Positive Health Online

Oral Health is crucial to the preservation of whole body health. Oral diseases, particularly periodontal disease, share many common risk factors with systemic diseases (e.g. inflammation, obesity, diabetes, hypertension, and elevated blood lipids and cholesterol).[1] Poor oral health may warrant the search for more serious underlying disease processes, as it has been documented that oral infections, particularly periodontitis, are associated with systemic disease pathogenesis: i.e. glucose intolerance, diabetes mellitus, insulin resistance,[1] cardiovascular conditions (e.g. atherosclerosis, heart attack, congestive heart failure and coronary artery disease),[2]-[4] respiratory conditions,[5] obesity,[6]-[7] hyperlipidemia, osteoporosis,[8] harmful pregnancy outcomes,[9] and rheumatoid arthritis.[10]

Several hundred billion bacteria can be found in a clean mouth, and if the mouth isn't satisfactorily cleaned, this quantity increases tenfold. These bacteria form firm clusters, dental plaque, that adhere to oral surfaces, and are not easily eliminated by the body's natural immune responses so must be mechanically removed. Dental plaque becomes more difficult to remove as it matures, forming a harder substance called calculus, which must be removed professionally by a dentist or dental hygienist.

The three most prevalent problems in the mouth are dental caries and the periodontal diseases, gingivitis and periodontitis. All are caused by numerous factors centring on dental plaque, nutrition and dietary factors, oral hygiene, genetics, environment and lifestyle. Dental caries, or missing teeth, can also make it difficult to bite and chew, thus compromising oral function, and consequently may worsen nutritional status and encourage systemic diseases, low self-esteem and a general decline in the quality of life.[11]-[12]

Peridontal Diseases (Gingivitis and Periodontitis)

Periodontal diseases are a group of related, but immensely diverse inflammatory diseases, involving the supporting structures that surround and anchor the teeth. Periodontitis will effect the majority of adults at some time in their lives.[13] They comprise two main categories: gingivitis and periodontitis, both of which are plaque-induced[14]-[20] inflammatory conditions that are considered infectious.[21] Gingivitis is a reversible condition that begins when the bacteria in plaque cause gum inflammation. If left untreated, it can progress to periodontitis. Gingivitis, inflammation of the gingival tissues only, can usually be reversed with daily brushing and flossing, and regular cleaning by a dentist or dental hygienist.

Periodontitis is an irreversible condition that destroys the jaw bone, and can lead to tooth loss. Susceptibility to periodontal disease varies among individuals,[22] and can be due to genetic factors,[23]-[24] poor host resistance (i.e. immune function), inadequate nutrition,[25] environmental and behavioural factors.[26] Some people are more prone to periodontal disease than others, but this doesn't mean that they will necessarily get the disease.

Clinical signs of gingivitis are redness, swelling, bleeding to touch, spontaneous bleeding, and/or visible pus; in the absence of any bone loss, periodontal pocketing, or apical tissue migration along the tooth root. These signs can typically be observed after 10-20days of plaque accumulation.[27]

Gingivitis can be divided into two varieties; those affected by local factors (plaque); and those that are affected by local factors and modified by specific host systemic factors. At the local level, frequent dietary sugar intake can be responsible for increased plaque accumulation and gingivitis.[28]-[29] Modifying factors for gingivitis include metabolic causes (e.g. hormonal disturbances present during puberty and pregnancy, and diabetes), genetic factors (e.g. Down's syndrome),[30]-[31] and environmental factors (e.g. vitamin C deficiency, calcium channel blockers – nifedipine – cyclosporine – an immuno-suppressive drug, phenytoin – used to control epilepsy), smoking, antibiotics, corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDS).[32] Other factors that can modify gingival inflammatory responses are immune deficiencies, HIV/AIDS, and psychological stress.[33] Psychological stress in adults leads to heightened gingivitis expression, and may be mediated by increased plaque accumulation.[34] Acute necrotizing ulcerative gingitivis (ANUG) has also been associated with stress.[35]

