A common misconception when thinking about teeth and their surrounding tissues, especially gingival/periodontal tissues, is that they are ‘lifeless’ and lack the vitality of other tissues in the body. Only when patients develop toothache or oral ulceration, do they appreciate how vital oral tissues are.

The gingival tissues have one of the richest blood supplies in the body and replace themselves faster than any other form of ‘skin’ in the body. Like other living tissues they are subjected to daily stresses. For teeth and gums these originate from diet, masticatory forces and bacteria within the plaque biofilm, or more specifically, the metabolic products of these bacteria. Gingival tissue ages like other skin tissues and needs nourishing and protecting from a variety of physical and biological stresses. One form of stress that contributes to aging and disease is ‘oxidative stress’, a process by which the excess free radicals in the periodontal tissues (generated either by accident or as part of an abnormal defence reaction to oral bacteria) exceed the tissues antioxidant defences and tissue damage results. There is now robust evidence that neutrophils within the peripheral blood stream of periodontitis patients appear to externally release excess oxygen radicals, even in their baseline state1 and this may contribute to the tissue-specific excess oxidative stress.

It has become clear in the last two to three years that periodontitis in its various forms is associated with oxidative stress within the periodontium2-5. Data from our own laboratories have shown a concomitant lowering of specific antioxidants and global antioxidant defence capacity in periodontitis patients and clear mechanisms linking antioxidants to periodontal tissue destruction, which were originally hypothesised 10 years ago are now emerging6-8.

Deficiencies in antioxidant micronutrients can arise at several levels, outside the cells within the tissue fluids, in the lipid membranes of cells and also within the cytoplasm of the cells themselves. The antioxidant barrier takes the form of specific enzymes within cells, antioxidant scavengers like vitamin E within cell membranes, and both scavenging, enzyme and iron-binding antioxidant systems within the extra-cellular fluids. These have also been shown to be depleted in periodontitis tissues as pocket depths increase9 as well as in gingival crevicular fluid. The antioxidant deficiencies in periodontitis demonstrated at the tissue level, appear at least in part, to arise secondary to excess oxygen radical release during periodontal inflammation10. Indeed, the antioxidant capacity of peripheral blood serum and plasma are also compromised in periodontitis patients11.

Another important barrier within the gingival tissues is the permeability barrier of the stratum corneum. The latter also needs replenishing and its function is dependent upon its lipid content, the predominant lipids within the stratum corneum of gingival epithelium being ceramides, cholesterol and fatty acids12. Linoleic acid is an essential fatty acid (also known as vitamin F) and plays a crucial role. Evidence suggests that it is required for the formation and maintenance of the barrier function of the stratum corneum13. The linoleate chain is essentially the only polyunsaturated chain in the stratum corneum, where it also appears to provide a degree of fluidity and plasticity to an otherwise saturated membrane14. Linoleic acid is a precursor of ceramide-1-linoleate, a structurally unusual ceramide that may be a significant determinant of stratum corneum permeability15. This ceramide is thought to act as a molecular rivet by stabilising the multilamellar lipid array in the intercellular spaces.

Over the last two to three decades toothpaste has been demonstrated to be an excellent delivery vehicle for active ingredients such as anti-bacterial agents and metal ions which effectively reduce plaque growth and promote gingival health. In the same way, the regular brushing with toothpaste can be exploited to deliver active ingredients which nourish gums by being incorporated into gingival tissues or by acting as antioxidants. These have the potential to provide additional benefits to the tissues by strengthening them at a cellular and sub-cellular level, to counteract day-to-day stresses like oxidative stress.

The beneficial effect of fluoride on dental hard tissue, i.e. tooth enamel and dentine, can be viewed in a similar way. The supply of the micro-nutrient fluoride16 not only prevents sound enamel from becoming decayed but it also helps to remineralise early caries lesions by incorporating fluoride and calcium into the enamel, and thus strengthens these areas against future challenges from dietary or bacterially generated acid attacks.

The history of fluoridated toothpastes classically demonstrates how cosmetic products can have a biological and scientific basis for their benefits and, based on that, a significant positive impact on the oral health of individuals and the population at large. Careful selection of the right active ingredients, and intelligent delivery to tissues, can only further improve the remarkable effects of modern dentifrices and oral care products. The constant drive to develop such exciting new healthcare products requires considerable investment in science, education and marketing.

In the reports included in this IDJ issue scientific evidence is provided which demonstrates that such micronutrients can be successfully delivered from a toothpaste formulation and incorporated into the relevant target tissues where they can exert their protective function.

References

1. Matthews JB, Wright HJ, Roberts A et al. Hyperactivity and reactivity of peripheral blood neutrophils in chronic periodontitis. Clin Exp Immunol 2007 147: 255-264.
2. Takane M, Sugano N, Iwasaki H et al. New biomarker evidence of oxidative DNA damage in whole saliva from clinically healthy and periodontally diseased individuals. J Periodontol 2002 73: 551-554.
3. Sugano N, Yokoyama K, Oshikawa M et al. Detection of Streptococcus anginosus and 8-hydroxydeoxyguanosine in saliva. J Oral Sci 2003 45: 181-184.
4. Sculley DV and Langley-Evans SC. Periodontal disease is associated with lower antioxidant capacity in whole saliva and evidence of increased protein oxidation. Clin Sci 2003 105: 167-172.
5. Panjamurthy K, Manoharan S, Ramachandran CR. Lipid peroxidation and antioxidant status in patients with periodontitis. Cell Mol Biol Lett 2005 10: 255-264.
6. Chapple ILC. Role of free radicals and antioxidants in the pathogenesis of the inflammatory periodontal diseases. Clin Mol Pathol 1996 49: M247-M255.
7. Chapple ILC, Brock G, Eftimiadi C et al. Glutathione in gingival crevicular fluid and its relation to local antioxidant capacity in periodontal health and disease. Mol Pathol 2002 55: 367-373.
8. Brock GR, Butterworth CJ, Matthews JB et al. Local and systemic total antioxidant capacity in periodontitis and health. J Clin Periodontol 2004 31: 515-521.
9. Ellis SD, Tucci MA, Serio FG et al. Factors for progression of periodontal diseases. J Oral Pathol Med 1998 27: 101-105. 10. Chapple ILC, Brock GR, Milward MR et al. Compromised GCF
total antioxidant capacity in periodontitis: cause or effect? J Clin Periodontol 2007 34: 103-110
11. Chapple ILC, Milward MR, Dietrich T. The Prevalence of Inflammatory Periodontitis is Negatively Associated with Serum Antioxidant Concentrations J Nutrition 2007 137: 657-664
12. Wertz PW, Swartzendruber DC Squier CA. Regional variation in the structure and permeability of oral mucosa and skin. Advanced Drug Delivery Reviews 1993 12: 1-12.
13. Ganem-Quintanar A, Falson-Rieg F, Buri P. Contribution of lipid components to the permeability barrier of oral mucosa. European Journal of Pharmaceutics and Biopharmaceutics 1997 44: 107-120.
14. Wertz PW, Squier CA. Cellular and molecular basis of barrier function in oral epithelium. Crit Rev Ther Drug Carrier Syst 1991 8: 237-269
15. Wertz PW, Downing DT. Ceramidase activity in porcine epidermis. FEBS Lett 1990 268: 110-112.
16. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington DC: The National Academic Press, 1997.

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