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 disease

S. \V. Hillson

Teeth come into contact with every part of the diet that enters the body. Such marks as are left by the passage of food should therefore act as reliable indicators for the diet eaten during life. Even while still being formed in childhood, teeth are affected by dietary factors. Teeth have additional advantages for archaeology. They are readily identifiable in isolation from the jaws that hold them. The hard and tough materials of which they are 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 about which much is now known and which are easily studied in ancient material.

Dental anatomy and pathology as dietary indicators

The structzlre of teeth
Both of the main components of teeth - enamel and dentine (fig. elements which may be used at least in part as dietary indicators.
I ) .-

have structural

Enamel Dental enan~elmay be thought of as being formed in layers. Initially, these layers 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 the structures known as Browz Striae of Retzius. Such striae arise from a cessation of growth which causes a flaw or break in the crystalline structure of the enamel. The flaw follows the outlines of the growth layers throughout the body of the crown. They can be seen clearly in microscope sections of teeth (plate aa). Outside the zone of dome-shaped layering, Brown Striae of Retzizts emerge on the surface of the tooth crown. Where they emerge the same process that causes the striae themselves also causes small dips in the crown surface. This gives rise to a pattern of waves, called perikymata (plate I). Thus the effects of the Brown Striae of Retxizls may WorM Arclzaeology Volunze 1 1 Number 2 Food arzd nutrition 0 R.K.P. 1979 0043--8~43/110z-o14~ $I.~o/I

been seen oil the surface, obviating the need to make a section. Both the striae and perikyr~.atabecome more marked in the cervical part of the crown than elseavherc, Bttv~een the brown striae are f~uncl, smai!er incremcu:tal sti.uctures. These s1.e r:aileci claossstriaCons and arc due to variation in speed rather than actual cessation of cilaxnef growth. Cross st:-i~.tocs i:ccur rhythmica.lly, with what i s aiur7ost certainly 21 daily

shapeci

layers
-.

I-

e r. Lo~lgi:utii:~aTsection t!i~.ouph hypoti~etiea;taoth

Fkrire :z. r.-l i he physiology o f dental 'piaqa<:

peric.clicijy. 'b'Icej can be s~c. o :TI m~croscopcscctlclnri e l tceti~ (but nrtoon the curface) ff the number betclacn the Bioa;z Strias o f Kslzilcs is cormrcd, the resrril mild give t1it" time eiapscd bctv een the fo~rnationof the latter sti-uctnrec;. By this means, brovri s t ~ i a eare a h a sbonn to be 1hy7thrnic~llyformed. 7'k.e tin-c betveerr fol-n~a~lor oi. stliae varies bztwecn eight and ten days, but secrns to be roughly constant for each individual, T h e cause of the tnro rhythms (dirrinal and 8-10 days) IS uncertain and compl~cated, Diet may play a part, especially in the case of the 8-10 elsy rhythm, but factors such as general body temperature are probably also invclved, Occasionally a particularly~severe disrupkiofi of growth occiirs at one, or several, of the brown striae. 'a'bis causes klie perilzymata to become much rnore pronounced, which may result in the crown being imperfectly formed (plate zb). Such deformity is called enamel bypoplasia and m a y bc