Gingivitis may resolve itself or lay quiet for an indeterminate period; however, the potential for periodontal pocket formation exists at any time. When pockets are detected clinically, they usually are associated with calculus present on the tooth's root surfaces. The progression from gingivitis to periodontitis requires varying amounts of time in different individuals, and may not happen at all in others.[36] Six months is typically required for gingivitis to advance to periodontitis,[37] pockets form between the gums and the tooth, trapping more harmful bacteria and food particles, and the gums may recede, exposing the root surfaces and increasing their sensitivity to heat and cold.[27] Teeth can loosen due to bone destruction. The body's host response prevents bacterial growth into the tissue, and removes bacterial products, by-products and enzymes that have penetrated the tissue.[38]-[39] But, it can also activate enzymes which can result in collagen loss and tissue breakdown, leading to a periodontal pocket.[40]-[41] Gingivitis precedes periodontitis, implying that the prevention of gingivitis is the key to preventing periodontitis. Prevention is the basis to good oral health.

Periodontitis frequently involve anaerobic bacteria (unable to survive in oxygen) found in dental plaque.[4]2 The three most common bacteria associated with periodontitis are Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia.[43]-[44] These bacteria discharge hydrogen sulfide, ammonia, amines, toxins, and enzymes that elicit inflammatory responses leading to periodontitis.[44]

Periodontitis is a cumulative condition. Once bone is lost, it is almost impossible to regain it, and most patients lose additional tooth-supporting (alveolar) bone over a period of years.[45]-[50] The bone destruction seen in periodontitis can be fairly even, and result in receding gum lines. However, more frequently, gaps are seen between an individual tooth and its socket; termed a periodontal pocket. Shallow periodontal pockets can deepen, eventually becoming deep enough to jeopardize the socket's support of adjacent teeth.[45]-[50] Of interest is that periodontitis which occurs over time only occurs at reasonably few dental sites that essentially undergo extensive periodontal destruction.[51]-[54]

Periodontitis may be overlooked until its later stages, or until abscesses, bleeding gums, loose teeth, spaces between teeth, bad breath and/or pain are present.[44] The reason why some people develop periodontitis more readily than others is highly elusive and is thought to involve many different reasons, some modifiable (behaviour, environment and nutrition) and others not modifiable (genetics).[55]

Prevention and Modifiable Risk Factors

Local risk factors include pre-existing disease, as evidenced by deep-probing depths, and plaque retentive areas associated with defective dental restorations,[47] and high fermentable dietary sugar. Therefore, defective dental restorations should also be replaced and dietary sugars should be reduced.

Vigilant bacterial plaque removal and infection control should be performed at least twice daily. If periodontal disease has progressed, the dentist, periodontist, or dental hygienist, removes plaque by cleaning the teeth (termed scaling and root planning). Medications, such as antibiotics, are sometimes used in conjunction with teeth cleaning. Surgery might be necessary if the inflammation and deep periodontal pockets remain following the above treatments. All of these treatments require the patient to maintain excellent daily home care.

Systemic and environmental factors, such as diabetes[50]-[56] and smoking[57] and other tobacco product use,[58]-[62] stress, depression,[26] and alcohol consumption,[63] have all been linked to periodontitis. Emotional stress often increases the severity of gingivitis[64] and periodontitis.[26] Modifying these behaviours, such as quitting tobacco use, drinking less alcohol, and improving dietary intake and nutritional status, improves periodontal health as well as treatment outcomes. Physical activity, in the form of walking, has been shown to be beneficial to periodontal health.[65]

Periodontitis can cause tooth loss, and may thus compromise your health by making eating difficult. Individuals who cannot chew or bite comfortably are less likely to consume high-fibre and nutrient-rich foods such as fruits and vegetables, thereby reducing their intake of essential nutrients, which can have very harmful effects on the body's general and oral health.

Nutritional and botanical therapies have demonstrated positive effects for people with gingivitis, gingival bleeding, periodontal pocketing and periodontal attachment and bone loss. Topical and systemic nutritional supplementation may be a beneficial adjunct to gingivitis and periodontitis therapy.

