- Email: [email protected]
Diet, nutrition and dental caries—A review
DIET, NUTRIHON AND DENTAL CARIES-A REVIEW By J. N. S W A L L O W . a.D.s. Lecturer in Children's Denlistr)' The London Hospital, Lond(m, E, 1, DENTAL carie~ is a disease that is affecting more individuals ever)" )'ear. 1"o quote from the report of the, Medical Officer of Health for Northumberland, 1959, in five year old children in 1948 the average number of aff~ted tc'eth per child was 4.3, in 1953 5.6 and in 1958 6,5. These figures are very similar to those reported by James and Parfitt (1954) who are observing London children, and Slack (1960) children in Liverpool. It is significant that tt~is increase does not produce the effect that a similar increase in the number ~f new cases of poliomyelitis or lung cancer would. The reason for this is that dental caries rarely is a direc~t cause of death, *~erious di~biIity of disfigurement. and like many chronic diseases is difficult to assess the effect it has on the well-being of the individual, it is significant too that dental di.~ase primarily affects civilised communities and that in these communities the demand for dental care and preventive medicine is greatest. Whilst the treatment of ~this disease is the responsib.~Jity of the dental surgeon, prevention is, in our present state of knowledge, primarily the responsibility of the individual, Therefore, it is the duty of the medical pre'~ssion, doctors, dentists, and nurses, to disseminate the knowledge required for prevention to be practicable.' THE
AI~TIOLOGY
O1'
DHNTAL
CARIES
In this modern world in which our knowledge of disease processes has increased by leaps and bounds, it may at first appear strange that there should still be some doubt as to the aetiology of what is apparently a simple problem, Dental caries like cancer is multifac[orial and the search for a single agent that is solely responsible for the disease process has hampered dental rese.arch for many years. The experimental work of Orland and co-workers (1954) ha~ verified that dental caries is the result of bacierial attack upon the teeth. They found that those animals which were reared in completely germ frec conditiotls did not develop the disease whilst similar animals with normal bacterial flora did. Nm only are bacteria necessary, but a b o a medium or substrate. Kite, Shaw and Sognnaes (1950) fed rats through a stomach tube a cariogenic diet, These animals developed no caries whils! the control animals fed the same diet by the normal route produced typical caries. S~eral theori~ t-uavc been advanced as to the mode of the bacterial attack. The acidogenic theory :of Miller (! 890) is one which to this day is accepted with modification by most re, earth workers. 443
#,44
PUIILIC
HEALTH
VOL
LXXIV
NO, 12
Basically it is sugg~t¢~l that acidogcnio bacteria act upon a substra~ to form acid which dissolves away the inorganic part of the enameL This breakdown occurs within a semipermeable "mcmbrane" called the dental plaque which adheres to the tooth surface in areas of stagnation. This plaque is formed by the deposition of protein constituents of the saliva and aggregation of microorganisms. The protcolytic theories depcnd upon the acc~tance that the initial lcsion is in the organic matrix, whilst tim chelation theory of Schatz (1957/) claims that certain oral bacteria produce chelating agents which remove the inorganic constituents of the enamel. The uncertainty of the mode of the initial attack does not prevent us from assessing caries from four view points : (1) the composition of the tooth, (2) the substrate, (3) the bacterial enzyme system, (4) the bacteria. It is intended in discussing the relationship of diet and nutrition and dcntal caries to consider only the first two factors, the tooth structure and the substrate. It should be mentioned that research work is at present going on to ncutralise the bacterial enzyme systems on the t~th surfaces without affecting the vital systems in the rest of the alimentary tract. It is possible that a simple answer to the problem :nay be found here. Attempts to control the oral bacteria, by the use, of.antiseptic mouthwashes and antibiotic tooth-pastes have becn tried, but without success. NUTRITION
AND
DENTAL
CARIES
Nutrition is the process by which the body assimilates and uses food, and attempts have been made to correlate structuraldefects in the teeth,nutritional deficiencies and dental caries. Most of this work has been performed upon animals, and in particular the rat, which, has been shown to have a similar caries process to that found in man. In this field,experimental methods are extremely oomplt~x as the increase of one dietary factor may result in the redla~tion of the intake of another. It is particularly easy to assume that the tinctwas responsible for the effect observvd rather than the second. Nutritional deficiencies then have been producxxl in these animals, and the effects of increasing various constituents of the diet during tooth developmerit studied firstlyfor structural changes and secondly changes in resistance to caries. The results obtained so far in the:~variation of protein intake during tooth development indicates a change in tooth morphology, Holloway (1960). This change in morphology is within the genetic lirnitations of the individual tooth and not due to an effect upon the gen~ the.mselves,
DIET,
NUTRITION
AND
DENTAL
CAR|ES--~
RE'~'IEW
44~
