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Compendium

February 2012, Volume 33, Issue 2
Published by AEGIS Communications


Biocorrosion Vs. Erosion: The 21st Century and a Time to Change

John O. Grippo, DDS

Abstract

The author’s objective is to precisely define the term “erosion” as a physical mechanism and to establish the mechanism of biocorrosion in the lexicon of dental terms. Using the prefix “bio” before corrosion differentiates it from corrosion, because it designates the chemical, biochemical, and electrochemical actions on enamel and dentin. Biocorrosion encompasses endogenous and exogenous acidic and proteolytic chemical degradation of enamel and dentin, as well as the piezoelectric electrochemical action on the collagen in dentin.

Since the earliest days of the study of dentistry, the term “erosion” has been misconstrued or misused in the designation of tooth surface lesions. This practice dates back to the time of Pierre Fauchard,1 who is widely acknowledged as the “Father of Modern Dentistry,” and was followed by Thomas Bell,2 Willoughby D. Miller,3 and Greene Vardiman Black.4 Furthermore, it has impeded the investigation of tooth-surface pathology, because the other types of chemical degradation in addition to acids—which are properly termed “biocorrosion”—have been ignored. The first use of the term “erosion” in relation to dental science can be traced to the publication of The Surgeon Dentist or Treatise on the Teeth by Pierre Fauchard in 1728.1 There Fauchard states:

The enamel of teeth is subject to disease which simulates caries, but it is however not caries. The external surface becomes uneven and rough like a grater but more irregular. I call this erosion of the surface of the enamel, or disposition to caries. From this it comes that the enamel is eaten by some corrosive, in the same way as rust corrodes the surface of metals. The cure for this is to polish the surface of the tooth.1

Bell, in Litch’s textbook, The Anatomy, Physiology and Diseases of the Teeth, which was published in 1831, was the second to use the term “erosion.”2 In 1907, Miller3 used the term “erosion,” and shortly thereafter, G.V. Black4 established the term “erosion” to designate the effects of acid on the hard tissues of teeth in a textbook published in 1908. That textbook has been widely used and has influenced the teaching in dental schools throughout most of the 20th century. It included an entire chapter entitled “Erosion of the Teeth.” In the book, Black stated, “The cause of erosion is involved in the utmost obscurity” and after “reaching back 200 years in the literature,” he proceeded to summarize eight causes. Among the causes cited were “faults in the formation of tissues during growth, friction, acid in someway but unknown, diseased glands in the mucous membrane, absorption, associated with gouty diathesis, alkaline fluids, or the enzyme of some microorganism.” Following his death, G.V. Black’s book was revised by his son, Arthur Black, who added these three additional possible causes of erosion: a disordered pulp due to an abnormal occlusion, an exudate from the gingival crevice due to traumatic occlusion, and excessive use of citrus fruits or acid beverages. These 11 causes of erosion cited in the revised book provoked concern in the dental community, as the term “erosion” had been continually used in his textbook until the 1970s.5

However, the term continues to be used today. Notwithstanding the confusion in its etiology since 1908, erosion is now being defined as “the chemically induced loss of enamel and dentin caused by the action of acids unrelated to bacterial action.”6,7 Numerous text books, oral pathology texts, and manuscripts continue to be published using this definition; however, it has caused confusion in other areas of the sciences, which find this definition incorrect and misleading. Recently, the term “erosion” has been preceded by the word “acid” by some authors,6,7 which this author finds odd, considering that the term erosion is defined as the acid dissolution of teeth.

Discussion

The term “erosion,” to be precise, is not a chemical mechanism but solely a physical mechanism, which causes friction, all by the action of flow or movement of a liquid, solid, gas, or a combination thereof. There is water erosion, which occurs from the force of the flow of water in a river moving over and eroding rocks, or when water moves over stones in a brook causing their surfaces to become worn smooth. Erosion can also involve wind, which can take a toll on areas of the world covered in desert. Although it may seem to be a small factor, wind over a period of time can even wear away stone. This is frequently noticed in graveyards, where the lettering of the stones becomes worn away by the movement of wind, in addition to the effect of rain, movement of snow, and sleet; over time, these elements erode away the surface of the stone by friction. The most common visible form of erosion is that of the sea as it moves the sands or soil in its powerful movement and continually changes the contour of beaches.

