Structural and Mechanical Factors

A British Conception of Caries Prevention

Nutritional and Other Causes of Dental Disease is Discussed by

J. D. King, Ph. D., D.P.D., L.D.S. in




Since 1932, Dr. J. D. King has been associated with Mrs. M. Mellanby, with a whole-time grant from the Medical Research Council, London. He has had the opportunity of examining all of Mrs. Mellanby’s experimental and clinical material, in addition to his own investigations of experimental caries and periodontal disease, nerve lesions, etc., with special reference to physical as well as nutritional factors on the diet.

Dr. King is a licentiate in Dental Surgery, Royal College of Surgeons, England, 1929. He has a diploma in Public Dentistry, University of St. Andrews, 1932. He received his Doctor of Philosophy degree from the University of Sheffield, 1935.

Dr. King has written numerous articles appearing in the following publications, in addition to many unpublished lectures before various dental societies.

Publications:–Brit. Dent. Journ., 56:538; Ibid., 57:233; Dent. Record, 55: 522; Brit. Dent. Journ., 59:233 & 305; Journ. Physiol., in press; Dent. Cosmos, in press.


                Modern theories of the etiology of dental caries are generally based upon the assumption that the health of the body as a whole to a large extent determines immunity or susceptibility to the disease. Such views were set upon a scientific basis by the experimental and clinical investigations of M. Mellanby (1918-34), and as a result our conception of the carious process has changed in many respects.

At the present time, the relationship of nutritional factors to lesion of the teeth and their supporting structures is being intensively studied in all parts of the world, and, although different opinions may be held as to the manner in which our diets affect the well-being of the teeth, it is generally agreed that certain food elements exert a beneficial effect upon these organs.


Volume 11, October, 1936.



Structure and Caries


M. Mellanby believes that defective tooth structure is largely responsible for the high incidence of dental caries in civilized communities, and that both conditions are directly related to specific nutritional factors. It was shown (Mellanby, 1918) that in experimental animals Vitamin D was of great importance in the formation of the calcified dental tissues, especially during the period of development. Ad deficiency of this vitamin resulted in poorly calcified enamel and dentine containing a large number of interglobular spaces.

These findings assumed a practical significance when it was observed that the majority of the teeth of civilized man were hypoplastic and, indeed, the structural defects were largely comparable to those associated with Vitamin D deficiency in experimental animals. Up to that time the incidence of hypoplasia had been assessed at about 3 per cent in the deciduous dentition, bur the less severe grades of the condition has been overlooked, only the very obvious pitting and loss of enamel being included under this heading.

M. Mellanby, however, by a critical examination of the surface enamel of a large number of human teeth—shed, extracted and in the mouth—by means of a probe and lens, observed that some teeth were much rougher than others, although on casual examination their naked-eye appearance in the mouth did not differ appreciably. Microscopic examination of such teeth demonstrated that the roughness (“surface texture”) of the enamel was associated with defective calcification of the enamel and dentine, and, conversely, the smoother the surface the better the histological structure.

Hypoplasia Predisposes to Caries

Furthermore, Mellanby noted that the worse the hypoplasia, judge by the surface texture and the calcification, the more susceptible was the tooth to decay, while smooth well-calcified teeth, which were in the minority, were relatively immune to the disease. For instance, of 1500 sectioned deciduous teeth, 78 per cent with well-calcified tissues were free from caries, as compared with only 6 per cent of the very hypoplastic, while 7.5 per cent of the former and 74 per cent of the latter had extensive disease.

As a result of these observations, it was considered probable that by improving the calcifying properties of the diet, (1) better formed teeth would be developed which would tend to resist the carious process, and (2) the resistance of teeth already formed before the special dieting might be increased, since in dogs it had been found that the amount and quality of secondary dentin laid down by the pulp in response to peripheral injury also largely depended upon the amount of Vitamin D available.

The results of the controlled dietary investigations in Sheffield (1924-32) and Birmingham (1928-35) have now been published. It is sufficient here to say that the addition of Vitamin D or Vitamin D-containing foods to the diets of institutional children markedly reduced the incidence of caries and also checked or arrested the disease in teeth which were affected before the Vitamin addition was made.

