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Dental Caries
D E N T A L CARIES* By CHARLES F. BÔDECKER, D.D.S., F.A.C.D., N ew York City
H E fact that the activity of dental caries varies greatly in different per sons has long been observed clinic ally. I t can now be reduced to exact figures by the use of the caries index .1 As an instance, H . H olliday and D . E. Ziskin, of the D epartm ent of O ral D iag nosis of the Columbia University, School of D ental and O ral Surgery, have shown in a group of 406 students of an average age of 17-19, a minimal caries index of 0 and a maximum of 54.375 per cent. Such extreme figures, showing the great differences in the activity of dental caries, can be duplicated in almost any dental practice. T h e thinking members of our profession, as well as the more advanced investigators, realize that food reten tion is not the sole cause of dental caries and consequently that oral hygiene is not the only method of combating this disease; for it is of no avail in prevent ing the progressive destruction of the teeth. O ther means are now being sought to improve the dental condition of pres ent and future generations.
T
*From the laboratory of Dental Histology and Embryology, Columbia University D en tal School. *Read before the Section on Mouth Hygiene and Preventive Dentistry at the SeventyFourth Annual Session of the American Dental Association, Buffalo, N. Y., Sept. 14, 1932. 1. Bodecker, C. F., and Bodecker, H. W . C .: Practical Index of Varying Susceptibility to Dental Caries in Man, D . Cosmos, 73 :707 (July) 1931. Bodecker, C. F .: Calcification of Modified Index of Dental Caries. D . Sur vey, 7:23 (D ec.) 1931.
Jour. A. D. A., May, 1933
T h e beneficial effect of a balanced diet can be rega'rded as definitely proved. But how can diet benefit fully formed teeth if these are considered as having no physiologic connection w ith the body? T h ere is a large group of investigators who, even though they realize th at the teeth are benefited by a well-balanced diet, do not admit a biologic connection w ith the body. T hey believe that the teeth are fully m atured on eruption, and that nothing can affect them for good or ill from the interior. T h e ir explanation of the mechanism of dental caries centers entirely in a change of oral conditions. Variations in the chemical constitution of the saliva through which a defective diet may harm the teeth, are therefore thought to be responsible. H ere again, there is a divergence of opinion. One group believes that an improper diet de velops an abnormality of the saliva; another group that the growth of Bacil lus acidophilus is stimulated by this means. T h e latter theory makes bacteria responsible for the increased activity of dental caries. Still another group be lieves in a combination of these two factors. T h e majority of investigators, as w ell as most of the dental profession, believe a variation of one or all of these factors to be the cause of dental caries. Let us now tu rn to the constitutional or internal factors. Broderick ,2 in his w ork “ D ental M edicine,” presents a great many arguments to the effect that
783
2. Broderick, F. W .: Dental Medicine, St. Louis: C. V. Mosby Company, 1928.
784
The Journal of the American D ental Association
the presence of bacteria and food reten tion around the teeth cannot wholly explain the varying activity of dental caries. H is statements on this subject are so clear and logical that they should convince the open minded. H e believes that the cause of dental caries is to be found in constitutional disturbances, par ticularly acidosis, and that this condition causes an abnormality of the saliva. H e does not entirely preclude the thesis of detrim ental influences affecting the den tal tissues from w ithin. Only a few investigators consider this to be possible. T h e m ajority maintain that no metabolic processes take place in the enamel and that therefore systemic disturbances can not harm the teeth by way of the pulp. T hey do not believe that a mechanism exists by which this could be effected. It is not yet generally adm itted that a fluid can penetrate from the pulp into the enamel, although the existence and per meability of channels leading from the pulp through the dentin and the enamel has been shown by Beust ,3 Fish ,4 Klein and Amberson ,5 Applebaum ,6 by me 7 and by others. T h e reason for this is that mem bers of the dental profession, as w ell as many investigators, are obsessed w ith the idea that erupted teeth need no supply of mineral salts and therefore receive none. Consequently,. they cannot understand 3. Beust, T . B.: Vascular System of Hard Substance of Teeth, D. Rec., 32:660, 1912. 4. Fish E. W .: Circulation of Lymph in Dentin and Enamel, J.A.D.A., 14:804 (M ay) 1927. 5. Klein, Henry, and Amberson, W . R .: Physico-Chemical Study of Structure of Den tal Enamel, J. D. Res., 9:667 (Oct.) 1929. 6. Applebaum, Edmund: Lymph Channels in Dentin and Enamel Stained by Amalgam, J. D. Res., 9:487 (A ug.) 1929. 7. Bodecker, C. F.: Permeability of Enamel in Relation to Stains, J.A.D.A., 1Q:60 (Jan.) 1923.
