Psychological stress has no association with salivary levels of β-defensin 2 and β-defensin 3
J Oral Pathol Med (2010) 39: 765–769 Background: Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down‐regulate the production of β‐defensins (antimicro...
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Published in | Journal of oral pathology & medicine Vol. 39; no. 10; pp. 765 - 769 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.11.2010
Wiley |
Subjects | |
Online Access | Get full text |
ISSN | 0904-2512 1600-0714 1600-0714 |
DOI | 10.1111/j.1600-0714.2010.00933.x |
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Abstract | J Oral Pathol Med (2010) 39: 765–769
Background: Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down‐regulate the production of β‐defensins (antimicrobial peptides produced in the oral cavity), the aim of the present study was to evaluate the association between stress and salivary levels of β‐defensin 2 (HBD‐2) and β‐defensin 3 (HBD‐3).
Methods: For this purpose, seventy five volunteers, classified as periodontally healthy, were submitted to a psychological evaluation using a validated questionnaire (Questionnaire of Lipp‐ISS). Following analysis of the questionnaires, the subjects were divided in two groups (Group A: Absence of stress and Group B: Presence of stress). Unstimulated saliva samples were collected and the concentration of total protein was determined using the BCA method, and the concentrations of HBD‐2 and HBD‐3 were determined by ELISA.
Results: The levels of total protein did not show a statistically significant difference between the groups. Analyses of HBD‐2 and HBD‐3 concentrations indicate that the stress condition was not associated with the levels of either peptide in saliva (P = 0.3664 for HBD‐2 and P = 0.3608 for HBD‐3).
Conclusion: In periodontally healthy subjects, HBD‐2 and HBD‐3 levels are not influenced by stress. |
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AbstractList | J Oral Pathol Med (2010) 39: 765–769
Background: Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down‐regulate the production of β‐defensins (antimicrobial peptides produced in the oral cavity), the aim of the present study was to evaluate the association between stress and salivary levels of β‐defensin 2 (HBD‐2) and β‐defensin 3 (HBD‐3).
Methods: For this purpose, seventy five volunteers, classified as periodontally healthy, were submitted to a psychological evaluation using a validated questionnaire (Questionnaire of Lipp‐ISS). Following analysis of the questionnaires, the subjects were divided in two groups (Group A: Absence of stress and Group B: Presence of stress). Unstimulated saliva samples were collected and the concentration of total protein was determined using the BCA method, and the concentrations of HBD‐2 and HBD‐3 were determined by ELISA.
Results: The levels of total protein did not show a statistically significant difference between the groups. Analyses of HBD‐2 and HBD‐3 concentrations indicate that the stress condition was not associated with the levels of either peptide in saliva (P = 0.3664 for HBD‐2 and P = 0.3608 for HBD‐3).
Conclusion: In periodontally healthy subjects, HBD‐2 and HBD‐3 levels are not influenced by stress. Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down-regulate the production of β-defensins (antimicrobial peptides produced in the oral cavity), the aim of the present study was to evaluate the association between stress and salivary levels of β-defensin 2 (HBD-2) and β-defensin 3 (HBD-3).BACKGROUNDRecent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down-regulate the production of β-defensins (antimicrobial peptides produced in the oral cavity), the aim of the present study was to evaluate the association between stress and salivary levels of β-defensin 2 (HBD-2) and β-defensin 3 (HBD-3).For this purpose, seventy five volunteers, classified as periodontally healthy, were submitted to a psychological evaluation using a validated questionnaire (Questionnaire of Lipp-ISS). Following analysis of the questionnaires, the subjects were divided in two groups (Group A: Absence of stress and Group B: Presence of stress). Unstimulated saliva samples were collected and the concentration of total protein was determined