Apart from the influence of Vitamin D upon the teeth, the calcium and phosphorus content of the diet are of course important. M. Mellanby found, however, that when sufficient Vitamin D was included in the food of experimental animals, these minerals were of much less significance than when the Vitamin was deficient. Finally, it was observed that cereals, particularly oatmeal, possessed anti-calcifying properties which could only be counter-acted by abundant supplies of the Vitamin. In the Sheffield investigations, reduction of the quantity of cereals consumed, as well as the addition of Vitamin D, still further increased the resistance of the teeth to decay (Mellanby and Pattison, 1924).

While confirmation has been obtained from many sources of the beneficialeffects of adequate nutrition in the prevention and control of dental caries (Boyd and Drain, 1928, 1929; McKeag, 1930; Bunting, 1931; McBeath, 1932; Price, 1934; Sprawson, 1934; Anderson et al., 1934, and others), the interpretation of such results in terms of improved tooth structure and tooth resistance has not been generally accepted, and, indeed, has been subjected to much criticism.

Correction of the Ca: P ratio and pH of the blood and saliva, reduction of the acid-forming bacteria in the oral cavity, and improvement of mouth hygiene have all at one time or another been  put forward to account for the reduction of caries by nutritional means. It is not the purpose of this paper to consider these theories, but rather to confine the discussion mainly to a consideration of the significance of the structural and mechanical factors in the caries syndrome.

Food Fermentation as the Exciting Cause of Caries

In 1890 Miller described a series of experiments in which he demonstrated that test-tube mixtures of bread, etc., and saliva fermented on incubation with the production of acids. A tooth immerse in such mixtures became decalcified and its tissues assumed an appearance similar to that seen in the human carious process. On this basis it was considered that dental caries in man was initiated by chemico-parasitic decalcification of the enamel, due to the fermentation of carbohydrate food debris retained about the teeth. This conception of the exciting factors in the etiology of the disease was whole-heartedly accepted by the dental accepted by the dental and medical professions, and as a result caries prophylaxis has largely consisted of measures designed to promote better cleanliness of the mouth and teeth by natural or by artificial means.

Natural and Artificial Caries

It must, however, be remembered that certain important differences exist between “test-tube caries” and the disease as seen clinically. The former is characterized by a simple decalcification and invasion of the dental tissues by bacteria and their products. In the mouth, on the other hand, the teeth are capable of defending themselves and arrest of the carious process may occur.

Such defensive reactions are associated with hypercalcified zones in the enamel (Mummery, 1922; Sprawson, 1930; Applebaum, 1935) and in the dentin (Tomes, 1848) and by deposits of secondary dentin at the pulp margin. The protection afforded by such means varies, but it seems probable that it is largely dependent upon the calcifying properties of the diet taken during the period of its formation, as indicated by the experimental and clinical investigations of M. Mellanby (1930, 1934).

The formation of so-called self-cleansing cavities, due to the breaking away of overhanging margins of carious enamel, may, by eliminating areas of food stagnation, contribute to arrest of the disease in its later stages. The work of Jeffrey (1932) and Thewlis (1932-36) also indicates that the composition of the enamel—especially at its periphery—may affect the potential resistance of a tooth to caries, but whether this is due to the degree of calcification or, as Gottlieb (1921) and Bibby and Van Huysen (1933) suggest, to the content of keratin-like-material, is as yet uncertain.

Experimental Caries in Animals

In 1922, McCollum, Simmonds, Kinney and Grieves noted lesions resembling dental caries in the molar teeth of some of the rats in their laboratory. As a result of this observation, much attention has been paid by research workers to the production and prevention of caries in these animals. At first the cause of the lesions was attributed to the fermentability of the carbohydrates in the diets employed (Shibata, 1929), or to the Vitamin D and mineral content of the rations (Klein and McCollum, 1931; Agnew, Agnew and Tisdall, 1933).

Hoppert, Webber and Canniff (1932), on the other hand, claimed that the size and hardness of the food particles was the dominating factor in the etiology of the disease, and this has now been amply confirmed (Rosebury, Karshan and Foley, 1933-34; Bibby and Sedwick, 1933; King, 1935; and others). Rosebury and his co-workers demonstrated the occurrence of two types of lesions, in the tooth cusps and in the fissures.

Bibby and Sedwick showed that cusp lesions were due to fracture by hard, coarse-particled food, this being facilitated by the pronounced forward inclination of the cusps of the lower molar teeth; further, they observed that the upper teeth were singularly free from such defects, irrespective of the physical or chemical qualities of the diet, and associated this immunity with the absence of such marked cusp inclination in the upper jaw.