that general metabolic disturbances may result in a derangement of the secretion of the dental pulp and that thus the den tal tissues may be harmed. Systemic disturbances will probably be shown to harm the teeth by abnormal changes in the dental pulp and mineral salt metabolism. These factors have been discussed at length elsewhere .8 I t is only necessary to mention them here. Sugges tions concerning a dental protective mech anism against decay likewise have been published .9 A brief recapitulation of a certain phase is necessary, as a modifica tion has been made since 1929. T he hypo thesis was then set up that the dental pulp in children and young adults secretes a lymph which permeates the dentin and the enamel. T his fluid was supposed to contain mineral salts which effect the posteruptive calcification of the dentin and enamel and maintain the high buffer power or alkali reserve of these tissues. T h a t these appear to have a high alkali reserve is indicated by the w ork of Karshan ,10 who showed a hydrogen-ion con centration of 7.8, 8.0 for the dentin and 7.3-7 .6 for the enamel. (Blood has a Pb. of 7.35-7.40.) O riginally ,11 it was thought that the dental lymph itself might neutralize oral acids and thus prevent the destruction of the enamel and dentin. Another more recently suggested possibility is that the 8. Bodecker, C. F., and Applebaum, Ed mund: M etabolism of Dentin; Its Relation to Dental Caries and to Treatm ent of Sen sitive Teeth, D. Cosmos, 73:995 (Oct.) 1931. 9. Bodecker, C. F .: N ew Theory of Cause of Dental Caries, D. Cosmos, 71:586 (June) 1929; Lipin Content of Dental T issues in Relation to Decay, J. D. Res., 11:277 (April) 1931. 10. Karshan, M.: Studies of Enamel and Dentin in Relation to Dental Caries, J. D. Res., 12:523 (June) 1932. 11. Footnote 9, first reference.
Bôdecker— D ental Caries lymph maintains the high alkali reserve in the dentin and enamel through a con stant supply of mineral salts (bicarbon ates?). T hus, under normally healthy conditions, dental caries would be pre vented in young persons. However this may be, the pulp and its secretion, the dental lymph, probably aided by a normal saliva (Eckerm ann ,12 Broderick2), ap pear to me to be the principal factors in maintaining the integrity of the teeth. Lester R. C ahn 13 now goes even far ther, believing that under pathologic con ditions, the dental pulp can decalcify the dentin and enamel from the interior, caries resulting in the areas of food reten tion. T h is has been shown to be possible by Blackberg and Berke ,14 who observed in young rachitic pups areas of décalci fication definable only by the roentgen rays, and extending from the pulp to the surface of the tooth. If these observations apply to human teeth, the cause of dental caries w ill be found to inhere, in systemic rather than in environmental conditions. I t appears that the activity of this disease is dependent on bodily conditions. T his does not mean that oral hygiene is unnec essary; for if mouth acid (due to food ferm entation) is the exciting cause of dental caries, the less food that is retained around the teeth (less acid), the less ac tive need be the protective mechanism to combat oral acid and still maintain the teeth intact. T h e close relation of the environmental causes of dental caries (food retention, the presence of bacteria and the condition 12. Eckermann, R .: Dental Caries and Os mosis, 1919. 13. Cahn, L. R .: Pulp and Its Influence on Dental Decay, D. Cosmos, to be published. 14. Blackberg, S. N., and Berke, J. D.: Posteruptive Changes in Teeth of Dogs on Rachitogenic Diets, J. D. Res., 12:695 (Oct.) 1932.