All of the aforementioned types of erosion have been cited to establish that these actions are physical, not chemical, as movement and flow are involved. The effects of erosion, or the wearing away by the flow of water on teeth, are insignificant in human dentistry, especially on the enamel. However, as has been seen by the author, they can affect the dentin-like teeth of sperm whales as a result of the huge volume and force of water flowing over their teeth when they seek and eat food such as the giant squid (Figure 1). As their teeth wear from the frictional effects of erosion from the water and abrasion from food, they continually erupt, thus providing more tooth structure (Figure 2).8

Corrosion and Biocorrosion

Corrosion is defined as “the metallic deterioration of a material by chemical or electrochemical attack in a particular environment.”9 As further stated in Perry’s Chemical Engineers’ Handbook, “Metallic materials, such as pure metals and their alloys, tend to enter into chemical union with the elements of a corrosive medium to form stable compounds similar to those found in nature.”9 When the metal loss occurs in this way, the compound is referred to as “the corrosion product” and the metal surface is spoken of as “being corroded.” Metallic corrosion applies specifically to chemical or electrochemical attack on metals. In order to appreciate the significance of the term “metallic corrosion,” one must recognize that there are many types of chemical and electrochemical reactions on materials,9 the most common of which in dentistry are galvanic10 and crevice11 corrosion in amalgam restorations.

As stated by Caputo and Standlee in their 1987 text, Biomechanics of Clinical Dentistry, “All dental tissues and structures follow the same laws of physics as any other material and structure.”12 It also may be added that teeth would follow the same laws of chemistry in that they would react with various agents. Biocorrosion is the chemical, biochemical, and/or electrochemical action, which causes the molecular degradation of the essential properties in a living tissue. The addition of the prefix “bio” to the word corrosion—implying action on living tissues, including teeth, which are non-metallic—differentiates it from metallic corrosion. The agents that cause the degradation of the hard tissue of teeth are referred to as “biocorrodents.”

There are four types of non-metallic corrosion affecting teeth, which will now be termed “biocorrosion.” They are endogenous (biochemical) and exogenous (chemical) acids, proteolysis (biochemical), and/or electrochemical action from the piezoelectric effect on dentin (Figure 3). Endogenous acids result from bacterial biocorrosion from acids created by the biofilm of plaque and have been recognized since W.D. Miller wrote about them in 1883.13 They would also include acids from the crevicular fluid14 and from hydrochloric acid from gastric secretions.15,16 Exogenous acids result from beverages in the diet, which include citric and phosphoric acids and acids from the atmosphere in some occupations.17 Exogenous biocorrosion can also occur as a result of acids from the frequent use of citric acid lozenges, carbonated beverages, sports drinks, and fruits containing citric acid.7,16-19 It also can result from the excessive consumption of wine,19 vitamin C tablets,20 and mouthrinses.21 The pooling of gastric acid on the teeth of bulimics, patients with gastroesophageal reflux disease (GERD), or those who vomit from alcoholism also causes erosion/biocorrosion and is designated as “perimylosis.”15

Proteolytic corrodents result from enzymatic lysis as in caries,22 as well as the production of proteases trypsin from the pancreas and pepsin from the stomach.23 It would also include the proteases collagenase24 and metalloproteinases from the crevicular fluid,25 as well as the electrochemical piezoelectric effects acting on the collagen in dentin.26-28 When either corrosion or biocorrosion combine with static stress or fatigue (cyclic) stress, these two mechanisms then exert a physicochemical action.29

Root Caries and Noncarious Cervical Lesions

In dental caries, it has been established that bacterial action-producing acids and proteolysis do occur during the degradation of tooth substance. The physicochemical mechanisms of static stress biocorrosion29 and fatigue (cyclic) stress biocorrosion,29 as well as the electrochemical action induced by stress by means of the piezoelectric action on the collagen in dentin, appear to be cofactors in the process of root caries formation.27,28 Furthermore, these aforementioned physicochemical mechanisms come into play during the etiology of non-carious cervical lesions (NCCLs) provided that the microfilm of bacterial plaque is consistently removed. If not, then the biocorrodent action of the bacteria-producing acid will simply progress as caries, as a close relationship does exist between root caries and NCCLs. A recent study by Schlueter et al23 has disclosed that trypsin from the pancreas and pepsin from the stomach, working in concert, play a role in the degradation of 33% organic protein of the dentin. This could account for the rapid progression of dentin destruction by proteolytic action in bulimics, patients with gastroesophageal reflux disease (GERD), or those who vomit from alcoholism.30