Fat variation during tooth development l~s not been fully investigated, but on the other hand the results of carbohydrate intake have been studied by many. This is to be expected as the rote of carbohydrates in the aetiology of caries has been accepted by workers for many years. Sognnaes (1948) felt that the ingestion of sucrose during the formati,~. period of the teeth affected the subsequent caries experience of these teeth. Later, in 1954 he reported that the addition of ashed food to the high sucrose diets produced a dead-eased amount of decay in the offspring. From this, it wa.~ suggested that the increase of caries found in animals fed on the refined diet could be due to the lack of some important unknow~a constituent of the diet. Steinman and Haley 0957) reported the results of the addition of carbo. hydrates to rats during the development of the molar teeth. They concluded that carbohydrates given during the calcification ot the teeth increased their caries susceptibility, that sucrose caused the greatest increase, and lactose the least. The importance of this woxk will be discussed later. The vi~min deficiencies have been stu~ed in great detail since the pioneer work of Mellanby (1928). To summarise the results obtained, it would appear that adequate vitamin intake d~Lring tooth development is essential for the proper formation of the teeth, but it would be dangerous to claim that a specific vitamin deficiency is solely responsible for susceptibility to decay. The ass~ation between poor enamel structure (hypoplasia) and caries reported by MeUanby (1934), and others has been contradicted by Staz (1934). Day (1944) doubted the evidence that the incidence of caries is reduced by an adequate intake of vitamin D'during tooth development claimed by Mellanby (1934) and others. Hartles and Slack (1959) staled that there was no direct evidence to support the view that hypoplasia was necessarily due to a deficiency of vitamin D or that adequate vitamin Dper se would prevent hypoplasia or reduce the incidence of dental c.¢a'ies. The confusion t ~ t surrounds this subject is due in ~ome part to the lack of precise knowledge as t o the actual mechanism of calcification, and the role of vitamin D in this process. For example, the rachitic children studied by Day may have had an adequate supply of vitamin D, although certainly a low calcium intake. The nutritional effects of minerals have been studied exten~vely since the discovery of the caries reducing power of fluorine. Sobel and Hanok (1948) showed that the variation of calcium and phosphorous in the diet resulted in variation of the composition of the teeth being formed. Kruger (I958) in Australia studied the effects of trace elements during ,tooth de¥~opment in rats, and ~he found that .fluorine produced the greatest reduction-i~ caries, but also that other dements produced signifier reductions, Many other, trace elements have beea stuch'ed; for example, Adler (1957) reported that minute quantities of molybdenum in water reduced the carie~ incid~ce,
446
PUBLIC
HEALTH
VOL
LXXIV
NO. 12
To return to the effects of fluorine, the actual method by which promotion is conferred is still debatable. Brudevold (1959) thinks that the production of the less soluble calcium fluor-apatite i s the main factor. Jenkins (1959) thinks that the effect is due to the fluorine released by acid attack acting as an enzyme inhibitor preventing further acid production and subsequent tooth destruction. Whatever the mode, it can be stated that the ingestion of the fluoride ion during tooth development provides a high degree of protection against the caries process. Thisprotection is gainedno matter what the original source of the fluoride i o n ; b e it naturally occurring or added to the domestic water supply. To summarise the evidence so far presented, it would appear that various deficiencies or excess of nutritional agents produce changes in the ability of the looth to withstand decay. Of these factors, the fluoride ion is of proven ~value in man, but others may well be shown to be .important at a later date, Hartles and Slack (I 959). Steinm a n and Hale)' (195"/) suggest that the high ;intake of sucrose during tooth development byAmerican children might play an important part in increasing their susceptibility, They thought too that the carbohydrate content of prepared milk feeds ~might be important because the calorific value of these feeds is increased by the addition ef sucrose whilst in human milk the sugar content is mainly lactose. LOCAL
FACTORS
]N
DENTAL.
CARIES
The formation of a bacterial substrate has long been associated with carbohydrates and in i~articuiar the fermentable short chain sugars. Research workers in both the human and animal fields have examined the factors which influence the behaviour of carbohydrates in the oral cavity. Gustafsson (1954) in the classic Vipeholm study produced:conclusive evidence that refined carbohydrates in the form of caramels produced an increase in dental caries proportional to the amount taken. The M.R.C. Report (I 955) indicated that by increasing the sucrose content of the diet, a t meal,times only, to a level considerably in excess of the average pre-war consumption, there was not~:a significant increase of the caries rate. This is supported by Mack (1949)whofoundthat an increase of sweets at meal-times did not produce an increase of caries activity: Sullivan and Goldsworthy (!958) in theHopewood House studies produced evidenceIhat children under a strict dietary Control with: !:minimal refined carbohydrates between meals, and a mainly vegetarian diet have minimal dental disease: Cran (1959) studied the teeth o r t he Australian Ab0H~e: and concluded that the~ine~tsed caries incidence was due:to an increcse of refined carbohydrate brought about by their closer contact voth white cavliisatlon, Asin'filareffeethas been reported in the Eskimo. It can be seen that the effect of the carbohydrate then depends on many
DIET,
NUTRITION
AND
DENTAL
CARIES~A
REVIEW
447
factors, the type and quantity of the food, the time and method of ingestion, and the availability for breakdown at the tooth surface. Work by Lundquist (1952) and others indicate that in man the rate of clearance of the sugar from the mouth is most important, and they describe tests to measure this. From the results obtained, attempts have been made to classify foodstuffs as to their rates~ of clearance and sugar availability, the so called caries potential. However, there are many factors which influence this clearance, not the least, being the variations from one person to another, especially the force of chewing, rate of flow and type of saliva, the arrangement of the teeth and the cleansing of the mouth by the tongue and cheeks. Apart from the role of the diet in providing the substrata, other local factors must be considered. 1.