Diet and dental disease

149

so severe that the shape of the crown is profoundly altered. I t has long been demonstrated that hypoplasia of this kind is related to vitamin D deficiency (Mellanby 19341, but it may also be caused by a general rise in body temperature, such as that occurring during fever. Thus it may be possible to use observations of enamel hypoplasia in ancient human teeth to indicate, if not diet alone, at least the general conditions of childhood. T h e age at which the events which caused the hypoplasia occurred is estimated in the following manner. Tooth crown surfaces may be divided (fig. 3, page 155) into rough zones (Hillson 1978), each covering a different period of crown formation and within each of which hypoplasia may be recorded. Microscope sections may be made of modern teeth and the number of Brown Striae o f Retzius between the boundaries of the crown surface zones counted. Average counts of cross striations are then determined between successive brown striae. I t is then possible to estimate the times taken in the formation of each zone. Ages for the start and finish of enamel formation are available (Scott and Symons 1976) and this allows estimation of the ages at which each zone boundary is reached. Many possibilities for error exist in this method, not least the widespread variation between individuals in the formation times of teeth. I t is, however, the only way at present available of estimating the ages of hypoplastic events and is likely to be reliable at least as a rough guide. I n this way, records of the severity of hypoplasia in each zone may be used to suggest dietary deficiencies or febrile conditions during given periods of an individual's development. Different teeth in the mouth. have different times of development, so that a scale of these childhood events may be constructed for each individual. For practical reasons, this scale is limited to the period between nine months and seven years of age. Dentine Like enamel, dentine grows in a rhythmical way. Finely spaced incremental structures in the dentine, the Lines o f oon Ehnev, are probably due to a diurnal rhythm. More widely spaced are the Contour Lines o f Owen, which may be due to a rhythm of upwards of ten days. Where a disturbance in growth occurs, of the kind producing the Brown Striae o f Retxius, patches of poorly mineralized dentine are formed. Such patches are known as interglobular dentine and have again long been demonstrated as connected 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. Dentine, however, can only be seen in a microscope section, and this limits its usefulness in archaeology, where lack of time or reluctance to damage ancient skeletal material may render section-making impossible. Plaque-related disease Soon after teeth erupt into the mouth, tliey are increasingly colonized by bacteria. These bacteria are highly specialized in adhering to dental surfaces and to each other; also in metabolizing the food entering the oral cavity. I n uncleaned teeth (which appears to be the case throughout most of antiquity) these bacteria build up on the surface of

the tooth into a layer which extends round the cerkical part of the crown, in contact with the gingivae. This layer is called plaque: and it is through the medium oi this connplex bacterial co:ony that many of the eEects of diet are expressed upon the teeth. 'l'he processes inuol\~ed in this may he srxmmarized under txvo headings: acid/alliali (pH) balance, allti inln~une response (fig. 2). The pf 1 of thc plaque varies according to the relative amount ,ilcid/c~lkali( p H ) b~zl~z~zce of protein as opposed to carbohydrate in the diet, When plaque bacteria rnetalnolizc protein, they produce alkaline waste products. Willen plaque bacteria metabolize carbohydrate, they produce lactic acid as a waste product. Z n this way, the pH of che plaquc changes throughout the clay. Pcriods of acidity alternate with alkalinity. Periods of particularlj high acidity, approaching pH 4, okcur when foods are eater? that conlain large quantities of sugars. Sugars are metabolized n ~ u c hmore rapidly man other carbohydrates and this causes more lactic acid to be produced rrlore quickly, It is thz relative balance between these Ilighly acidic and alkaline periods that determines whether the disease dental carics occurs. Ilrrring the acid phases, the millera1 of the er~amelis dissolved. During allialine periods, the minzral is replaced from a store which is maintained in solution in the saliva. If acid periods outnumber and outlast alkaline ones, a steacil 10s:; of mineral occurs from the enamel underneath the 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. rI7 he sugar sucrose is particularly effective in causing dental caries because of its specific involvement in the rapid growth of plaqv,~. Conversely, if lnuclz of the food consists of protein arrd the plaque is tE~usalltaliae for most of the cime, extra mineral is deposited in plaque on the surface of the tooelr. As stated above, the saliva contains rnuch dissolved mineral, which crystallizes within the plaque \$hen there are insufEcient acid episodes to cause it to redissolve. Silch mineralized plaque builds up into a layer that, in ~~ncleaned teeth, can be quite thick and which is called dental calculus or tartar (plate 3b). Dental caries and dental calculus tend to bc mutually exclusive because of this relationship with plaque pH, For this reasorr, mhen their frequency is recorded in ancient teeth, they should make particularly good indicators of the protein versus carbobycirate content ol the diet. I t should be emphasized that this is a much simplified description of the disease processes; beside diet other aspects of physiology, both genetic and eilvironmental, are involved.