Erosion/Biocorrosion

The most common means by which erosion occurs is when it combines with an acidic biocorrodent as erosion/biocorrosion. This would be the case during the frequent consumption and movement over teeth of highly acidic beverages, such as sport drinks and colas containing citric and phosphoric acid, which are frequently swished around in the mouth.6,31 Erosion/biocorrosion occurs during the regurgitation of acidic stomach contents, as seen in patients who vomit due to bulimia or chronic alcoholism.6,30 These combined effects of erosion and biocorrosion, which are referred to as “perimylosis,” cause severe loss of tooth substance in the palatal area of the anterior teeth.6,15

Piezoelectric Effects on Collagen in Dentin

Although many studies of the piezoelectric electrochemical effects on bone have been conducted, little has been done on teeth.26,32-34 Because enamel is not piezoelectric,26,34 it is possible that such effects on the collagen in the dentin may play a role in the genesis of NCCLs,27-29 root caries,27-29 and cervical dentin hypersensitivity (CDH).35,36 The potential difference (positive surface charge) produced by eccentric loading on the dentin and cementum may cause calcium ions to be displaced from zones of tensile cervical stress, to be displaced into the saliva.27,28 The electrokinetic phenomenon referred to as “streaming potential,” which is dependent on the nature of the electrokinetic potential existing at the solid-liquid interface, has been proposed as the cause of CDH.37,38 “It is possible that the deformation in dentin by biomechanical loading may produce changes of the outward fluid movements in dentinal tubules, and that electrokinetic potential induced at this time may promote changes in localized calcium ion activity in the cervical regions.”39 The piezoelectric effects may be minor and difficult to quantify, as the salivary remineralization of dentin could have a neutralizing effect on any ionic loss that may be induced by these effects.

Combined Mechanisms

In bioengineering, it must be recognized that when teeth interact through the dynamics of occlusion, loading forces generate stress to the teeth and their supporting structures. Whenever stress combines with a biocorrodent—whether it is a protease or an acid—it is termed either “static stress biocorrosion” or “fatigue (cyclic) stress biocorrosion” (Figure 4).40 Studies using acid, conducted mostly in Australia, have demonstrated that these mechanisms do occur.41-44

Conclusion

The use of the term “biocorrosion”—which is the chemical, biochemical, and electrochemical action on teeth—to replace “erosion” is fitting because it is a more precise term. Biocorrosion embraces the action of endogenous acids from plaque, crevicular fluid, and gastric mucosa, in addition to exogenous acids from diet and due to some occupations. It also includes proteolysis, as in the degradation of the 33% organic protein of the dentin by the digestive enzyme proteases, trypsin from the pancreas, and pepsin from the stomach, working synergistically. Biocorrosion also embraces both the proteolytic action in caries as well as proteases in the crevicular fluid. The effects of biocorrosion combined with stress is a plausible reason as to why root caries progresses so rapidly. Furthermore, biocorrosion appears to play a role in the loss of ions from the collagen in dentin, which has piezoelectric properties and could be a cofactor in the genesis of CDH.

In short, now in the 21st century, it is time to place the term “biocorrosion” into the lexicon of dental terms and “erosion” in its rightful place as a physical mechanism in the loss of tooth substance by friction.

Acknowledgements

The following respondents from various countries have supported the publication of this paper: Gordon Christensen, DDS, MSD, PhD; Thomas A. Coleman, DDS; Babacar Faye, DDS, PhD; Roberto Gatto, MD, DMD; Robert Gettens, PhD; Kyu-Bok Lee, DDS, PhD; Karl Lyons, MDS, FRACDS; James V. Masi, PhD; Antonello Messina, DDS; Gene D. Mc Coy, DDS; E. Bradley Moynahan, PhD; Daniel S. Oh, PhD; Bradley T. Piotrowski, DDS, MS; Paul H. Rigali, DDS; Martin J Tyas, DDSc, PhD, FRACDS; David J. Zegarelli, DDS; Adriaan J.J. Zonnenberg, LDS.

References

1. Fauchard P. The Surgeon Dentist or Treatise on the Teeth. Lindsay L, translation from 1746 2nd ed. London, England: Butterworth; 1946:20,21,40,46,47.

