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Salivary antioxidants and periodontal disease status

Published online by Cambridge University Press:  28 February 2007

Dean V. Sculley*
Affiliation:
Centre for Healthcare Education, University College Northampton, Boughton Green Road, Northampton NN2 7AL, UK
Simon C. Langley-Evans
Affiliation:
Division of Nutritional Biochemistry, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK
*Corresponding
*Corresponding Author: D. V. Sculley, fax +44 1604 791114, email Dean.Sculley@Northampton.ac.uk
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Abstract

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Periodontal disease is a common chronic adult condition. The bacterium Porphyromonas gingivalis has been implicated in the aetiology of this disease, which causes destruction of the connective tissue and bone around the root area of the tooth. It has been observed that invading P. gingivalis bacteria trigger the release of cytokines such as interleukin 8 and tumour necrosis factor α, leading to elevated numbers and activity of polymorphonucleocytes (PMN). As a result of stimulation by bacterial antigens, PMN produce the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. Patients with periodontal disease display increased PMN number and activity. It has been suggested that this proliferation results in a high degree of ROS release, culminating in heightened oxidative damage to gingival tissue, periodontal ligament and alveolar bone. Antioxidant constituents in plasma have been well-documented, being chiefly ascorbate, albumin and urate, and these are known to display sensitivity to dietary antioxidant intakes. The concentration of antioxidants in saliva does not appear to mirror those of plasma. The extent of dietary influence upon salivary antioxidant status is unclear. Urate is the predominant salivary antioxidant, with albumin and ascorbate providing minor contributions. Previous research has found reduced salivary antioxidant activity in patients suffering from periodontal disease. An improved understanding of the role antioxidants play in periodontitis, and the influence of nutrition on antioxidant status, may lead to a possible nutritional strategy for the treatment of periodontal disease.