Concurrently with other investigations, since 1932 the present writer has been studying the problem of experimental “caries” in rats, in the hope that some information might be obtained which would assist in the elucidation of the cause of the disease in man. A preliminary report of the experimental findings has already been published (King, 1935) and it is sufficient here to give a very brief description of the principal results and conclusions so far obtained.

The findings indicated that both cusps and fissure lesions in the molar teeth of rats are initiated by mechanical means, such conditions being dependent upon the size and hardness of the food particles and the morphological characteristics of the teeth. When the animals are given diets containing a preponderance of hard coarse-particled food, a high incidence of caries-like lesions is observed in the lower jaw after 2-6 months.

The cusp lesions originate as fractures of the enamel in those regions where the cusp inclination is most marked—that is, where the brittle enamel is insufficiently supported by the more elastic dentin. Fissure lesions are also caused by enamel fracture, but in this instance the injury is due to the forcible wedging of hard coarse food into the deep and narrow fissures of the lower teeth; as a result the walls of the fissures are levered apart and splits are produced in the enamel at their base, where the disruptive stresses exert their greatest effect. The upper teeth are relatively immune to both types of the disease, presumably because neither the inclination of their cusps no the depth of their fissures is sufficiently pronounced.

If, on the other hand, rats are given food in a finely-divided state, irrespective of its chemical composition, for as long as 15 months or more, their molar teeth remain free from “caries.” The stagnation of food debris about the teeth  and decalcification and invasion of the dental tissues by bacteria and their products appear to play little or no part in the initial stages of the disease, but, if the dentin be exposed to these agencies by traumatic injury of the enamel, then phenomena resembling those characteristics of the carious process in man are observed.

Hoppert, Webber and Canniff (1932) have stated that the vitamin and mineral content of the diet has no effect upon the susceptibility of the rat’s teeth to “caries.” Rosebury, Karshan and Foley (1934), however, believe that the Vitamin D-calcium-phosphorus complex in some way retards, though does not prevent, the occurrence of the lesions.

In some preliminary experiments the present writer has noted that defective tooth structure may facilitate the “carious” process in rats, as might be expected from the mechanical nature of its etiology. The crowns of the molar teeth of these animals are formed before weaning, so that variations in their developmental structure are controlled by the nutrition of their parents. When the parents are given rations deficient in Vitamin D, the teeth of the offspring are defectively calcified and may become diseased even when their diets are composed of relatively soft and finely-divided food.

The Possible Relationship of the Experimental Lesions to Dental Caries in Man

The question now arises as to whether the lesions produced in the molar teeth of rats are comparable to dental caries in man. It is generally believed that the earliest stage of the human carious process is a disintegration of the tooth surface by the acid products of food fermentation in the mouth. In the rat, on the other hand, mechanical injury of the teeth appears to precede decalcification and, indeed. It would seem that the latter does not occur unless fractures or cracks in the enamel are present. At first sight, therefore, the initial stage of the disease in rats appears to differ from that in man.

The work of Malleson (1925), however, strongly suggests that in man also traumatic injury of the teeth plays an important predisposing role in the etiology of caries. This worker clearly demonstrated the existence of enamel cracks in large numbers in human teeth, and it was his opinion that in those regions where food stagnation and caries were common—as, for example, in deep fissures and on the approximal surfaces of the teeth—the presence of such cracks was a significant factor in caries susceptibility.



Many Causes For Defects

As to origin of these defects, Malleson considered that some may be developmental and others may occur after tooth eruption, due possibly to the unresistant nature of the enamel surrounding the highly organic and elastic dentin, or to traumatism in the process of mastication.

It will be seen, therefore, that the fundamental differences in the etiology of experimental “caries” in rats and the human disease may, perhaps, be more apparent than real. It is true that the human diet seldom contains a preponderance of food-particles as coarse and hard as those which were found to cause the rat lesions. On the analogy, however, of the experiments in which rats with defectively calcified teeth succumbed to the disease when the food-particles were relatively soft, it seems possible that the teeth of “civilized” man, the majority of which are structurally defective (M. Mellanby, 1934), may also become injured—though perhaps to a less extent—during the mastication even of the soft food—stuff of the modern dietary.

