J. Anat. (1998) 193, pp. 431–442, with 16 figures Printed in the United Kingdom 431

Pathological bone changes in the mandibles of wild red deer

(Cervus elaphus L.) exposed to high environmental levels of

fluoride

MICHAEL SCHULTZ1, UWE KIERDORF2, FRANTISEK SEDLACEK3 AND HORST KIERDORF4

"Zentrum Anatomie, UniversitaX t GoX ttingen, GoX ttingen, Germany, # Institut fuX r Allgemeine und Spezielle Zoologie, Justus-

Liebig-UniversitaX t Giessen, Giessen, Germany, $ Institute of Landscape Ecology, Ceske Budejovice, Czech Republic, and

%Zoologisches Institut, UniversitaX t zu KoX ln, KoX ln, Germany

(Accepted 2 June 1998)

A macroscopic, microscopic and scanning electron microscope study was performed on the pathological

bone changes of the mandibles of wild red deer (n¯ 61) exhibiting severe dental fluorosis. The animals

originated from a highly fluoride polluted area in Central Europe (Ore mountains and their southern

foreland, Czech-German border region) and constituted 11±2% of the studied red deer sample (n¯ 545)

from this area. Pathologically increased wear and fracture of fluorosed teeth caused a variety of mandibular

bone alterations, including periodontal breakdown, periostitis, osteitis and chronic osteomyelitis. As a

further consequence of severe dental attrition, opening of the pulp chamber and formation of periapical

abscesses were occasionally observed. In case of severe periodontal breakdown, loss of teeth from the

mandibles was found. In addition to the inflammatory bone changes, the occurrence of osteofluorotic

alterations was also diagnosed in the specimens with the highest bone fluoride concentrations (" 4000 mg

F−}kg dry wt). These changes comprised extended apposition of periosteal bone onto the mandibular cortex

as well as deformation of the mandibular body, which was attributed to a fluoride-induced osteomalacia.

The present study provided circumstantial evidence that, in addition to fluoride induced dental lesions, the

occurrence of marked periodontal disease and tooth loss is an important factor responsible for a reduction

of life expectancy in severely fluorotic wild red deer.

Key words : Dental fluorosis ; skeletal fluorosis ; periodontal disease ; bone pathology; environmental pollution.

Fluorosed dental hard tissues of deer exhibit a variety

of pathological alterations, including enamel sub-

surface hypomineralisation of different depth and

extent, occurrence of enamel hypoplasias, presence of

large amounts of interglobular dentine and accen-

tuation of the incremental lines in enamel and dentine

(Kierdorf et al. 1993, 1996c, 1997; Appleton et al.

1996; Kierdorf & Kierdorf, 1997). As a consequence

of enamel hypomineralisation, severely fluorosed deer

teeth show markedly increased wear, eventually

leading to the loss of a functional tooth shape. In

addition, fracturing of severely fluorosed teeth and

tooth loss were occasionally observed in wild deer

exposed to increased levels of fluoride (Kierdorf et al.

Correspondence to Dr Horst Kierdorf, Zoologisches Institut, Universita$ t zu Ko$ ln, Weyertal 119, D-50923 Ko$ ln, Germany. Tel. : ­49-221-

470-2606; fax: ­49-221-470-4987.

1996c). Recently, a strong positive correlation be-

tween the degree of dental fluorosis and mandibular

bone fluoride content was found in a sample of red

deer exposed to elevated levels of fluoride, thus

demonstrating the usefulness of dental fluorosis as a

biomarker of increased fluoride exposure for bio-

monitoring studies in deer (Kierdorf & Kierdorf,

1998). During research in the heavily fluoride-polluted

area of the Ore mountains and their southern foreland

(Czech-German border region) (Kierdorf et al.

1996a, b, c), a high prevalence of pathological bone

changes was also found in the mandibles of fluorotic

red deer. So far, these bone alterations have not been

described in great detail, nor has any other work on

wild mammals focused on mandibular bone pathology

related to the occurrence of dental fluorosis.

Fig. 1. Right hemimandible of a 10-y-old red deer stag, bucco-occlusal view. Bone fluoride content 3647 mg F−}kg dry wt. Severe attrition

of P$, P

%and M

#, and fracturing of M

$. Note roughening of the cortex (arrowhead) beneath the P

$due to periosteal bone apposition.