Oral tissues have a higher turnover rate than other tissues of the body. This rapid turnover time, together with the ongoing repair of damaged tissues, demands a higher nutrient requirement than other body tissues. Consuming a healthy diet, high in essential nutrients, can help the health of your teeth, gums and supporting oral bone. If you are unable to obtain these nutrients that are in demand during periodontal stress from your diet, you should consider supplementing your diet with key nutrients that are known to be helpful in maintaining the health of teeth, gums and their supporting bone (alveolar bone). These suggestions must not be seen as an alternative to dental treatment or dental advice.

Malnutrition has the potential to influence the prognosis of periodontal infections adversely,[66] and elicits adverse alterations in the oral microbial ecology, and in the volume, antibacterial and physicochemical properties of saliva.[67]

Individuals with periodontitis have diets that are deficient in many essential nutrients including; calcium, thiamin, vitamin A, riboflavin, niacin, folic acid, zinc and magnesium, when compared to the RDAs (Recommended Daily Allowance) for these nutrients.[68] Gum disease may benefit from the following supplements: vitamin C, bioflavonoids, coenzyme Q10, vitamin E, vitamin A, selenium, zinc, vitamin B complex, calcium, magnesium, and other nutrients.

Key Nutrients and Supplements

Topical Considerations

Clinically, topical application of coenzyme Q10 (CoQ10) to periodontal pockets significantly reduced gingivitis, bleeding and gingival enzyme activity.[69] Clinical studies showed that topical application of CoQ10 was extraordinarily effective in reducing periodontal pocket depths,[70] and clinical symptoms of gingivitis and periodontitis.[71] Lactoferrin was shown to reduce the adhesion of several oral bacteria,[72],[32] stop the growth of certain periodontitis causing bacteria, and kill certain periodontitis and cavity causing bacteria.[73]

Extensive clinical trials, using oral rinses and toothpaste products containing Mexican Sanguinaria extract (derived from bloodroot),[74] have shown its effectiveness in reducing plaque build-up and gingivitis.[75]-[80] Other studies using a combination of Sanguinaria extract and zinc chloride were also beneficial,[81]-[82] and suggested that zinc may provide a mild enhancement of Sanguinaria extract effectiveness against gingivitis.[82]

Green tea, which contains the polyphenol (-) Epigallocatechin gallate, and green tea extract applied topically, can also help prevent periodonitis.[83]-[85] Using non-human primates, vitamin B3-supplemented toothpaste showed a similar improvement in gingival health as the 0.5% chlorhexidine (antimicrobial) toothpaste group, but significant improvement over the control toothpaste group.[86] Two independent clinical trials using a herbal mouth rinse versus distilled water,[87] and herbal tooth paste versus Colgate® Total,[88] showed significant improvements in gingivitis and gingival bleeding; the herbal toothpaste also significantly reduced plaque and stain relative to Colgate® Total.[88] Mouth care products which contain essential oils, such as tea tree oil, eucalyptus oil and menthol, significantly reduced both gingival inflammation and bleeding when compared to fluoride-containing products.[89] Hydrogen peroxide has been shown to inhibit plaque formation and reduce gingivitis, promoting healthy gums and teeth.[90]

Folic acid-containing mouthwash has been used in the treatment of gingivitis and its accompanying inflammation; it significantly reduced gingival redness and bleeding in subjects whose dietary intakes of folic acid were mostly below 200 milligrams daily.[91] In a double-blind study, of the effects of folic acid supplemented at 2mg twice daily for 30 days, revealed that folic acid supplementation may increase gingival resistance to local irritants,[92] however, in mouthwash form, it can improve gingival health, and showed significantly greater local effects rather than systemic influences.[93]-[96]

Systemic Considerations:

Nutritional supplements are best taken in combination and should contain adequate levels of zinc, copper, calcium, phosphorus, magnesium, selenium, vitamins A, C, D and E, vitamin B complex, bioflavonoids, additional antioxidants, botanicals and other nutrients.

