L. Scott Brooksby, DDS, DICOI
680 W. Washington St Ste. E102
Sequim, WA 98382
How ozone is the missing link in caries control and reversal
Subject: How ozone is the missing link in caries control and reversal
I have been asked by several members of the group to explain exactly how the application of ozone leads to caries reversal and remineralisation.
For those of you who have your units, please accept this as revision, and if you want to comment, mail me! I am away from the end of this week until Wednesday next week; Prof Lynch and I are lecturing in Hong Kong from where I hope to send you an update on this symposium.
Caries reversal using ozone.
Caries is a multi-factorial disease process. Fermentable carbohydrates alone do not cause caries. Other ingredients are required, like bacteria, surfaces for attachment, proteins, and a supply of substrate that the bugs can use to live. Far from being simple, bugs are very complex, which of course would explain why they have existed for many millions of years almost unchanged, compared to humans who have occupied a very small time-scale period of the world's history. We know from some of the work carried out at Porton Down Government Labs, that bugs talk to each other with chemical messages. For example, when a collection of bugs find a niche to exploit, they send out messages to attract more bugs into the area. And if the host tries to change the environment to make it less favourable for them, chemical messages are sent out that attract different bug species that attempt to change the environment back to the status quo. Clever bugs eh!
Up to the last few years, as I am sure you are aware, there has been a large volume of research looking for the `perfect' treatment regime to halt and reverse decay. But if you read this research, there is no simple system, and even where it could be shown that caries reversal could be achieved, it was unpredictable, and often could not be taken from one study area to another and made to work in the new location. The early research looking at chlorhexidine, fluoride, oral hygiene, triclosan and so on all showed the same results; ie unpredictable, and for the main, no positive results! But it was shown that carious lesion could re-mineralise given the right conditions. The concept of a balance between mineral loss and gain as the oral environment changed from basic to acidic to basic was well researched and established, and the concept that saliva contains all the minerals a tooth surface needs to re-mineralise was accepted by the profession.
But lets face it, for the vast majority of patients, the regime required was time consuming and required a huge amount of time investment on the part of the dental profession and the patient. Sadly, in the UK and other countries, patients just are not prepared to make this investment, despite the clear benefits.
Then came along a whole series of studies that showed the dental profession that we were not actually measuring the disease process correctly, so there were a number of studies that laid down clinical criteria for diagnosis and classification of carious lesions.
Then in the late 90's came the first results of studies looking at the effect of ozone on microorganisms. 20 seconds, for example gave a log reduction from 7 to 0.4, or in plain English, 7,000,000 colony- forming units, to 0.4 CFU. In other words, as you cannot have less than one bug, this must be background contamination.
Then the ground breaking PhD by A Baysan and Primary Root Carious Lesions (PRCL's) in 2001, and since then a growing number of papers and abstracts from research areas showing the effects not just on bugs, but the bio-molecules (their waste products) they produce to form the acid niche environment ANE.
The key to understanding how ozone has revolutionised dental caries management is from the H NMR studies. In these studies, small samples of caries are exposed to high magnetic fields. Samples before ozone treatment show high spikes of pyruvic acids for example, one of the most important acids that is involved it the establishment of the ANE. Samples after ozone treatment show acetates and carbon dioxide, known break down products of these bio-molecules.
So what is happing at the caries site?
Ozone is delivered at a concentration of 2,100(+/- 10%) ppm. At this concentration, it first de-natures the protein coat, the pellicle. Studies have shown that this `protects' the ANE and does not allow pharmaceutical products to penetrate it to knock out the bugs. Once denatured, ozone then oxidises the micro-flora. Then as there is a continual feed of ozone into the cup area, the ozone begins to penetrate the carious lesion, oxidising the bio-molecules, so neutralising the ANE to its entire depth.
Of course in deep lesions, more time is required to allow full depth penetration, so for those of you in the early days who did not get a good result with large lesions at 10 and 20 seconds, this is why; the ENE was left intact in the deeper lesions, and the carious lesion re- established within the 14 weeks in preference to remineralisation. Also, as the ANE still existed at the base of the lesion, it could be postulated that this prevented mineral penetration into this base area. So the idea of 40 or more seconds for the large lesions, and continual treatment for the 99+ lesions seems to have sorted the poor results some of the early users were having with large lesions.
