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Guthrow, C. E.,
Johnson, L. B. and Lawless, K. R., “Corrosion of Dental Amalgam and its
Component Phases”, J. Dent. Res. 46(6): 1372-1381, 1967
The effects of artificial
saliva on the surfaces of the individual phases of dental amalgam have been
observed by optical and electron microscopy and have been correlated with
measured corrosion potentials and currents. The 2 phase (Sn8Hg) had
the most active potential and was observed to be the most severely attacked
phase, the type of attack being general pitting. The phase (Ag3Sn)
had an almost neutral potential and observations showed little attack or
deposition, as there was only light etching. The 1 phase (Ag2Hg3)
had a noble potential and was observed to develop a deposit, identified as AgCl,
during anodic polarization.
Although some hindrance to
dissolution was found as the potential was increased, no true passivity
developed. It appeared, therefore, that little protection was offered by film
formation in an oral environment.The measured corrosion current of about 9µ
amp./cm2 for dental amalgam in artificial saliva indicated a
potentially rather drastic corrosion rate. Evidently, the high circuit
resistance in a true oral environment is the factor that limits the amount of
corrosion that actually occurs.
Von Fraunhofer,
J. A. and Staheli, P. J., “Corrosion of Dental Amalgam”, Nature 240, 304
- 306 (01 December 1972)
DENTAL amalgam is incorporated
into about 80% of all dental restorations. It is prepared by grinding or
triturating a silver−tin alloy (Ag3Sn, the phase) with mercury in the
proportions 1 : 1 or 5 : 6 of alloy to mercury. The setting reaction of dental
amalgam has been studied by many workers1−4 and is now accepted to be Excess
mercury is removed from the amalgam both before and during insertion into the
cavity. There is, however, some controversy over whether the 2 phase is
continuous throughout the matrix5 or whether it is present in discrete clumps or
clusters (G. Wing, personal communication).
References
1. Ryge, G. , Fairhurst, C. W.
, and Fischer, C. M. , Int. Dent. J., 11, 181 (1961).
2. Wing, G. , and Ryge, G. , J.
Dent. Res., 44, 1325 (1965).
3. Wing, G. , Aust. Dent. J.,
11, 105 (1966).
4. Allan, F. , Asgar, K. , and
Peyton, F. , J. Dent. Res., 44, 1002 (1965).
5. Jorgensen,
K. D. , Acta Odont. Scand., 23, 347 (1965).
6. Schoonover, I. C. , and
Souder, W. , J. Amer. Dent. Ass., 28, 1278 (1941).
7. Schriever, W. , and Diamond,
L. E. , J. Dent. Res., 31, 205 (1952).
8. Mumford, J. M. , Br. Dent.
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Res., 36, 632 (1957).
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11. Fusayama, T. , Katayori, T.
, and Nomoto, S. , J. Dent. Res., 42, 1183 (1963).
12. Guthrow, C. E. , Johnson,
L. B. , and Lawless, K. R. , J. Dent. Res., 46, 1372 (1967).
13. Carter, D. , Ross, T. , and
Smith, D. , Br. Corros. J., 2, 199 (1967).
14. von Fraunhofer, J. A. , and
Staheli, P. J. , Br. Dent. J., 130, 522 (1971).
15. von Fraunhofer, J. A. , and
Staheli, P. J. , Br. Dent. J., 132, 357 (1972).
16. Jenkins, G. N. , The
Physiology of the Mouth, third edition, 317 (Oxford, Blackwell, 1967).
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