Moreover, it should be noted that the most frequent sites of origin of the disease in the rat and in man show striking similarities. In the rat, the lesions occur in those parts of the cusps which are insufficiently supported by dentin and in the base of deep fissures. In man, too, deep pits and fissures are very susceptible, as are also the approximal contact points of the cusps and at the bucco-cervical margin where, owing to the convexity of the tooth surface, the dentin gives less support to the more brittle enamel; actual fracture of the tooth cusps does not, of course, occur in man, but the enamel cracks demonstrated by Malleson (1925) may be regarded merely as injuries of a lesser grade.

Maddern (1930), from a study of the forces of occlusion, as judged by the position and extent of attrition facets, in relation to the morefrequent sites of caries, comes to the conclusion that in man the disease is primarily caused by the action of unevenly distributed mechanical stresses upon the teeth. He believes that such stresses result in a splitting of the outer border of the dentin, thus facilitating fracture on the enamel and, finally, invasion of the tissues by micro-organisms.

He claims that the comparative immunity of the permanent lower incisors is due to the slender nature of the surrounding alveolar bone, so that, instead of work being done on the teeth, the application of force results in movement of the alveolus itself. Further, he argues that this conception would account for the susceptibility of the lower incisors to periodontal disease and that the apparent antagonism between the latter and caries may be explained along similar lines.

It is well-known that the crowns of the teeth of those primitive peoples who are comparatively immune to caries become rapidly worn down during mastication. Such attrition, however, in marked contrast to the small attrition facetson the teeth of modern man, is relatively evenly distributed over the whole of the occlusal surface of all the teeth, so that no one part of the denture is subjected to much more stress than another.

It is interesting here to note that attrition is normally a marked feature of the teeth of rats, but in itself does not lead to “caries”; if, on the other hand, the forces of mastication are concentrated on some particular area of the crown instead of being distributed over the whole occlusal surface, then the dental tissues give way under such mechanical stress and “caries” results.

Local and Systemic Factors Cause Dental Disease

Other investigators, such as Stillman and McCall (1930), while contending that “traumatic occlusion” plays and important part in both caries and periodontal disease believe that the diseases are brought about by the resultant interference with the circulation of blood in the dental pulps and gingivae. Some of the factors influencing the occlusion of the teeth of experimental animals have been described in a previous publication (King, 1936).


The author has suggested that mechanical injury of the teeth may be an important factor in the initiation of dental caries, not only in rats, but also in man. The evidence in favor of this hypothesis is as yet inconclusive, but, on the other hand, the production of “test-tube caries” or the results of clinical and other investigations have by no means proved that chemico-parasitic decalcification of the enamel is the initial stage in the disease process.

In caries of the tooth fissures, there would appear to be no doubt that the depth of the fissures to a large extent determines their liability to decay. This, it is believed, may in the first place be due to the powerful disruptive forces in these regions rather than to the retention of food debris.

Bossert (1933) by measuring the angle of the mesio-occlusal valley in stone models of one hundred human upper molars, found that the steeper the walls of the pits and fissures the more susceptible were the teeth to decay, while the shallower the depressions the more immune were the teeth. Further, M. Mellanby (1934) observed not only that dental hypoplasia was an important factor in caries susceptibility, but also that the floor of the depressions between cusps of well-calcified molars was more rounded and less deep than those of the abnormal or hypoplastic.

It is usually stated that approximal cusp caries is caused by the trapping and subsequent fermentation of food between the teeth, but, again the morphology of the teeth of mans is such that mechanical injury of the enamel at the contact points may occur owing to deficient support from the more elastic dentin beneath. When the disease attacks the cusps, however, it is possible that the compressive, shear and tensile stresses described by Maddern (1930) may be the more important factors. His suggested explanation of the relative immunity of the permanent lower incisors is worthy of further investigation, although here, too, the shape of the teeth—that is, the “non-bublous” nature of the mesial and distal surfaces—may be concerned.

It has been argued that where caries attacks a tooth almost immediately after eruption, and therefore traumatism in the mouth would be expected, the disease could not have been due to mechanical agencies; but, as Maddern has remarked, in certain cases the forces encountered even before or during eruption may also be injurious.

If, then, mechanical factors are involved in the production of carious lesions in man, it becomes obvious that the high incidence of structural defects found by M. Mellanby (1934) must assumegreat significance in the etiology of the disease, and the relationship between tooth structure and caries susceptibility becomes more readily understood.