Pi~rszz~ne response. The presence of large colonies of bartcria next to the gingivae stimulates a response in the tissues of the jaw (Macl'hes and Cowley 1975). Bacteria produce potentially toxic molecules called antigens, which cause tliie body's defence mechanisms to be activated. Local innate immune response includes an inl'larnrnatory reaction, with the arrival of white blood cells which ingest bacteria and thus destroy them. There is also an acquired immune response, in which specialized white hlood cells arrive and produce antibodies, n~oleculesspecific to individual antigens, wbiclr

Diet and dental disease

I5I

bind to them and thus neutralize them. Slight localized inflammation and a mild, acquired immune response are a normal finding in the gingival tissues of most individuals. This normal, slight response involves very little tissue damage. When the plaque deposits 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 the hypersensitive response large numbers of white blood cells arrive, including the specialized antibody-producing cells. Although immune response is designed to combat bacteria and their effects, rather than to damage body cells, it can have a disastrous result when elevated to a hypersensitive level. Hypersensitivity is essentially an overreaction to what is in fact not an especially dangerous stimulus. Processes involved in massive bacterial destruction and neutralization of antigens also destroy body cells and interfere with body metabolism. In this way, the collagen fibres which attach both the gingivae and teeth to the underlying bone of the jaw are lost. This bone is probably maintained in a shape suitable for retention of teeth (i.e. with tooth sockets) by the functional stimulation of the attaching collagen fibres. When the bone is relieved of this 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 are eventually lost, and the bone remodels to a smooth, flattened and socketless surface. The effects of this resorption and remodelling are termed periodontal disease and are commonly found in ancient skeletal material.

Wear patterns
Food contains many abrasive elements. These may be mineral, as in bone or the gritty contaminants from querns in stone-ground flour. They may also be due to the tough cellulose molecules of plant tissue, or the collagen of animal tissue. Contact with these abrasive constituents inevitably wears down the surfaces of teeth, as food is ground between them (plate 4b). This process is called attrition. Very little information can be gained about the rate of wear in ancient skeletal material. This is due to difficulties in ageing adult individuals precisely enough. All that is possible at present is an examination of the pattern of wear throughout the dentitions of each individual. Molar attrition may be compared with that of the premolars, canines and incisors. Differences are found between populations in this pattern and dietary differences can sometimes be inferred as the cause. Too little work with dental attrition has been done with modern populations, of known diet, for Inore than general inferences to be made.

Example: dental disease in Ancient Egypt and Nubia

Using skeletal material from Egyptian and Nubian cemeteries, a sample represcnting 941 individuals has been investigated (Hillson 1978). The cemeteries ranged in date from Predynastic at Badari and A Group in Nubia, to Christian burials, also in Nubia (table I).

Diet and dental disease The people

153

T h e term 'population' when applied to man is a rather vague one which implies ;a geographically definable group of individuals who interbreed mostly with each other. A comparison between populations of the frequencies of oral diseases should indicate any differences in the type of diet most commonly eaten in either group. In this way, it may be possible to reconstruct a regional and temporal picture of the diet. The difficulty in archaeology is the uncertainty of what ancient living population a group of skeletons may represent. A group of burials within one cemetery may indeed represent a local human population. I t may, however, just as easily represent only one section of that population, or include individuals from populations not genetically closely related to the local one. The only way in which this problem can be approached is by examining the genetic relationships of the individuals buried in each cemetery. Genetic differences between members of the same cemetery, or similarities between members of different cemeteries, may indicate the nature of the population being studied. Blood grovlps arid other biochemical factors are the best guide to genetic relationships. Although there are claims for the detectjoil or' such factors in ancient skeletal material (e.g. Lengyel r g ? ~ ) , for most practical purposes similarities and differences in the form of the skeleton must be used instead. Variation in shape of the skull alone is still almost universally used for such work. The skull is relatively easy to measure. I t appears to be less affected by environmental pressures during development than are post-cranial bones and may thus act as an indicator for the genetic make-up of an individual. Although the sIrulls used in the present study varied considerably in shape, no groupings of individuals within a cemetery, or remarkable differences between cemetery groups were found. Skulls of different sexes of course differed, but all skulls of one sex were similar in their measured shape. Comparison was by principal components analysis, discriminant analysis and multidimensional scaling. This finding is consisteilt with other studies (summarized in Hillson 1978) of the ancient populations of the Nile valley. I t appears that sliull shape has been remarkably constant both in time and space. While it is uncertain that this represents a genetic constancy, the general morphological similarity does at least suggest that. differences in disease frequency may be explairled by diet rather than by structural variation.

The diet
Three main studies have been carried out that attempt to summarize information about the diet of the ancient Egyptians: Ruffer ( ~ g ~ gSaffirio ), (1972) and Darby et al. (1977). I n all of these studies, textual, pictorial and archaeological evidence are used, but only rarely is there any indication of the numbers of people who habitually ate a particular foodstuff. So as a guide to the nutritional status of the Egyptians, they are of little use. For the most part, an indication of the range of foodstuffs available is given: chronological changes in diet are not discussed. Domestic animals - cattle, sheep, goats and pigs - were kept from Neolithic times.