Vitamin C is important for collagen synthesis, and also promotes healthy cell development, proper calcium absorption, normal tissue growth and repair, strengthens blood capillaries, protects against infection, and can also enhance immune function. Those with a history of ANUG are known to ingest less vitamin C compared to healthy people.[97] Clinical studies, using vitamin C deficient diets, revealed that measures of gingival inflammation were directly related to their plasma vitamin C deficiency status,[98] and vitamin C supplementation did improve gingival health in these people.[99] However, megadoses of vitamin C in normal human subjects did not positively affect the gingival response to periodontal cleaning and scaling.[100] Vitamin C deficiency is known to lead to severe periodontal disease in certain individuals such as the elderly and cigarette smokers.[101] Therefore, these individuals should consider taking a vitamin C supplement. Vitamin C is more effective taken with bioflavonoids, calcium and magnesium, and other antioxidants. Citrus bioflavonoid supplementation has been shown to encourage jaw bone formation[102]-[103] and can enhance the effectiveness of vitamin C. Bioflavonoids should be taken with vitamin C and calcium.

Vitamins E and A are potent antioxidants, as they protect cells by neutralizing free radicals that cause oxidative cellular damage. Vitamin E also exhibits anti-inflammatory properties which may limit inflammation-induced tissue destruction.[104] Vitamin E should be taken with a range of antioxidants, including vitamin C, beta-carotene and selenium. Vitamin A is essential for normal growth and maintenance of oral tissues and bones, is important in protein synthesis, and assists immune function. Vitamin A deficiency has been associated with periodontal pocket formation.[105] Vitamin A should be taken with B group vitamins, vitamins C, D, and E, choline, essential fatty acids, calcium, phosphorus and zinc for the best results.

Oral tissues are composed of rapidly growing cells with a high turnover rate, as a consequence increasing the need for B complex vitamins, vitamin B1, B2, B3, B5, B6, B9, B12, and biotin. Vitamin B complex helps maintain the body's normal immune function. Lower levels of B complex vitamins are associated with tooth loss.[106] The B vitamins are usually taken in the form of vitamin B complex with vitamin C.

Calcium intake of 800mg or more daily is essential to the normal development and maintenance of teeth, and their supporting structures. Calcium deficiency has been associated with gingival inflammation, pocket formation and alveolar bone resorption.[107] Vitamin D is also essential for the development and maintenance of teeth and oral bone. Vitamin D, in its proper form, also promotes intestinal absorption of calcium. Magnesium is essential for the mobilization of calcium from bone and assists in bone maintenance, formation and regeneration. Magnesium deficiency can lower the rate of jaw bone formation and lead to widening of the periodontal ligament (which connects the tooth to alveolar bone).[108]

Selenium helps fight infections,[109] and works best with vitamins E, and A. Zinc is important in bone metabolism, including alveolar bone, and is vital for wound healing, immune function, cell division and general growth of all tissues. Zinc is also the natural enemy of bacteria.[110] Other micronutrients important to good gum and oral health are copper, molybdenum and vanadium. Copper helps to stabilize newly formed collagen tissues in the mouth. Molybdenum is important in the growth and development of alveolar bone, dentin, and enamel.[111] Vanadium is required for cellular metabolism and the formation of healthy bones and teeth.

Depending on the condition of your gums and teeth, I recommend you see your dentist at least twice, possibly four times a year, to limit the progression of plaque and periodontal problems, and to be examined for oral cancer. Proper oral care, lifestyle and dietary adjustments, as well as nutritional supplementation, can help many individuals reduce the risk of gum disease and tooth loss.