Many people at both the courses and lectures Prof Lynch and I have been at, have asked what is the point of sterilising the tooth surface and lesion, if when the patient licks the tooth, it will be re-infected. Of course this will happen. But having eliminated the ANE, and restored the balance of oral flora of the lesion to a balance between good / bad bugs, reinforced oral health, prescribed remineralising washes and pastes, the lesion has little alternative than to go through the process of mineral gain, ie remineralisation and caries reversal. The whole balance has been shifted from that of mineral loss, to that of mineral gain.
By slightly modifying the way the HealOzone Patient kit is used, it can be made to be even more effective. These products have a large concentration of bio-available minerals. If the paste is smeared over the treated lesions, and the pump spray used 3-4 times each day (just two puffs at each application) the bio available mineral concentration in the saliva is so huge that remineralisation has to occur in preference to mineral loss and re-establishment of the ANE, leading to active caries. My study just sent for publication shows 100% reversal of PRCL's in the treated group. Compare this to those lesions not ozone treated. They are in the same mouth, are exposed to the same oral hygiene care, mineral washes, etc, etc, but only 1% reversed, 59% stayed the same, and 40% got worse. Hence a recent comment that `the elimination of the biofilm is just a small part of treatment' is essentially correct, but misses the whole point of the system that the key to successful caries reversal is elimination of the ANE.
The references for those who want to do a little more reading around this posting are below. This does concentrate on PRCL's but will give you a firm basis on which to understand the concepts and issues that I have discussed above.
Regards, Julian
References:
1. Steele JG, Walls AW, Ayatollahi SM, et al. Major clinical findings from a dental survey of elderly people in three different English communities. Brit Dent J 1996; 180:17-23.
2. O'Mullane DM, Whelton H. Oral health in Irish adults 1899-90. Government Publications Stationery Office, Dublin, 1992.
3. Hellyer PH, Beighton D, Heath MR, et al. Root caries in older people attending a general dental practice in East Sussex. Br Dent J 1990; 169: 201-206.
4. Galan D, Lynch E. Epidemiology of root caries. Gerodontology 1993; 10: 59-71.
5. Downer MC. The improving dental health of United Kingdom adults and prospects for the future. Brit Dent J 1991; 170: 154-158.
6. Banting DW, Ellen RP, Fillery ED. Prevalence of root surface caries among institutional older persons. Community Dent Oral Epidemiol 1980; 8: 84-88.
7. Beck JD. The epidemiology of root surface caries: North American Studies. Adv Dent Res 1993; 7: 42-51.
8. Hand JS, Hunt RJ, Beck JD. Incidence of coronal and root caries in an older adult population. J Public Health Dent 1988; 48: 14-19.
9. Silwood CJ, Lynch EJ, Seddon S,et al. 1H-NMR analysis of microbial- derived organic acids in primary root carious lesions and saliva. NMR Biomed. 1999; 12: 345-356.
10. Silwood CJ, Lynch E, Claxson AW, et al. 1H NMR investigations of the molecular nature of low-molecular-mass calcium ions in biofluids. J Biol Inorg Chem. 2002; 7: 46-57.
11. Silwood CL, Grootveld M, Lynch E. 1H and 13C NMR spectroscopic analysis of human saliva. J Dent Res. 2002; 81: 422-427.
12. Beighton D, Lynch E, Heath MR. A microbiological study of primary root caries lesions with different treatment needs. J Dent Res 1993;73: 623-629.
13. Lynch E, Beighton D. Relationships between mutans streptococci and perceived treatment needs of primary root carious lesions. Gerodontology 1993; 10: 98-104.
14. Ship JA, Fox PC, Baum BJ. How much saliva flow is enough? "Normal" function defined. J Am Dent Assoc 1991; 122: 63-69
15. Brailsford SR, Lynch E, Beighton D. The isolation of Actinomyces naeslundii from sound root surfaces and root carious lesions. Caries Res. 1998; 32:100-106.
16. Lynch E, Beighton D. Short term effects of Cervitec on the microflora of primary root carious lesions requiring restoration. Caries Res 1993; 27: 106
17. Lynch E. Relationships between clinical criteria and microflora of primary root caries. Proceedings of the First Annual Indiana Conference, Indianapolis. Indiana University School of Dentistry (ISBN 0-9655149), 1996; 195-242.