CONSISTENCY
The consistency of the diet has been investigated with regard to dental caries. Slack and Martin (1958) reported the result o f ending a meal with a portion of apple and concluded that the effect on the reduction of caries incidence was encouraging, though it was ffointed o u t that the limitations of the study necessitated caution in the interpretation of the results. They suggested that the action o f the apple is two-fold, firstly stimulating salivary flow, and secondly producing some mechanical cleansing, 2.
THE
ROLE
OF
DIET
SUPPLEMENTS
Recent work by Harris andalso McClure (1959) indicates that tile phosphate of the diet might be a factor in dental caries. The mode of action is unsettled but it may well be an ionic exchange at the tooth surface as is found in the reaction between enamel and topically applied fluoride solutions. Certain foods are taken by modern m a n for no apparent reason but enjoyment, the nutritional value being little, if any. Such products a s fruit drinks have a grave local effect upon the teeth producing, because o f their low pH and high: titratable acidity, decalcification and subsequent caries breakdown, Holloway, Mellanby and Stewart (1958). Sweets, chewing gum, and:similar substances have only slight nutritional value, but their high refined carbohydrate content and the habit of eating them between meals are potent factors i n the production o f caries. PREVENTION
OF
DENTAL
D IETARY
DISEASE
BY
~M E A N S
So f a r a n attempt has been made to reviewthe recent evidence:on the role of nutrition-anddiet in dental caries, The problem that faces us now is to correlate theexpen~entat results, and from them to formulate methods of preventing the disease process. I t i s important to investigate the motivation behind dietary habit, and to
448
PUBLIC
HEALTH
VOL
LXXIV
NO,
12
study methods by which these habits can be adapted to include and to exclude those products which have been shown to be linked with caries. The factors which influence the diet ofan individual are extremely complex. Davidson, Meikeljohn, and Passmore (1959) list the following :--insufficient food production, climatic irregularities, soil erosion, war, ineflicient farming, unequal distribution of food (poverty), lack of kitchen facilities and equipment, lack of leisure, lack of t~nsport, ignorance, and religious customs. From this formidable list, it can be seen that "the prevention of nutritional disorders is to a large extent outside the powers of the medical profession. The only practical method available to us is education. The Committee o n Nutrition (1950)said : " T o persons accustomed to the traditional British diet, certain constituents of this diet may have a psychological importance out of proportion to their value when regarded from a nutrition aspect." Although this statement referred mainly to the effect of food shortages, it is true in general of many of the dietary hat3its which we may wish to alter. During the war, because of food shortage, rationing was a means of'exerting dietary restrictions upon the whole population. One effect of sugar rationing, as studies by Toverud (1949) have shown, w a s a great improvement in the dent/if ~i~ealthof children in several countries. With the end of rationing, the intake of sweets has increased to a level now far higher than before the war. The reasons for this include a rise in the averagc standard of living with an incrcasc of spending money for luxuries, and displacqment activity to relieve tension, boredom, frustration, all under the influence of high powered advertising that affects every 6he today. In as much as dietary habits, good and bad arc developed early in life it would seem that here is an obvious place to introduce any proposed change. Toverud (1948) investigated the effect o f dietary instruction on: dental caries. He advised pregnant~women as to the correct diet for hersdf and unborn child and continued this instruction after ~ e child was born, The results were most impressive and showed a definitclreduction :in the caries incidence over that found in the control. The welfare services then provid~ us with a means of educating the general public at a time when they are particuiarlyprone to suggestion. It is important that th,s work should begin early in!:pregnancy so that the :mother'to-be becomes conscious o f the dietary needs~of her unborn child and herself. ~The value of carbohydrate restrictions fromlthc:weight point of view/is obvi0us to the mother, ibut has: far more i m p a c t i f i t s beneficial effe~: upon thechild, is explained. Slmilarly,~iico'operation in ~ e use of mitk an d l v i ~ i n supplements can be bcstachiev¢~i ~ t h e ~ i l d is reader he primary obj¢ct. Afterbirth. mothersshould be encouragcdto give codIiver oilandorang¢ juice and to breast fc~!!their •babies:i This is~not because i t is believedthat
"natural" fecding:improve~ the s t r ~
and size of the jaws~as Was once
DIET,
NUTRITION
AND
DENTAL
CARIES--A
REVIEW
449