432 M. Schultz and others

In an attempt to further characterise the con-

sequences of increased fluoride exposure on free-living

deer the aims of the present study have been: (1) to

provide a detailed description of the pathological

changes to the mandibular bone of red deer from this

highly fluoride polluted area, (2) to study the aetiology

and pathogenesis of these lesions and (3) to discuss the

consequences of the pathological mandibular bone

alterations for the individual and the population.

Specimens

A total of 61 defleshed, cleaned and dried red deer

mandibles (n¯ 43) or hemimandibles (n¯ 18) ex-

hibiting marked to severe dental fluorosis (for details

of tooth classification see Kierdorf et al. 1996b) were

at our disposal. Except for 1 specimen, all mandibles

originated from male animals. The analysed material

represented 11±2% of the total number of red deer

specimens (n¯ 545, of which 410 showed dental

fluorosis of varying degrees) with a completed per-

manent dentition, that were inspected in the course of

our above-mentioned biomonitoring studies (Kierdorf

et al. 1996a, b). The study area is exposed to severe

fluoride pollution, originating mainly from emissions

of the large brown-coal fired power plants situated in

the north-Bohemian basin (Reuter et al. 1997).

Except for 2 animals, which were found dead, all

red deer had been taken during normal hunting

operations. Their mandibles were collected, cleaned

and provided for study by the local hunters. The age

of the individuals was assessed independently by 3

experienced persons, based on the wear of the first

molats. The ages given in this paper are the means of

these 3 values, rounded to the nearest full year. The

M"

was used for age estimation since in red deer

exposed to high fluoride levels during dental de-

velopment this tooth is the only one exhibiting normal

enamel mineralisation and, thus, also normal, i.e. age

related wear (Kierdorf et al. 1996c). This has

previously been attributed to the fact that crown

formation in the M"takes place prenatally and during

the period of milk feeding and that, contrary to the

Fig. 2. Left hemimandible of an 8-y-old red deer hind, bucco-occlusal view. Bone fluoride content 4167 mg F−}kg dry wt. Formation of deep

alveolar bone pockets with partial or total root exposure between the molars and between P%and M

". Loss of interdental contact between,

and slight mesial inclination of, the molars. Also note roughening and dilatation of the corticalis and deformation of the mandibular body.

Fig. 3. Left hemimandible of an 8-y-old red deer stag, bucco-occlusal view. Bone fluoride content 4680 mg F−}kg dry wt. Pronounced loss

of alveolar bone, especially between M"

and M#, leading to total or partial root exposure. Loss of interdental contact between the molars

and between P%

and M". Also note deformation of the mandibular body.

Fig. 4. Left hemimandible of a 6-y-old red deer stag, lingual view. Bond fluoride content 2262 mg F−}kg dry wt. Normal enamel appearance

of M"

(asterisk), whereas the other teeth exhibit enamel discolouration and moderately (premolars) to severely (M#) increased wear. Note

wedging of forage into interdental gap between P%

and M".

other, later mineralising permanent cheek teeth, it is

therefore not exposed to markedly elevated plasma

fluoride levels during development, even in individuals

from highly fluoride-polluted habitats (Kierdorf et al.

1996 a, c). The estimated ages of the specimens

forming our sample ranged between 5 and 13 y.

Crown formation in the permanent dentition in red

deer is completed at C 26 mo of age (Brown &

Chapman, 1991).

Samples of mandibular bone were obtained and

analysed for fluoride content with a fluoride ion

specific electrode (Orion model 96-09, Cambridge,

MA) as described previously (Kierdorf et al. 1996c).

Compared with age matched controls from an

unpolluted area (highest concentration 1026 mg

F−}kg dry wt in a 14-y-old animal), the bone fluoride

levels recorded in the present sample were increased

by factors of 4±0 to 8±1 (Kierdorf et al. 1995, 1996c).

The highest value (4680 mg F−}kg dry wt) was

measured in an 8-y-old individual.

Examination of bone changes

All mandibles were first inspected for gross mor-

phological bone changes and photographed. After-

wards, buccolingually oriented -rays were taken

from selected specimens. For histopathological analy-

sis, epoxy resin embedded, buccolingual ground

sections of 70 µm thickness were prepared from

segments of some of the mandibles according to the

method described by Schultz & Drommer (1983) and

Schultz (1988). The sections were viewed and photo-

graphed in normal and polarised transmitted light.

For scanning electron microscopy, bone samples were

removed from the mandibles, mounted on aluminium

stubs, sputter-coated with gold-palladium and viewed

in a scanning-electron microscope Zeiss DSM 250,

operated at 15 kV.

