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Diet and Dental Disease

S. W. Hillson

World Archaeology, Vol. 11, No. 2, Food and Nutrition. (Oct., 1979), pp. 147-162.

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Diet and dental diseaseS. \V. Hillson

Teeth come into contact with every part of the diet that enters the body. Such marksas are left by the passage of food should therefore act as reliable indicators for the dieteaten during life. Even while still being formed in childhood, teeth are affected bydietary factors.

Teeth have additional advantages for archaeology. They are readily identifiable inisolation from the jaws that hold them. The hard and tough materials of which theyare made often allow their preservation where other parts of the skeleton do not survive.They have a wide range of reactions to the constituents of the diet, reactions aboutwhich much is now known and which are easily studied in ancient material.

Dental anatomy and pathology as dietary indicators

The structzlre of teethBoth of the main components of teeth - enamel and dentine (fig. I ) .- have structuralelements which may be used at least in part as dietary indicators.Enamel Dental enan~elmay be thought of as being formed in layers. Initially, theselayers are dome-shaped (fig. I). Later, the domes are surrounded by sleeve-like layers,svhich become ever shorter until the enamel crown of the tooth is completed.This layered pattern of growth is given physical expression in enamel by thestructures known as Browz Striae of Retzius. Such striae arise from a cessation ofgrowth which causes a flaw or break in the crystalline structure of the enamel. Theflaw follows the outlines of the growth layers throughout the body of the crown. Theycan be seen clearly in microscope sections of teeth (plate aa).Outside the zone of dome-shaped layering, Brown Striae of Retzizts emerge on thesurface of the tooth crown. Where they emerge the same process that causes the striaethemselves also causes small dips in the crown surface. This gives rise to a pattern ofwaves, called perikymata (plate I). Thus the effects of the Brown Striae of Retxizls may

Wo rM Arclzaeology Volunze11 Number 2 Food arzd nutrition0 R.K.P. 1979 0043--8~43/110z-o14~I . ~ o / I

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been seen oil the surface, obviating the need to make a section. Both the striae andperikyr~.atabecome more marked in the cervical part of the crown than elseavherc,

Bttv~een he brown striae are f ~ u n c l ,smai!er incremcu:tal sti.uctures. These s1.e r:aileciclaoss striaCons and arc due to variation in speed rather than actual cessation of cilaxnefgrowth. Cross st:-i~.tocs :ccur rhythmica.lly, with what i s aiur7ost certainly 2 daily

shapec i

l aye rs-.

II0

- .

e r. Lo~lgi:utii:~aTsection t!i~.ouph Fkrire :z. r.-lihe physiology of dental 'piaqa

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Diet an d den tal disease 149so severe that the shape of the crown is profoundly altered. I t has long been dem onstratedthat hypoplasia of this kind is related to vitamin D deficiency (Mellanby 19341, but itmay also be caused by a general rise in body temperature, su ch as that occurring duringfever.T h u s it may be possible to use observations of enam el hypoplasia in ancient hu m anteeth t o indicate, if not diet alone, at least th e general conditions of childhood. T h eage at which the events which caused the hypoplasia occurred is estimated in thefollowing manner. Tooth crown surfaces may be divided (fig. 3, page 1 5 5 ) into roughzones (Hillson 1 978), each covering a different period of crown form ation and with in eachof which hypoplasia may be recorded. Microscope sections may be made of modernteeth and th e num ber of Brown Striae of Retzius between the boundaries of th e crownsurface zones counted. Average counts of cross striations are then determine d betweensuccessive brown striae. I t is then possible to estimate the times taken in th e form ationof each zone. Ages for the start and finish of enamel formation are available (Scottand Sym ons 1976) and this allows estimation of th e ages at which each zone bo undaryis reached. Many possibilities for error exist in this method, not least the widespreadvariation between individuals in the formation times of teeth. It is, however, the onlyway at present available of estimating the ages of hypoplastic events and is likely to bereliable at least as a rough guide.I n this way, records of the severity of hypoplasia in each zone may be used to suggestdietary deficiencies or febrile conditions d uring given periods of an individual's develop-me nt. Different teeth i n the m outh. have different times of development, so tha t ascale of these childhood events may be constructed for each individual. For practicalreasons, this scale is limited to the period between nine months and seven years ofage.Dentine Like enamel, dentine grows in a rhythmical way. Finely spaced increm entalstruc tures in the den tine, the Lines of oon Ehnev, are probably du e to a diurnal rhyth m.M ore widely spaced are the Contour Lines of Owen, which may be du e to a rhythm ofupwards of ten days. Where a disturbance in growth occurs, of the kind producing theBrown Striae of Retxius, patches of poorly mineralized dentine are formed. Su chpatches are known as interglobular dentine and have again long been demonstrated asconnected with vitamin D deficiency (Mellanby 1934).It is possible to use these interglobular dentine patches in a similar way to the

hypoplasia of enamel, in reconstructing the sequence of events during childhood.De ntin e, however, can only be seen in a microscope section, an d this limits its usefulnessin archaeology, where lack of time or reluctance to damage ancient skeletal materialmay render section-making impossible.

