CLINICAL EVALUATION OF UREA-AMMONIATED DENTIFRICES 65 SUMMARY' While the mechanism by which ammoniated dentifrices function is not yet entirely clear, they have been shown to have therapeutic value in reducing Lactobacillus acido- philus in the mouth. Further, a high urea formula used for nearly four years in a controlled study has lowered the average rate of cavity formation 37.8%. These denti- frices, like other methods of caries reduction, are no panacea but should be co-ordinated with other means of combating dental disease where the attack is appreciable. Experiments with ammoniated dentifrices are now in progress in Aurora, Peoria, Mahopac, Philadelphia, and Los Alamos. Of these experiments, only in the work covered by our three- and four-year reports and at Ma- hopac is dentifrice use unsupervised. Results from prescribed and policed use of a dentifrice, while valid, may not be duplicated in average general use unless hasty home care is altered to the conditions and techniques of the experiment. Ammoniated for- mulas should contain a sufficient quantity of active ingredients so that when used in the mouth they maintain a 3 to 5% concentration during the hygiene period. Liquids may contain just under 10%, pastes between 15% and 20%, and powders between 25% and 30%. Lower concentrations are being tested at Aurora and Peoria * the efficacy of "high" urea concentrations is now confirmed. *"In the interim the findings of the Kesel Aurora and Peoria experiment (14) have been published. There was approxi- mately 12% caries reduction, which would seem to support the contention that such re- duction would be somewhat proportionate to the available ammoniated ingredients i.e.: 12% from an 8% formula, 37-40% from a 27.5 formula." BIBLIOGRAPHY (1) Grove, C. T., and Grove, C. J., Dental Cosmos., 76, 1029 (1934). (2) Hill, T. J., y. ,4m. Dental ,4ssoc., 26, 239 (1939). (3) Stephan, R. M., Science, 92, 578, (1940). (3a)Stephan, R. M., and Miller, B. F., Proc. Soc. Exp. BIG/. Med., 55, 101 (1944). (4) Henschel, C. J., N.Y. 3. Dentistry, 16, 102 (1946). (5) Schmidt-Nielsen, B. and K., Sci. Monthly, 69, 180 (1949). (6) Kesel, R. G., et al., •7. Arm. Dental .dssoc., 33, 695 (1946). (7) Kesel, R. G.,, et al., .rim. •7. Orthodontics OralSurg., 33, 80 (1947). (8) Henschel, C. J., and Lieher, L., Dental Research, 28,248 (1949). (9) Easlick, K. A., "Dental Caries," C. V. Mosby Co. (1948), 74 pp., Bibby, B. G. (10) Volker, J. F., N.Y. 3. Dentistry, 19, 104 (1949). (11) Stephan, R. M., •7. Dental Research, 23, 257 (1944). (12) Stephan, R. M., Ibid., 22, 63 (1943). (13) Gottlieb, B., "Dental Caries," Lea & Febiger, Philadelphia (1947). (14) Kesel, R. G., et al., •7. .rim. Dental .dssoc., 41, No. 4, 482 (1950).

AMMONIATED DENTIFRICES* By ROBERT G. KESEL, M.S., D.D.S. University of Illinois College of Dentistry, Chicago, Ill. THE MAJORITY of those study- ing the very prevalent disease, dental caries, believe that it de- velops principally because of the dissolution of the hard or inorganic substance of the teeth, in acids that are produced through the action of bacteria on refined carbohydrates in contact with the tooth surface. A conference on the etiology and con- trol of dental caries was held at the University of Michigan about two years ago. It was attended by 114 individuals representing the various sciences and professions concerned with the caries problem and after a week of study and discussion the following conclusion was adopted unanimously: "Dental caries is a disease of the calcified tissues of the teeth. It is caused by acids result- ing from the action of micro-organ- isms on carbohydrates, is charac- terized by a decalcification of the inorganic portion and is accom- panied or followed by a disintegra- tion of the organic substance of the tooth. The lesions of the disease predominantly occur in particular regions of the tooth, and their type * Presented at the Dec. 8, 1949, Meeting, New York City. is determined by the morphologic nature of the tissue in which they appear" (1). There is a minority group who believes that tooth destruction is brought about by the digestion of the organic matrix of enamel and den- tin, but their evidence is based largely on personal interpretation of the appearance of extracted teeth prepared for histopathologic study. The majority belief is based on the accumulation of much diversified evidence in support of the acid con- cept. This evidence can be classified as clinical, chemical, bacteriological, and dietary, as well as histopatho- logical. There is general agreement that caries is a bacterially produced dis- ease resulting from the action of bacteria that are contained in the plaque or film present on the sur- faces of the teeth which are not self- cleansing. These areas are along the gum line, the adjoining sur- faces of the teeth in the region of their contact or in defects such as pits and grooves that afford me- chanical protection. Decay occurs in these areas where bacteria can col- lect and remain more or less undis-