In the fluorotic red deer mandibles only the 1st molar

exhibited normal wear, whereas the other permanent

cheek teeth showed pathologically increased attrition

Pathological bone changes in fluorotic deer mandibles 433

Fig. 5. Lingual mandibular surface of the specimen shown in Fig. 3. Note pitting of the cortex and numerous impressions of small blood

vessels.

Fig. 6. Scanning electron micrograph of the bone surface shown in Fig. 5. Impressions of small blood vessels (asterisk), blood vessel openings

(arrowhead) and numerous microfistulae are discernible. ¬22.

Fig. 8. Apposition of periosteal bone onto the original cortical surface of the mandible shown in Fig. 3. Scanning electron micrograph. ¬50.

(Figs 1–4). In consequence, a marked and often

irregular reduction of crown height and crown length

was observed in the fluorosed teeth, leading to the

formation of dysfunctional, sometimes sharp-edged

tooth crowns. Fracturing of M#or M

$was seen in 15

of the 61 (¯ 24±6%) specimens (Figs 1, 12, 13). In the

434 M. Schultz and others

complete mandibles, tooth fractures mostly occurred

in a bilaterally symmetric fashion.

As a sequel of severe dental attrition and tooth

fracturing, advanced periodontal lesions and signs of

dentoalveolar abscess formation were found in 32 of

the 61 (¯ 52±5%) specimens forming our sample. In

the (macerated) specimens an initial sign of perio-

dontal disease was a slight bone loss at the alveolar

crest, leading to exposure of cancellous bone and of

the proximal parts of the tooth roots (Figs 2, 3). A

more pronounced reduction in height of the alveolar

process was typically associated with loss of contact

and the occurrence of gaps between adjacent teeth

(Figs 2, 3). Such diastema formation was most

frequently found between the 1st molar, possessing

enamel of normal hardness, and its neighbouring

teeth (P%and M

#), whose hypomineralised enamel had

been rapidly eroded due to interdental and occlusal

wear. Gap formation between P%and M

"was further

promoted by the fact that the contact face between the

crowns of these 2 teeth is rather small and confined to

their more occlusal portions. In 1st and 2nd molars,

the loss of contact with their neighbouring teeth often

led to a mesial drift and sometimes also to a slight

mesial inclination, leading to additional gap form-

ation within the tooth row (Figs 2, 3). Wedging of

forage into the interdental gaps (Fig. 4) was associated

with further resorption of alveolar bone, thereby

creating more space for additional food impaction.

In specimens exhibiting severe periodontitis and

alveolar bone loss, the basal portions of the tooth

sockets were also affected, and advanced bone

resorption concomitant with complete exposure of

individual tooth roots as well as formation of deep

and distended bone pockets were observed (Figs 2, 3).

Gross morphological bone changes related to the

suppurative inflammatory processes included

roughening and pitting of the buccal and lingual bone

cortex due to penetration by small blood vessels and

presence of numerous microfistulae (Figs 2, 5, 6).

Inspection of ground sections taken from the

affected regions revealed pathological changes of the

mandibular cortex resulting from the inflammatory

processes. Thus in the specimen shown in Figure 3

apposition of layers of woven bone onto the original

lingual surface of the mandibula was observed

(Fig. 7a). As a consequence, a highly porous outer

bone layer had been formed. This finding marks a

chronic inflammation which seemingly acted with

recidivation.

In some specimens, new cortical bone formation

was confined to areas affected by the inflammation

and the bone apposition was thus regarded as resulting

from a periosteal reaction triggered by the inflam-

matory processes. However, in 2 specimens with very

high bone fluoride levels (4680 and 4167 mg F−}kg

dry wt, respectively) a more generalised apposition of

a layer of periosteal bone onto the original mandibular

surface occurred (Figs 7b, 8). Also, in 3 of the 4

specimens with bone fluoride levels exceeding 4000 mg

F−}kg dry wt present in our sample, an abnormal

curvature of the mandibular body was observed (Figs

2, 3). This deformation indicated a weakening of the

mandibular bone in the affected individuals.

In cases of excessive dental attrition, the occurrence

of pulpits and periapical inflammation, causing the

formation of chronic periapical abscesses, was also

occasionally observed. Thus in the specimen shown in

Figures 9–11, opening of the pulp chamber of the

severely worn P%

had caused the formation of a

periapical abscess associated with the distal root of

this tooth (Figs 9, 11). Deep-seated suppuration at

this location then produced an opening fistula in the

buccal cortex of the mandibular body, the relatively

large sinus opening being surrounded by a rim of

newly formed woven bone (Fig. 10), indicative of a

reactive periostitis. Microscopic examination revealed

that the abscess had penetrated through the bottom of

the tooth socket into the mandibular canal (Fig. 7c).