785
of the saliva) to the protective mechanism situated in the dental tissues, primarily in the pulp, explains some puzzling clinical observations: 1. T h e increase of the susceptibility to dental caries in persons during preg nancy or systemic illness in spite of rigor ous oral hygiene. 2. T he fact that unclean teeth do not necessarily decay if the activity of the protective mechanism is normal. 3. U nilateral approximal decay. T his condition, although rare, may be noted occasionally in dental roentgenograms. It is incomprehensible, if we regard dental caries as being due solely to food reten tion, the presence of bacteria or even to changes in the saliva, for all these condi tions must affect both closely contacting approximal surfaces. If, on the other hand, we accept the thesis that the alkali reserve of the calcified dental tissues is maintained by the pulp, and further that a pathologic pulp may abstract mineral salts from the dentin and enamel, uni lateral approximal decay is readily ex plained. In this case, systemic conditions are probably not far below normal. T h e pulp in the affected tooth is pathologic (owing possibly to some local irritation) and therefore is decalcifying the dentin and enamel, making this tooth more sus ceptible to attack from without. T h e supposition that the teeth may be affected by some internal mechanism which is in close physiologic connection w ith the body is considered by some to be pure speculation. In answer to this, I shall briefly enumerate the data on which the existence of a protective mech anism is based: 1. T h e odontoblasts of the pulp send dentinal fibrils throughout the dentin which join w ith the organic structures of the enamel rod sheaths .7 2. T h e dentinal fibrils are tubular,
786
T he Journal of the American D ental Association
thus allowing a greater flow of lymph .15 3. A n organic m atrix is present in the enamel. I t is composed of: (a) tufts, ( b ) enamel rod sheaths, (c) lamellae and (d ) enamel cuticle .16 4. T h e dentinal fibrils are seen to pass into the enamel, if the angle of the sec tion is correct.17 5. D entinal fibrils connect w ith (a) tufts, ( b ) sheaths and, occasionally (c) lamellae and (d ) enamel cuticle (histo logic evidence). 6 . T h is entire system of channels pen etrating the dentin and enamel is perme able from w ithin in newly erupted teeth (shown by animal and human experi ments. ) 18 7. T h e dental lymph can be noted w ith a low-powered binocular microscope in newly exposed dentin of noncarious, young, vital teeth. Excavated cavities in carious teeth show very little lymph, as the dentin has become irritated by the decay and its permeability has been greatly reduced .19 T h e presence of a slight amount of lymph is shown by the following com mon clinical observation: when a com pletely excavated cavity in a vital tooth has been dried w ith alcohol and hot air, 15. H anazawa, K anae: Study of Minute Structure of Dentin Especially of Relation Between Dentinal Tubules and Fibrils, D. Cosmos, 59:125 (Feb.) 1917. Bodecker, C.F.: Soft Fiber of Tomes a Tubular Structure, D . Cosmos, 56:1378 (D ec.) 1914; J.N.D.A., 9:281 (A pril) 1922. 16. Bodecker, C. F .: Enamel of Teeth Decalcified by Celloidin D ecalcifying Method, and Examined with Ultra Violet Light, D. Rev., 20:317 (A p ril) 1906. 17. Kato, Seiji: H istological Study of H u man Enamel, D . Cosmos, 7 1 :1139 (D ec.) 1929. 18. Fish, E. W .: A ge Changes in Permea bility of D og’s Enamel, J. Physiol., 72 321326 (July) 1931. 19. Footnotes 2-8.
the dentin takes on a chalky w hite opac ity and a minute or two after desiccation, the dentin turns a translucent yellow. I t appears that only the slowly exuding lymph can be responsible for this change in color. T h e secretion of dental lymph must be greatest during youth, because the odon toblasts are then largest and most active and the dental tissues most permeable. Youth is also the time when the posteruptive calcification of the tooth occurs. F urther, it is the period at which caries is highly active. T his may indicate that the function of the pulp and the permeability of the dental tissues bear some relation to the activity of the disease at this time. Recent data are based on the fact that 1. T h e observations of Blackberg and Berke 14 indicate that the dentin and enamel in rachitic dogs may be decalcified from w ithin by the presence of an abnor mal pulp. Hence, it is possible that the activity of the dental pulp may be harm ful under certain conditions. 2. It has been shown by the elaborate w ork of K arlstrom 20 that enamel varies in hardness. H e observed that this tissue was less hard in the interior than on the surface. Further, he proved that the enamel of matured, erupted teeth was markedly harder than that of newly erupted teeth, particularly in the interior. H e came to the conclusion that the min eral salts for the posteruptive calcification of the enamel originated in the interior and not on the exterior (salivary salts). H e also found that the dental enamel of pregnant women was not so hard as that of the “norm al,” particularly if the con dition were complicated by systemic ill ness or improper diet. 20. Karstrom, S.: ologic Studies of Dental Reference to Question Tandlak.-Tidskr., 1931,
Physiologic and Path Enamel with Special of Vitality, Svensk Sup. 1.