using the BCA method, and the concentrations of HBD-2 and HBD-3 were determined by ELISA.METHODSFor this purpose, seventy five volunteers, classified as periodontally healthy, were submitted to a psychological evaluation using a validated questionnaire (Questionnaire of Lipp-ISS). Following analysis of the questionnaires, the subjects were divided in two groups (Group A: Absence of stress and Group B: Presence of stress). Unstimulated saliva samples were collected and the concentration of total protein was determined using the BCA method, and the concentrations of HBD-2 and HBD-3 were determined by ELISA.The levels of total protein did not show a statistically significant difference between the groups. Analyses of HBD-2 and HBD-3 concentrations indicate that the stress condition was not associated with the levels of either peptide in saliva (P=0.3664 for HBD-2 and P=0.3608 for HBD-3).RESULTSThe levels of total protein did not show a statistically significant difference between the groups. Analyses of HBD-2 and HBD-3 concentrations indicate that the stress condition was not associated with the levels of either peptide in saliva (P=0.3664 for HBD-2 and P=0.3608 for HBD-3).In periodontally healthy subjects, HBD-2 and HBD-3 levels are not influenced by stress.CONCLUSIONIn periodontally healthy subjects, HBD-2 and HBD-3 levels are not influenced by stress. Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown. Considering that psychological stress can down-regulate the production of β-defensins (antimicrobial peptides produced in the oral cavity), the aim of the present study was to evaluate the association between stress and salivary levels of β-defensin 2 (HBD-2) and β-defensin 3 (HBD-3). For this purpose, seventy five volunteers, classified as periodontally healthy, were submitted to a psychological evaluation using a validated questionnaire (Questionnaire of Lipp-ISS). Following analysis of the questionnaires, the subjects were divided in two groups (Group A: Absence of stress and Group B: Presence of stress). Unstimulated saliva samples were collected and the concentration of total protein was determined using the BCA method, and the concentrations of HBD-2 and HBD-3 were determined by ELISA. The levels of total protein did not show a statistically significant difference between the groups. Analyses of HBD-2 and HBD-3 concentrations indicate that the stress condition was not associated with the levels of either peptide in saliva (P=0.3664 for HBD-2 and P=0.3608 for HBD-3). In periodontally healthy subjects, HBD-2 and HBD-3 levels are not influenced by stress. |
Author | Costa, Fernando Oliveira Cortelli, Sheila Cavalca De Brito Penna Forte, Lilibeth Ferraz Cortelli, José Roberto De Campos, Maria Valéria Costa Cogo, Karina Aquino, Davi Romeiro Franco, Gilson Cesar Nobre |
Author_xml | – sequence: 1 givenname: Lilibeth Ferraz surname: De Brito Penna Forte fullname: De Brito Penna Forte, Lilibeth Ferraz organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 2 givenname: Sheila Cavalca surname: Cortelli fullname: Cortelli, Sheila Cavalca organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 3 givenname: José Roberto surname: Cortelli fullname: Cortelli, José Roberto organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 4 givenname: Davi Romeiro surname: Aquino fullname: Aquino, Davi Romeiro organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 5 givenname: Maria Valéria Costa surname: De Campos fullname: De Campos, Maria Valéria Costa organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 6 givenname: Karina surname: Cogo fullname: Cogo, Karina organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil – sequence: 7 givenname: Fernando Oliveira surname: Costa fullname: Costa, Fernando Oliveira organization: Department of Dentistry, Federal University of Minas Gerais, Belo Horizonte/MG, Brazil – sequence: 8 givenname: Gilson Cesar Nobre surname: Franco fullname: Franco, Gilson Cesar Nobre organization: Department of Dentistry, University of Taubaté, Taubaté/SP, Brazil |
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Keywords | beta-defensin salivary proteins Periodontal disease Association Stomatology ENT periodontal diseases Defensin Protein Stress |
