Does Periodontal Disease Reflect Atherosclerosis in Continuous Ambulatory Peritoneal Dialysis Patients?

Cengiz, Murat; Bal, Seda; Gökçay, Sibel; Cengiz, Kuddusi

doi:10.1902/jop.2007.060499

Cited by 37 publications

(41 citation statements)

References 34 publications

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“…Severe periodontitis and poor dental status were associated with low serum albumin levels and PEW in both HD and PD adult patients (46,82). A latter study in HD patients described signs of poor oral health status in 80% of the patients who often had severe periodontitis associated with both poor nutritional status and systemic inflammation (48).…”

Section: Poor Oral Health As a Contributor To Protein-energy Wastingmentioning

confidence: 96%

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Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Akar

Carrero

et al. 2011

Clinical Journal of the American Society of Nephrology

168

136

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SummaryChanges in the oral cavity, such as periodontitis and other manifestations of poor oral health, are common in patients with chronic kidney disease (CKD) and may contribute to increased morbidity and mortality because of systemic consequences such as inflammation, infections, protein-energy wasting, and atherosclerotic complications. Poor oral health in CKD patients may thus represent an important, but often overlooked, problem. Several studies show that uremic patients have higher rates of decayed, missing, and filled teeth, loss of attachment, and periapical and mucosal lesions than the general population. The consequences of poor oral health may be more severe in CKD patients because of advanced age, common comorbidities such as diabetes, concurrent medications, and a state of immune dysfunction that may increase the risk for systemic consequences of periodontitis and other oral and dental pathologic conditions. Poor dentition and other signs of poor oral health should be an alarm clock also at early stages of CKD. However, it remains to be determined whether more successful management of poor oral health and periodontitis will reduce the risk of inflammation, infection, protein-energy wasting, and atherosclerotic complications in CKD patients. This review explores etiological factors and potential systemic consequences of poor oral health in CKD patients as well as possible preventive and therapeutic strategies.

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Section: Poor Oral Health As a Contributor To Protein-energy Wastingmentioning

confidence: 96%

“…Namely, poor oral health in CKD patients relates to PEW and inflammation (46,48,82,87), and moderate-to-severe periodontal disease predisposes to CVD-related mortality fivefold (4).…”

Section: Proposed Measures To Prevent and Treat Poor Oral Health In Cmentioning

confidence: 99%

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Akar

Carrero

et al. 2011

Clinical Journal of the American Society of Nephrology

168

136

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“…In addition to the oral manifestation of periodontitis, periodontal pathogens such as Porphyromonas gingivalis are associated with a variety of other systemic disorders such as atherosclerosis, pneumonia, rheumatoid arthritis, and nephritis (7,10,12,23,24,26,28,29,34). However, colonization of the subgingival pocket by P. gingivalis can occur only after the organism first becomes established in the supragingival biofilm or on tissue surfaces.…”

mentioning

confidence: 99%

Structural Dissection and In Vivo Effectiveness of a Peptide Inhibitor of Porphyromonas gingivalis Adherence to Streptococcus gordonii

et al. 2011

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The interaction of the minor fimbrial antigen (Mfa) with streptococcal antigen I/II (e.g., SspB) facilitates colonization of the dental biofilm by Porphyromonas gingivalis. We previously showed that a 27-mer peptide derived from SspB (designated BAR) resembles the nuclear receptor (NR) box protein-protein interacting domain and potently inhibits this interaction in vitro. Here, we show that the EXXP motif upstream of the NR core ␣-helix contributes to the Mfa-SspB interaction and that BAR reduces P. gingivalis colonization and alveolar bone loss in vivo in a murine model of periodontitis. Substitution of Gln for Pro 1171 or Glu 1168 increased the ␣-helicity of BAR and reduced its inhibitory activity in vitro by 10-fold and 2-fold, respectively. To determine if BAR prevents P. gingivalis infection in vivo, mice were first infected with Streptococcus gordonii and then challenged with P. gingivalis in the absence and presence of BAR. Animals that were infected with either 10 9 CFU of S. gordonii DL-1 or 10 7 CFU of P. gingivalis 33277 did not show a statistically significant increase in alveolar bone resorption over sham-infected controls. However, infection with 10 9 CFU of S. gordonii followed by 10 7 CFU of P. gingivalis induced significantly greater bone loss (P < 0.01) than sham infection or infection of mice with either organism alone. S. gordonii-infected mice that were subsequently challenged with 10 7 CFU of P. gingivalis in the presence of BAR exhibited levels of bone resorption similar to those of sham-infected animals. Together, these results indicate that both EXXP and the NR box are important for the Mfa-SspB interaction and that BAR peptide represents a potential therapeutic that may limit colonization of the oral cavity by P. gingivalis.Periodontal disease is an oral inflammatory disorder that is initiated by a microbial biofilm that forms in the subgingival pocket. In addition to the oral manifestation of periodontitis, periodontal pathogens such as Porphyromonas gingivalis are associated with a variety of other systemic disorders such as atherosclerosis, pneumonia, rheumatoid arthritis, and nephritis (7,10,12,23,24,26,28,29,34). However, colonization of the subgingival pocket by P. gingivalis can occur only after the organism first becomes established in the supragingival biofilm or on tissue surfaces. Colonization of the supragingival biofilm occurs through interspecies interactions of P. gingivalis with specific species of oral streptococci (e.g., Streptococcus oralis and Streptococcus gordonii but not the mutans streptococci) (11,20), and these initial interactions thus represent viable targets for therapeutic intervention to limit colonization of the oral cavity by P. gingivalis.The selective adherence of P. gingivalis to specific oral streptococcal species is driven by a protein-protein interaction that occurs between the minor fimbrial antigen (Mfa) of P. gingivalis and the streptococcal antigen I/II, and inactivation of mfa completely prevents P. gingivalis adherence and formation of biofil...

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“…Inflammatory periodontal diseases represent a risk factor for several chronic and serious systemic conditions, such as vascular diseases including stroke (107)(108)(109)(110), pulmonary disease (111)(112)(113), nephritis (114) and pre-term birth (115,116).…”

Section: Periodontal Diseasesmentioning

confidence: 99%

Tobacco-induced changes to Porphyromonas gingivalis gene expression, phenotype and host-pathogen interactions.

Bagaitkar¹

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Does Periodontal Disease Reflect Atherosclerosis in Continuous Ambulatory Peritoneal Dialysis Patients?

Abstract: Periodontal health is poor in CAPD patients and correlates with markers of malnutrition, inflammation, and atherosclerosis. The diagnosis and treatment of periodontal diseases require better awareness.

Cited by 37 publications

References 34 publications

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Structural Dissection and In Vivo Effectiveness of a Peptide Inhibitor of Porphyromonas gingivalis Adherence to Streptococcus gordonii

Tobacco-induced changes to Porphyromonas gingivalis gene expression, phenotype and host-pathogen interactions.

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