18. Lynch E, Beighton D: A comparison of primary root caries lesions classified according to colour. Caries Res 1994; 28: 233-239.
19. Baysan A. Management of Primary Root Caries using Ozone Therapies. PhD Thesis, University of London, 2002.
20. Lynch E. The measurement of root caries for research purposes. J Dent Res 1986; 65: 510.
21. ten Cate JM, van Amerongen JP. Caries diagnosis, conventional methods. Proceedings of the First Annual Indiana Conference, Indianapolis. Indiana University School of Dentistry (ISBN 0- 9655149), 1996, 27-37.
22. Nyvad B, Fejerskov O. Scanning electron microscopy of early microbial colonization of human enamel and root surfaces in vivo. Scand J Dent Res 1987; 95: 287-296.
23. Lynch E. The diagnosis and management of primary root caries. PhD. thesis, University of London, 1994.
24. Hellyer P, Lynch E. Diagnosis of root caries - a critical review. Gerodontology 1991; 9: 95-102.
25. Hazen SP, Chilton NW, Mumma RD. The problem of root caries; 1. Literature review and clinical description. J Amer Dent Assoc 1973; 86: 137-144.
26. Taylor MJ, Lynch E. Microleakage. J Dent. 1992; 20:3-10.
27. Taylor MJ, Lynch E. Marginal adaptation. J Dent. 1993; 21: 265- 73.
28. Lynch E, Tay WM. Glass ionomer cements part III- clinical properties II. J Irish Dent Assoc 1989; 35: 66-73.
29.Vehkalahti M, Rajala M, Tuominen R, et al. Prevalence of root caries in the adult Finnish population. Community Dent Oral Epidemiol 1983; 11: 188-190.
30. Manji F, Fejerskov O, Baelum V. Pattern of dental caries in an adult rural population. Caries Res 1989; 23: 55-62
31.Stamm JW, Banting DW, Imrey PB. Adult root caries survey of two similar communities with contrasting natural water fluoride levels. J Am Dent Assoc 1990; 120: 143-149.
32. Katz RV. The clinical diagnosis of root caries. Issues for the clinician and researcher. Am J Dent 1995; 8: 335-341.
33. Galan D, Lynch E. Prevention of root caries in older adults. J Can Dent Assoc. 1994; 60::422 433
34. Papas A, Joshi A, Giunta J. Prevalence and intraoral distribution of coronal and root caries in middle-aged and older adults. Caries Res 1992; 26: 459-465.
35. Beighton D, Lynch E. Relationships between yeasts and primary root-caries lesions. Gerodontology. 1993; 10::105-108.
36.Collier FI, Heath MR, Lynch E, et al. Assessment of the clinical status of primary root carious lesions using an enzymic assay. Caries Res. 1993; 27: 60-64.
37. Beighton D, Hellyer PH, Lynch EJ, et al. Salivary levels of mutans streptococci, lactobacilli, yeasts, and root caries prevalence in non-institutionalized elderly dental patients. Community Dent Oral Epidemiol. 1991; 19: 302-307
38. Fure S. Five-year incidence of caries, salivary and microbial conditions in 60-, 70- and 80-year-old Swedish individuals. Caries Res 1998; 32: 166-174.
39. Beighton D, Lynch E. Comparison of selected microflora of plaque and underlying carious dentine associated with primary root caries lesions. Caries Res. 1995; 29::154-158
40. Allen EP, Bayne S, Becker I, et al. Annual review of selected dental literature: Report of the Committee on scientific investigation of the American Academy of Restorative Dentistry. J Prosthet Dent 1999; 83: 27-66.
41. Lynch E. Antimicrobial management of primary root carious lesions: a review. Gerodontology. 1996; 13: 118-129.
42. Baysan A, Lynch E. Management of primary root caries with a high fluoride dentifrice. Tissue Preservation and Caries Treatment. Quintessence Book 2001, Chapter 2, 37-48.
43. Lynch E, Baysan A, Ellwood R et al. Effectiveness of two fluoride dentifrices to arrest root carious lesions. Am J Dent. 2000; 13: 218- 220.