thought, but because from a dental point of view artificialmilk fccds contain a high proportion of sucrose which may well have a delclcriouseffectupon the developing teeth. Advice as to weaning is frequently sought by mothcrs, especially with the first child. They should bc discoura~cd from using fruit cordials, sugar water, or honey on a pacifier.The cffccts of these upon the teeth has been we!I described by James, Parfitt and Faulkncr (1957). In this context it should bc mentioned that the habit of allowing the child to go Io slecp with a bottle of swcctcned milk in itsmouth is not only dangerous from a dental point of view, but also a potential cause of asphyxiation. In the toddler stage, mothers are tempted to give their children sweets to obtain for themselves a few moments respite. At this age a piece of apple or carrot is just as much appreciated and far cheaper. Now, too, the child is subjected to a constant attack with refined carbohydrates by wcll-meanin8 relatives especially grandparents. The mother has to bc particularly tactful in such circumstances, not only then but later when the child goes to school. Here he comes under the influence of others and good dietary habits can bc ruined by unthinking school teachers. One cannot deny that even the perfect child ~411 at times indulge in something that has bccn forbidden at home, and for this reason it is suggested that parents bc advised to provide swccts :at the table to be eaten when the mid-day and evening meals have bcen fmishcd. This will prevent the child from feeling differentwith all the adverse effectsupon its personality and popularity in its socialgroup. In discussing the school lifeof the child some mention has to be made of the increasing number of tuck shops that are to be found even in the primary schools. The provision of refined'carbohydrates between meals not only affcctsthe dental health of the child, but also ruins his appetite for the midday meal. This is a problem that school dentists and the school meal service have in common. The great difficultyis that quite often, these tuck shops are financially extremely profitable,and arc used to supply the school with additional facilitiessuch as film projectors and tape recorders. One can, however, get over this problem by advising the substitution of non-cariogenic foods such as apples. The responsibilityof the school teacher does not end in the provisiom of a scholastic education, In thesedays when most children take school meals, a great deal of dietary teaching fallsinto theirhands. The need for the teachers receiving training in this field is obvious. Some colleges arc including the subject in their curriculum. Howcvcr, thc responsibility for the teaching of the teachers rests for a large part in the hands of the school medical officers and the school dental officers. This requires a great deal of co.operation from the principals of the schools whose help is essential for the introduction of any preventive measures. A briefoutline has been made of the methods of dietary control of dental
450
PUBLIC
HEALTH
VOL
LXXIV
NO.
12
disease. The problem is both complex and serious. It requires the fullest cooperation between doctors and dentists especially those directly concerned with the school child. Acknowledgment is made to Professor G. U Slack, o.n.E., T,D., F.D.S.R.C.S., t>~e. nAcr., for his advice and help in the writing of this paper. REFERENCES A D L~ R, P. (1957). Odont. Revy. 8, 202. B R u D r. v o L t) F I r~ t~. (I959). J. Der~;. Child. 26, I86. C R A ~, J. A. (1959). Austral. dent. J. 4, 182. D A v i O S O ~4, S., M ~ I K E I. J o r s r~, A. P., & P A s s M OR E, R. (1959). "' H u m a n Nutrition and Dietetics," Livingstone, L o n d o n p. 690. D A v, C. D. M. (1944). Brit. dent. J. 76, 115. G u s T ^ F s s o r~, B. E. et aL (1954). Acta odont. Scand. I1, 232. H o L t. o W A ~, P. J., M I~ LI. AN nY M A Y, & STEWART, R. J. C. (1958). Brit. dent.J. 104, 305. .......... . (1960). Personal C o m m u n i c a t i o n . JAMES, P. M, C,, PARF1TT, G. J.~ d~, F A L K N E R FRANK. (1957). Brit. dent. J. 103, 37. ~-.-, & . . . . . , (1957), Ibid. 103, 214. J j~.r~ s: J r~ s, G. N. (1959). Arch. oral BioL 1, 33. K l N o , J. D., M1ELI. ANBY, M., S T O N E s , . H . H . , & G R E E N , H. V. (1955). Spec. Rep. Set. Med. Res. Coun: (Lond.) No~ 288. K I T V., O. W., S H A W, J. H., & S o G N ~r A E S, R. F. (1950). J. Nutrition 42, 89. K It u o r. R, B. J, (I958). Austral dent. J. 3, 236. L u N D O u I s T, C. (1952), Odont, Revy. 33, Suppl. 1. M A c X, P. B. (1959). Soc, Re,¢. in Child Development, 13, 62. M c C t. u ~ i~, F. J., & M u I, I~E g, A. Jx. (1959). 3". dent. Res. 38, 394. M E b L Ar¢ g ~', M, (1928). Brit, dent.J. 49, 769. ----~--.. (1934), @ee. Rep,.Ser. Med. Res. Coun. (Lond.) No. 191. M 1L L ~ rt, W. D. (1890). " T h e Micro-organisms of the H u m a n M o u t h . " Philadelphia, S.S, White Dental Mfg. Co. 0 R L A N D, F. J., etal. (1954). J. dent. Res. 33, 147. Rep, ~ f C o m m . on Nutrit. (1950). Brit. Med. Ass., L o n d o n p. 97. S c H ^ T z, A. (1957). Anna&. Dent. 16, 37. S h ^ c K, G. L, (1960)~ Personal Communication. .... :r:......., & M A r t T I N , W, J. (1958). Brit, dent. J. 105, 366 S oBv. t., A. E., & H A N o g , A. (i948). J. biol. Chem. 176, 1.103. S o o NN A I~ S, R. F. (!948), J, Anwr. dent. Ass. 37, 676. S T ^ a% J. (1934). S, Afr. med.J, i7, 1. S T la I N M A N, R. R., & H A L 1~Y, M. 1. (1957), .I. Dent. Child. 24, 21 !. S U Lt. ~ v AN, H. R., & G o L D S W O P. T tt ",', N, E. (1958). Austral dent. J. 3, 395. T o v I~n U D , G , (I949). Proe~ roy. Sot',/~¢ed.:42, 249. T o V I~R U O, K . V, (1948). Acta paediat. (Uppsala~ 36, 257.