Type
Meeting Report
Copyright
Copyright © The Nutrition Society 2002

References

Abbey, M (1995) The importance of vitamin-E in reducing cardiovascular risk. Nutrition Reviews 53, S28S32.Google ScholarPubMed
Ainamo, J, Barmes, D, Beagrie, G, Cutress, T, Martin, J & Sardo-infiri, J (1982) Development of the World Health Organization community periodontal index of treatment needs (CPITN). International Dental Journal 32, 281291.Google Scholar
Asman, B (1987) Peripheral PMN cells in juvenile periodontitis. Journal of Clinical Periodontitis 15, 360364.CrossRefGoogle Scholar
Bartold, PM, Wiebkin, OW & Thonard, JC (1984) The effect of oxygen-derived free radicals on gingival proteoglycans and hyaluronic acid. Journal of Periodontal Research 19, 390400.CrossRefGoogle ScholarPubMed
Benzie, IFF & Strain, JJ (1996) The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": The FRAP assay. Analytical Biochemistry 239, 7076.CrossRefGoogle ScholarPubMed
Beutler, E (1979) Glutathione peroxidase. In Red Cell Metabolism: A Manual of Biochemical Methods, 2nd ed., pp. 7173 [Beutler, E, editor]. New York: Grune and Stratton.Google Scholar
Beutler, BA & Cerami, A (1989) Recombinant interleukin-1 suppresses lipoprotein lipase activity in 3T3-L1 cells. Journal of Immunology 135, 39693971.Google Scholar
Chapple, ILC, Mason, GI, Garner, I, Matthews, JB, Thorpe, GH, Maxwell, SRJ & Whitehead, TP (1997) Enhanced chemiluminescent assay for measuring the total antioxidant capacity of serum, saliva and crevicular fluid. Annals of Clinical Biochemistry 34, 412421.CrossRefGoogle ScholarPubMed
Edgar, WM (1992) Saliva: Its secretion, composition and functions. British Dental Journal 172, 305312.CrossRefGoogle ScholarPubMed
Frank, RM & Voegel, JC (1978) Bacterial bone resorption in advanced cases of human periodontitis. Journal of Periodontal Research 13, 251261.CrossRefGoogle ScholarPubMed
Fravalo, P, Menard, C & Bonnaure-Mallet, M (1996) Effect of Porphyromonas gingivalis on epithelial cell MMP-9 type IV collagenase production. Infection and Immunity 64, 49404945.Google ScholarPubMed
Frei, B (1991) Ascorbic acid protects lipids in human plasma and low density lipoprotein against oxidative damage. American Journal of Clinical Nutrition 54, 1113S1118S.CrossRefGoogle ScholarPubMed
Gainet, J, Chollet-Martin, S, Brion, M, Hakim, J, Gougerot-Pocidalo, M & Elbim, C (1998) Interleukin-8 production by polymorphonuclear neutrophils in patients with rapidly progressive periodontitis: An amplifying loop of polymorphonuclear neutrophil activation. Laboratory Investigation 78, 755761.Google ScholarPubMed
Gamble, JR, Harlan, JM & Klebanoff, SJ (1985) Stimulation of the adherence of neutrophils to umbilical vein endothelium by human recombinant tumor necrosis factor. Proceedings of the National Academy of Sciences USA 82, 86678671.CrossRefGoogle ScholarPubMed
Greenstein, G & Lamster, I (1997) Bacterial transmission in periodontal diseases: a critical review. Journal of Periodontology 68, 421431.CrossRefGoogle ScholarPubMed
Greenwald, RA & Moy, WW (1979) Inhibition of collagen gelation by action of the superoxide radical. Arthritis and Rheumatism 22, 251259.CrossRefGoogle ScholarPubMed
Guarnieri, C, Zucchelli, G, Bernardi, F, Scheda, M, Valentini, AF & Calandriello, M (1991) Enhanced superoxide production with no change of the antioxidant activity in gingival fluid of patients with adult periodontitis. Free Radical Research 15, 1116.CrossRefGoogle ScholarPubMed
Haffajee, AD & Socransky, SS (1994) Microbial etiological agents of destructive periodontal diseases. Periodontology 5, 78111.CrossRefGoogle ScholarPubMed
Halliwell, B (1988) Albumin – An important extracellular antioxidant? Biochemical Pharmacology 37, 569571.CrossRefGoogle ScholarPubMed
Halliwell, B (1991) Reactive oxygen species in living systems: source, biochemistry, and role in human disease. American Journal of Medicine 91, Suppl. 3C, 1422.CrossRefGoogle ScholarPubMed
Haraszthy, VI, Zambon, JJ, Trevisan, M, Zeid, M & Genco, RJ (1998) Identification of pathogens in atheromatous plaques (abstract). Journal of Dental Research 77B, 273Abstr.Google Scholar
Havemose-Poulsen, A & Holmstrup, P (1997) Factors affecting IL-1-mediated collagen metabolism by fibroblasts and the pathogenesis of periodontal disease: a review of the literature. Critical Reviews in Oral Biology and Medicine 8, 217236.CrossRefGoogle ScholarPubMed
Jenkinson, HF & Dymock, D (1999) The microbiology of periodontal disease. Dental Update 26, 191197.CrossRefGoogle ScholarPubMed
Kadowaki, T, Nakayama, K, Okamoto, K, Abe, N, Baba, A, Shi, Y, Ratnayake, DB & Yamamoto, K (2000) Porphyromonas gingivalis proteinases as virulence determinants in progression of periodontal disease. Journal of Biochemistry 128, 153159.CrossRefGoogle Scholar
Katz, J, Sambandam, V, Wu, JH, Michalek, SM & Balkovetz, DF (2000) Characterisation of. Porphyromonas gingivalis-induced degradation of epithelial junction complexes. Infection and Immunity 68, 14411449.CrossRefGoogle Scholar
Kaufman, E & Lamster, IB (2000) Analysis of saliva for periodontal diagnosis. Journal of Clinical Periodontology 27, 453465.CrossRefGoogle ScholarPubMed
Kinane, DF & Lowe, GDO (2000) How periodontal disease may contribute to cardiovascular disease. Periodontology 2000 23, 121126.CrossRefGoogle ScholarPubMed
Lamont, RJ & Jenkinson, LRJ (1998) Life below the gum line: Pathogenic mechanisms of. Porphyromonas gingivalis. Microbiology and Molecular Biology Reviews 62, 12441263.Google ScholarPubMed
Lamont, RJ & Jenkinson, LRJ (2000) Subgingival colonization by Porphyromonas gingivalis. Oral Microbiology and Immunology 15, 341349.CrossRefGoogle ScholarPubMed
Moore, S, Calder, KAC, Millar, NJ & Rice-Evans, CA (1994) Antioxidant activity of saliva and periodontal disease. Free Radical Research 21, 417425.CrossRefGoogle ScholarPubMed
Navazesh, M (1993) Methods for collecting saliva. Annals of the New York Academy of Science 694, 7277.CrossRefGoogle ScholarPubMed
Novak, MJ & Cohen, HJ (1991) Depolarization of polymorphonuclear leukocytes by Porphyromonas (Bacteroides) gingivalis 381 in the absence of respiratory burst activation. Infection and Immunity 59, 31343142.Google ScholarPubMed
Nuttall, NM, Steele, JG, Pine, CM, White, D & Pitts, NB (2001) The impact of oral health on people in the UK in 1998. British Dental Journal 190, 121126.Google ScholarPubMed
Ridgeway, EE (2000) Periodontal disease: Diagnosis and management. Journal of the American Academy of Nurse Practitioners 12, 7983.CrossRefGoogle ScholarPubMed
Rotstein, OD, Pruett, TL, Fiegel, VD, Nelson, RD & Simmons, RL (1985) Succinic acid, a metabolic by-product of Bacteriodes species, inhibits polymorphonuclear leukocyte function. Infection and Immunity 48, 402408.Google Scholar
Smalley, JW, Birss, AJ & Silver, J (2000) The periodontal pathogen orphyromonas gingivalis harnesses the chemistry of the u-oxo bishaem of iron protoporphyrin IX to protect against hydrogen peroxide. FEMS Microbiology Letters 183, 159164.Google ScholarPubMed
Smalley, JW, Silver, J, Marsh, PJ & Birss, AJ (1998) The periodontopathogen Porphyromonas gingivalis binds iron protoporphyrin IX in the u-oxo dimeric form: an oxidative buffer and possible pathogenic mechanism. Biochemistry Journal 331, 681685.CrossRefGoogle ScholarPubMed
Theilade, E (1990) Factors controlling the microflora of the healthy mouth. In Human Microbial Ecology, pp. 156 [Hill, MJ and Marsh, PD, editors]. Boca Raton, FL: CRC Press, Inc.Google Scholar
Tobias, PS, Gegner, J, Tapping, R, Orr, S, Mathison, J, Lee, KJD, Kravchenko, V, Han, J & Ulevitch, RJ (1997) Lipopolysaccharide dependant cellular activation. Journal of Periodontal Disease 32, 99103.CrossRefGoogle Scholar
Travis, J, Potempa, J & Maeda, H (1995) Are bacterial proteinases pathogenic factors? Trends in Microbiology 3, 405407.CrossRefGoogle ScholarPubMed
Wu, T, Trevisan, M, Genco, RJ, Dorn, JP, Falkner, KL & Sempos, T (2000) Periodontal disease and risk of cerebrovascular disease. Archives of International Medicine 160, 27492755.CrossRefGoogle ScholarPubMed
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