Plaque-related diseaseSoon after teeth erupt into the mouth, tliey are increasingly colonized by bacteria.Th ese bacteria are highly specialized in adhering to dental surfaces and to each o the r;also in metabolizing the food entering th e oral cavity. I n uncleaned teeth (which appearsto be the case throughout most of antiquity) these bacteria build up on the surface of

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the tooth into a layer which extends round the cerkical part of the crown, in contactwith the gingivae.This layer is called plaque: and it is through the medium oi this connplex bacterialco:ony that many of the eEects of diet are expressed upon the teeth. 'l'he processesinuol\~ed n this may he srxmmarized under txvo headings: acid/alliali (pH) balance, allti

inln~uneesponse (fig. 2).,ilcid/c~lkali( p H )b~zl~z~zcehe pf 1of thc plaque varies according to the relative amountof protein as opposed to carbohydrate in the diet, When plaque bacteria rnetalnolizcprotein, they produce alkaline waste products. Willen plaque bacteria metabolize carbo-hydrate, they produce lactic acid as a waste product. Zn this way, the pH of che plaqucchanges throughout the clay. Pcriods of acidity alternate with alkalinity. Periods ofparticularlj high acidity, approaching pH 4, okcur when foods are eater? that conlainlarge quantities of sugars. Sugars are metabolized n ~u chmore rapidly man othercarbohydrates and this causes more lactic acid to be produced rrlore quickly,It is thz relative balance between these Ilighly acidic and alkaline periods thatdetermines whether the disease dental carics occurs. Ilrrring the acid phases, themillera1 of the er~amel s dissolved. During allialine periods, the minzral is replacedfrom a store which is maintained in solution i n the saliva. If acid periods outnumberand outlast alkaline ones, a steacil 10s:; of mineral occurs from the enamel underneaththe plaque. Eventually, the characteristic pit-like lesions of dental caries occur (plate 3a).In most cases, regular cating of sugary foods, anci thus regldar highly acid plaqiie

periods, is required before much evidence of dental caries appears. r 7I he sugar sucroseis particularly effective in causing dental caries because of its specific involvement inthe rapid growth of plaqv,~.Conversely, if lnuclz of the food consists of protein arrd the plaque is tE~us lltaliaefor most of the cime, extra mineral is deposited in plaque on the surface of the tooelr. Asstated above, the saliva contains rnuch dissolved mineral, which crystallizes within theplaque \$hen there are insufEcient acid episodes to cause it to redissolve. Silch mineralizedplaque builds up into a layer that, in ~~ nc le an edeeth, can be quite thick and which iscalled dental calculus or tartar (plate 3b). Dental caries and dental calculus tend to bcmutually exclusive because of this relationship with plaque pH, For this reasorr, mhentheir frequency is recorded in ancient teeth, they should make particularly goodindicators of the protein versus carbobycirate content ol the diet.It should be emphasized that this is a much simplified description of the diseaseprocesses; beside diet other aspects of physiology, both genetic and eilvironmental,are involved.Pi~rszz~neesponse. The presence of large colonies of bartcria next to the gingivaestimulates a response in the tissues of the jaw (Macl'hes and Cowley 1975). Bacteriaproduce potentially toxic molecules called antigens, which cause tliie body's defencemechanisms to be activated. Local innate immune response includes an inl'larnrnatoryreaction, with the arrival of white blood cells which ingest bacteria and thus destroythem. There is also an acquired immune response, in which specialized white hloodcells arrive and produce antibodies, n~oleculesspecific to individual antigens, wbiclr

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Diet and dental disease I 5 Ibind to them and thus neutralize them. Slight localized inflammation and a mild,acquired immune response are a normal finding in the gingival tissues of mostindividuals.This normal, slight response involves very little tissue damage. When the plaquedeposits are extensive, however, a much more severe response, called hypersensitivity,is triggered off. The way in which this happens is not well known, but ciuring thehypersensitive response large numbers of white blood cells arrive, including thespecialized antibody-producing cells. Although immune response is designed to combatbacteria and their effects, rather than to damage body cells, it can have a disastrousresult when elevated to a hypersensitive level. Hypersensitivity is essentially an over-reaction to what is in fact not an especially dangerous stimulus. Processes involved inmassive bacterial destruction and neutralization of antigens also destroy body cellsand interfere with body metabolism. In this way, the collagen fibres which attach boththe gingivae and teeth to the underlying bone of the jaw are lost. This bone is probablymaintained in a shape suitable for retention of teeth (i.e. with tooth sockets) by thefunctional stimulation of the attaching collagen fibres. When the bone is relieved ofthis stimulation, it reverts to a form not suitable for tooth retention.