AI~TIOLOGY
O1'
DHNTAL
CARIES
In this modern world in which our knowledge of disease processes has increased by leaps and bounds, it may at first appear strange that there should still be some doubt as to the aetiology of what is apparently a simple problem, Dental caries like cancer is multifac[orial and the search for a single agent that is solely responsible for the disease process has hampered dental rese.arch for many years. The experimental work of Orland and co-workers (1954) ha~ verified that dental caries is the result of bacierial attack upon the teeth. They found that those animals which were reared in completely germ frec conditiotls did not develop the disease whilst similar animals with normal bacterial flora did. Nm only are bacteria necessary, but a b o a medium or substrate. Kite, Shaw and Sognnaes (1950) fed rats through a stomach tube a cariogenic diet, These animals developed no caries whils! the control animals fed the same diet by the normal route produced typical caries. S~eral theori~ t-uavc been advanced as to the mode of the bacterial attack. The acidogenic theory :of Miller (! 890) is one which to this day is accepted with modification by most re, earth workers. 443
#,44
PUIILIC
HEALTH
VOL
LXXIV
NO, 12
Basically it is sugg~t¢~l that acidogcnio bacteria act upon a substra~ to form acid which dissolves away the inorganic part of the enameL This breakdown occurs within a semipermeable "mcmbrane" called the dental plaque which adheres to the tooth surface in areas of stagnation. This plaque is formed by the deposition of protein constituents of the saliva and aggregation of microorganisms. The protcolytic theories depcnd upon the acc~tance that the initial lcsion is in the organic matrix, whilst tim chelation theory of Schatz (1957/) claims that certain oral bacteria produce chelating agents which remove the inorganic constituents of the enamel. The uncertainty of the mode of the initial attack does not prevent us from assessing caries from four view points : (1) the composition of the tooth, (2) the substrate, (3) the bacterial enzyme system, (4) the bacteria. It is intended in discussing the relationship of diet and nutrition and dcntal caries to consider only the first two factors, the tooth structure and the substrate. It should be mentioned that research work is at present going on to ncutralise the bacterial enzyme systems on the t~th surfaces without affecting the vital systems in the rest of the alimentary tract. It is possible that a simple answer to the problem :nay be found here. Attempts to control the oral bacteria, by the use, of.antiseptic mouthwashes and antibiotic tooth-pastes have becn tried, but without success. NUTRITION
AND
DENTAL
CARIES
Nutrition is the process by which the body assimilates and uses food, and attempts have been made to correlate structuraldefects in the teeth,nutritional deficiencies and dental caries. Most of this work has been performed upon animals, and in particular the rat, which, has been shown to have a similar caries process to that found in man. In this field,experimental methods are extremely oomplt~x as the increase of one dietary factor may result in the redla~tion of the intake of another. It is particularly easy to assume that the tinctwas responsible for the effect observvd rather than the second. Nutritional deficiencies then have been producxxl in these animals, and the effects of increasing various constituents of the diet during tooth developmerit studied firstlyfor structural changes and secondly changes in resistance to caries. The results obtained so far in the:~variation of protein intake during tooth development indicates a change in tooth morphology, Holloway (1960). This change in morphology is within the genetic lirnitations of the individual tooth and not due to an effect upon the gen~ the.mselves,
DIET,
NUTRITION
AND
DENTAL
CAR|ES--~
RE'~'IEW
44~
Fat variation during tooth development l~s not been fully investigated, but on the other hand the results of carbohydrate intake have been studied by many. This is to be expected as the rote of carbohydrates in the aetiology of caries has been accepted by workers for many years. Sognnaes (1948) felt that the ingestion of sucrose during the formati,~. period of the teeth affected the subsequent caries experience of these teeth. Later, in 1954 he reported that the addition of ashed food to the high sucrose diets produced a dead-eased amount of decay in the offspring. From this, it wa.~ suggested that the increase of caries found in animals fed on the refined diet could be due to the lack of some important unknow~a constituent of the diet. Steinman and Haley 0957) reported the results of the addition of carbo. hydrates to rats during the development of the molar teeth. They concluded that carbohydrates given during the calcification ot the teeth increased their caries susceptibility, that sucrose caused the greatest increase, and lactose the least. The importance of this woxk will be discussed later. The vi~min deficiencies have been stu~ed in great detail since the pioneer work of Mellanby (1928). To summarise the results obtained, it would appear that adequate vitamin intake d~Lring tooth development is essential for the proper formation of the teeth, but it would be dangerous to claim that a specific vitamin deficiency is solely responsible for susceptibility to decay. The ass~ation between poor enamel structure (hypoplasia) and caries reported by MeUanby (1934), and others has been contradicted by Staz (1934). Day (1944) doubted the evidence that the incidence of caries is reduced by an adequate intake of vitamin D'during tooth development claimed by Mellanby (1934) and others. Hartles and Slack (1959) staled that there was no direct evidence to support the view that hypoplasia was necessarily due to a deficiency of vitamin D or that adequate vitamin Dper se would prevent hypoplasia or reduce the incidence of dental c.