2. Bell T. Abrasion and erosion on the teeth, part 3. Litch WF, ed. The Anatomy, Physiology and Diseases of the Teeth. Philadelphia, PA: Carey & Lea; 1831.

3. Miller WD. Experiments and observations on the wasting of tooth tissue previously designated as erosion, abrasion, chemical abrasion, denudation, etc. Dental Cosmos 1907; XLIX No. 1:1-23, XLIX No. 2:109-124, XLIX No. 3:225-247.

4. Black GV. A work on operative dentistry. Vol. 1. Pathology of the Hard Tissues of the Teeth. 1st ed. Chicago, IL: Medico-Dental Publishing; 1907:39-59.

5. Blackwell RE. Operative Dentistry Vol. I. Black A, ed. 9th ed. South Milwaukee, WI: Medical-Dental; 1955:156-180.

6. Bartlett DW, Phillips K, Smith B. A difference in perspective—The North American and European interpretations of tooth wear. Int J of Prosthodont. 1999;12(5):401-408.

7. Bartlett DW. Etiology and prevention of acid erosion. Compend Contin Educ Dent. 2009;30(9):616-620.

8. Klevezal GS, Kleinenberg SE. Age Determination of Mammals from Annual Layers in the Teeth and Bones. Academy of Sciences of the USSR. Moscow: Severtsov Institute of Animal Morphology; 1967. Translated from Russian by the Israel Program for Scientific/Translations; Jerusalem, 1969.

9. Perry R, Green D. Perry’s Chemical Engineers’ Handbook. 6th Edition. New York, NY: McGraw Hill Co.; 1984:Section 23;1,23-25.

10. Fusayama T, Katayori T, Nomoto S. Corrosion of gold and amalgam placed in contact with each other. J Dent Res. 1963;42:1183-1197.

11. Sutow EJ, Jones DW, Hall GC. Correlation of dental amalgam crevice corrosion with clinical ratings. J Dent Res. 1989;68(2):82-88.

12. Caputo AA, Standlee JP. Biomechanics of Clinical Dentistry. Hanover Park, IL: Quintessence Publishing; 1987:19.

13. Miller WD. The etiology of dental caries. Barrett WC, ed. The Independent Practitioner. 1883;12:629-644.

14. Bodecker CF. Local acidity: a cause of local erosion-abrasion. Ann Dent. 1945;4(6):50-55.

15. Holst JJ, Lange F. Perimylosis: a contribution toward the genesis of tooth wasting from non-mechanical causes. Acta Odontal Scand. 1939;1:36-48.

16. Zero DT. Etiology of dental erosion—extrinsic factors. Eur J Oral Sci. 1996;104(2[pt2]):162-174.

17. Bartlett DW. The role of erosion in tooth wear: aetiology, prevention, and management. Int Dent J. 2005;55(4 suppl 1):277-284.

18. Stafne EC, Lovestadt SA. Dissolution of tooth substance by lemon juice, acid beverages and acids from other sources. J Am Dent Assoc. 1947;34(9):586-592.

19. Bartlett DW. Acid erosion: why is it important to your patients? Inside Dentistry. 2009;5(2)67-69.

20. Giunta JL. Dental erosion resulting from chewable vitamin C tablets. J Am Dent Assoc. 1983;107(2):253-256.

21. Noonan V, Kabani S. Dental erosion. J Mass Dent Soc. 2010;59(2):43.

22. Roth G. Proteolytic organisms of the carious lesion. Oral Surg Oral Med Oral Pathol. 1957;10(10):1105-1117.

23. Schlueter N, Hardt M, Klimek J, Ganss C. Influence of digestive enzymes trypsin and pepsin in vitro on the progression of erosion in dentine. Arch Oral Biol. 2010;55(4):294-299.

24. Kawasaki K, Featherstone JDB. Effects of collagenase on root demineralization. J Dent Res. 1997;76(1):588-595.

25. Tjaderhane L, Larjava H, Sorsa T, et al. The activation and function of host matrix metalloproteinases in dentin matrix breakdown in caries lesions. J Dent Res. 1998;77(8):1622-1629.