Rone round the tooth sockets is resorbed (plate 4a), the teeth become loose and areeventually lost, and the bone remodels to a smooth, flattened and socketless surface.The effects of this resorption and remodelling are termed periodontal disease and arecommonly found in ancient skeletal material.

We ar patternsFood contains many abrasive elements. These may be mineral, as in bone or the grittycontaminants from querns in stone-ground flour. They may also be due to the toughcellulose molecules of plant tissue, or the collagen of animal tissue. Contact with theseabrasive constituents inevitably wears down the surfaces of teeth, as food is groundbetween them (plate 4b). This process is called attrition.

Very little information can be gained about the rate of wear in ancient skeletalmaterial. This is due to difficulties in ageing adult individuals precisely enough. Allthat is possible at present is an examination of the pattern of wear throughout thedentitions of each individual. Molar attrition may be compared with that of the pre-molars, canines and incisors. Differences are found between populations in this patternand dietary differences can sometimes be inferred as the cause. Too little work withdental attrition has been done with modern populations, of known diet, for Inore thangeneral inferences to be made.

Example: dental disease in Ancient Egypt and NubiaUsing skeletal material from Egyptian and Nubian cemeteries, a sample represcnting941 individuals has been investigated (Hillson 1978). The cemeteries ranged in datefrom Predynastic at Badari and A Group in Nubia, to Christian burials, also in Nubia(table I).

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Diet and dental disease 153

Th e peopleT h e term 'population' when applied to m an is a rather vague one which implies ;ageographically definable group of individuals who interbreed mostly with each other.A comparison between populations of the frequencies of oral diseases should indicateany differences in the type of diet most commonly eaten in either group. In this way,it may be possible to reconstruc t a regional and tem poral picture of the diet.

The difficulty in archaeology is the uncertainty of what ancient living population agroup of skeletons may represent. A group of burials within one cemetery may indeedrepresent a local hu ma n population. I t may, however, just as easily represent only onesection of that population, or include individuals from populations not geneticallyclosely related to the local one.

The only way in which this problem can be approached is by examining the geneticrelationships of the individuals buried in each cemetery. Genetic differences betweenmem bers of the sam e cemetery, or similarities between m emb ers of different cemeteries,may indicate the nature of the population being studied. Blood grovlps arid otherbiochemical factors are th e best gu ide to genetic relationships. Althoug h there are claimsfor th e detectjoil or' such factors in ancient skeletal material (e.g. Lengyel r g ? ~ ) , ormost p ractical purposes similarities and differences in th e form of the skeleton m ust beused instead.

Variation in shape of the skull alone is still almost universally used for such work.T h e skull is relatively easy to measure. I t appears to be less affected by environ men talpressures during development than are post-cranial bones and may thus act as anindicator for the genetic make-up of an individual. Although the sIrulls used in thepresent study varied considerably in shape, no groupings of individuals within acemetery, or remarkable differences between cemetery groups were found. Skulls ofdifferent sexes of co urse differed, bu t all skulls of o ne sex were similar in their measu redshape. Comparison was by principal components analysis, discriminant analysis andmultidimensional scaling.

This finding is consisteilt with other studies (summarized in Hillson 1978) of theancient populations of the Nile valley. It appea rs that sliull shape has been remark -ably constant bot h in tim e a nd space. W hile it is uncertain tha t this represen ts agenetic constancy, the general morphological similarity does at least suggest that.differences in disease frequency may be explairled by diet rather than by structuralvariation.The dietT hr ee main studies have been carried o ut that attemp t to summarize information abou tthe d ie t of the ancient Egyptians : Ruffe r ( ~ g ~ g ) ,affirio (1972) and Darby et al. (1977).In all of these studies, textual, pictorial and archaeological evidence are used, but onlyrarely is there any indication of the numbers of people who habitually ate a particularfoodstuff. So as a guide to the nutritional statu s of t he Egy ptians, they are of little use.For the most part, an indication of the range of foodstuffs available is given: chrono-logical changes in diet are not discussed.

Dom estic animals - cattle, sheep, goats and pigs - were kept from Neolithic times.