¢a'ies. The confusion t ~ t surrounds this subject is due in ~ome part to the lack of precise knowledge as t o the actual mechanism of calcification, and the role of vitamin D in this process. For example, the rachitic children studied by Day may have had an adequate supply of vitamin D, although certainly a low calcium intake. The nutritional effects of minerals have been studied exten~vely since the discovery of the caries reducing power of fluorine. Sobel and Hanok (1948) showed that the variation of calcium and phosphorous in the diet resulted in variation of the composition of the teeth being formed. Kruger (I958) in Australia studied the effects of trace elements during ,tooth de¥~opment in rats, and ~he found that .fluorine produced the greatest reduction-i~ caries, but also that other dements produced signifier reductions, Many other, trace elements have beea stuch'ed; for example, Adler (1957) reported that minute quantities of molybdenum in water reduced the carie~ incid~ce,
446
PUBLIC
HEALTH
VOL
LXXIV
NO. 12
To return to the effects of fluorine, the actual method by which promotion is conferred is still debatable. Brudevold (1959) thinks that the production of the less soluble calcium fluor-apatite i s the main factor. Jenkins (1959) thinks that the effect is due to the fluorine released by acid attack acting as an enzyme inhibitor preventing further acid production and subsequent tooth destruction. Whatever the mode, it can be stated that the ingestion of the fluoride ion during tooth development provides a high degree of protection against the caries process. Thisprotection is gainedno matter what the original source of the fluoride i o n ; b e it naturally occurring or added to the domestic water supply. To summarise the evidence so far presented, it would appear that various deficiencies or excess of nutritional agents produce changes in the ability of the looth to withstand decay. Of these factors, the fluoride ion is of proven ~value in man, but others may well be shown to be .important at a later date, Hartles and Slack (I 959). Steinm a n and Hale)' (195"/) suggest that the high ;intake of sucrose during tooth development byAmerican children might play an important part in increasing their susceptibility, They thought too that the carbohydrate content of prepared milk feeds ~might be important because the calorific value of these feeds is increased by the addition ef sucrose whilst in human milk the sugar content is mainly lactose. LOCAL
FACTORS
]N
DENTAL.
CARIES
The formation of a bacterial substrate has long been associated with carbohydrates and in i~articuiar the fermentable short chain sugars. Research workers in both the human and animal fields have examined the factors which influence the behaviour of carbohydrates in the oral cavity. Gustafsson (1954) in the classic Vipeholm study produced:conclusive evidence that refined carbohydrates in the form of caramels produced an increase in dental caries proportional to the amount taken. The M.R.C. Report (I 955) indicated that by increasing the sucrose content of the diet, a t meal,times only, to a level considerably in excess of the average pre-war consumption, there was not~:a significant increase of the caries rate. This is supported by Mack (1949)whofoundthat an increase of sweets at meal-times did not produce an increase of caries activity: Sullivan and Goldsworthy (!958) in theHopewood House studies produced evidenceIhat children under a strict dietary Control with: !:minimal refined carbohydrates between meals, and a mainly vegetarian diet have minimal dental disease: Cran (1959) studied the teeth o r t he Australian Ab0H~e: and concluded that the~ine~tsed caries incidence was due:to an increcse of refined carbohydrate brought about by their closer contact voth white cavliisatlon, Asin'filareffeethas been reported in the Eskimo. It can be seen that the effect of the carbohydrate then depends on many
DIET,
NUTRITION
AND
DENTAL
CARIES~A
REVIEW
447
factors, the type and quantity of the food, the time and method of ingestion, and the availability for breakdown at the tooth surface. Work by Lundquist (1952) and others indicate that in man the rate of clearance of the sugar from the mouth is most important, and they describe tests to measure this. From the results obtained, attempts have been made to classify foodstuffs as to their rates~ of clearance and sugar availability, the so called caries potential. However, there are many factors which influence this clearance, not the least, being the variations from one person to another, especially the force of chewing, rate of flow and type of saliva, the arrangement of the teeth and the cleansing of the mouth by the tongue and cheeks. Apart from the role of the diet in providing the substrata, other local factors must be considered. 1.
CONSISTENCY
The consistency of the diet has been investigated with regard to dental caries. Slack and Martin (1958) reported the result o f ending a meal with a portion of apple and concluded that the effect on the reduction of caries incidence was encouraging, though it was ffointed o u t that the limitations of the study necessitated caution in the interpretation of the results. They suggested that the action o f the apple is two-fold, firstly stimulating salivary flow, and secondly producing some mechanical cleansing, 2.