Wild animals were also hunted, includlng hare, anrelope, ~9.jldfow\-9 and fish, Cereal crops included wheat, barley and millet, 'These werc used to make bread, for mbicln there is ample evidence. Bread was apparently as important then a. it Is n o ~ v(14atwardhan and Darby 1972). On a stele commemorating an expedltion of Seti l ( ( r 309 xzgr B.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 bread yields 4,483 kcal (R'lin. Ag. Fish and Food ~ 9 7 6 which )~ is an adequate daily provision of calories. IVJany dizerent kinds of vegetables mere eaten, including pulses, and It is likely that the ancient Egyptian peasants gained most of their protein from this source, as do the present dayjellnhin. Fruit uTasalso grown, but there is Iittlc information about its importance to the diet. f ~ in s Egypt today (Patwardhan and Darby ~ 9 7 2 it )~ idlikely that dried fruit n7as eaten more than frcsh fruit. i n the cemetery of Deir-el-Medlna, M here workers engaged in building the royal necropolis were apparently buried, cr~ished dried figs were baked into bread (Safirio 1g.j~). Sweetening agefits included honey, dried carob, dates and figs, 2nd grape-juice concentrates. A11 contain large quantities of sugar, dried carob having a particularly high concentration of sucrose (M'lnton and 'Vcvinton 1945), the sugar mainly responsible for dental caries today. "8iegetaPdr oils were available in ancient Egypt, perhaps eaten on bread, as by the modern Jellahin. Th-~ls the 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 e a s probably bread (most likely wheaten) ancl the main source of protein, vegetables perhaps with some fish. The wealthier people probably had rnore protein from mammal meat and other such h~xurics.Even poor people are unliltely to have been especially undernourished, except in times of faminc.

The teeth

Plaque- elated diseases "6he first problem in stuclyin-igthe pathology of a large skeletal sanlple is in devising a method o C recording that allows individuals to be comparec! statistically (fig. 3, table 2). Much time was also spent investigating the best way in which to present the informafion, The final method used was to produce a percentage ol: individuals affected by a given disease at each cemetery. IrTistograms and table5 were constructed for each degree of severity of each disease, showing the percentage of individuals at each site who had more than 10 per cent of their permanent t x t h aflected. This solved the problems of ~nissingteeth and ~ncornpletejaws, giving 23 comparable index between all sites. I n 1946, a survey of dental health in Abassia Fever Hospital, Cairo, was coanductcci by Damson (1948). Approximately go per cent of 944 individuals, aged between r 5 and 55 years, had some evidence of dental caries. On average 0.95 teeth were affected per individual. Periodontal disease of some kind was almost universal, biit especially severe and chronic disease of the kind likely to produce bone changes occurred in abo~lt 4 r pet cent of cases. Dental calculus deposits mere also almost universal. This pattern of disease is presumably due to the diet described above, and to lack of oral hygiene. Vegetable products form the staple foods. Most of such foods contain

Diet and dental disease

155

Dental Caries Severity Coding

ENAMEL

PULP
DENTINE REPAIR

Caries Position

OCCLUSAL.

Dental Calculus

3RD MOLAR

1ST. INCISOR

MESIAL INTERPROXIMAL

DISTAL
INTERPROXIMAL.

grades

Zones for recording Enamel Hypoplasia

Right Half Permanent Dentition

INCISORS

Upper

Lower

MOLARS

PREMOLARS CANINE

INCISORS

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

TABLE 2

Coding for periodontal disease and attrition Periodontal disease o = no bone resorption or remodelling as a result of periodontal disease.

bone resorption in the crest of the alveolar process (the part of the jaw that actually
supports the tooth) only. 2 = bone resorption in the whole of the alveolar process round the tooth. 3 = some deposition of new bone (healing), but areas of destruction still visible. 4 = areas of bone destruction covered by new bone. j = remodelling complete - bone surface conlpact and smooth.
I =