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Wild animals were also hunted, includlng hare, anrelope, ~9.jldfow\-9nd fish, Cerealcrops included wheat, barley and millet, 'These werc used to make bread, for mbiclnthere is ample evidence. Bread was apparently as important then a. it Is no~v 14at-wardhan and Darby 1972). On a stele commemorating an expedltion of Seti l ( ( r 309 xzgrB.c.) to a stone quarry in Nubia, ~ , o o omen were said ro have bcen given 2,o deben( I,860 gm.) of bread each per day (SaErio 1972). 1,860 gin. of wholelneal wheaten breadyields 4,483 kcal (R'lin. Ag. Fish and Food ~ 9 7 6 ) ~hich is an adequate daily provisionof calories. IVJany dizerent kinds of vegetables mere eaten, including pulses, and It islikely that the ancient Egyptian peasants gained most of their protein from this source,as do the present dayjellnhin. Fruit uTas lso grown, but there is Iittlc information aboutits importance to the diet. f ~ sn Egypt today (Patwardhan and Darby ~ 9 7 2 ) ~t idlikelythat dried fruit n7as eaten more than frcsh fruit. in the cemetery of Deir-el-Medlna,Mhere workers engaged in building the royal necropolis were apparently buried, cr~isheddried figs were baked into bread (Safirio 1g . j ~ ) .Sweetening agefits included honey,dried carob, dates and figs, 2nd grape-juice concentrates. A11 contain large quantitiesof sugar, dried carob having a particularly high concentration of sucrose (M'lntonand 'Vcvinton 1945), the sugar mainly responsible for dental caries today. "8iegetaPdroils were available in ancient Egypt, perhaps eaten on bread, as by the modernJellahin.

Th-~lshe nlost likely diet of the aniclent Egyptian pezsaxlt was like that o l peasants ol'recent times (l'arwardhan and Darby 1972). The rnain source of carbohydrate easprobably bread (most likely wheaten) ancl the main source of protein, vegetables -perhaps with some fish. The wealthier people probably had rnore protein from mammalmeat and other such h~xurics.Even poor people are unliltely to have been especiallyundernourished, except in times of faminc.

The teethPlaque- elated diseases "6he first problem in stuclyin-ig the pathology of a large skeletalsanlple is in devising a method oC recording that allows individuals to be comparec!statistically (fig. 3, table 2). Much time was also spent investigating the best way inwhich to present the informafion, The final method used was to produce a percentageol: individuals affected by a given disease at each cemetery. IrTistograms and table5were constructed for each degree of severity of each disease, showing the percentageof individuals at each site who had more than 10 per cent of their permanent tx t haflected. This solved the problems of ~nissing eeth and ~ncornplete aws, giving 23comparable index between all sites.

In 1946, a survey of dental health in Abassia Fever Hospital, Cairo, was coanductcciby Damson (1948). Approximately go per cent of 944 individuals, aged between r 5 and 55years, had some evidence of dental caries. On average 0.95 teeth were affected perindividual. Periodontal disease of some kind was almost universal, biit especially severeand chronic disease of the kind likely to produce bone changes occurred in abo~lt r petcent of cases. Dental calculus deposits mere also almost universal.

This pattern of disease is presumably due to the diet described above, and to lackof oral hygiene. Vegetable products form the staple foods. Most of such foods contain

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--

Diet and dental disease 155

Denta l Caries Sever i t y Cod ingE N A M E L

5

P U L PDENTINE REPAIR

Car ies Pos i t ion OCCLUSAL. Den ta l Ca lcu lus

1ST. INCISOR 3R D MOLAR

0 1 2 3MESIAL DISTAL INTERPROXIMAL I NT E RP RO X I M A L . grades Zones for reco rd ing Enamel Hypop las ia Right H a l f Perm anent Dentition

INCISORSUpper

Lower MOLAR S PREMOLARS INCISORSCANINE

Figure 3. Scoring for dental caries severity and position. Zones forrecording enamel hypoplasia

T A B L E 2

Coding for periodonta l disease and attritionPeriodontal diseaseo = no bone resorption or remodelling as a result of periodontal disease. I = bone resorption in th e crest of t he alveolar process (the pa rt of the jaw that actually

supports the tooth) only.2 = bone resorption in th e whole of the alveolar process round t he tooth.3 = some d eposition of new bone (healing), bu t areas of destru ction still visible.4 = areas of bone destruction covered by new bone.j = remodelling complete - bone surface conlpact and sm ooth.AttritionSeverity of attrition was scored by the pattern of dentine that was exposed on the occlusalsurface of th e crown, using a system similar to that of M urp hy (1959).

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both carbohydrate and protein, thus allowing the plaque growtla necessary for perio-dontal disease and the frequent alkaline episodes necessary for calculus deposition,Sugar intake is presumably large enough for the common occurrence of dentalcaries.