THE
ROLE
OF
DIET
SUPPLEMENTS
Recent work by Harris andalso McClure (1959) indicates that tile phosphate of the diet might be a factor in dental caries. The mode of action is unsettled but it may well be an ionic exchange at the tooth surface as is found in the reaction between enamel and topically applied fluoride solutions. Certain foods are taken by modern m a n for no apparent reason but enjoyment, the nutritional value being little, if any. Such products a s fruit drinks have a grave local effect upon the teeth producing, because o f their low pH and high: titratable acidity, decalcification and subsequent caries breakdown, Holloway, Mellanby and Stewart (1958). Sweets, chewing gum, and:similar substances have only slight nutritional value, but their high refined carbohydrate content and the habit of eating them between meals are potent factors i n the production o f caries. PREVENTION
OF
DENTAL
D IETARY
DISEASE
BY
~M E A N S
So f a r a n attempt has been made to reviewthe recent evidence:on the role of nutrition-anddiet in dental caries, The problem that faces us now is to correlate theexpen~entat results, and from them to formulate methods of preventing the disease process. I t i s important to investigate the motivation behind dietary habit, and to
448
PUBLIC
HEALTH
VOL
LXXIV
NO,
12
study methods by which these habits can be adapted to include and to exclude those products which have been shown to be linked with caries. The factors which influence the diet ofan individual are extremely complex. Davidson, Meikeljohn, and Passmore (1959) list the following :--insufficient food production, climatic irregularities, soil erosion, war, ineflicient farming, unequal distribution of food (poverty), lack of kitchen facilities and equipment, lack of leisure, lack of t~nsport, ignorance, and religious customs. From this formidable list, it can be seen that "the prevention of nutritional disorders is to a large extent outside the powers of the medical profession. The only practical method available to us is education. The Committee o n Nutrition (1950)said : " T o persons accustomed to the traditional British diet, certain constituents of this diet may have a psychological importance out of proportion to their value when regarded from a nutrition aspect." Although this statement referred mainly to the effect of food shortages, it is true in general of many of the dietary hat3its which we may wish to alter. During the war, because of food shortage, rationing was a means of'exerting dietary restrictions upon the whole population. One effect of sugar rationing, as studies by Toverud (1949) have shown, w a s a great improvement in the dent/if ~i~ealthof children in several countries. With the end of rationing, the intake of sweets has increased to a level now far higher than before the war. The reasons for this include a rise in the averagc standard of living with an incrcasc of spending money for luxuries, and displacqment activity to relieve tension, boredom, frustration, all under the influence of high powered advertising that affects every 6he today. In as much as dietary habits, good and bad arc developed early in life it would seem that here is an obvious place to introduce any proposed change. Toverud (1948) investigated the effect o f dietary instruction on: dental caries. He advised pregnant~women as to the correct diet for hersdf and unborn child and continued this instruction after ~ e child was born, The results were most impressive and showed a definitclreduction :in the caries incidence over that found in the control. The welfare services then provid~ us with a means of educating the general public at a time when they are particuiarlyprone to suggestion. It is important that th,s work should begin early in!:pregnancy so that the :mother'to-be becomes conscious o f the dietary needs~of her unborn child and herself. ~The value of carbohydrate restrictions fromlthc:weight point of view/is obvi0us to the mother, ibut has: far more i m p a c t i f i t s beneficial effe~: upon thechild, is explained. Slmilarly,~iico'operation in ~ e use of mitk an d l v i ~ i n supplements can be bcstachiev¢~i ~ t h e ~ i l d is reader he primary obj¢ct. Afterbirth. mothersshould be encouragcdto give codIiver oilandorang¢ juice and to breast fc~!!their •babies:i This is~not because i t is believedthat
"natural" fecding:improve~ the s t r ~
and size of the jaws~as Was once
DIET,
NUTRITION
AND
DENTAL
CARIES--A
REVIEW
449
thought, but because from a dental point of view artificialmilk fccds contain a high proportion of sucrose which may well have a delclcriouseffectupon the developing teeth. Advice as to weaning is frequently sought by mothcrs, especially with the first child. They should bc discoura~cd from using fruit cordials, sugar water, or honey on a pacifier.The cffccts of these upon the teeth has been we!I described by James, Parfitt and Faulkncr (1957). In this context it should bc mentioned that the habit of allowing the child to go Io slecp with a bottle of swcctcned milk in itsmouth is not only dangerous from a dental point of view, but also a potential cause of asphyxiation. In the toddler stage, mothers are tempted to give their children sweets to obtain for themselves a few moments respite. At this age a piece of apple or carrot is just as much appreciated and far cheaper. Now, too, the child is subjected to a constant attack with refined carbohydrates by wcll-meanin8 relatives especially grandparents. The mother has to bc particularly tactful in such circumstances, not only then but later when the child goes to school. Here he comes under the influence of others and good dietary habits can bc ruined by unthinking school teachers. One cannot deny that even the perfect child ~411 at times indulge in something that has bccn forbidden at home, and for this reason it is suggested that parents bc advised to provide swccts :at the table to be eaten when the mid-day and evening meals have bcen fmishcd. This will prevent the child from feeling differentwith all the adverse effectsupon its personality and popularity in its socialgroup. In discussing the school lifeof the child some mention has to be made of the increasing number of tuck shops that are to be found even in the primary schools. The provision of refined'carbohydrates between meals not only affcctsthe dental health of the child, but also ruins his appetite for the midday meal. This is a problem that school dentists and the school meal service have in common. The great difficultyis that quite often, these tuck shops are financially extremely profitable,and arc used to supply the school with additional facilitiessuch as film projectors and tape recorders. One can, however, get over this problem by advising the substitution of non-cariogenic foods such as apples. The responsibilityof the school teacher does not end in the provisiom of a scholastic education, In thesedays when most children take school meals, a great deal of dietary teaching fallsinto theirhands. The need for the teachers receiving training in this field is obvious. Some colleges arc including the subject in their curriculum. Howcvcr, thc responsibility for the teaching of the teachers rests for a large part in the hands of the school medical officers and the school dental officers. This requires a great deal of co.operation from the principals of the schools whose help is essential for the introduction of any preventive measures. A briefoutline has been made of the methods of dietary control of dental
450
PUBLIC
HEALTH
VOL
LXXIV
NO.