44. Lynch E, Baysan A. Reversal of primary root caries using a dentifrice with a high fluoride content. Caries Res. 2001; 35::60-64.
45. Baysan A, Lynch E, Ellwood R et al. Reversal of primary root caries using dentifrices containing 5,000 and 1,100 ppm fluoride. Caries Res. 2001; 35: 41-46.
46. Duckworth R. The science behind caries prevention. Int Dent J 1993; 43: 529-539.
47. Lynch E., Brailsford S.R., Morris-Clapp C.et al. Effect on Cervitec on the treatment needs of primary root-caries. J Dent Res 1995;73: 535
48. Keltjens HMAM, Schaeken MJM, van der Hoeven H. Preventive aspects of root caries. Int Dent J 1993; 43: 143-148.
49. Wright PS, Hellyer PH, Beighton D, et al. Relationship of removable partial denture use to root caries in an older population. Int J Prosthodont. 1992; 5: 39-46
50. Baysan A, Lynch E, Grootveld M. The use of ozone for the management of primary root carious lesions. Tissue Preservation and Caries Treatment. Quintessence Book 2001, Chapter 3, 49-67.
51. Baysan A, Whiley R, Lynch E. Anti-microbial effects of a novel ozone generating device on microorganisms associated with primary root carious lesions in vitro. Caries Res 2000; 34: 498-501.
52. Baysan A, Lynch E Effect of ozone on the oral microbiota and clinical severity of primary root caries Am J Dent, 2004, Accepted for publication
53. Lynch E. Kariesbehandlung mit Ozon. Die Quintessenz 2003; 54: 608- 610
54. Lynch E. Leczenie prochnicy za pomoca ozonu. Quintessence dla lekarzy stomatologow 2003; 11:198-200
55. Bocci V. Ozonization of blood for the therapy of viral diseases and immunodeficiencies. A hypothesis. Med Hypothesis 1992; 39: 30-34.
56. Bocci V, Luzzi E, Corradeschi F, et al. Studies on the biological effects of ozone: 4. Cytokine production and glutathione levels in human erythrocytes. J Biol Regul Homeost Agents 1993; 7: 133-138.
57. Bocci V. Does ozone therapy normalize the cellular redox balance? Implications for therapy of human immunodeficiency virus infection and several other diseases. Med Hypotheses 1996; 46: 150-154.
58. Bocci V. Ozone as a bioregulator. Pharmacology and toxicology of ozonetherapy today. J Biol Regul Homeost Agents 1996; 10: 31-53
59. Bocci V. Biological and clinical effects of ozone. Has ozone therapy a future in medicine? Br J Biomed Sci 1999; 56: 270-279.
60. Lynch E, Tay WM. Glass ionomer cements part III- clinical properties II. J Irish Dent Assoc 1989; 35: 66-73.
61. Arneberg P. Dental caries in the elderly. 2. Root caries. Symptoms and treatment guidelines. Nor Tannlaegeforen Tid 1989; 99: 676-679.
62. Nyvad B, Fejerskov O. Active root surface caries converted into inactive caries as a response to oral hygiene. Scand J Dent Res 1986; 94: 281-284
63. Bradshaw DJ, McKee AS, Marsh PD. Prevention of population shifts in oral microbial communities in vitro by low fluoride concentrations. J Dent Res 1990; 69: 436-441.
64. Papas A, Russell D, Singh M, et al. Double blind clinical trial of a remineralizing dentifrice in the prevention of caries in a radiation therapy population. Gerodontology 1999; 16: 2-10.
65. Nunn J, Morris J, Pine C, et al. The condition of teeth in the UK in 1998 and implication for the future. Br Dent J 2000; 23: 613-644.
66. Anusavice KJ. Need for early detection of caries lesions: A United States Perspective. Proceedings of the 4th Annual Indiana Conference, Indianapolis. Indiana University School of Dentistry (ISBN 0-9655 149-2-7), 2000, 13-29.
67. Emilson CG, Ravald N, Birkhed D. Effects of a 12-month prophylactic programme on selected oral bacterial populations on root surfaces with active and inactive carious lesions. Caries Res 1993; 27: 195-200.
Comments on how Ozone affects caries by Julian Holmes