As is shown in Figures 1 and 7d, a chronic

inflammatory process, established as a consequence of

severe dental attrition, could also induce a periosteal

reaction, leading to the apposition of woven bone

onto the buccal cortex.

Tooth fractures constituted another pathological

condition causing periodontal disease in the fluorotic

mandibles. In the specimen depicted in Figure 1,

molar fracturing must have occurred shortly before

death, since the associated periodontal lesion is still

rudimentary. A much more advanced stage of perio-

dontal disease resulting from tooth fracture is shown

in Figures 12 and 13. In these cases, inflammation

following tooth fracture had led to deep-seated

suppuration and partial destruction of the tooth

sockets of both M$. In the left hemimandible, opening

of the mandibular canal had occurred (Fig. 12).

Beneath the fractured teeth, the lingual face of the

mandible’s outer cortex exhibited an irregular pitting

and impressions caused by small blood vessels.

Inspection of ground sections revealed signs of severe

bone inflammation in the tooth socket of the 3rd

molar. On the lingual face of the mandibular body a

thin external basic lamella covering the original cortex

was observed. In the pitted area, the bone surface was

structured by partly very flat, partly deeper foveolar,

this being indicative of healed inflammation. On the

Pathological bone changes in fluorotic deer mandibles 435

Fig. 7. Thin ground sections (70 µm) viewed in polarised light using a hilfsobjekt-I (quartz) (a, b, d–h) or in normal transmitted light (c).

(a) Apposition of layers of woven bone onto the original lingual alveolar cortex, marking a chronic inflammation; arrows: original bone

surface ; specimen shown in Fig. 3 ; ¬57. (b) Periosteal bone deposited onto the original cortical surface of the mandibular body, interpreted

as a fluoride-induced osteoblastic reaction; asterisk: blood vessel canal ; specimen shown in Fig. 3 ; ¬228. (c) Destruction of the bony plate

436 M. Schultz and others

buccal side, the original bone surface was covered by

a layer of woven bone (Fig. 7e). The external basic

lamella and a narrow area of the external osteonal

bone (Fig. 7e) as well as the roof of the mandibular

canal (Fig. 7 f ) were destroyed by osteoclastic activity.

These findings demonstrate the presence of severe

chronic inflammatory processes, including early

chronic osteomyelitis, that were still active when the

animal died.

A very severe case of chronic osteomyelitis and

concomitant osteitis, periostitis and periodontitis was

observed in the mandible of a 9-y-old stag found dead

(Figs 14–16). In this specimen, both M$were missing.

Since the remnants of their former alveoli were almost

completely filled with cancellous bone, loss of these

teeth, probably as a consequence of tooth fracture,

must have occurred long before death. In addition,

the P$, P

%and M

#were worn down to their roots. In

the left hemimandible, opening of the mandibular

canal had occurred in the region of the 3rd molar. On

the right side, destruction of the 3rd premolar tooth

socket and opening of the mandibular canal at this

location were noted (Fig. 14). In the affected area, the

mandibular body formed a large, bulging capsule with

a highly porous surface structure (Fig. 15). At the

level of the M", a wide fistula opening was present in

the lingual cortex. Within the distended mandibular

canal, a large bony sequestrum was found, which

extended from the level of the 2nd premolar to that of

the 1st molar (Fig. 16). This sequestrum represented

part of the original lingual alveolar cortex, which had

become displaced and partly destroyed due to a severe

inflammatory process associated with dentoalveolar

abscess formation. Histological study further pro-

vided evidence of (1) apposition of woven bone onto

the surface of the sequestrum (Fig. 7g), (2) advanced

osteoclastic bone resorption that had caused de-

struction of the former lingual alveolar corticalis, and

(3) formation of new periosteal bone constituting the

highly porous bulging capsule (involucrum) now

forming the lingual cortical surface of the mandible

(Fig. 7h). As a consequence of intense suppuration,

the premolar and molar roots of the specimen

exhibited a very marked hypercementosis (Fig. 16).

separating the tooth sockets from the mandibular canal due to a chronic periapical abscess ; asterisk: root cement ; specimen shown in Fig.