12
disease. The problem is both complex and serious. It requires the fullest cooperation between doctors and dentists especially those directly concerned with the school child. Acknowledgment is made to Professor G. U Slack, o.n.E., T,D., F.D.S.R.C.S., t>~e. nAcr., for his advice and help in the writing of this paper. REFERENCES A D L~ R, P. (1957). Odont. Revy. 8, 202. B R u D r. v o L t) F I r~ t~. (I959). J. Der~;. Child. 26, I86. C R A ~, J. A. (1959). Austral. dent. J. 4, 182. D A v i O S O ~4, S., M ~ I K E I. J o r s r~, A. P., & P A s s M OR E, R. (1959). "' H u m a n Nutrition and Dietetics," Livingstone, L o n d o n p. 690. D A v, C. D. M. (1944). Brit. dent. J. 76, 115. G u s T ^ F s s o r~, B. E. et aL (1954). Acta odont. Scand. I1, 232. H o L t. o W A ~, P. J., M I~ LI. AN nY M A Y, & STEWART, R. J. C. (1958). Brit. dent.J. 104, 305. .......... . (1960). Personal C o m m u n i c a t i o n . JAMES, P. M, C,, PARF1TT, G. J.~ d~, F A L K N E R FRANK. (1957). Brit. dent. J. 103, 37. ~-.-, & . . . . . , (1957), Ibid. 103, 214. J j~.r~ s: J r~ s, G. N. (1959). Arch. oral BioL 1, 33. K l N o , J. D., M1ELI. ANBY, M., S T O N E s , . H . H . , & G R E E N , H. V. (1955). Spec. Rep. Set. Med. Res. Coun: (Lond.) No~ 288. K I T V., O. W., S H A W, J. H., & S o G N ~r A E S, R. F. (1950). J. Nutrition 42, 89. K It u o r. R, B. J, (I958). Austral dent. J. 3, 236. L u N D O u I s T, C. (1952), Odont, Revy. 33, Suppl. 1. M A c X, P. B. (1959). Soc, Re,¢. in Child Development, 13, 62. M c C t. u ~ i~, F. J., & M u I, I~E g, A. Jx. (1959). 3". dent. Res. 38, 394. M E b L Ar¢ g ~', M, (1928). Brit, dent.J. 49, 769. ----~--.. (1934), @ee. Rep,.Ser. Med. Res. Coun. (Lond.) No. 191. M 1L L ~ rt, W. D. (1890). " T h e Micro-organisms of the H u m a n M o u t h . " Philadelphia, S.S, White Dental Mfg. Co. 0 R L A N D, F. J., etal. (1954). J. dent. Res. 33, 147. Rep, ~ f C o m m . on Nutrit. (1950). Brit. Med. Ass., L o n d o n p. 97. S c H ^ T z, A. (1957). Anna&. Dent. 16, 37. S h ^ c K, G. L, (1960)~ Personal Communication. .... :r:......., & M A r t T I N , W, J. (1958). Brit, dent. J. 105, 366 S oBv. t., A. E., & H A N o g , A. (i948). J. biol. Chem. 176, 1.103. S o o NN A I~ S, R. F. (!948), J, Anwr. dent. Ass. 37, 676. S T ^ a% J. (1934). S, Afr. med.J, i7, 1. S T la I N M A N, R. R., & H A L 1~Y, M. 1. (1957), .I. Dent. Child. 24, 21 !. S U Lt. ~ v AN, H. R., & G o L D S W O P. T tt ",', N, E. (1958). Austral dent. J. 3, 395. T o v I~n U D , G , (I949). Proe~ roy. Sot',/~¢ed.:42, 249. T o V I~R U O, K . V, (1948). Acta paediat. (Uppsala~ 36, 257.