In ancient Egypt and Nubia, there is no textual or archaeological evidence for oralhygiene, nor was there any biological evidence for this. Plaque deposits could thereforegrow7until limited by the polishing effects of chewing. For sites of the Dynastic periodand later, the incidence of dental caries was 10 per cent or less, of individuals beingaffected in more than 10per cent of their teeth, Dental calculus deposits were observedon the teeth of 50 per cent of the individuals studied. Bone destruction and repair dueto periodontal disease occurred in fewer than zo per cent of individuals,

I t is difficult to make comparisons between the skeletal material and Da\~son's rg48)results for recent Egypt. Fllethods sf study are necessar~lydifitrent and the indicesof disease occurrence must also be different. Despite this, there is a large differchncebetween the two sets of figures. All the plaque-related diseases seen1 less common irathe ancient material than the recent. This piesumably reflects less extensive plaquedeposits or, the anc,ent teeth. 19 major difference in the basic diet is not necessary as anexplanation, since ihe high frequency of calculus still suggests consumption of vegetablefoodstuffs (see beloa) during the Dynastic period. Sugars play a large role in plaquegrowth and the difference could be due to increased sugar consunlption in recentEgypt, perhaps a reflection of the modern widespread habit of drinking heavilysweetened tea. Such an explanation is supported by the especially low incidence ofcaries in the ancient material. So T postulate from the evidence ;a general diet similar tothat of today's fell~shia,but with sugar less widely consrrmed,

The incidence of the plaque-related diseases in ancient material is broadly sln~ilarbetween sexes. Females, however, generally have a slightly higher incidence (table 3)of these diseases than males. This is perhaps due to great consumption of sugar byfemales, or to physiological dlgerences. 'The diseases are Jess comrnorl in childre11 andsub-adults (table q ) ;han in adults, presumably also due to less eutensivc plaque deposits

That is the position for Dynastic tin:es on\? arcls. The three Predynastic sites, Abydos,El-'Annra and Badari, have l o ~ e i .reqi ~ecciesC plaque-related diseases tha? t h ~atcrcemeteries. This agam is presurrrably due to less extensive plaque deposits, which mayhave been caused by even lower sugar consumption. Another reason might be that moremeat was eaten than ~ ege tabl e oods. Most meats contain almost no carbohytirate(Min. Ag. Fish and Food 1976). This smld generally cut down the size of plaquedeposits and thus the incidence of all diseases equally. 'The floodplain of the Wile waswider and rainfall higher in Pretlynastic times than later (Hillson 1978) and it is likelythat vegetation cover was more extensive outside tlie valley. Game may have been morereadily avaiiable, or the do~nestic nimals which are found as bones on Predynasticsites more vi-idespread.Support for thrs idea of differences in basic diet during Predynastic times may comefrom the pattern of dental attrition, which differs from that of later pznods. Wear oithe anterior teeth relative to cheek teeth is less severe in the Predynastic skrrlls, l\!leatcontains fewer abrasive constituents than vegetable foods and is thus less likely to causetooth wear.

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I ' l a t ~ i I 'er ikymata, shomn on a rub be r latex cas t f rom th e s rr rface of a canlne f rom Kerrr lah u b l a (c. 17za-I550 B.c.)

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Platr r ( a ) Section through dtntal enamel of a canine from Kerma, Xubia ( c . 1720-1j.jo B.c.)rI7he sectton is longitudinal and observed between crossed polarizers, the plate being madeup of a rriosaic of sevcral photomicrographs. B~ozcr7zS fr iae qf Rrtzius may be seen as aseries of darker lines in the body of the enamel. The worn, occlusdl surface is on the left ofthe plate, the cervical region further to the right

Plate ~ ( b )Enamel hypoplasia in the lower left canine of an individual from the Romancemetery at I-Iawara in Egypt

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I ' l a t~ j(u) ,Ll~lddental carles In t h e left 'tuppet i t co~l t i i r rd th l rc i t no l a r s o t ,In ~ n d i \ ~ d l r d lroirlKcrtna, Uubia ( 6 . 1720 I j;o u.c.)

Plate 3(6) Th e eroded remains of extensive dental calc~~luseposits on thc upper lett nlnlars(and second premolar) o f an individual frorn Kernlib

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Plate # ( a ) Kesorp t~ondue t o perioclontal d~srasen thr upper jaw of an lndiviitual fromKerma

Plate q(b) Attrition in the upper left molars and second premolar of the same individual asin plate 3(b)

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Diet and dental disease I 5 7T A B L E 3D$+j%rences in overa ll incidence of plaque-related diseases between sexes

Male FemaleY o Yo

Slight dental caries (Grade I )Severe dental caries (Grade 3)Occlusal den tal cariesDistal interproximal dental cariesPeriodontal disease -destruction (Grade 2)Periodontal disease --

repair (Grade 5)Calculus (Grades I, 2 or 3)