9 ; ¬57. (d ) Newly formed bone spicules covering the original buccal cortical surface, the bone formation representing a periostitis caused

by a chronic inflammatory process ; specimen shown in Fig. 1 ; ¬57. (e) Original mandibular buccal surface covered by a secondary layer

of woven bone. The external basic lamella and a thin layer of the external haversian systems have been destroyed by osteoclastic resorption;

specimen shown in Fig. 12; ¬57. ( f ) Howship’s lacunae (arrows) in the roof of the mandibular canal denoting osteoclastic bone resorption;

specimen shown in Fig. 12; ¬228. (g) Bone apposition (asterisk) onto the surface of the bony sequestrum representing part of the original

lingual alveolar cortex; specimen shown in Fig. 14; ¬57. (h) Newly formed porous bone, representing an involucrum, covering the remnants

of the original outer cortical plate ; asterisk: resorption cavity within the original cortex; specimen shown in Fig. 14; ¬57.

The present study revealed that reduced enamel

hardness and the resulting increased wear of fluorosed

deer teeth caused a variety of pathological mandibular

bone changes in the affected animals. Rapid occlusal

and interdental attrition led to diastema formation,

the resulting increase in tooth mobility causing an

imbalance in periodontal tension and in consequence

a drift of individual teeth away from their normal

positions, leading to an enlargement of interdental

gaps. Mechanical trauma to the gingiva, due to

wedging of forage into these gaps and}or occurrence

of injury caused by the sharp-edged tooth crowns,

promoted the establisment of periodontal inflam-

mation. Periodontal breakdown with damage to and

recession of the alveolar bone occurred as a sequel to

this process.

Severe periodontal lesions were also frequently

observed as a consequence of tooth fracture. Fur-

thermore, the occurrence of periapical abscesses,

caused by exaggerated attrition of the fluorosed teeth

and, in consequence, an opening and infection of the

pulp cavity, was occasionally observed in our material.

Similar lesions have previously been described on a

macroscopic scale in deer (Karstad, 1967; Kay et al.

1975), sheep (Roholm, 1937; Milhaud & Gras, 1978),

horses (Shupe & Olson, 1971) and cattle (Gru$ nder,

1972; Lasarov et al. 1972; Shupe & Olson, 1983) with

severe dental fluorosis. As already stated by Shupe &

Olson (1971), in contrast to the typical tooth changes,

the periodontal lesions present in fluorotic animals are

not pathognomonic of a chronic fluoride intoxication.

Prevalence and severity of periodontal lesions

present in our sample of red deer exhibiting marked

dental fluorosis substantially differed from the situ-

ation in a population not exposed to increased levels

of fluoride. Thus Geiger et al. (1992), who studied 431

red deer mandibles from the Harz mountains

(Germany) found only 3 cases (¯ 0±7%) of perio-

dontal disease, all affected individuals being 13 or

more years of age. In 267 complete red deer skulls

from the same area, the lower jaw was significantly

less affected by periodontal lesions than the upper

Pathological bone changes in fluorotic deer mandibles 437

Fig. 9. Right hemimandible of a 13-y-old red deer stag, bucco-occlusal view. Bone fluoride content 4223 mg F−}kg dry wt. Severe dental

disfigurement. Note formation of a periapical abscess associated with the distal root of the P%

as a consequence of opening of the tooth’s

pulp cavity (arrow). A large sinus opening penetrates the buccal cortex.

Fig. 10. Newly formed woven bone caused by reactive periostitis surrounding the large sinus opening shown in Fig. 9. Asterisk, distal root

of P%.

Fig. 11. Radiograph of the hemimandible shown in Fig. 9. Note radiolucent space around the tip of the distal root of the P%

(arrowhead)

and marked hypercementosis on the roots of this tooth.

438 M. Schultz and others

Figs 12, 13. Left (12) and right (13) hemimandibles of a 6-y-old red deer stag, bucco-occlusal views. Bone fluoride content 2670 mg F−}kg

dry wt. Fracturing of both M$

in a symmetric fashion and opening of the mandibular canal in the left hemimandible (arrow). In the right

hemimandible, the distal column of the 3rd molar has not been shed. Note marked loss of alveolar bone at the fracture site (arrowhead).

jaw. In the complete skulls, periodintal changes

affecting only the lower jaw were not observed.

Furthermore, occurrence of tooth fractures was not

reported in the 698 specimens studied by Geiger et al.

(1992).