References

1. Grossi S and Genco R. Periodontal disease and diabetes mellitus: a two- way relationship. Ann Periodontol. 3: 51-61. 1998.
2. Beck J et al. Dental infections and atherosclerosis. Am Heart J. 138: S528-S533.1999.
3. Loesche W et al. Assessing the relationship between dental disease and coronary heart disease in elderly US veterans. J Am Dent Assoc. 129: 301-311. 1988.
4. Arbes S et al. Association between extent of periodontal attachment loss and self-reported history of heart attack: an analysis of NHANES III data. J Dent Res. 78: 1777-1782. 1999.
5. Scannapieco F. Role of oral bacteria in respiratory infection. J Periodontol. 70: 793-802. 1999.
6. Saito T et al. Relationship between upper body obesity and periodontitis. J Dent Res. 80: 1631-1636. 2001.
7. Wood N et al. Comparison of body composition and periodontal disease using nutritional assessment techniques: third National Health and Nutrition Examination Survey (NHANES III). J Clin Periodontol. 30: 321-327. 2003.
8. Jeffcoat M. Osteoporosis: a possible modifying factor in oral bone loss. Ann Periodontol. 3: 312-21.1998.
9. Offenbacher S et al. Periodontal infection as a possible risk factor for pre-term low birth weight. J Periodontol. 67: 1103-1113. 1996.
10. Mercado F et al. Inter-relationships between rheumatoid arthritis and periodontal disease: A review. J Clin Periodontol. 30: 761-72. 2003.
11. Gift H and Redford M. Oral health and quality of life. Clin Geriatr Med. 8: 673-683. 1992.
12. Hollister M and Weintraub J. The association of oral status with systemic health, quality of life, and economic productivity. J Dent Educ. 57: 901-912. 1993.
13. Genco R et al. Periodontal disease and cardiovascular disease. Epidemiology and possible mechanisms. J Am Dent Assoc. 133: 14S-22S. 2002.
14. Loe H et al. Experimental gingivitis in man. J Periodontol. 36: 177-187. 1965.
15. Theilade E et al. Experimental gingivitis in man. II. Longitudinal clinical and bacteriological investigation. J Periodontal Res. 1: 1-13. 1966.
16. Lindhe J et al. Experimental periodontitis in the beagle dog. J Periodontal Res. 8: 1-10. 1973.
17. Slots J and Hausmann E. Longitudinal study of experimentally induced periodontal disease in Macaca arctoides: relationship between microflora and alveolar bone loss. Infection and Immunity. 23: 260-269. 1979.
18. Holt S et al. Implantation of Bacteroides gingivalis in non-human primates initiates progression of periodontitis. Science. 239: 55-57. 1988.
19. Breuer M and Cosgrove R. The relationship between gingivitis and plaque levels. J Periodontol. 60: 172-175. 1989.
20. Persson G et al. Immunization against Porphyromonas gingivalis inhibits progression of experimental periodontitis in non-human primates. Infection and Immunity. 62: 1026-1031. 1994.
21. Williams R. Periodontal disease. New England Journal of Medicine. 332: 373-382. 1990.
22. Loe H et al. Natural history of periodontal disease in man. Rapid, moderate and no loss of attachment in Sri Lankan labourers 14 to 46 years of age. J Clin Periodontol. 13: 431-445. 1986.
23. Hart T and Kornman K. Genetic factors in the pathogenesis of periodontitis. Periodontol 2000. 14: 202-215. 1997.
24. Michalowicz B et al. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol. 71: 1699-1707. 2000.
25. Neiva R et al. Effects of specific nutrients on periodontal disease onset, progression and treatment. J Clin Periodontol. 30: 579-89. 2003.
26. Grossi S. Smoking and Stress: common denominators for periodontal disease, heart disease, and diabetes mellitus. Compend Contin Educ Dent Suppl. 30: 31-9. 2000.
27. Loesche W. Association of the oral flora with important medical diseases. Curr Opin Periodontol. 4: 21-28. 1997.
