Thomas C. Grubb
University of Maryland, Baltimore
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Journal of Dental Research | 1945
Thomas C. Grubb
The most generally accepted conception of dental caries etiology at present is that certain oral microorganisms ferment carbohydrates on the tooth surface producing sufficient acid to decalcify the enamel. The microorganisms most frequently implicated are the lactobacilli (1) and streptococci (2) because they are so frequently isolated from carious teeth, and are both aciduric and acidogenic. It is not proposed to discuss which is the more important for there is good evidence implicating both genera; and, quite possibly, both may be equally involved. On the basis of this conception of caries etiology, modern investigators have introduced a number of substances tending to inhibit or prevent microbic fermentation in the mouth. It is believed that such substances as sodium fluoride, synthetic vitamin K, iodoacetic acid, etc. block various enzymic reactions produced by acidogenic bacteria and thus the end products, acids, are not formed. The introduction of such substances for the prevention or control of caries is indeed a logical procedure but sufficient time has not elapsed to judge adequately the value of these measures. The purpose of this report is to present another method of attacking the problem of caries prevention and control. Whereas previous methods have sought to restrict or inhibit the action of microorganisms on carbohydrates, the method introduced here consists of substituting a sugar-alcohol which is but slowly attacked by acidogenic organisms. This new approach to the problem was suggested by one of our colleagues3 on the basis of the following reasoning. Bergeys Manual of Determinative Bacteriology (3) states that sorbitol is not fermented by Lactobacillus acidophilus. Since L. acidophilus is thought to be one of the most important causes of caries, and since sorbitol is sufficiently sweet to be substituted for sucrose in most instances where the latter is now used for sweetening purposes it was logical to believe that the substitution of this sugar-alcohol for sucrose or glucose would reduce or prevent acid production in the mouth. Although a preliminary study of the problem showed that one of the premises in our reasoning was incorrect for the literature reveals many
The Journal of Infectious Diseases | 1936
Howard J. Shaughnessy; Thomas C. Grubb
Journal of Bacteriology | 1947
Thomas C. Grubb; Marie L. Miesse; Bruno Puetzer
The Journal of Infectious Diseases | 1935
Thomas C. Grubb
Journal of The American Pharmaceutical Association | 1959
Thomas C. Grubb
The Journal of Infectious Diseases | 1946
Bruno Puetzer; Thomas C. Grubb
The Journal of Infectious Diseases | 1942
George P. Hager; Thomas C. Grubb
Journal of The American Pharmaceutical Association | 1942
Richard H. Barry; Walter H. Hartung; Thomas C. Grubb
The Journal of Infectious Diseases | 1941
Leonard Karel; Thomas C. Grubb; C. W. Chapman
Journal of The American Pharmaceutical Association | 1950
John A. Scigliano; Thomas C. Grubb; Donald E. Shay