Attrition
Severity of attrition was scored by the pattern of dentine that was exposed on the occlusal surface of the crown, using a system similar to that of Murphy (1959).
-

both carbohydrate and protein, thus allowing the plaque growtla necessary for periodontal disease and the frequent alkaline episodes necessary for calculus deposition, Sugar intake is presumably large enough for the common occurrence of dental caries. I n ancient Egypt and Nubia, there is no textual or archaeological evidence for oral hygiene, nor was there any biological evidence for this. Plaque deposits could therefore grow7until limited by the polishing effects of chewing. For sites of the Dynastic period and later, the incidence of dental caries was 10 per cent or less, of individuals being affected in more than 10per cent of their teeth, Dental calculus deposits were observed on the teeth of 50 per cent of the individuals studied. Bone destruction and repair due to 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 indices of disease occurrence must also be different. Despite this, there is a large differchnce between the two sets of figures. All the plaque-related diseases seen1 less common ira the ancient material than the recent. This piesumably reflects less extensive plaque deposits or, the anc,ent teeth. 1 9 major difference in the basic diet is not necessary as an explanation, since ihe high frequency of calculus still suggests consumption of vegetable foodstuffs (see beloa) during the Dynastic period. Sugars play a large role in plaque growth and the difference could be due to increased sugar consunlption in recent Egypt, perhaps a reflection of the modern widespread habit of drinking heavily sweetened tea. Such an explanation is supported by the especially low incidence of caries in the ancient material. So T postulate from the evidence ;a general diet similar to that of today's fell~shia,but with sugar less widely consrrmed, The incidence of the plaque-related diseases in ancient material is broadly sln~ilar between 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 by females, or to physiological dlgerences. 'The diseases are Jess comrnorl in childre11 and sub-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, Aby dos, El-'Annra and Badari, have l o ~ e i rreqi . ~eccies o C plaque-related diseases tha? t h latcr ~ cemeteries. This agam is presurrrably due to less extensive plaque deposits, which may have been caused by even lower sugar consumption. Another reason might be that more meat was eaten than ~egetablefoods. Most meats contain almost no carbohytirate (Min. Ag. Fish and Food 1976). This s m l d generally cut down the size of plaque deposits and thus the incidence of all diseases equally. 'The floodplain of the Wile was wider and rainfall higher in Pretlynastic times than later (Hillson 1978) and it is likely that vegetation cover was more extensive outside tlie valley. Game may have been more readily avaiiable, or the do~nesticanimals which are found as bones on Predynastic sites more vi-idespread. Support for thrs idea of differences in basic diet during Predynastic times may come from the pattern of dental attrition, which differs from that of later pznods. Wear oi the anterior teeth relative to cheek teeth is less severe in the Predynastic skrrlls, l\!leat contains fewer abrasive constituents than vegetable foods and is thus less likely to cause tooth wear.

I'lat~ i I'erikymata, shomn on a rubber latex cast from the srrrface of a canlne from Kerrrla h u b l a (c. 17za-I550 B.c.)

Platr r ( a ) Section through dtntal enamel of a canine from Kerma, Xubia ( c . 1720-1j.jo B.c.) I he sectton is longitudinal and observed between crossed polarizers, the plate being made up of a rriosaic of sevcral photomicrographs. B~ozcr7zSfriae qf Rrtzius may be seen as a series of darker lines in the body of the enamel. T h e worn, occlusdl surface is on the left of the plate, the cervical region further to the right
r
7

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

I'lat~ j(u) ,Ll~lddental carles I n the left 'tuppet i t c o ~ l t i ,irrd thlrci tnolars ot ,In ~ n d i \ ~ d l r d froirl l Kcrtna, Uubia ( 6 . 1720 I j;o u.c.)

Plate 3(6) T h e eroded remains of extensive dental c a l c ~ ~ l u deposits s on thc upper lett nlnlars (and second premolar) o f an individual frorn Kernlib

Plate # ( a ) Kesorpt~on due t o perioclontal d~srase in thr upper jaw of an lndiviitual from

Kerma

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

Diet and dental disease

TABLE

I57

3 D$+j%rences in overall incidence of plaque-related diseases between sexes

Male
Yo

Female

Yo

Slight dental caries (Grade

I)

Severe dental caries (Grade 3) Occlusal dental caries Distal interproximal dental 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 more than 10 per cent of their permanent dentition affected by each disease, with the total number of individuals from which the percentage was calculated in brackets underneath.