28. Jalil R et al. Effect of variation in dietary sucrose intake on plaque removal by mechanical means. J Clin Periodontol. 10: 389-398. 1983.
29. Sidi A and Ashley F. Influence of frequent sugar intakes on experimental gingivitis. J Periodontol. 55: 419-423. 1984.
30. Reuland-Bosma W and van Dijk J. Periodontal disease in Down's syndrome: a review. J Clin Periodontol. 13: 64-73. 1986.
31. Reuland-Bosma W et al. Experimental gingivitis around deciduous teeth in children with Down's syndrome. J Clin Periodontol. 13: 294-300. 1986.
32. Loesche W and Grossman N. Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment. Clin Microbiol Rev. 14: 727-52, 2001.
33. Tatakis D and Trombelli L. Modulation of clinical expression of plaque-induced gingivitis. J Clin Periodontol. 31: 229-238.2004.
34. Nares S. The genetic relationship to periodontal disease. Periodontol 2000. 32: 36-49. 2003.
35. Schoor R and Havrilla J. Acute necrotizing ulcerative gingivitis: etiology and stress relationships. Int J Psychosom. 33: 35-40, 1986.
36. Albandar J et al. Destructive periodontal disease in adults 30 years of age and older in the United States, 1988-1994. J Periodontol. 70: 13-29. 1999.
37. Brecx M et al. Stereological observations on long term experimental gingivitis in man. J Clin Periodontol. 15: 621-627. 1988.
38. Califano J et al. Antibody reactive with Actinobacillus actinomycetemcomitans leukotoxin in early-onset periodontitis patients. A Oral Microbiol Immunol. 12: 20-26, 1997.
39. Ebersole J et al. Longitudinal dynamics of infection and serum antibody in A. actinomycetemcomitans periodontitis. Oral Dis. 1: 129-138. 1995.
40. Sorsa T et al. Identification of proteases from periodontopathogenic bacteria as activators of latent human neutrophil and fibroblast-type interstitial collagenases. Infect Immun. 60: 4491-4495, 1992.
41. Uitto V et al. Collagenolytic enzymes in periodontal diseases. Proc Finn Dent Soc. 83: 119-130. 1987.
42. Page R. The pathobiology of periodontal diseases may affect systemic diseases: inversion of a paradigm. Ann Periodontol. 3: 108-20. 1998.
43. Asikainen S and Alaluusua S. Bacteriology of dental infections. Eur Heart J. 14: 43-50. 1993.
44. Haffajee A and Socransky S. Microbial etiological agents of destructive periodontal diseases. Periodontology 2000. 5: 78-111. 1994.
45. Grossi S et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol. 66: 23-29. 1995.
46. Brown L et al. Early-onset periodontitis: progression of attachment loss during six years. J Periodontol. 67: 968-975. 1996.
47. Grossi S et al. Assessment risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol. 65: 260-267. 1994.
48. Loe H and Brown L. Early onset periodontitis in the United States of America. J Periodontol. 62: 608-612. 1991.
49. Oliver R et al. Periodontal diseases in the United States population. J Periodontol. 69: 269-278. 1998.
50. Papapanou P. Periodontal diseases: epidemiology. Ann Periodontol. 1: 1-36. 1996.
51. Lindhe J et al. Progression of periodontal disease in adult subjects in the absence of periodontal therapy. J Clin Periodontol. 10: 433-42. 1989.
52. Jenkins W and Kinane D. The 'high risk' group on periodontitis. Br Dent J. 167: 168-171. 1989.
53. Lindhe J et al. Periodontal loser sites in untreated adult subjects. J Clin Periodontol. 16: 671-678. 1989.
54. Socransky S et al. New concepts of destructive periodontal disease. J Clin Periodontol. 11: 21-32. 1984.
55. Loesche W and Grossman N. Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment. Clin Microbiol Rev. 14: 727-52. 2001.
56. Shlossman M et al. Type 2 diabetes melltius and periodontal disease. J Am Dent Assoc. 121: 532-536. 1990.