B'ódecker— D ental Caries O n the foregoing data 21 is based the idea that the varying activity of dental caries observed in different individuals is dependent principally on a dysfunction of the pulp and its secretion, the dental lymph. (Secondarily, the chemical con stitution of the saliva may affect the caries susceptibility of the teeth, and influ ence the direction of the flow of lymph. ) An abnormal pulp probably secretes an abnormal dental lym ph; and instead of effecting the posteruptive calcification of the young tooth, it may even cause a décal cification, thus aggravating or even ini tiating dental caries. CO N CLU SION
W hether we regard dental enamel as a vital or a dead tissue in its reaction to dental caries seems to be a m atter of definition. It is perhaps a question of whether the term “vitality” should be applied to a noncellular tissue (enamel) in which apparently metabolic activity occurs through the cellular processes of an enclosed organ (p u lp ). T o me, it seems that the enamel does possess a low 21. Footnotes 1-9.
787
degree of vitality. D o we not consider dentin as vital or not vital, this depend ing on the presence or absence of a live pulp? And yet dentin is an “acellular” tissue, as far as it contains no nucleated cells. T h e entire question revolves around the following: 1. Are newly erupted teeth less highly calcified than m ature ones? 2. Do the mineral salts which effect the posteruptive calcification of the teeth, originate from the blood in the dental pulp? 3. Can fully erupted teeth be harmed by systemic disturbances by way of the pulp? A nd can this explain the varying activity of dental caries in different indi viduals and at different ages? If we answer these questions in the affirmative, and I think some of us can, we must regard the enamel as a tissue closely dependent for its welfare on its physiologic connection w ith the body, particularly during youth. T hus dental caries w ill finally prove to be caused mainly by systemic disturbances. 630 W est 168th Street.
H E fact that the activity of dental caries varies greatly in different per sons has long been observed clinic ally. I t can now be reduced to exact figures by the use of the caries index .1 As an instance, H . H olliday and D . E. Ziskin, of the D epartm ent of O ral D iag nosis of the Columbia University, School of D ental and O ral Surgery, have shown in a group of 406 students of an average age of 17-19, a minimal caries index of 0 and a maximum of 54.375 per cent. Such extreme figures, showing the great differences in the activity of dental caries, can be duplicated in almost any dental practice. T h e thinking members of our profession, as well as the more advanced investigators, realize that food reten tion is not the sole cause of dental caries and consequently that oral hygiene is not the only method of combating this disease; for it is of no avail in prevent ing the progressive destruction of the teeth. O ther means are now being sought to improve the dental condition of pres ent and future generations.
T
*From the laboratory of Dental Histology and Embryology, Columbia University D en tal School. *Read before the Section on Mouth Hygiene and Preventive Dentistry at the SeventyFourth Annual Session of the American Dental Association, Buffalo, N. Y., Sept. 14, 1932. 1. Bodecker, C. F., and Bodecker, H. W . C .: Practical Index of Varying Susceptibility to Dental Caries in Man, D . Cosmos, 73 :707 (July) 1931. Bodecker, C. F .: Calcification of Modified Index of Dental Caries. D . Sur vey, 7:23 (D ec.) 1931.