26. Fukuda E, Yasuda I. On the piezo electric effect of bone. Jap J Appl Phys. 1964;2(3):117.

27. Grippo JO, Masi JV. The Role of Stress Corrosion and Piezoelectricity in the Formation of Root Caries. Proceedings of the Thirteenth Annual Northeast Bioengineering Conference. Vol.I. Foster KR, ed. University of Pennsylvania, Philadelphia, PA: 1987.

28. Grippo JO, Masi JV. Role of biodental engineering factors (BEF) in the etiology of root caries. J Esthet Den. 1991;33(2):71-76.

29. Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction revisited: A new perspective on tooth surface lesions. J Am Dent Assoc. 2004;135(8):1109-1118.

30. Smith BGN, Robb ND. Dental erosion in patients with chronic alcoholism. J Dent. 1989;17(5):219-221.

31. Abrahamsen TC. The worn dentition pathognomonic—patterns of abrasion and erosion. Int Dent J. 2005;55(4):268-276.

32. Marino AA, Gross BD. Piezoelectricity in cementum, dentine and bone. Arch Oral Biol. 1989;34(7):507-509.

33. Braden M, Bairstow A, Beider I, Ritter B. Electrical and piezo-electrical properties of dental hard tissues. Nature. 1966;212(5070):1565-1566.

34. Shamos MH, Lavine LS. Physical bases for biolectric effects in mineralized tissues. Clin Orthop Relat Res. 1964;35:177-188.

35. Coleman TA, Grippo JO, Kinderknecht K. Cervical dentin hypersensitivity. Part II: associations with abfractive lesions. Quintessence Int. 2000;31(7):466-473.

36. Coleman TA, Grippo JO, Kinderknecht K. Cervical dentin hypersensitivity. Part III: resolution following occlusal equilibration. Quintessence Int. 2003;34(6):427-434.

37. Horiuchi H, Matthews B. In-vitro observations on fluid flow through human dentine caused by pain-producing stimuli. Arch Oral Biol. 1973;18(2):275-294.

38. Griffiths H, Morgan G, Williams K, Addy M. Dentin hypersensitivity: the measurement in vitro of streaming potentials with fluid flow across dentine and hydroxyapaptite. J Periodontal Res. 1993;28(1):60-64.

39. Hanaoka K, Nagao D, Mitsui K, et al. A biomechanical approach to the etiology and treatment of noncarious dental cervical lesions. Bull Kanagawa Dent College. 1998;26(2):103-113.

40. Faye B, Kane AW, Sarr M, et al. Noncarious cervical lesions among a non-toothbrushing population with Hansen's disease (leprosy): initial findings. Quintessence Int. 2006;37(8):613-619.

41. Palamara D, Palamara JE, Tyas MJ, et al. Effect of stress on acid dissolution of enamel. Dent. Mater. 2001;17(2):109-115.

42. Mishra P, Palamara JE, Tyas MJ, Burrow MF. Effect of loading and pH on the subsurface demineralization of dentin beams. Calcif Tissue Int. 2006;79(4):273-277.

43. Mishra P, Palamara JE, Tyas MJ, Burrow MF. Effect of static loading of dentin beams at various pH levels. Calcif Tissue Int. 2006;79(6):416-421.

44. Staninec M, Nalla RK, Hilton JF, et al. Dentin erosion simulation by cantilever beam fatigue and pH change. J Dent Res. 2005;84(4):371-375.

About the Author

John O. Grippo, DDS
Adjunct Faculty
Department of Biomedical Engineering
Western New England University
Springfield, Massachusetts


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Image Gallery

Figure 1  A sperm whale’s tooth showing erosion caused by the flow of water on its coronal surface. This short segment becomes very smooth from the friction of the water and consumption of food such as the giant squid. These whales have been report

Figure 1

Figure 2  The root surface of the sperm whale’s tooth depicting the area where the tooth grows as the exposed coronal surface erodes from friction.

Figure 2

Figure 3  The schema of pathodynamic mechanisms indicating the various initiating etiologic factors that produce lesions in the enamel and dentin. (Source: Grippo JO, Simring M, Coleman TA. Abfraction, abrasion, biocorrosion and the enigma of noncari

Figure 3

Figure 4  Advanced combined bioocorrosion/abfractions in tooth Nos. 6, 8, 9, and 11 through 14 caused by both static stress and fatigue (cyclic) stress, and the consumption of a highly acidic beverage called Bissap (sorrel) in a 69-year-old male with

Figure 4