57. Genco R. Current view of risk factors for periodontal diseases. J Periodontol. 67: 1041-1049. 1996.
58. Albandar JM et al. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol. 71: 1874-81. 2000.
59. Bergstrom J et al. Exposure to tobacco smoking and periodontal health. J Clin Periodontol. 27: 61-8. 2000.
60. Bergstrom J et al. A ten-year prospective study of tobacco smoking and periodontal health. J Periodontol. 71: 1338-47. 2000.
61. Tomar S. Dentistry's role in tobacco control. J Am Dent Assoc. 132: 30S-35S. 2001.
62. Tomar S and Asma S. Smoking-attributable periodontitis in the United States: Findings from NHANES III. National Health and Nutrition Examination Survey. J Periodontol. 71: 73-78. 2000.
63. Tezal M et al. Alcohol consumption and periodontal disease. The Third National Health and Nutrition Examination Survey. J Clin Periodontol. 31: 484-8. 2004.
64. Deinzer R. Increase in gingival inflammation under academic stress. J Clin Periodontol. 25: 431-3. 1998.
65. Merchant A et al. Increased physical activity decreases periodontitis risk in men. Eur J Epidemiol. 18: 891-8, 2003.
66. Enwonwu C. Cellular and molecular effects of malnutrition and their relevance to periodontal diseases. J Clin Periodontol. 21: 643-657. 1994.
67. Enwonwu C. Interface of malnutrition and periodontal diseases. Am J Clin Nutr. 61: 430S-436S. 1995.
68. Neill D and Phillips H. The masticatory performance, dental state, and dietary intake of a group of elderly army pensioners. Br Dent J. 128: 581-585. 1970.
69. Hanioka T et al. Effect of topical application of coenzyme Q10 on adult periodontitis. Mol Aspects Med. 15: S241-8. 1994.
70. Wilkinson E et al. Bioenergetics in clinical medicine. II. Adjunctive treatment with coenzyme Q in periodontal therapy. Res Commun Chem Pathol Pharmacol. 12: 111-23. 1975.
71. Iwamoto Y et al. Study of periodontal disease and coenzyme Q. Res Commun Chem Pathol Pharmacol. 11: 265-71.1975.
72. Fine D and Furgang D. Lactoferrin iron levels affect attachment of Actinobacillus actinomycetemcomitans to buccal epithelial cells. J Periodontol. 73: 616-23. 2002.
73. Kalfas S et al. Human lactoferrin binding to Porphyromonas ginvgivalis, Prevotella intermedia and Prevotella melaninogenica. Oral Microbiol Immunol. 6: 350-5. 1991.
74. Harkrader R et al. The history, chemistry and pharmacokinetics of Sanguinaria extract. J Can Dent Assoc. 56: 7-12. 1990.
75. Gonzalez Begne M et al. Clinical effect of a Mexican sanguinaria extract (Polygonum aviculare L) on gingivitis. J Ethnopharmacol. 74: 45-51. 2001.
76. Wennstrom J and Lindhe J. Some effects of a sanguinarine-containing mouth rinse on developing plaque and gingivitis. J Clin Periodontol. 12: 867-72. 1985.
77. Munro I et al. Viadent usage and oral leukoplakia: a spurious association. Regul Toxicol Pharmacol. 30: 182-96. 1999.
78. Tenenbaum H et al. Effectiveness of a sanguinarine regimen after scaling and root planning. J Periodontol. 70: 307-311. 1999.
79. Cullinan M et al. Efficacy of a dentifrice and oral rinse containing sanguinaria extract in conjunction with initial periodontal therapy. Aust Dent J. 42: 47-51. 1997.
80. Kopczyk R et al. Clinical and microbiological effects of a sanguinaria-containing mouth rinse and dentifrice with and without fluoride during six months of use. J Periodontol. 62: 617-22. 1991.
81. Harper D et al. Clinical efficacy of a dentifrice and oral rinse containing sanguinaria extract and zinc chloride during six months of use. J Periodontol. 61: 352-8. 1990.
82. Southard G et al. The relationship of sanguinaria extract concentration and zinc ion to plaque and gingivitis. J Clin Periodontol. 14: 315-9. 1987.