Jour. A. D. A., May, 1933
T h e beneficial effect of a balanced diet can be rega'rded as definitely proved. But how can diet benefit fully formed teeth if these are considered as having no physiologic connection w ith the body? T h ere is a large group of investigators who, even though they realize th at the teeth are benefited by a well-balanced diet, do not admit a biologic connection w ith the body. T hey believe that the teeth are fully m atured on eruption, and that nothing can affect them for good or ill from the interior. T h e ir explanation of the mechanism of dental caries centers entirely in a change of oral conditions. Variations in the chemical constitution of the saliva through which a defective diet may harm the teeth, are therefore thought to be responsible. H ere again, there is a divergence of opinion. One group believes that an improper diet de velops an abnormality of the saliva; another group that the growth of Bacil lus acidophilus is stimulated by this means. T h e latter theory makes bacteria responsible for the increased activity of dental caries. Still another group be lieves in a combination of these two factors. T h e majority of investigators, as w ell as most of the dental profession, believe a variation of one or all of these factors to be the cause of dental caries. Let us now tu rn to the constitutional or internal factors. Broderick ,2 in his w ork “ D ental M edicine,” presents a great many arguments to the effect that
783
2. Broderick, F. W .: Dental Medicine, St. Louis: C. V. Mosby Company, 1928.
784
The Journal of the American D ental Association
the presence of bacteria and food reten tion around the teeth cannot wholly explain the varying activity of dental caries. H is statements on this subject are so clear and logical that they should convince the open minded. H e believes that the cause of dental caries is to be found in constitutional disturbances, par ticularly acidosis, and that this condition causes an abnormality of the saliva. H e does not entirely preclude the thesis of detrim ental influences affecting the den tal tissues from w ithin. Only a few investigators consider this to be possible. T h e m ajority maintain that no metabolic processes take place in the enamel and that therefore systemic disturbances can not harm the teeth by way of the pulp. T hey do not believe that a mechanism exists by which this could be effected. It is not yet generally adm itted that a fluid can penetrate from the pulp into the enamel, although the existence and per meability of channels leading from the pulp through the dentin and the enamel has been shown by Beust ,3 Fish ,4 Klein and Amberson ,5 Applebaum ,6 by me 7 and by others. T h e reason for this is that mem bers of the dental profession, as w ell as many investigators, are obsessed w ith the idea that erupted teeth need no supply of mineral salts and therefore receive none. Consequently,. they cannot understand 3. Beust, T . B.: Vascular System of Hard Substance of Teeth, D. Rec., 32:660, 1912. 4. Fish E. W .: Circulation of Lymph in Dentin and Enamel, J.A.D.A., 14:804 (M ay) 1927. 5. Klein, Henry, and Amberson, W . R .: Physico-Chemical Study of Structure of Den tal Enamel, J. D. Res., 9:667 (Oct.) 1929. 6. Applebaum, Edmund: Lymph Channels in Dentin and Enamel Stained by Amalgam, J. D. Res., 9:487 (A ug.) 1929. 7. Bodecker, C. F.: Permeability of Enamel in Relation to Stains, J.A.D.A., 1Q:60 (Jan.) 1923.
that general metabolic disturbances may result in a derangement of the secretion of the dental pulp and that thus the den tal tissues may be harmed. Systemic disturbances will probably be shown to harm the teeth by abnormal changes in the dental pulp and mineral salt metabolism. These factors have been discussed at length elsewhere .8 I t is only necessary to mention them here. Sugges tions concerning a dental protective mech anism against decay likewise have been published .9 A brief recapitulation of a certain phase is necessary, as a modifica tion has been made since 1929. T he hypo thesis was then set up that the dental pulp in children and young adults secretes a lymph which permeates the dentin and the enamel. T his fluid was supposed to contain mineral salts which effect the posteruptive calcification of the dentin and enamel and maintain the high buffer power or alkali reserve of these tissues. T h a t these appear to have a high alkali reserve is indicated by the w ork of Karshan ,10 who showed a hydrogen-ion con centration of 7.8, 8.0 for the dentin and 7.3-7 .6 for the enamel. (Blood has a Pb. of 7.35-7.40.) O riginally ,11 it was thought that the dental lymph itself might neutralize oral acids and thus prevent the destruction of the enamel and dentin. Another more recently suggested possibility is that the 8. Bodecker, C. F., and Applebaum, Ed mund: M etabolism of Dentin; Its Relation to Dental Caries and to Treatm ent of Sen sitive Teeth, D. Cosmos, 73:995 (Oct.) 1931. 9. Bodecker, C. F .: N ew Theory of Cause of Dental Caries, D. Cosmos, 71:586 (June) 1929; Lipin Content of Dental T issues in Relation to Decay, J. D. Res., 11:277 (April) 1931. 10. Karshan, M.: Studies of Enamel and Dentin in Relation to Dental Caries, J. D. Res., 12:523 (June) 1932. 11. Footnote 9, first reference.