T h e table shows the percentage of individuals w ith more tha n 10 per cent of their permanentdentition affected by each disease, with the total number of individuals from which thepercentage was calculated in brackets underneath.T A B L E 4DiJ'yerences n overa ll incidence of plaque-related diseases between 10-year age grozq s

10-20Y e a ~ s 20-30Years 30-40Years 40-50Years 50-60Years% Yo Yo % Yo

Slight dental caries(Grade I)

Severe dental caries(Grade 3)Occlusal dental caries

Distal interproximaldental caries

Periodontal disease -destruction (Grade 2)

Periodontal disease .-repair (Grade 5)

Calculus (Grades I, 2 or 3)

T h e table shows the percentage of individuals with m ore than 10 per cent of their permanentdentition affected by each disease, with the total number of individuals from which thepercentage was ca!culated in brackets und erneath .

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So ine D ynas t i c s i t es d id no t f'ollccv th e genera l t r cn b . Car i es f r equenc y i s higher a tS idm an t , 53185 a nd H awa ra t ha n a t o ther s i t es (fig, 4). ' r h i s s u g g e s ts t h a t i n o r e e v t e n s i r eac id p l aque depos i t s ex i s t ed on the t ee th o f i nd iv idua l s bu r i ed the re . Wow is thissup po r t ed by th e ev idence of o ther d i seases?

De nta l Car ies, Grade 1 Se ver i t y Den ta l Car ies, Grade 3 Sever i t y100, 100,

Per iodon ta i D~sease ,Grade 2 Pcr iodo nta l D isease, Grade 5100 1oc

b 9 5 5 4? E Y i t 9 1E 2 % 50 hi' 1 9 7.1 hDental Calculus, Indiv iduals Unat fecteci1C0 , ABY Abydos

ELA El - - 'Am raB A D B a d a r i277 S i t e 277 (S.J.E.)SED S ~ d m a n tI

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- - -

Diet und dentul disease r gg

. I""C 60 1 Badari ............... ................,

6 3 :~~~ - I40 ~-....... i...

20 . .... t ..... .-..-C i

01-. _ 7 - ,5 4 3 2 1 3 2 5 4 3 2 1L O W E R R IG H T F IR S T h l O L A R UPPER R IG H T C A N IN E U PP ER R IG H T S E C O N D M O L A R

Years after 01-ti,o/lOOl Wawara r'' 804 . . . . . . . . . t

401 - 1 7--0 7 1-i , 1 1 ---,0 : - - _ -- - 4 - f i -- 1I - -4 3 2 1 3 5 4 3 ' 2 1

L O h E R R l G l i T F IR S T M O L A R UPPER R IGHT CANINE UPPER R IGHT SECOND MOL AR

o ) ' ~ ~Kermalo01604 ...................... 401 7 - - - - ----i ................ ...[I------.--- i , .................. .....L-i ............................. . . .-1 .__?_-- -..A--..---_--_.-.5 4 3 2 1 3 2 5 4 3 2 1 b - . - 7 7 - 7 - 1 7 - - - T V T - T ? T - l v r - m i

0 1 2 3 4 5 6 7 Years a f te r Birth

Figuve 5. The sequence of enamel hypoplasia at Eadari, Sidmant, Hawara and Kerma.Percentages of individilals at these sites affected by enamel hypoplasia in zones $,'I., 3,2 and I of the Low er Right First Molar , zones 3 and z of the Upper Right Canine, zonesj,4, 3 , 2 and I of the Upper Right Second A.Iolar. Dotted lines above and below thetop of each bas of the histograms define the gj per cent C onfidence Limits.r Plaque thickness Periodontal disease requires extensive plaque deposits , but isrelatively independent of pH. Bone des t iuc t ion i s common a t S idm ant and the repa i rphase of periodontal disease (fig. 4) common at S185. Hawara is omit ted owing todifficult ies with recording, but the thickness of plaque deposits is generally supported.2 Plaque pH Dental calculus should bear an inverse relatioiiship to dental caries,Sid m an t, S185 a nd Ha wa ra a re all especially low i n ca1cl;Ius (fig. 4).

T h e most l ikely cause for suc h extensive, acid plaque deposits is increased con-sumpt ion of sugar . Both Hawara and S idmant apparent ly conta ined the bodies ofmoderate ly well - to-do townspeople an d S185 conta ined Egy pt ianized Nubian s , o r