83. Hirasawa M et al. Improvement of periodontal status by green tea catechin using a local delivery system: a clinical pilot study. J Periodontal Res. 37: 433-8. 2002.
84. Lee M et al. Delivery of tea polyphenols to the oral cavity by green tea leaves and black tea leaves. Cancer Epidemiol Biomarkers Prev. 13: 132-7. 2004.
85. Sakanaka S and Okada Y. Inhibitory effects of green tea polyphenol on the production of virulence factor of the periodontal-disease-causing anaerobic bacterium Porphyromonas gingivalis. J Agric Food Chem. 52: 1688-92. 2004.
86. Tagushi S. Effects of nicotinate ethyl ester treatment on gingival blood circulation of experimental gingivtitis in monkeys. Nippon Shishubyo Gakkai Kaishi. 1: 184-199. 1989.
87. Scherer W et al. The ability of an herbal mouth rinse to reduce gingival bleeding. J Clin Dent. 9: 97-100. 1988.
88. Beiswanger B et al. The comparative efficacy of stabilized stannous fluoride dentifrice, peroxide/baking soda dentifrice and essential oil mouth rinse for the prevention of gingivitis. J Clin Dent. 8: 46-53. 1997.
89. Estafan D et al. Clinical efficacy of an herbal toothpaste. J Clin Dent. 9: 31-33. 1988.
89. Rosin M et al. Effects of SCN-/H2O2 combinations in dentifrices on plaque and gingivitis. J Clin Periodontol. 28: 270-6. 2001.
90. Marshall M et al. Hydrogen peroxide: a review of its use in dentistry. J Periodontol. 66: 786-796. 1995.
91. Pack A. Folate mouthwash: effects on established gingivitis in periodontal patients. J Clin Periodontol. 11: 619-28. 1984.
92. Vogel R and Wechsler S. The effect of folic acid on gingival health. J Periodontol. 11: 667-668. 1976.
93. Pack A. Effects of topical and systemic folic acid supplementation on gingivitis in pregnancy. J Clin Periodontol. 5: 402-414. 1980.
94. Thompson M. The influence of nutritional factors on periodontal disease: a philosophical review. J New Zealand Soc Periodontol. 51: 15-19. 1981.
95. Thompson M. Effects of extended systemic and topical folate supplementation on gingivitis in pregnancy. J Clin Periodontol. 3: 275-280. 1982.
96. Pack A. Folate mouthwash: effects on established gingivitis in periodontal patients. J Clin Periodontol. 9: 619-628. 1984.
97. Melnick S et al. A case-control study of plasma ascorbate and acute necrotizing ulcerative gingivitis. J Dent Res. 5: 855-860. 1988.
98. Leggott P et al. The effect of controlled ascorbic acid depletion and supplementation on periodontal health. J Periodontol. 8: 480-485. 1986.
99. Leggott P et al. Effects of ascorbic acid depletion and supplementation on periodontal health and subgingivial microflora in humans. J Dent Res. 12: 1531-1536. 1991.
100. Woolfe S et al. Relationship of ascorbic acid levels of blood and gingival tissue with response to periodontal therapy. J Clin Periodontol. 3: 159-165. 1984.
101. Basu J et al. Plasma reduced and total ascorbic acid in healthy women: effects of smoking and oral contraception. Contraception. 39: 85-93. 1989.
102. Wood N. The effects of dietary bioflavonoid (rutin, quercetin and naringin) supplementation on physiological changes in molar crestal alveolar bone-cemento-enamel junction distance in young rats. J Med Food. 7: 192-6. 2004.
103. Wood N. The effects of dietary naringenin supplementation on physiological changes in molar crestal alveolar bone-cemento-enamel junction distance in young rats. J Med Food. 8: 31-5. 2005.
104. Singh U et al. Vitamin E, oxidative stress, and inflammation. Ann Rev Nutr. 25: 151-74. 2005.
105. Bailey R et al. Persistent oral health problems associated with comorbidity and impaired diet quality in older adults. J Am Diet Assoc. 104: 1273-6. 2004.
106. Yoshihara A et al. The relationship between dietary intake and the number of teeth in elderly Japanese subjects. Gerontology. 22: 211-218. 20