Bôdecker— D ental Caries lymph maintains the high alkali reserve in the dentin and enamel through a con stant supply of mineral salts (bicarbon ates?). T hus, under normally healthy conditions, dental caries would be pre vented in young persons. However this may be, the pulp and its secretion, the dental lymph, probably aided by a normal saliva (Eckerm ann ,12 Broderick2), ap pear to me to be the principal factors in maintaining the integrity of the teeth. Lester R. C ahn 13 now goes even far ther, believing that under pathologic con ditions, the dental pulp can decalcify the dentin and enamel from the interior, caries resulting in the areas of food reten tion. T h is has been shown to be possible by Blackberg and Berke ,14 who observed in young rachitic pups areas of décalci fication definable only by the roentgen rays, and extending from the pulp to the surface of the tooth. If these observations apply to human teeth, the cause of dental caries w ill be found to inhere, in systemic rather than in environmental conditions. I t appears that the activity of this disease is dependent on bodily conditions. T his does not mean that oral hygiene is unnec essary; for if mouth acid (due to food ferm entation) is the exciting cause of dental caries, the less food that is retained around the teeth (less acid), the less ac tive need be the protective mechanism to combat oral acid and still maintain the teeth intact. T h e close relation of the environmental causes of dental caries (food retention, the presence of bacteria and the condition 12. Eckermann, R .: Dental Caries and Os mosis, 1919. 13. Cahn, L. R .: Pulp and Its Influence on Dental Decay, D. Cosmos, to be published. 14. Blackberg, S. N., and Berke, J. D.: Posteruptive Changes in Teeth of Dogs on Rachitogenic Diets, J. D. Res., 12:695 (Oct.) 1932.
785
of the saliva) to the protective mechanism situated in the dental tissues, primarily in the pulp, explains some puzzling clinical observations: 1. T h e increase of the susceptibility to dental caries in persons during preg nancy or systemic illness in spite of rigor ous oral hygiene. 2. T he fact that unclean teeth do not necessarily decay if the activity of the protective mechanism is normal. 3. U nilateral approximal decay. T his condition, although rare, may be noted occasionally in dental roentgenograms. It is incomprehensible, if we regard dental caries as being due solely to food reten tion, the presence of bacteria or even to changes in the saliva, for all these condi tions must affect both closely contacting approximal surfaces. If, on the other hand, we accept the thesis that the alkali reserve of the calcified dental tissues is maintained by the pulp, and further that a pathologic pulp may abstract mineral salts from the dentin and enamel, uni lateral approximal decay is readily ex plained. In this case, systemic conditions are probably not far below normal. T h e pulp in the affected tooth is pathologic (owing possibly to some local irritation) and therefore is decalcifying the dentin and enamel, making this tooth more sus ceptible to attack from without. T h e supposition that the teeth may be affected by some internal mechanism which is in close physiologic connection w ith the body is considered by some to be pure speculation. In answer to this, I shall briefly enumerate the data on which the existence of a protective mech anism is based: 1. T h e odontoblasts of the pulp send dentinal fibrils throughout the dentin which join w ith the organic structures of the enamel rod sheaths .7 2. T h e dentinal fibrils are tubular,
786
T he Journal of the American D ental Association
thus allowing a greater flow of lymph .15 3. A n organic m atrix is present in the enamel. I t is composed of: (a) tufts, ( b ) enamel rod sheaths, (c) lamellae and (d ) enamel cuticle .16 4. T h e dentinal fibrils are seen to pass into the enamel, if the angle of the sec tion is correct.17 5. D entinal fibrils connect w ith (a) tufts, ( b ) sheaths and, occasionally (c) lamellae and (d ) enamel cuticle (histo logic evidence). 6 . T h is entire system of channels pen etrating the dentin and enamel is perme able from w ithin in newly erupted teeth (shown by animal and human experi ments. ) 18 7. T h e dental lymph can be noted w ith a low-powered binocular microscope in newly exposed dentin of noncarious, young, vital teeth. Excavated cavities in carious teeth show very little lymph, as the dentin has become irritated by the decay and its permeability has been greatly reduced .19 T h e presence of a slight amount of lymph is shown by the following com mon clinical observation: when a com pletely excavated cavity in a vital tooth has been dried w ith alcohol and hot air, 15. H anazawa, K anae: Study of Minute Structure of Dentin Especially of Relation Between Dentinal Tubules and Fibrils, D. Cosmos, 59:125 (Feb.) 1917. Bodecker, C.F.: Soft Fiber of Tomes a Tubular Structure, D . Cosmos, 56:1378 (D ec.) 1914; J.N.D.A., 9:281 (A pril) 1922. 16. Bodecker, C. F .: Enamel of Teeth Decalcified by Celloidin D ecalcifying Method, and Examined with Ultra Violet Light, D. Rev., 20:317 (A p ril) 1906. 17. Kato, Seiji: H istological Study of H u man Enamel, D . Cosmos, 7 1 :1139 (D ec.) 1929. 18. Fish, E. W .: A ge Changes in Permea bility of D og’s Enamel, J. Physiol., 72 321326 (July) 1931. 19. Footnotes 2-8.