The suggestions put forward in this paper are necessarily of a tentative nature and depend in part upon the relationship of experimental “caries” to the carious process in man. It is believed, however, that a still closer knowledge (1) of the disease in experimental animals; (2) of the factors which control tooth development; (3) of the chemical composition and histology of the enamel periphery, where caries, as we know it, is first observed; and (4) of the reaction of the enamel to physical as well as bacterio-chemical agencies, would provide further valuable data for the control and prevention of this widespread affliction.

At the present time, however, it would seem that our best means of controlling the incidence and spread of dental caries is by ensuring the formation of well-calcified teeth in proper occlusion—that is, by including in the diet a liberal supply of fat-soluble vitamins and mineral salts, especially during the period of development of the teeth and jaws.



  1. Agnew, M.C., Agnew, R.G., and Tisdall, F.F. (1933), J. Amer. Dent. Assoc., 20:193.
  2. Anderson, P.G., Williams, C.H.M., Halderson, Armer, Dent. Assoc., 21:1349.
  3. Applebaum, E. (1935), Dent. Cosmos, 77:931.
  4. Bibby, B.G., and Sedwick, H.J. (1933), J. Dent. Res., 13:429.
  5. Bibby, B.G., and Van Huysen, G. (1933), J. Amer. Dent. Assoc., 20:828.
  6. Bossert, W.A. (1933), J. Dent. Res., 13:125.
  7. Boyd, J.D., and Drain, C.L. (1928), J. Amer. Med. Assoc., 90:1867.
  8. Boyd, J.D., Drain, C.L., and Nelson, M.V. (1929), Amer, J. Dis. Child., 38L721.
  9. Bunting, R.W. (1931), J. Amer. Dent. Assoc., 18:785.
  10. Gottlieb, B. (1921), Zeitschr. f. Stomatol., 19:129.
  11. Hoppert, C.G., Webber, P.A., and Canniff, T.L. (1932), J. Dent. Res., 12:161.
  12. Jeffrey, G.E.S. (1932), Brit. Dent. J., 53:65.
  13. King, J.D. (1935), Brit. Dent. J., 59:233 and 305. — (1936), J. Physiol. (in press).
  14. Klein, H., and McCollum, E.V. (1931), J. Dent. Res., 11:745.
  15. Maddern, C.B. (1930), Dent. J. of Austral., 2:504.
  16. Malleson, H.C. (1924), Brit. Dent. J., 45:601. – (1925), Ibid., 46:907.
  17. McBeath, E.C. (1932), J. Dent. Res., 12:723.
  18. McCollum, E.V., Simmonds, N., Kinney, E.M., and Grieves, C.J. (1922), Bull. Johns Hopkins Hosp., 33:202.
  19. McKeag, R.H. (1930), Brit. Dent. J., 51:281.
  20. Mellanby, M. (1918), Lancet, 2:767. – (1923), Proc. Roy. Soc. Med. (Sect. Odont.), 16:74.

—- (1927), Brit. Dent. J., 48:1481.

—- (1929), Sp. Rep. Ser. Med. Res. Coun. London, No. 140.

—- (1930), Ibid., No. 153.

—- (1934), Ibid., No. 191.

  1. Mellanby, M., and King, J.D. (1934), Brit. Dent. J., 56:538.
  2. Mellanby, M., and Pattison, C.L. (1924), Brit. Med. J., ii:354.

—- (1926), Brit. Dent. J., 47:1045.

—- (1932), Brit, Med. J., i:507.

  1. Miller, W.D. (1890), Micro-organisms of the Human Mouth.
  2. Mummery, J.H. (1922), Sp. Rep. Ser. Med. Res. Coun., London, No. 70.
  3. Price, W.A. (1934), Dent. Comos, 76:871.
  4. Rosebury, T., Karshan, M., and Foley, G. (1933), J. Dent. Res., 13:379.

—- (1934), J. Amer. Dent. Assoc., 21:1599.

  1. Shibata, M. (1929), Japanese J. Exper. Med., 7:247.
  2. Sprawson, E.C. (1930), Proc. Roy. Soc., B, 106:376.

—- (1934), Brit. Dent. J., 56:125.

  1. Stillman, P.R., and McCall, J. O. (1930), J. Dent. Res., 10:255.
  2. Thewlis, J. (1932), Brit. Dent. J., 53:655.

—- (1934), Ibid., 57:457>

—- (1936), Brit. J. Radio1., 9: New Series, No. 101 (May).

  1. Tomes, J. (1848), A Course of Lectures on Dental Physiology and Surgery, London, p. 103.