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Egyptian immigrants to Nubia. Thus the increased occurrence of sugar eating may beexplained by social diflerences.Tooth slructzc~e Work was also carried out on the structural defects of the teeth, Scrrracpreparation and examination of ground sections was undertalcen, but this vras time-consuming and poor dentine preservation made observation difi-cult. j;or this rcasorz,work was concentrated upon the enamel hypoplasia visible on the sudacc of 3'1(, toothcrown. Three site.; proved to have especially high Scquenclies of s.rci-1 ItypopiasiaBadari, Sidmanr and Hawara. As stated above, difirenl teeth can bc arranged i q asequeacc to show how the incidence of hypoplasia varied with age. Figure !; s11:awrshistogranls constructed horn such a series: crown zones (i;lg, 3) 5, 4, 3 , a and r oC tileLo7:ver Righ.t First ?+d\uolar,zones 3 ant1 a of the 'lippcr Right Ca~ine, ones 5,q., 3, 2a11d i of the Upper Right Second hiIolar. T h i s provides the sequence from nin:: monthsto seven years after birth,

Histograms are shown for Badari, Sid~narrtand Ra.wasa, the t h r e exceptionl-il site:;,and for K-errna, a n example of the r:ernaiader, At Il(-ernaa and most other c~-lll;ei:eries~there is a rna.xi:nwn hypoplasia frequency a f 40 pcr cent of individuals. 7'he frequex~c:yis at this Ici:el, or slightly iosver, throughout ~ o s tf the graph, Also shown 2.t Rernr;iis the x~~eaknessf t ~vo arts of the scale - zones 5 and 4. of the ko\ver Right First IVlolarand zones 5 and 4 of the Upper Right Second Nholar. 'These zones are formed early i i sthe development of the teeth and show less evidence of hypoplasia than the later zones(this is due to their mrrdl faster growtli). 'This is tlrc rrlost likely yeason for .[:he qowfrequencies in these parts of the gt aphs a t all four sites.Tn addition to this qa per cent 'backgrounds frequency of hypoplasia, Badari, Uidmzrrrtand IBawara have peaks of incidence, some higher than per cent of ~n~ihiduals,between three and five years of age, Badari awrd Hawara also have troughs of inci3er~c.t.just before this period at about two and a half years. 'khe peak may be due t o a greatersusceptibility oor "ce canine to hypoplasia, bu t rhe iack of this peak at other. sites arguesagainst this explanation. The trough is also unlikely to be due to lower.ed s~ ts cc p~bi li tyat zone I of the Lower Right First Molar, as this should rbeore-ticallybe a partictxlarlysusceptible part of the tooth.

'Fhe 4-0 per cent background frequency of hypoplasia could be due to constantlyoccurring dietary deficiencies and febrile disease. The three-to five-year peak at eadari,Sidmant and Mawara could then be superimposed upon this by additional factors. Apossible additional cause may be hrtlaer vitanlin BP deficiency, Three possible reasonsfor such a deficiency exist:T Vitamin D is manufactured in the skin by sianl~ght. a?suficient exposure to suniighi

may thus cause a deficiency.z Breast milk contains some vitamin P). Poorly-nourished mothers produce vitanlirr Ibdeficient breast milk.

Vitamin D in later childhood comes directly from the diet, This diet may veryeasily be deficient.

T,ength of breast feeding in modern societies varies between about 18 anonrlas andq. years after birth. Some societies today often retain breast feeding for longer periodts.

3

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Diet and dental disease 161

This may be due to the use of lactation as a contraceptive method, or to an attempt tointroduce a deficient adult diet slowly. Thus in the ancient Nile valley, it is quitepossible that weaning occurred at three to four years. When the supply of breast milkwas cut off, the other sources of vitamin D may not even have compensated for the lossof this relatively small supply. At Sidmant and Hav~ara,where parents may have beenrelatively well-to-do, children may have been especially heavily clothed, or confinedindoors, causing insufficient sunlight to reach the skin. Other causes, such as particularsusceptibility to childhood diseases and particular environmental or genetic predis-positions must not be forgotten.

The high incidence of hypoplasia at Sidmant and Hawara may have played a partin the high frequency of dental caries at these two sites. Hypoplasia provides flaws inthe enamel which may be exploited by the solution process.

This work formed part of a P1i.D. project at the Institute of Archaeology, Universityof London. It was supported by studentships from the University of Birmingham andthe Medical Research Council. I would like especially to thank: Mr D. W. Brothwell,Dr A. Boyde, Dr I. D. Graham, Dr C. Stringer, Mr 13. Denston and Dr 0. V. Nielsenfor their help during the work; also Mr R. C. Turner for preparing the drawings inthis paper.