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References | Dale BA, Kimball JR, Krisanaprakornkit S, et al. Localized antimicrobial peptide expression in human gingiva. J Periodontal Res 2001; 36: 285-94. Kido J, Nakamura T, Kido R, et al. Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease. J Clin Periodontol 1999; 26: 653-7. Navazesh M, Kumar SK. Measuring salivary flow: challenges and opportunities. J Am Dent Assoc 2008; 139(Suppl): 35S-40S. Ouhara K, Komatsuzawa H, Shiba H, et al. Actinobacillus actinomycetemcomitans outer membrane protein 100 triggers innate immunity and production of beta-defensin and the 18-kilodalton cationic antimicrobial protein through the fibronectin-integrin pathway in human gingival epithelial cells. Infect Immun 2006; 74: 5211-20. Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996; 67: 1041-9. Schroder JM. Epithelial peptide antibiotics. Biochem Pharmacol 1999; 57: 121-34. Breivik T, Thrane PS, Murison R, Gjermo P. Emotional stress effects on immunity, gingivitis and periodontitis. Eur J Oral Sci 1996; 104: 327-34. Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress and inadequate coping behaviors to periodontal disease. J Periodontol 1999; 70: 711-23. Ganz T, Lehrer RI. Defensins. Immunology 1994; 6: 584-9. Goldammer T, Zerbe H, Molenaar A, et al. Mastitis increases mammary mRNA abundance of beta-defensin 5, toll-like-receptor 2 (TLR2), and TLR4 but not TLR9 in cattle. Clin Diagn Lab Immunol 2004; 11: 174-85. Yang D, Chertov O, Bykovskaia SN, et al. Beta-defensins: linking innate and adaptive immunity through dendritic and T cell CCR6. Science 1999; 286: 525-8. Aberg KM, Radek KA, Choi EH, et al. Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice. J Clin Invest 2007; 117: 3339-49. Yang EV, Glaser R. Stress-induced immunomodulation and the implications for health. Int Immunopharmacol 2002; 2: 315-24. Krisanaprakornkit S, Kimball JR, Weinberg A, Darveau RP, Bainbridge BW, Dale BA. Inducible expression of human beta-defensin 2 by Fusobacterium nucleatum in oral epithelial cells: multiple signaling pathways and role of commensal bacteria in innate immunity and the epithelial barrier. Infect Immun 2000; 68: 2907-15. Mizukawa N, Sugiyama K, Ueno T, Mishima K, Takagi S, Sugahara T. Level of human defensin-1, an antimicrobial peptide in saliva of patients with oral inflammation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87: 539-43. Witthöft T, Pilz CS, Fellermann K, Nitschke M, Stange EF, Ludwig D. Enhanced human beta-defensin-2 (hBD-2) expression by corticosteroids is independent of NF-kappaB in colonic epithelial cells (CaCo2). Dig Dis Sci 2005; 50: 1252-9. Hugo FN, Hilgert JB, Corso S, et al. Association of chronic stress, depression symptoms and cortisol with low saliva flow in a sample of south-Brazilians aged 50 years and older. Gerodontology 2008; 25: 18-25. Lu Q, Jin L, Darveau RP, Samaranayake LP. Expression of human beta-defensins-1 and -2 peptides in unresolved chronic periodontitis. J Periodont Res 2005; 39: 221-7. Vedolin GM, Lobato VV, Conti PC, Lauris JR. The impact of stress and anxiety on the pressure pain threshold of myofascial pain patients. J Oral Rehabil 2009; 36: 313-21. Harder J, Bartels J, Christophers E, Schröder JM. A peptide antibiotic from human skin. Nature 1997; 387: 861. Dommisch H, Açil Y, Dunsche A, Winter J, Jepsen S. Differential gene expression of human beta-defensins (hBD-1, -2, -3) in inflammatory gingival diseases. Oral Microbiol Immunol 2005; 20: 186-90. Carvalho AL, Cury AA, Garcia RC. Prevalence of bruxism and emotional stress and the association between them in Brazilian police officers. Braz Oral Res 2008; 22: 31-5. Terai K, Sano Y, Kawasaki S, et al. Effects of dexamethasone and cyclosporin A on human beta-defensin in corneal epithelial cells. Exp Eye Res 2004; 79: 175-80. Kurland AR, Schreiner H, Diamond G. In vivo beta-defensin gene expression in rat gingival epithelium in response to Actinobacillus actinomycetemcomitans infection. J Periodontal Res 2006; 41: 567-72. Lipp MEN, Guevara AJH. Validação empírica do Inventário de Sintomas de Stress (ISS). Estudos de Psicologia 1994; 11: 43-49. Peruzzo DC, Benatti BB, Antunes IB, et al. Chronic stress may modulate periodontal disease: a study in rats. J Periodontol 2008; 79: 697-704. López