4 DiJ'yerencesin overall incidence of plaque-related diseases between 10-year age grozqs

TABLE
10-20

20-30

30-40

40-50

50-60

Yea~s

Years

Years

Years

Years

%
Slight dental caries (Grade I) Severe dental caries (Grade 3) Occlusal dental caries Distal interproximal dental caries Periodontal disease destruction (Grade 2) Periodontal disease .repair (Grade 5) Calculus (Grades I, 2 or 3)

Yo

Yo

Yo

T h e table shows the percentage of individuals with more than 10 per cent of their permanent dentition affected by each disease, with the total number of individuals from which the percentage was ca!culated in brackets underneath.

Soine Dynastic sites did not f'ollccv t h e general trcnb. Caries frequency is higher at Sidmant, 53185 a n d Hawara than a t other sites (fig, 4). ' r h i s suggests that inore evtensire acid plaque deposits existed on the teeth of individuals buried there. Wow is this supported by the evidence of other diseases?
Dental Caries, Grade 1 Severity Dental Caries, Grade 3 Severity

100,

100,

100

Periodontai D~sease, Grade 2

1oc

Pcriodontal Disease, Grade 5

55

4?

EY

it9

1E

2%

50

hi'

19

7.1

1C0

Dental Calculus, Individuals Unatfecteci

ABY ELA BAD 277 SED I< Rll A S35 270 SHL 185 H \IVA BG A S25

Abydos El --'Amra Badari S i t e 277 (S.J.E.) S~dmant Iccrma Site 3.5 (S.J.E.) Site 270 (S.J E,) Shallal S~tc i 8 5 (S.J.E.) Hawai-a Biga Slre 25 (S.J.E.)

Fkure 4. Plaque-related disease. Percentage of individuals at each site wit11 more than lo per cent of the permanent dentition affected by Grades I and 3 caries, Grades 2 and 5. periodontal
disease, unaffected by calculus. Dotted lines above and below thc top of each bar of ahc histograms define the 9.5 per cent Confidence Limits. Each site is denoted by an abbreviation; the associated numbers give thc total of individw~lsfrom which the percentages were calaxlated.

Diet und dentul disease

r gg

.
C

I"";

60 1
63:

Badari
~~~

................

. . . . . . . . . . . . . . .
~-

4 0I
20.

. . . . . . . ..... ....
t
.-..-

I
i
C i

...

01 . _
5 4

,
2

LOWER RIGHT FIRST h l O L A R

UPPER RIGHT C A N I N E

UPPER RIGHT SECOND M O L A R

o/lOOl '' 804

Wawara
.........

Years a f t e r 01-ti,

rt

401 20 0 5 4

7
:
-

1-i
-

1
- 4 -5 f i 4
,

7--

1
3 '

--

I--

1 - -, --

L O h E R R l G l i T FIRST M O L A R

UPPER RIGHT CANINE

UPPER RIGHT SECOND M O L A R

o ) ' ~ ~

lo 801
604 401

Kerma
. . . . . . . . . . . . . . . . . . . . . .

. . .
[ I r . i

.....
,. . . . . . . . . . . . . . . . . .

~. . . . . . . . . . . . . . . . . . . . . . . . .
...
1
7----

----i

................

..
5
- l - t -b

L-i

.__?_--

-..A--..---_--_.-.
1

2
2

2
?

5
T

4
l

3
v r

2
-

m i

- . - 7 7 - 7 - 1 7 - - - T V T - T

Years after 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 Lower Right First Molar, zones 3 and z of the Upper Right Canine, zones j,4, 3, 2 and I of the Upper Right Second A.Iolar. Dotted lines above and below the top of each bas of the histograms define the gj per cent Confidence Limits.

r Plaque thickness Periodontal disease requires extensive plaque deposits, but is relatively independent of pH. Bone destiuction is common at Sidmant and the repair phase of periodontal disease (fig. 4) common at S185. Hawara is omitted owing to difficulties with recording, but the thickness of plaque deposits is generally supported.
Plaque pH Dental calculus should bear an inverse relatioiiship to dental caries, Sidmant, S185 and Hawara are all especially low in ca1cl;Ius (fig. 4). T h e most likely cause for such extensive, acid plaque deposits is increased consumption of sugar. Both Hawara and Sidmant apparently contained the bodies of moderately well-to-do townspeople and S185 contained Egyptianized Nubians, or
2

Egyptian immigrants to Nubia. Thus the increased occurrence of sugar eating may be explained by social diflerences.

Tooth slructzc~e Work was also carried out on the structural defects of the teeth, Scrrrac preparation and examination of ground sections was undertalcen, but this vras timeconsuming 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 ( , tooth crown. Three site.; proved to have especially high Scquenclies of s.rci-1 Itypopiasia Badari, Sidmanr and Hawara. As stated above, difirenl teeth can bc arranged i q a sequeacc to show how the incidence of hypoplasia varied with age. Figure ! ; s11:awrs histogranls constructed horn such a series: crown zones (i;lg, 3) 5, 4, 3, a and r oC tile Lo7:ver Righ.t First ?+d\uolar, zones 3 ant1 a of the 'lippcr Right C a ~ i n e ,zones 5, q., 3, 2 a11d i of the Upper Right Second hiIolar. T h i s provides the sequence from nin:: months to seven years after birth, Histograms are shown for Badari, Sid~narrt a nd Ra.wasa, the t h r e exceptionl-ilsite:;, 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:y is at this Ici:el, or slightly iosver, throughout ~ o s of t the graph, Also shown 2.t Rernr;i is the x~~eakness of t ~ v o parts of the scale - zones 5 and 4. of the ko\ver Right First IVlolar and zones 5 and 4 of the Upper Right Second Nholar. 'These zones are formed early i i s the 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 qow frequencies in these parts of the gt aphs a t all four sites. Tn addition to this qa per cent 'backgrounds frequency of hypoplasia, Badari, Uidmzrrrt and 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 greater susceptibility oor' "ce canine to hypoplasia, but rhe iack of this peak at other. sites argues against this explanation. The trough is also unlikely to be due to lower.ed s~tsccp~bility at zone I of the Lower Right First Molar, as this should rbeore-tically be a partictxlarly susceptible part of the tooth. 'Fhe 4-0 per cent background frequency of hypoplasia could be due to constantly occurring 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. A possible additional cause may be hrtlaer vitanlin B P deficiency, Three possible reasons for such a deficiency exist:
Vitamin D is manufactured in the skin by sianl~ght.ba?suficient exposure to suniighi may thus cause a deficiency. ) . Poorly-nourished mothers produce vitanlirr Ib z Breast milk contains some vitamin P deficient breast milk. 3 Vitamin D in later childhood comes directly from the diet, This diet may very easily be deficient.
T

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

Diet and dental disease

161

This may be due to the use of lactation as a contraceptive method, or to an attempt to introduce a deficient adult diet slowly. Thus in the ancient Nile valley, it is quite possible that weaning occurred at three to four years. When the supply of breast milk was cut off, the other sources of vitamin D may not even have compensated for the loss of this relatively small supply. At Sidmant and Hav~ara, where parents may have been relatively well-to-do, children may have been especially heavily clothed, or confined indoors, causing insufficient sunlight to reach the skin. Other causes, such as particular susceptibility to childhood diseases and particular environmental or genetic predispositions must not be forgotten. The high incidence of hypoplasia at Sidmant and Hawara may have played a part in the high frequency of dental caries at these two sites. Hypoplasia provides flaws in the enamel which may be exploited by the solution process.

This work formed part of a P1i.D. project at the Institute of Archaeology, University of London. I t was supported by studentships from the University of Birmingham and the Medical Research Council. I would like especially to thank: M r D. W. Brothwell, D r A. Boyde, D r I. D. Graham, D r C. Stringer, Mr 13. Denston and Dr 0. V. Nielsen for their help during the work; also Mr R. C. Turner for preparing the drawings in this paper.
Department of CIassics and Archaeology, TJniversity of Lancaster

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Abstract

Diet and dental disease

Diet is a controlling hcfor is1 several co~uillongroups of (lentdl diseases. 'These include ehosc
due to bacterial cleposits on the teeth .ind to defects of dcntai structure. MLIC~I recent
r cxr-en:i.t~ has been carried out, so that the ~elatronshipof diet to these diseases is now well ~ P I O ~ ~ I I , 'I'his a!lou s the frequencies of occurrence or dellral diseases in ancient skeletal nlaterlal to Ilr used as indicators of the diet eaten by the population dul ing life. A dcsei iption i s given (,:t l ~ e theory behind this method and an examplr of its applications to slieletal m ~ t e r i a from l Egyytlan ancl Nubian cemereries