the dentin takes on a chalky w hite opac ity and a minute or two after desiccation, the dentin turns a translucent yellow. I t appears that only the slowly exuding lymph can be responsible for this change in color. T h e secretion of dental lymph must be greatest during youth, because the odon toblasts are then largest and most active and the dental tissues most permeable. Youth is also the time when the posteruptive calcification of the tooth occurs. F urther, it is the period at which caries is highly active. T his may indicate that the function of the pulp and the permeability of the dental tissues bear some relation to the activity of the disease at this time. Recent data are based on the fact that 1. T h e observations of Blackberg and Berke 14 indicate that the dentin and enamel in rachitic dogs may be decalcified from w ithin by the presence of an abnor mal pulp. Hence, it is possible that the activity of the dental pulp may be harm ful under certain conditions. 2. It has been shown by the elaborate w ork of K arlstrom 20 that enamel varies in hardness. H e observed that this tissue was less hard in the interior than on the surface. Further, he proved that the enamel of matured, erupted teeth was markedly harder than that of newly erupted teeth, particularly in the interior. H e came to the conclusion that the min eral salts for the posteruptive calcification of the enamel originated in the interior and not on the exterior (salivary salts). H e also found that the dental enamel of pregnant women was not so hard as that of the “norm al,” particularly if the con dition were complicated by systemic ill ness or improper diet. 20. Karstrom, S.: ologic Studies of Dental Reference to Question Tandlak.-Tidskr., 1931,
Physiologic and Path Enamel with Special of Vitality, Svensk Sup. 1.
B'ódecker— D ental Caries O n the foregoing data 21 is based the idea that the varying activity of dental caries observed in different individuals is dependent principally on a dysfunction of the pulp and its secretion, the dental lymph. (Secondarily, the chemical con stitution of the saliva may affect the caries susceptibility of the teeth, and influ ence the direction of the flow of lymph. ) An abnormal pulp probably secretes an abnormal dental lym ph; and instead of effecting the posteruptive calcification of the young tooth, it may even cause a décal cification, thus aggravating or even ini tiating dental caries. CO N CLU SION
W hether we regard dental enamel as a vital or a dead tissue in its reaction to dental caries seems to be a m atter of definition. It is perhaps a question of whether the term “vitality” should be applied to a noncellular tissue (enamel) in which apparently metabolic activity occurs through the cellular processes of an enclosed organ (p u lp ). T o me, it seems that the enamel does possess a low 21. Footnotes 1-9.
787
degree of vitality. D o we not consider dentin as vital or not vital, this depend ing on the presence or absence of a live pulp? And yet dentin is an “acellular” tissue, as far as it contains no nucleated cells. T h e entire question revolves around the following: 1. Are newly erupted teeth less highly calcified than m ature ones? 2. Do the mineral salts which effect the posteruptive calcification of the teeth, originate from the blood in the dental pulp? 3. Can fully erupted teeth be harmed by systemic disturbances by way of the pulp? A nd can this explain the varying activity of dental caries in different indi viduals and at different ages? If we answer these questions in the affirmative, and I think some of us can, we must regard the enamel as a tissue closely dependent for its welfare on its physiologic connection w ith the body, particularly during youth. T hus dental caries w ill finally prove to be caused mainly by systemic disturbances. 630 W est 168th Street.