NJ, Smith PC, Gutierrez J. Periodontal therapy may reduce the risk of preterm low birth weight in women with periodontal disease: a randomized controlled trial. J Periodontol 2002; 73: 911-24. Nieminen A, Nordlund L, Uitto VJ. The effect of treatment on the activity of salivary proteases and glycosidases in adults with advanced periodontitis. J Periodontol 1993; 64: 297-301. Niyonsaba F, Iwabuchi K, Matsuda H, Ogawa H, Nagaoka I. Epithelial cell-derived human beta-defensin-2 acts as a chemotaxin for mast cells through a pertussis toxin-sensitive and phospholipase C-dependent pathway. Int Immunol 2002; 14: 421-6. Cortelli SC, Cortelli JR, Holzhausen M, et al. Essential oils in one-stage full-mouth disinfection: double-blind, randomized clinical trial of long-term clinical, microbial and salivary effects. J Clin Periodontol 2009; 36: 333-42. Varoga D, Tohidnezhad M, Paulsen F, et al. The role of human beta-defensin-2 in bone. J Anat 2008; 213: 749-57. Levy O. Antibiotic proteins of polymorphonuclear leukocytes. Eur J Haematol 1996; 56: 263-77. Book M, Chen Q, Lehmann LE, et al. Inducibility of the endogenous antibiotic peptide beta-defensin 2 is impaired in patients with severe sepsis. Crit Care 2007; 11: R19. Dunsche A, Acil Y, Siebert R, Harder J, Schroder JM, Jepsen S. 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References_xml | – reference: Navazesh M, Kumar SK. Measuring salivary flow: challenges and opportunities. J Am Dent Assoc 2008; 139(Suppl): 35S-40S. – reference: Yang D, Chertov O, Bykovskaia SN, et al. Beta-defensins: linking innate and adaptive immunity through dendritic and T cell CCR6. Science 1999; 286: 525-8. – reference: Nieminen A, Nordlund L, Uitto VJ. The effect of treatment on the activity of salivary proteases and glycosidases in adults with advanced periodontitis. J Periodontol 1993; 64: 297-301. – reference: Hugo FN, Hilgert JB, Corso S, et al. Association of chronic stress, depression symptoms and cortisol with low saliva flow in a sample of south-Brazilians aged 50 years and older. Gerodontology 2008; 25: 18-25. – reference: Book M, Chen Q, Lehmann LE, et al. Inducibility of the endogenous antibiotic peptide beta-defensin 2 is impaired in patients with severe sepsis. Crit Care 2007; 11: R19. – reference: Kurland AR, Schreiner H, Diamond G. In vivo beta-defensin gene expression in rat gingival epithelium in response to Actinobacillus actinomycetemcomitans infection. J Periodontal Res 2006; 41: 567-72. – reference: Yang EV, Glaser R. Stress-induced immunomodulation and the implications for health. Int Immunopharmacol 2002; 2: 315-24. – reference: Aberg KM, Radek KA, Choi EH, et al. Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice. J Clin Invest 2007; 117: 3339-49. – reference: Niyonsaba F, Iwabuchi K, Matsuda H, Ogawa H, Nagaoka I. Epithelial cell-derived human beta-defensin-2 acts as a chemotaxin for mast cells through a pertussis toxin-sensitive and phospholipase C-dependent pathway. Int Immunol 2002; 14: 421-6. – reference: Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress and inadequate coping behaviors to periodontal disease. J Periodontol 1999; 70: 711-23. – reference: Carvalho AL, Cury AA, Garcia RC. Prevalence of bruxism and emotional stress and the association between them in Brazilian police officers. Braz Oral Res 2008; 22: 31-5. – reference: Vedolin GM, Lobato VV, Conti PC, Lauris JR. The impact of stress and anxiety on the pressure pain threshold of myofascial pain patients. J Oral Rehabil 2009; 36: 313-21. – reference: Levy O. Antibiotic proteins of polymorphonuclear leukocytes. Eur J Haematol 1996; 56: 263-77. – reference: Ouhara K, Komatsuzawa H, Shiba H, et al. Actinobacillus actinomycetemcomitans outer membrane protein 100 triggers innate immunity and production of beta-defensin and the 18-kilodalton cationic antimicrobial protein through the fibronectin-integrin pathway in human gingival epithelial cells. Infect Immun 2006; 74: 5211-20. – reference: Mizukawa N, Sugiyama K, Ueno T, Mishima K, Takagi S, Sugahara T. Level of human defensin-1, an antimicrobial peptide in saliva of patients with oral inflammation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87: 539-43. – reference: Kido J, Nakamura T, Kido R, et al. Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease. J Clin Periodontol 1999; 26: 653-7. – reference: Harder J, Bartels J, Christophers E, Schröder JM. A peptide antibiotic from human skin. Nature 1997; 387: 861. – reference: Witthöft T, Pilz CS, Fellermann K, Nitschke M, Stange EF, Ludwig D. Enhanced human beta-defensin-2 (hBD-2) expression by corticosteroids is independent of NF-kappaB in colonic epithelial cells (CaCo2). Dig Dis Sci 2005; 50: 1252-9. – reference: Varoga D, Tohidnezhad M, Paulsen F, et al. The role of human beta-defensin-2 in bone. J Anat 2008; 213: 749-57. – reference: Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996; 67: 1041-9. – reference: Lu Q, Jin L, Darveau RP, Samaranayake LP. Expression of human beta-defensins-1 and -2 peptides in unresolved chronic periodontitis. J Periodont Res 2005; 39: 221-7. – reference: Breivik T, Thrane PS, Murison R, Gjermo P. Emotional stress effects on immunity, gingivitis and periodontitis. Eur J Oral Sci 1996; 104: 327-34. – reference: Dommisch H, Açil Y, Dunsche A, Winter J, Jepsen S. Differential gene expression of human beta-defensins (hBD-1, -2, -3) in inflammatory gingival diseases. Oral Microbiol Immunol 2005; 20: 186-90. – reference: Dunsche A, Acil Y, Siebert R, Harder J, Schroder JM, Jepsen S. Expression profile of human defensins and antimicrobial proteins in oral tissues. J Oral Pathol Med 2001; 30: 154-8. – reference: Schroder JM. Epithelial peptide antibiotics. Biochem Pharmacol 1999; 57: 121-34. – reference: Cortelli SC, Cortelli JR, Holzhausen M, et al. Essential oils in one-stage full-mouth disinfection: double-blind, randomized clinical trial of long-term clinical, microbial and salivary effects. J Clin Periodontol 2009; 36: 333-42. – reference: Terai K, Sano Y, Kawasaki S, et al. Effects of dexamethasone and cyclosporin A on human beta-defensin in corneal epithelial cells. Exp Eye Res 2004; 79: 175-80. – reference: Krisanaprakornkit S, Kimball JR, Weinberg A, Darveau RP, Bainbridge BW, Dale BA. Inducible expression of human beta-defensin 2 by Fusobacterium nucleatum in oral epithelial cells: multiple signaling pathways and role of commensal bacteria in innate immunity and the epithelial barrier. Infect Immun 2000; 68: 2907-15. – reference: Peruzzo DC, Benatti BB, Antunes IB, et al. Chronic stress may modulate periodontal disease: a study in rats. J Periodontol 2008; 79: 697-704. – reference: Ganz T, Lehrer RI. Defensins. Immunology 1994; 6: 584-9. – reference: Goldammer T, Zerbe H, Molenaar A, et al. Mastitis increases mammary mRNA abundance of beta-defensin 5, toll-like-receptor 2 (TLR2), and TLR4 but not TLR9 in cattle. Clin Diagn Lab Immunol 2004; 11: 174-85. – reference: López NJ, Smith PC, Gutierrez J. Periodontal therapy may reduce the risk of preterm low birth weight in women with periodontal disease: a randomized controlled trial. J Periodontol 2002; 73: 911-24. – reference: Dale BA, Kimball JR, Krisanaprakornkit S, et al. Localized antimicrobial peptide expression in human gingiva. J Periodontal Res 2001; 36: 285-94. – reference: Lipp MEN, Guevara AJH. Validação empírica do Inventário de Sintomas de Stress (ISS). 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Snippet | J Oral Pathol Med (2010) 39: 765–769
Background: Recent studies suggest that stress can predispose an individual to the development of periodontal disease,... Recent studies suggest that stress can predispose an individual to the development of periodontal disease, but the exact biological mechanism is unknown.... |
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SubjectTerms | Adaptation, Physiological Adolescent Adult beta-defensin beta-Defensins - immunology beta-Defensins - metabolism Biological and medical sciences Cross-Sectional Studies Facial bones, jaws, teeth, parodontium: diseases, semeiology Female Humans Male Medical sciences Non tumoral diseases Otorhinolaryngology. Stomatology periodontal diseases Reference Values Saliva - immunology Saliva - metabolism salivary proteins Salivary Proteins and Peptides - immunology stress Stress, Psychological - immunology Stress, Psychological - metabolism Young Adult |
Title | Psychological stress has no association with salivary levels of β-defensin 2 and β-defensin 3 |
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