, and L. Brayer. 1982. Phase contrast microscopic evaluation of subgingival plaque in combination with either conventional or antimicrobial home treatment of patients with periodontal inflammation. J Periodontal Res 17:537. 7. Robertson, M. R., F. R. Saglie, F. A. Carranza, Jr., and M. G. Newman. 1985. [Bacterial invasion and disease activity in human periodontitis (I)]. Av Odontoestomatol 1:200. 8. Tanner, A. C., C. Haffer, G. T. Bratthall, R. A. Visconti, and S. S. Socransky. 1979. A study of the bacteria associated with advancing periodontitis in man. J Clin Periodontol 6:278. 9. Newman MG. Classification and epidemiology of periodontal diseases. In: Newman MG, Takei H, Carranza FA, editors. Carraza's Clinical Periodontology. 10th ed. Philadelphia: WB Saunders Company; 2007. pp. 100–29. 10. Pihlstrom B. Periodontal risk assessment, diagnosis and treatment planning. J Periodontol. 2001;25:37–58 11.Albandar 2011 Underestimation of periodontitis in NHANES surveys. J Periodontol. 2011 Mar;82 (3):337-41. 12.Eke PI, Dye BA, Wei L, Slade GD, Thornton-Evans GO, Borgnakke WS, Taylor GW, Page RC, Beck JD, Genco RJ. Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 to 2012. J Periodontol. 2015 May;86(5):611-22. 13.Kassebaum NJ, Bernabé E, Dahiya M, Bhandari B, Murray CJ, Marcenes W. Global burden of severe periodontitis in 1990-2010: a systematic review and meta-regression. J Dent Res. 2014 Nov;93(11):1045-53
  • 8. 14.Flemmig TF, Beikler T. 2013 Economics of periodontal care: market trends, competitive forces and incentives.Periodontol 2000. Jun;62(1):287-304. 15.Paquette DW. The periodontal infection-systemic disease link: A review of the truth or myth. J Int Acad Periodontol. 2002;4:101–9. 16.Moutsopoulos NM, Madianos PN. Low-grade inflammation in chronic infectious diseases: Paradigm of periodontal infections. Ann N Y Acad Sci. 2006;1088:251–64. 17.Fowler EB, Breault LG, Cuenin MF. Periodontal disease and its association with systemic disease. Mil Med. 2001;166:85–9. 18. DeBowes LJ. The effects of dental disease on systemic disease. Vet Clin North Am Small Anim Pract.1998;28:1057–62 19.Ohyama H, Nakasho K, Yamanegi K, Noiri Y, Kuhara A, Kato-Kogoe N, et al. An unusual autopsy case of pyogenic liver abscess caused by periodontal bacteria. Jpn Infect Dis. 2009;62:381–3. 20.Taylor GW. Bidirectional interrelationships between diabetes and periodontal diseases: An epidemiologic perspective. Ann Periodontol. 2001;6:99–12. 21.Loos BG. Systemic markers of inflammation in periodontitis. J Periodontol. 2005;76:2106–15. 22.Genco R, Offenbecker S, Beck J. Periodontal disease and cardiovascular disease: Epidemiology and possible mechanisms. J Am Dent Assoc. 2002;133:145–25. 23. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and coronary heart disease risk. J Am Dent Assoc. 2000;284:1406–10. 24. Danesh J, Collins R, Peto R. Chronic infections and coronary heart disease: Is there a link? Lancet.1997;350:430–6.
  • 9. 25. Madianos PN, Bobetsis GA, Kinane DF. Is periodontitis associated with an increased risk of coronary heart disease and preterm and/or low birth weight births? J Clin Periodontol. 2002;29:22–36. 26. Geismar K, Stoltze K, Sigurd B, Gyntelberg F, Holmstrup P. Periodontal disease and coronary heart disease. J Periodontol. 2006;77:1547–54. 27. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol. 2000;71:1554–60. 28. Chiu B. Multiple infections in carotid atherosclerotic plaques. Am Heart J. 1999;138:534–6. 29.Fong IW. Infection and their role in artherosclerotic vascular disease. J Am Dent Assoc. 2002;133:7–3. 30.Willershausen B, Adrian K, Willershausen I, Zahorka D, Briseňo B, Blettner M, et al. Association between chronic dental infection and acute myocardial infarction. J Endod. 2009;35:626–30. 31.Saini R, Marawar PP, Shete S, Saini S. Periodontitis a true infection. J Glob Infect Dis. 2009;1:149–51. 32.Madianos PN1, Lieff S, Murtha AP, Boggess KA, Auten RL Jr, Beck JD, Offenbacher S.Maternal periodontitis and prematurity. Part II: Maternal infection and fetal exposure. Ann,Periodontol. 2001 Dec;6(1):175-82. 33.McGaw T. Periodontal diseases and pre-term delivery of low birth weight infants. J Can Dent Assoc.2002;68:165–9. 34.Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC. Periodontal infection and preterm birth: Results of a prospective study. J Am Dent Assoc. 2001;132:875–80 35.Yeo BK, Lim LP, Paquette DW, Williams RC. Periodontal disease – the emergence of a risk for systemic conditions: Pre-term low birth weight. Ann Acad Med Singapore Azarpazhooh A, Leake JL. Systematic review of the association between respiratory diseases and oral health. J Periodontol. 2006;77:1465–82. 36.Scannapieco FA. Potential associations between chronic respiratory disease and periodontal disease: Analysis of National Health and Nutrition Examination Survey III. J Periodontol. 2000;71:1528–34.[
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