Departmen t of CIassics an d Archaeology,TJniversity of Lan caster

ReferencesArchaeological Survey of Nubia 1910-11'.Report for 1907-8. 2 vols i- Plates. Cairo: SurveyOflice.Brothwell, D. R. 1972. Digging up Bones. London: British Museum (Natural History).Brunton, 6 . 1925-4. Interim report on Badari. Proceedings of British Association. Sessions 192,sand 1926.Brunton, 6. 1928. Qau and Badari. London: British School of Archaeology in Egypt.Darby, W. J., Ghaliounghui, P. and (;rivetti, L. 1977. Food: the Gift of Osiris. London:Academic Press.Dawson, C . E. 1948. Dental defects and periodontal disease in Egypt 1944-47. Journal ofDental Research. 27 ~512-23 .Hillson, S. W . 1978. Hu ma n Biological Varia tion i n the Nile Val ley , in R elation to En*ciironmentalFactors. Ph.D. thesis, University of London.Lengyel, I. A. 1975. Palaeoserology. Blood Typ ing with the Fluorescent Antibo dy Meth od.Budapest: AlradCmia Kiad6.MacPhee, T. and Cowley, G. 1975. Essentials of Periodontology and Poiod ontics. 2nd Edition.Oxford: Blackwell Scientific Publications.

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:,~pedition

Llellanby, 31. 1934. Dirt and t ee th : an expe ri men ta l s t ~ d y . a r t 141: the effect oi diel orr thcdental s t ructure and disease in man. llfedical Researrh Councfl Spe ck1 R e p o ~ f et iec lib r o r ,L o n d o n : l-Il\ISO.YIin. of Ag.,Fish. and Food. 1976, Manua! o f 2Yzf~i t ion ,th Edit ion . L ondo n: I3:MSC).Korcfstrom, H. A. and I l a l a r~d ,R . Keolithic a n d A Group si tes . Scan&fial/ian 'Joirii

Copenhagen : Xlunksgaarcl .Patwardhan, V. H. and Darby, W. J. 197a. 7'he State o f ,Vutsltion i n thc Aiali d/iidciIe Pd'~esi., N aslivilit~Vand erbilt e'niversity Press. Petr ie, W. 31. F. 1889. Piazcasa, Biahanu and .Arsi720&.London: Fie ld and 'l'ne!.. Petr ie, IT.R1. F. ancl Brunton, G. rgzq. Seriinenf. Londoir: British School of L+rc!2.aeology in Egypt . Porter , R. and Moss , R. L,. B. 1927 -51. l ; )~~ogra~~/~l) / l icd and .Anriciai I I i e ro ~ ~ ~ p h ic i l ~ l i ~ ~ y r a ~ l z yTe.vis, Rezefs an d Fabrtinjis. London r O ~ f o r d .%.!~ii~iersityress.Ranciall-MacIver, D. and Mace, A. C, 1902. E! Ainrah n:tii illy tlo s. h,ontlon: Eg ypt Explora'iic~ri F u n d . Reisner, 6.A. 1923. Bxc:avations at Kerrna. F I ~ i e a r dAfricaia Studies. 1' and VI. Ruffer, M. A. 1919. Food in Egypt . lWi~:inoii.esprisentis 2 l ' f izsiitut ~ d ~ E ~ ~ p f r . :l-Re.Saffirio, L. 1972. Food and dietary habi ts in ancient Egypt.. ;7ourfaal o; Pfa?nan R'i'oblio!~. 1 :297--305. Save Siiderbergh, T, i962 . Pre!in-iil~ary Re po rt of the iicandinavian Joi nt E xpe dition, ig6r . Kush. X:76-105, Save Soderhergh, 'r. 1963. Preliminary Report of t h e Scandlnaviax_i Jo int Fk pe ditio n: archaeologica! investigations betwcen Faras and Gemai, ihjovcmber 19 6 r - h l a r c h :gbz , k ush, XI :u-hg Save Sbcierbergh, T. 1.964. Preiiminasy Report of tile Ge and i~ia via n ;joint Ex.peditior1: archaeological investigations between Faras an d G em ai, Novem ber r9bz--.lMarcli 1963. Rush.XII::g-39. Scott , J. H. and Symon:;, 'id'. B. B. 1976. Introdz!zlceion o Dental -4rrato~tzy.5 th E di tio n , 37di.i-. bu rgh : Churchill Livingstone. Winton, A. %. and \ i7 in ton, K. B. r o q j , Analysis oo .Foo/lss.London : C hapman .

Abstract

Diet and dental diseaseDiet is a controll ing hcfo r is1 several c o~ uill on ro ups of (lentdl diseases. 'These includ e ehosc due to bacterial cleposits on the teeth .ind to defects of dcntai s t ructure. MLIC~I ecent r cxr-en:i.t~has been carr ied out , so that the ~e latr on sh ip f diet to these diseases is now well ~ P I O ~ ~ I I ,'I'his a!lou s th e freq uenc ies of occu rren ce or dellral diseases in ancient sk eletal nlaterlal to I l rused as indicators of th e diet eaten by th e population dul ing life. A dcsei iptio n i s given (,:t l ~ etheory behind this method a nd an exam plr of i ts applications to s lieletal m ~ te ri a lrom Egyytlanancl Nubian cemereries