As was previously shown (Kierdorf et al. 1996c),

severely fluorosed premolars and molars of red deer

are characterised by the loss of a functional crown

shape. In analogy to the situation reported for severely

fluorotic cattle (Shupe & Olson, 1983), an impairment

of body condition can be expected in this situation.

Severe periodontal disease and its sequels (tooth loss,

pain, abscess formation, etc.) will exacerbate this

fitness reduction due to further limitations in food

intake and processing as well as a general deterioration

of the animal’s health, especially in case of acute or

chronic abscess formation. A corresponding loss of

body condition resulting from dental and periodontal

disease was previously described in chamois

(Rupricapra rupricapra) (Pekelharing, 1974) and rein-

deer (Rangifer tarandus) (Leader-Williams, 1980), the

latter animals probably suffering from lumpy jaw

disease. It is reasonable to assume that in severely

fluorotic red deer emaciation resulting from the

pathological conditions described above will eventu-

ally lead to premature death, especially of older

individuals. This situation is thus an example of an

initially sublethal effect (fluoride induced dental

changes) becoming lethal under certain conditions

(Heinz, 1989), in this case as a consequence of

Pathological bone changes in fluorotic deer mandibles 439

Fig. 14. Right hemimandible of a 9-y-old red deer stag, bucco-occlusal view. Bone fluoride content 3555 mg F−}kg dry wt. Loss of M$and

very severe attrition of the other cheek teeth, except M". Remnants of the former alveolar cavity of the M

$almost completely filled by woven

bone (asterisk). Opening of the mandibular canal at the bottom of the alveolar cavity of the P$

(arrowhead).

Fig. 15. Lingual view of hemimandible shown in Fig. 14. The cortical bone forms a large bulging capsule with a porous surface structure.

A large sinus opening is present and a sequestrum lying in the mandibular canal is discernible.

Fig. 16. Radiograph of the hemimandible shown in Fig. 14. The sequestrum extends from the level of the P#to that of the M

"(arrowheads).

Also note very pronounced hypercementosis on the tooth roots.

440 M. Schultz and others

established severe pathological bone changes and

tooth loss with advanced age.

Premature death can also occur as a direct result of

dentoalveolar abscess formation. According to Miles

& Grigson (1990), opening of an abscess into the oral

cavity commonly leads to a septic pneumonia due to

inhalation of septic discharges. Also a generalized

septicaemia due to spreading of the infection via the

blood stream could lead to the animal’s death.

Some of the pathological bone alterations observed

in the animals with the highest skeletal fluoride levels

are regarded as resulting from of a systemic effect of

the ingested fluoride on bone formation and turnover.

Thus the generalised apposition of periosteal new

bone, which was observed in some of the fluorotic red

deer, is a well-known consequence of chronic fluoride

intoxication (Roholm, 1937; Shupe & Olson, 1983;

Shupe et al. 1992; Vikøren & Stuve, 1996), due to a

fluoride induced stimulation of osteoblastic activity.

The abnormal curvature of the mandibular body seen

in 3 red deer specimens with bone fluoride contents

exceeding 4000 mg F−}kg dry wt denotes a weakening

of the bone, leading to its deformation upon mech-

anical loading. As was shown in clinical and ex-

perimental animal studies, prolonged uptake of

increased amounts of fluoride leads to osteomalacia

and decreased biomechanical competence of bone

(Boivin et al. 1989; Chavassieux et al. 1991; Søgaard

et al. 1994, 1995; Lundy et al. 1995; Turner et al.

1995). On the basis of these findings, the mandibular

deformation observed in the highly fluoride exposed

red deer is supposed to be the result of a fluoride

induced osteomalacia. However, in addition the severe

inflammatory changes present in these mandibles may

have contributed to the weakening of the mandibular

bone.

The present study provides circumstantial evidence

that in addition to the fluoride induced dental lesions

the occurrence of severe periodontal disease (including

tooth loss) is also a potential factor limiting the life-

span of severely fluorotic red deer. In populations

from highly fluoride polluted habitats a shift in age

structure compared to populations from uncontam-

inated areas is therefore likely to occur. This view is in

principal accordance with the findings of Kay et al.

(1975), who reported a shift to younger age classes in

mule deer (Odocoileus heminonus) and white-tailed

deer (Odocoileus virginianus) inhabiting a severely

fluoride polluted area. Since the red deer inhabiting

our study area are under considerable hunting

pressure, effects of regional fluoride pollution on

population structure are however difficult to assess.

The expert technical assistance of M. Brandt, A. Heise

and I. Hettwer-Steeger is gratefully acknowledged.

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